ICD-11: Draft Proposal for Changes in the Classification of Mental and Behavioural Disorders
Indian Psychiatric Society (IPS)
Department of Psychiatry,
All India Institute of Medical Sciences, New Delhi
ICD-11: Draft Proposal for Changes in the Classification of Mental and Behavioral Disorders
This report should be cited as:
Department of Psychiatry, AIIMS (2008). ICD-11: Draft Proposal for Changes in the Classification of Mental and Behavioural Disorders
Department of Psychiatry,
AIIMS, New Delhi
Chief, National Drug Dependence Treatment Centre and Head, Department of Psychiatry,
AIIMS, New Delhi
Dr Pratap Sharan had full access to all of the materials in this report and takes responsibilityfor the integrity and accuracy of its summarization.
Classification of Psychiatric Disorders: General Issues
Organic, including Symptomatic, Mental Disorders
Mental and Behavioural Disorders due to Psychoactive Substance Use
Schizophrenia, Schizotypal and Delusional Disorders
Neurotic, Stress Related and Somatoform Disorders
Behavioural Syndromes associated with Physiological Disturbances and Physical Factors
Categories ‘F70 – F98’
The draft proposal for changes in the classification of mental and behavioural disorders towards ICD 11 was prepared under the aegis of the Department of Psychiatry, All India Institute of Medical Sciences for consideration in an Indian Psychiatric Society (IPS) Committee, which will send its recommendations to the World Psychiatric Association (WPA). The draft proposal is also available on the Departmental website.
Each chapter was prepared by faculty members, who were assisted by residents of the department. In preparing their suggestions the authors often referred to the Robins and Guze criteria to evaluate the validity of various categories and specifiers. The initial suggestions made by the authors were discussed in a series of departmental meetings comprising of the entire professional staff of the department and thus the final draft proposal has received inputs from more than 30 trained professional staff from various disciplines (Psychiatry, Clinical Psychology, and Biochemistry) and another 20 professionals in training.
Each chapter of the draft proposal ha the following structure:
· The first section lists the suggested changes.
· The next section provides supportive evidence for the proposed changes.
· Some authors have included a closing section consisting of initial suggestions made by them that were discussed but not accepted by the whole group for final recommendation.
CLASSIFICATION OF PSYCHIATRIC DISORDERS: GENERAL ISSUES
Pratap Sharan, MD, PhD, Shiv Prakash, MD
1. Public health issues should be addressed while revising the ICD classification.
2. There is a need for better conceptualization of positive mental health and to develop/derive indicators of mental health in the framework of classification.
3. An axis for risk and protective factors should be added.
4. Prevention relevant subthreshold categories should be included in various phenomenological groups, e.g. depressive disorder, eating disorder, etc.
5. Some categories can be combined, e.g. the category of adjustment disorders could be merged with subthreshold categories in relevant phenomenological groups (e.g. depression, the presence or absence of stressors could be coded on the risk and protective factor axis).
6. A system that provides a longitudinal framework is required. Two changes are proposed: (1) use of diagnostic criteria that are developmentally informed, and (2) listing of relevant information on risk and protective factor axis.
7. The diagnostic system should become more culturally sensitive: three changes are proposed: (1) use of diagnostic criteria that are culturally informed (alternative criteria could be derived to connect with specific cultural contexts), (2) recognition of conditions that are considered pathological in one culture and non pathological in another (e.g. dissociative possessions limited to a religious context that enhances prestige), and (3) crosswalks between categories in the ICD mental health chapter with systems in force in other countries (e.g. USA, China, Latin America, etc.) should be provided.
8. An axis for classification of agreed upon dimensions should be provided.
9. Multiaxial classification comprising of the following should be provided:
· Axis I: Categorical diagnoses related to health and illhealth
· Axis II: Dimensions related to health and illhealth
· Axis III: Protective and risk and factors
· Axis IV: Function and dysfunction (ICF)
· Axis V: Quality of life
10. To facilitate use in primary care three versions of the classification should be drawn, in which the categories of the more complex version are nested in the broader categories of the less complex system. To facilitate use in general health setting crosswalks (at the level of diagnostic codes) between categories in the ICD mental health chapter with those in the other systems (e.g. international classification of epileptic seizures, sleep disorders, etc.) should be provided.
Supporting evidence for proposed changes
I. Public health issues should be addressed while revising the ICD classification
The clinician is focused on treatment and rehabilitation of individuals or groups while the public health expert seeks to employ a broader range of health interventions which include promotion, preventive, curative or rehabilitative strategies aimed at populations and groups at risk. Thus, the clinicians have a relatively greater interest in the current condition of the patient, and diagnostic categories that are narrow and which predict treatment response; while the public mental health expert is relatively more interested in risk/ causative/ developmental factors toward pathology, service delivery to the population, diagnostic categories that vary in breadth (broad for communicating with non-experts and narrow for some specific interventions) and are predictive of response to the entire range of preventive efforts. Public health experts also look at the broader spectrum of health and their determinants (Mezzich 2002a, 2002b).
Classificatory systems have public mental health implications, e.g. concept of diagnosis is crucial to epidemiology and surveillance of population health (Mezzich 2002a). However, since public health is not the explicit focus of the classificatory exercises, many issues that are relevant to public health, have not been addressed. For example, diagnoses like mixed anxiety depression and age-related cognitive decline are disputed because they are below an ‘appropriate’ threshold, but they contribute significantly to disorder burden. Within the spectrum of mental health intervention, prevention and promotion have become realistic and evidence-based alternatives. These bring new challenges to classification system - the challenge of defining boundaries of disorders, risk categories and normality (Mrazek and Hagerty 1994; Mrazek and Hosman 2002).
Public health also has much to contribute to classification. In an effort to move from descriptive criteria based approach to an etiology based approach, epidemiology serves as the bridge between proposed aetiologies or disease mechanisms and potential manifestations (Caine 2003).
II. There is a need for better conceptualization of positive mental health and to develop/derive indicators of mental health in the framework of classification
Mental health has been conceptualized in two broad ways: ‘positive’ mental health (Jahoda, 1958; Maslow 1968; Tudor 1996) and ‘functional’ metal health (Hosman 1997). The former considers mental health in terms of qualities such as self-confidence, identity, ability to love, happiness, etc. that are seen as worthwhile to promote because they represent a fundamental human values in themselves. The ‘functional model’ considers mental health more in terms of psychological resources and abilities, that people need to have for a satisfying and productive life e.g. in the domains of health, relationships, work, ability to cope with stress, etc.. For this last part, the functional model of mental health coincides with the concept of protective factors.
A growing body of cross-cultural evidence indicates that various psychological, social and behavioural factors such as secure attachment, an optimistic outlook on life with a sense of purpose and direction, effective strategies for coping with challenge, emotionally rewarding social relationships, etc. are protective of health and supportive to positive mental health (Cacioppo et al 2000; Ryff and Singer 2003). Such protection facilitates resistance (resilience) to disease (disorder), minimizes and delays the emergence of disabilities and promotes more rapid recovery from illness (WHO 2002). Good mental health may also be facilitated by religious/ spiritual feelings, experience, orientation and world view (Bhugra and Osbourne, 2004). Thus, it has to be borne in mind that definition of mental health may be at least partially culture-bound with both commonalities and differences between cultures.
The recognition of positive mental health features in psychiatric patients would also substantially reduce the stigma associated with mental illness. A similar reorientation with reference of classification was achieved in the transformation of International Classification of Impairments, Disabilities and Handicaps (WHO 1980) to International Classification of Functioning (WHO 2001b).
III. An axis for risk and protective factors should be added
In many situations prevention enhances options for managing disorders e.g. it may be possible to prevent many cases of conduct disorders, while it may be fairly difficult to treat them (Reid 1993). Prevention may also be significant for many individuals, who do not have access to treatment or those who receive inappropriate services. A growing number of randomized controlled prevention trials and community trials have offered evidence for significant changes on a wide variety of targeted outcome indicators, including indicators for risk and protective factors, mental and behavioural disorders and improvements in mental health (Mrazek and Haggerty 1994; Clarke et al 1995; Hosman and Llopis 1999).
Risks do not occur in isolation; in fact many risks cannot be disentangled in order to be considered in isolation as they act at different levels which vary over time. Clearly, one outcome can be caused by many risk factors (equifinality – multiple pathways to the same disorder), but similarly one risk factor can lead to many outcomes (multifinality – overlapping pathways to different disorders). Further, there is a non-linear relationship between risk factors and outcomes. Although one or two risk factors may show little prediction to poor outcome, there are rapidly increasing rates of disorders with additional risk factors (Rutter 1979; Greenberg et al 2001). Another point that needs to be borne in mind about risks is that some of the distal risks cannot appropriately be defined at the individual level (e.g. social disintegration).
Addition of an axis for risk and protective factors in the classificatory system could serve as the link between etiological understanding of disorders and promotive, preventive, curative and rehabilitative interventions. Risk factors may help in identifying subtypes that may aid in the exploration of pathophysiology and etiology (Andreasen and Carpenter, 1993). The axis on risk factors could be used as a matrix with Axis I (clinical diagnosis), to eliminate the need for some specifiers. For example, postpartum depression could be labelled as depression on Axis I and the specifier 'postpartum' would appear on the axis for risk factors. This axis could replace the Axis III and IV of DSM IV and Axis III of ICD-10 as it is broader in scope. It will end the artificial mind-body divide in relation to etiological factors. In addition, it will emphasize distal social and developmental causes of disorders which are not emphasized in the present classification systems and can be major foci of public mental health policies.
IV. Prevention relevant subthreshold categories should be included in various phenomenological groups, e.g. depressive disorder, eating disorder, etc
A substantial volume of literature suggests that subthreshold conditions have considerable public health importance. Subthreshold depressions (e.g. mixed anxiety depression, recurrent brief depression, minor depression, etc.) are reported to occur in up to 24% of the general adult (Horwath et al 1992) and 52% of the elderly (Pincus et al 1999) populations. Further, it is difficult to differentiate subthreshold depression and major depressive disorder on the basis of demographic and clinical characteristics; medical and psychiatric comorbidity; dysfunction (subtheshold depression cause five-times more disability days than major depressive disorders and dysthymia combined); follow up studies; outcome (in terms of chronicity and suicide), and a family vulnerability for major depression (Broadhead et al 1990; Johnson et al 1992; Judd et al 1998).
However, since less than one-fourth of subjects with minor depression develop major depression (Broadhead et al 1990; Wells et al 1992) in most cases subthreshold depression should be considered as an indicator of risk for developing threshold depression - a focus for indicated prevention (a subcategory of primary prevention). Subthreshold depressive categories should therefore be included in the classification under the rubric of prevention relevant categories.
Regier et al (2002) suggest that the diagnostic thresholds in current classificatory systems reflect an emphasis on treatment over prevention. Altering the threshold for caseness will change the latitude for prevention and treatment within the public mental health spectrum. Assignment of boundaries between normal states, high risk states and disorders can be made on the basis of empirical studies of risk (Vasan et al 2002). Definition of prevention relevant categories would encourage studies aimed at understanding their causation (Pincus et al 1999; 2003) and early intervention for those at risk for future morbidity, comorbidity and mortality rather than limiting intervention to after significant morbidity has occurred.
V. Some categories can be combined, e.g. the category of adjustment disorders could be merged with subthreshold categories in relevant phenomenological groups (e.g. depression - the presence or absence of stressors could be coded on the risk and protective factor axis)
The preoccupation with over-refined categories and subcategories has led to complex diagnostic systems that are difficult to use in the community setting. Moreover, the evergrowing list of types/subtypes contains many conditions that are rarely diagnosed (Bertelsen 2002).
Definition of broad categories would be useful from the promotion and prevention perspective. Over the last 3 decades, the majority of evidence-based promotive and preventive trials have focused on common or generic protective and risk factors, e.g. interventions for increasing self-esteem, emotional resilience, problem-solving and coping skills (Mrazek and Haggerty 1994; Hosman & Llopis, 1999); and prevention of broad categories such as depression (Rutz et al 1992a; 1992b), anxiety symptoms and disorders (Dadds et al 1999), externalising problems and substance abuse (Wolchik et al 2000), or suicidal behavior (Zenere and Lazarus, 1997). When varying clinical presentation have major risk factors in common, subtyping is less relevant from the preventive perspective.
The increase in number of disorders has added to the problems of comorbidity – nearly one-third of cases in the general population have comorbid psychiatric problems (Wittchen 1996). At least some of these would be artefacts, a function of the number of available categories. Data suggest that much comorbidity in the mental health field is due to shared antecedents (genetic and environmental, e.g. childhood adversity) (Kendler et al 1992; Brown et al 1996; Livesley et al 1998; Mineka et al 1998), a fact that goes against the possibility of independence and chance co-occurrence of disorders. Thus, Krueger et al (1998) found support for a 2-factor model for explaining comorbidity – a latent internalizing factor (depression and anxiety) and a latent externalizing factor (conduct disorder, marijuana and alcohol dependence). The lack of independence between diagnoses could explain the absence of diagnostic specificity of treatment response (Regier et al 2002).
The argument for definition of broad categories is not against the existence of narrower categories. When subtypes have major subtype–specific and malleable determinants, fine divisions of categories could be relevant for prevention, treatment and rehabilitation, wherein strategies are targeted to reduction in number of episodes, duration, severity and dysfunction associated with illnesses and secondary morbidity (McGorry 1992). Hence, close attention should be paid to the number, hierarchy and specificity of categories during revision of classifications.
VI. A system that provides a longitudinal framework is required. Two changes are proposed: (1) use of diagnostic criteria that are developmentally informed, and (2) listing of relevant information on risk and protective factor axis
A life-course approach to study of health and illness has come to dominate public health following the recognition of the fact that risks as well as symptomatic expression of disorders vary across developmental spans (Ingram and Price, 2001) and that exposure to disadvantageous experiences and environments accumulate throughout life to increase the risk of illnesses (WHO 2002).
The need for a developmentally informed diagnostic system is most acute for definition of psychopathology in children and adolescents because most of the current diagnostic systems are based solely on models of adult psychopathology. Ryan et al (1987) and Kashani et al (1997) found that children especially pre-schoolers with depressive disorders presented with somatic complaints and aggressive behaviour and most showed psychomotor agitation. The diagnosis may be overlooked because of the presence of these associated symptoms that are suggestive of an externalising disorder. These findings combined with the observation of Kovacs (1986) that younger children may not be capable of experiencing or reporting the symptoms thought to be representative of major depression, emphasize the need to have developmentally relevant criteria for diagnosis.
Other studies have emphasized the need for greater attention to the life course approach to mental disorders. The results of several prospective longitudinal studies of population based samples of children and adolescents show that retrospective adult studies may seriously overestimate the age at onset of many disorders (Costello et al 1999, Lewinsohn et al 2000). In addition, some disorders e.g. ADHD and major psychoses may show early prodromes (Pine et al 2002). An episode of depression or anxiety is a risk factor for further episodes of same general type of disorder, e.g. major depression and suicide (Kovacs and Devlin 1998; Mineka et al 1998), and attention deficit hyperactivity disorders is a predictor of conduct disorder/antisocial personality disorder, substance use disorder and bipolar disorder (Biederman e al 1998; Faraone et al 1998). Some heterotypic associations are also apparent. High levels of anxiety in children predicted increase in depression over time, however high levels of reported depression in children did not predict increase in anxiety (Kolvin and Trowell 2002). Tic disorder shows longitudinal association with obsessive compulsive disorder with tic decreasing and obsessive symptoms increasing over time (Pine et al 2002). Interplay of biological and environmental risk factors could influence courses both singly and across related disorders, e.g. childhood sexual abuse for externalizing disorders (Brown et al 1996) and kindling for schizophrenia, bipolar and other disorders (Frances and Egger, 1999). Failure to take a life course approach makes the occurrence of such comorbidity perplexing.
VII. The diagnostic system should become more culturally sensitive: three changes are proposed: (1) use of diagnostic criteria that are culturally informed (alternative criteria could be derived to connect with specific cultural contexts), (2) recognition of conditions that are considered pathological in one culture and non pathological in another (e.g. dissociative possessions limited to a religious context that enhances prestige), and (3) crosswalks between categories in the ICD mental health chapter with systems in force in other countries (e.g. USA, China, Latin America, etc.) should be provided.
Current data show that 85% of the variation in DNA sequence is common to ethnic groups. Such observations suggest that the risk of common illnesses including mental illnesses largely derive from alleles shared across all group of humans, supporting the possibility of having universal syndromes. But variations at the genetic level across ethnic groups (15%) and environmental risk factors provide for the possibility of substantial phenotypic variations across cultures and across time spans (Hyman 2002).
ICD 10 and DSM-IV do not adequately consider the possibility that context affects prototypical manifestations of an illness. It would be desirable to develop a system of classification that is flexible for local and cultural adaptations. For example, in some cultures people may not volunteer sadness as a symptom because a conceptually equivalent term may not exist in the language, or because of stigma attached to it, or because it is not recognized as an illness (Patel 2001). In such circumstances it would be better to use local concepts, e.g. 'Kufungisisa' (thinking too much) in Shona language of Zimbabwe or 'Neurasthenia' in China (Kleinman and Kleinman 1985; Patel 2001). Application of a universally defined criteria set in such cultures in an inflexible way, would lead to gross underestimation of prevalence of somatic symptoms related to depression and also of the prevalence of depression in the population studied (Alarcón et al 2002).
Avoidance of the concept of cultural variations in common psychiatric disorders leads to paradoxical situations. ICD-10 emphasizes adverse medical and psychological consequences in dependence and harmful use categories to ease application across different cultures and countries (Rounsaville 2002). However, development of social consequences more often predates physical and psychological problems in the natural history of pathological substance use disorders. As a consequence, rates as well as test-retest reliability of ICD-10 harmful use were lower than that of DSM-IV abuse (Chatterji et al 1997; Rounsaville 2002). On the other hand, acute and transient psychosis, a culturally informed diagnosis has been shown to have some genetic (Das et al 1999), epidemiological and prognostic validity (Susser et al 1996).
A simple system of psychiatric classification that can readily be translated into indigenous categories of illness is highly desirable. Attempts at crosswalks between ICD-10 and indigenous categories can be seen in Chinese Classification for Mental Disorders-3rd Edition (CCMD-3) (Chen 2002), Latin American Guide for Psychiatric Diagnosis (GLDF) (Berganza et al 2002) and Third Cuban Glossary of Psychiatry (GC-3) (Otero-Ojeda 2002).
VIII. An axis for classification of agreed upon dimensions should be provided
The relative validity of these categorical and dimensional approaches rests on a number of empirical considerations (Widiger & Samuel, 2005). An especially important issue concerns the nature of the underlying distributions. Taxometric studies suggest that both latent categories and dimensions are widely distributed. Dimensional models receive extensive support in the broad neurotic spectrum, predominating among the mood and anxiety disorders, e.g. chronic worry and posttraumatic stress (Ruscio et al, 2001). Analyses of depression have yielded mixed results but generally have found evidence of continuity rather than discontinuity (Haslam & Beck, 1994; Ruscio & Ruscio, 2002). However, melancholic depression appears to be better understood as a latent category and there are indications of latent categories in the domain of social anxiety and inhibition. Also, categorical models enjoy more support in the domain of personality disorders than might not have been anticipated.
Dimensional systems allow one to model the severity of dysfunction, not simply its presence versus absence (Clark et al, 1995). A large body of evidence also indicates that the artificial dichotomization of continuous measures leads to substantial losses in reliability, stability and validity (Widiger, 1992). Dimensional approach may also help in preparing for the future inclusion of genetic, imaging, and biochemical elements to psychiatric diagnoses.
IX. Multiaxial classification comprising of the following should be provided:
· Axis I: Categorical diagnoses related to health and illhealth
· Axis II: Dimensions related to health and illhealth
· Axis III: Protective and risk and factors
· Axis IV: Function and dysfunction (ICF)
Axis V: Quality of life
Multiaxial evaluation provides a vehicle for describing different aspects of a patient’s condition in order to improve our understanding of the condition and thereby to improve its management. Many multiaxial systems have been proposed and there is much variance among them regarding specific axes (Mezzich et al 1987). However, only a limited number of axes can be included in a system that is manageable in regular work internationally. Economizing arrangements could be considered to accommodate information within the multiaxial system, e.g. Mezzich et al (1987) found two broad and pervasive themes in their review of multiaxial systems: phenomenology and etiological/ associated factors. The latter could accommodate sub themes like biological, psychological, cultural, and spiritual aspects. Axes which cannot be accommodated within a given list could be considered as special - for use with particular populations or situations.
Axis I (categorical diagnoses related to health/ illhealth) would comprise of:
· mental disorders (including subsyndromal illnesses, mental retardation, personality disorders and also general medical conditions),
· mental conditions (not amounting to disorders) requiring preventive/treatment intervention, e.g. self-harm (Z codes),
· mental condition similar to disorders that do not require treatment interventions, e.g. dissociation occurring only in the context of religious ceremonies that enhances prestige, and
· health conditions (targets for health protection/promotion), e.g. well being, maturity.
Axis II (dimensions related to health/ illhealth) would comprise of consensually agreed upon dimensions. Some dimensions that can be considered are:
· negative syndrome, positive syndrome, and disorganization;
· positive affect, negative affect, and physiological hyperarousal;
· personaility (e.g. 5-factor model) and personality disorders (e.g. Livesley, 1998);
· internalizig and externalizing syndrome; and
· health (socioemotional intelligence, well being, resilience, etc).
The axis could also accomodate endophenotypes, cognitive structures, defence mechanisms, etc. for which consensus can be obtained.
Axis III (risk, protective and contextual factors) would include consensually agreed upon risk/protective, formative, precipitating and perpetuating factors. The axis would be subdivided into the following dimensions:
· biological (e.g. genetic, drug use);
· psychological (e.g. avoidant coping);
· social (e.g. social disintegration); and
· transcendental (e.g. spirituality, sense of coherence).
Axes IV and V are self-explanatory.
X. To facilitate use in primary care three versions of the classification should be drawn, in which the categories of the more complex version are nested in the broader categories of the less complex system. To facilitate use in general health setting crosswalks (at the level of diagnostic codes) between categories in the ICD mental health chapter with those in the other systems (e.g. international classification of epileptic seizures, sleep disorders, etc.) should be provided.
DSM-IV and ICD-10 were not particularly well suited for use in non-speciality settings. It is noteworthy that in the 'Beyond Blue' Project, an Australian initiative to combat depression, 'depression' and 'anxiety disorders' were the two major categories used in the skill focused training provided to general practitioners and in media advocacy work (Beyond Blue 2001). Neither ICD-10 nor DSM-IV was adopted.
Primary Care: The ICD-10 has two primary care versions - a concise version (containing 25 conditions) for those with medical training and prescription responsibility and a brief version (containing 6 conditions) for other primary care workers with limited medical training (WHO 1996). Similarly, a primary care version exists for the DSM-IV (APA 1996). The problem with ICD-10 PHC versions is that the categories in the two versions do not match each other and the detailed version of the ICD-10; however, they provide a simple way of classifying mental disorders. The DSM-IV primary care version on the other hand maintains its ties with the detailed DSM-IV but it does not simplify the classification per se, focusing instead on simplifying the process of reaching the DSM-IV classification by following a workbook style, wherein symptoms branch out into diagnostic algorithms (Pingitore and Sansone 1998).
The best solution would be to have three versions of increasing complexity, in which the categories of the more complex version are nested in the broader categories of the less complex system.
General Medical Health System: Trimble (2002) has suggested that ICD/DSM should have links to other classificatory systems, e.g. the international classification of epileptic seizures, movement disorders, lobar atrophies, dementia and sleep disorders (ASDA 1990; Mckeith et al 1996; McKhann et al 1984; Neary et al 1998). This could be achieved in many different ways. One could be to reproduce those classificatory systems/diagnostic criteria within the published ICD/DSM volumes. Another could be providing crosswalks between categories in one system with those in the other system. There is also the case for the provision of similar crosswalk to the classification used by nurses, e.g. Contemprory Nursing Diagnosis Manual of North American Nursing Diagnosis Association (NANDA 1994). Guidance is also needed for linking individual diagnosis to the International Classification of Functioning (ICF) as suggested by Kopelman and Fleminger (2002) and Jenkins et al (2002).
· Alarcón RD, Bell C, Kirmayer LJ, et al. Beyond the funhouse mirrors: research agenda on culture and psychiatric diagnosis. In Kupfer DJ, First MB, Regier DA (Eds.): A Research Agenda for DSM-V. Washington DC: American Psychiatric Association 2002; pp219-281.
· American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Ed 4, Primary Care Version. Washington DC: APA, 1996.
· American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Ed 4. Washington DC: APA, 2000.
· American Sleep Disorders Association. International Classification of Sleep Disorders: Diagnostic and Coding Manual. Rochester, Minnesota: ASDA, 1990.
· Andreasen NC, Carpenter WT Jr. Diagnosis and classification of schizophrenia. Schizophr Bull 1993; 19:199-214.
· Berganza C, Mezzich JE, Jorge MR. Latin American Guide for Psychiatric Diagnosis (GLDP). Psychopathology 2002; 35:185-190.
· Bertelsen A. Schizophrenia and related disorders: experience with current diagnostic systems. Psychopathology 2002; 35:89-93.
· Beyond Blue. beyondblue: the national depression initiative 2001. Available at: http://www.beyondblue.org.au/site/.
· Bhugra D, Osbourne TR. Spirituality and psychiatry. Indian J Psychiatry 2004; 46:5-6.
· Biederman J, Wilens TE, Mick E, et al. Does attention-deficit hyperactivity disorder impact the developmental course of drug and alcohol abuse and dependence? Biol Psychiatry 1998; 44:269-273.
· Broadhead E, Blazer D, George L, et al. Depression, disability days, and days lost from work in a prospective epidemiologic survey. JAMA 1990; 264:2524-2528.
· Brown GW, Harris TO, Eales MJ. Social factors and comorbidity of depressive and anxiety disorders. Br J Psychiatry 1996; 168 (Suppl 30):50-57.
· Cacioppo JT, Berntson GG, Sheridan JF, et al. Multi-level integrative analyses of human behaviour. Social neuroscience and the complementing nature of social and biological approaches. Psychol Bull 2000; 126:829-843.
· Caine ED. Determining causation in psychiatry. In Philips KA, First MB, Pincus HA (Eds.): Advancing DSM Dilemmas in Psychiatric Diagnosis. Washington DC: American Psychiatric Association 2003; pp 1-22.
· Chatterji S, Saunders JB, Vrasti R, et al. Reliability of the alcohol and drug modules of the Alcohol Use Disorder and Associated Disabilities Interview Schedule-Alcohol/Drug - Revised (AUDADIS-ADR): an international comparison. Drug Alcohol Depend 1997; 47:171-185.
· Chen Y-F. Chinese Classification of Mental Disorders (CCMD-3): towards integration in international classification. Psychopathology 2002; 35:171-175.
· Clarke GN, Hawkins W, Murphy M, et al. Targeted prevention of unipolar depressive disorder in an at‑risk sample of high school adolescents: a randomized trial of a group cognitive intervention. J Am Acad Child Adolesc Psychiatry 1995; 34:312‑321.
· Costello E J, Erkanli A, Federman E, et al. Development of psychiatric comorbidity with substance abuse in adolescents: effects of timing and sex. J Clinical Child Psychol 1999; 28:298-311.
· Dadds MR, Holland DE, Laurens KR, et al. Early intervention and prevention of anxiety disorders in children: results at 2-year follow-up. J Consult Clin Psychol 1999; 67:145-150.
· Das SK, Malhotra S, Basu D. Family study of acute and transient psychotic disorders: comparison with schizophrenia. Soc Psychiatr Psychiatr Epidemiol 1999; 34:328-332.
· Faraone SV, Biederman J, Mennin D, et al. Attention-deficit hyperactivity disorder with bipolar disorder: a familial subtype? J Am Acad Child Adolesc Psychiatry 1998; 37:459-460.
· Frances AJ, Egger HL. Wither psychiatric diagnosis. Aust N Z J Psychiatry 1999; 33:161-165.
· Greenberg MT, DomitrovichC, Bumbarger B. The prevention of mental disorders in school-aged children: current state of the field. [Prevention & Treatment, 4, Article 1]. 2001. Available at: http://journals.apa.org/prevention/volume4/pre0040001a.html.
· Haslam N, Beck AT. Subtyping major depression: A taxometric analysis. J Abnormal Psychol 1994; 103:686–692.
· Horwath E, Johnson J, Klerman GL, et al. What are the public health implications of subclinical depressive symptoms? Psychiatr Q 1992; 65:323-337.
· Hosman CMH. Conceptual clarifications on promotion and prevention: a plea for functionally related fields. In Trent DR, Reed CA (Eds.: Promotion of Mental Health, Vol 6. Aldershot: Ashgate 1997; pp 179 -204.
· Hosman CMH, Llopis JE. Effective Mental Health Promotion and Mental Disorders Prevention. European Union for Health Promotion and Education, 1999.
· Hyman SE. Neuroscience, genetics, and the future of psychiatric diagnosis. Psychopathology 2002; 35:139-144.
· Ingram RE, Price JM. Vulnerability to Psychopathology: Risks across the Life Span. New York: Guilford Press 2001.
· Jahoda M. Current Concepts of Positive Mental Health. New York: Basic Books 1958.
· Jenkins R, Goldberg D, Kiima D, et al. Classification in primary care: experience with current diagnostic systems. Psychopathology 2002; 35:127-131.
· Johnson J, Weissman M, Klerman G. Service utilization and social morbidity associated with depressive symptoms in the community. JAMA 1992; 267:1478-1483.
· Judd LL, Akiskal HS, Maser JD, et al. A prospective 12-year study of subsyndromal and syndromal depressive symptoms in unipolar major depressive ddisorders. Arch Gen Psychiatry 1998; 55: 694-700.
· Kashani JH, Allan WD, Beck NC Jr. Dysthymic disorder in clinically referred preschool children. J Am Acad Child Adolesc Psychiatry 1997; 36:1426-1433.
· Kendler KS, Neale MC, Kessler RC, et al. Major depression and generalized anxiety disorder: same genes, partly different environments. Arch Gen Psychiatry 1992; 49:716-722.
· Kleinman A, Kleinman J. Somatization: the interconnections in Chinese society among culture, depressive experiences, and the meaning of pain. In Kleinman A, Good B (Eds.): Culture and Depression. Berkeley, CA: University of California Press 1985; pp 429-490.
· Kolvin I, Trowell J. Diagnosis and classification in child and adolescent psychiatry: the case of unipolar affective disorder. Psychopathology 2002; 35:117-121.
· Kopelman MD, Fleminger S: Experience and perspectives on the classification of organic mental disorders. Psychopathology 2002; 35:76-81.
· Kovacs M. A developmental perspective on methods and measures in the assessment of depressive disorders: the clinical interview. In Rutter M, Izard CR (Eds.): Depression in Young People: Developmental and Clinical Perspectives. New York: Guildford Press 1986; pp 435-465.
· Kovacs M, Devlin B. Internalizing disorders in childhood. J Child Psychol Psychiatry 1998; 39:47-63.
· Krueger RF, Caspi A, Moffitt TE, et al. The structure and stability of common mental disorders (DSM-III-R): a longitudinal–epidemiological study. J Abnorm Psychol 1998; 107:216-227.
· Lewinsohn PM, Rohde P, Seeley JR, et al. Natural course of adolescent major depressive disorder in a community sample: predictors of recurrence in young adults. Am J Psychiatry 2000; 157:1584-1591.
· Livesley WJ, Jang KL, Vernon PA. Phenotypic and genetic structure of traits delineating personality disorder. Arch Gen Psychiatry 1998; 55:941-948.
· Maslow AH. Towards a Psychology of Being. New York: Van Nostrand 1968.
· McGorry PD. The concept of recovery and secondary prevention in psychotic disorders. Aust N Z J Psychiatry 1992; 26:3-17.
· McKeith IG, Galasko D, Kosaka K, et al. Consensus guidelines for the clinical and pathological diagnosis of dementia with Lewy bodies (DLB): Report of the consortium on DLB international workshop. Neurology 1996; 47:1113-1124.
· McKhann G, Drachman D, Folstein M, et al. Clinical diagnosis of Alzheimer’s disease: report of the NINCDS-ADRDA work group under the auspices of the Department of Health and Human Services Task Force of Alzheimer’s disease. Neurology 1984; 34:939-944.
· Mezzich JE. Comprehensive diagnosis: a conceptual basis for future diagnostic systems. Psychopathology 2002a; 35:162-165.
· Mezzich JE. The WPA International Guidelines for Diagnostic Assessment. World Psychiatry 2002b; 1:36-39.
· Mezzich JE, Fabrega H, Mezzich AC. On the clinical utility of multiaxial diagnosis. Experience and perspectives. In Tischler GL (Ed.): Diagnosis and Classification in Psychiatry: A Critical Appraisal of DSM-III. Cambridge: Cambridge University Press 1987; pp 449-463.
· Mineka S, Watson D, Clark LA. Comorbidity of anxiety and unipolar mood disorders. Annu Rev Psychol 1998; 49:387-412.
· Mrazek P, Haggerty RJ. Reducing Risks for Mental Disorder: Frontiers for Preventive Intervention Research. Washington DC: National Academy Press 1994.
· Mrazek P, Hosman CMH. Toward a Strategy for World-wide Action to Promote Mental Health and Prevent Mental and Behavioral Disorders. Alexandria, VA: The World Federation for Mental Health 2002.
· Neary D, Snowden JZ, Gustafson K, et al. Frontotemporal lobar degeneration: a consensus on clinical diagnostic criteria. Neurology 1998; 51:1546-1554.
· North American Nursing Diagnosis Association. Contemporary Nursing Diagnosis Manual. Philadelphia: NANDA 1994.
· Otero-Ojeda AA. Third Cuban Glossary of Psychiatry (GC-3): key features and contributions. Psychopathology 2002; 35:181-184.
· Patel V. Cultural factors and international epidemiology.Br Med Bull 2001; 57:33-45.
· Pincus HA, Davis WW, McQueen LE. 'Subthreshold' mental disorders. A review and synthesis of studies on minor depression and other 'brand names.' Br J Psychiatry 1999; 174: 288-296.
· Pincus HA, McQueen LE, Ellison L. Subthreshold mental disorders: nosological and research recommendations. In Philips KA, First MB, Pincus HA (Eds.): Advancing DSM Dilemmas in Psychiatric Diagnosis. Washington DC: American Psychiatric Association, 2003; pp 129-144.
· Pine DS, Alegria M, Cook, Jr. EH, et al. Advances in developmental science and DSM-V. In Kupfer DJ, First MB, Regier DA (Eds.): A Research Agenda for DSM-V. Washington DC: American Psychiatric Association 2002, pp 85-122.
· Pingitore D, Sansone RA. Using DSM-IV primary care version: a guide to psychiatric diagnosis in primary care. Am Fam Physician 1998; 58:1347-1352.
· Regier DA, Narrow WE, First MB, et al. The APA classification of mental disorders: future perspectives. Psychopathology 2002; 35:166-170.
· Reid JB. Prevention of conduct disorder before and after school entry: relating interventions to developmental findings. Dev Psychopathol 1993; 5:243-262.
· Ruscio AM, Borkovec TD, Ruscio J. A taxometric investigation of the latent structure of worry. J Abnorm Psychol 2001; 110:413–422.
· Ruscio AM, Ruscio J. The latent structure of analogue depression: Should the Beck Depression Inventory be used to classify groups? Psychol Assess 2000; 14:135–145.
· Rutter M. Protective factors in children's responses to stress and disadvantage. In Kent MW, Rolf J (Eds.): Primary Prevention of Psychopathology, Vol 3. Social Competence in Children. Hanover NH: University Press of New England 1979, pp 49–74.
· Rutz W, Carlsson P, Von Knorring L, et al. Cost-benefit analysis of an educational program for general practitioners given by the Swedish Committee for the Prevention and Treatment of Depression. Acta Psychiatr Scand 1992b; 85:457-464.
· Rutz W, Von Knorring L, Walinder J. Long‑term effects of an educational program for general practitioners given by the Swedish Committee for the Prevention and Treatment of Depression. Acta Psychiatr Scand 1992a; 85:83‑88.
· Rounsaville BJ. Experience with ICD-10/DSM-IV substance use disorders. Psychopathology 2002; 35:82-88.
· Ryan ND, Puig-Antich J, Amborsini P, et al. The clinical picture of major depression in children and adolescents. Arch Gen Psychiatry 1987; 44:854-861.
· Ryff CD, Singer B. The role of emotions on pathways to positive health. In Davidson RJ, Goldsmith HH, Scherer K (Eds.): Handbook of Affective Science. New York: Oxford University Press 2003, pp 1083-1104.
· Sigvardsson S, Bohman M, von Knorring AL, et al. Symptom patterns and causes of somatization in men. I. Differentiation of two discrete disorders. Genet
· Susser E, Finnarty MT, Sohler N. Acute psychoses: a proposed diagnosis for ICD-11 and DSM-V. Psychiatr Q 1996; 67:165-176.
· Trimble M. Clinical presentations in neuropsychiatry. Semin Clin Neuropsychiatry 2002; 7:11-17.
· Tudor K. Mental Health Promotion: Paradigms and Practice. London: Routledge 1996.
· Vasan RS, Beiser A, Seshadri S, et al. Residual lifetime risk for developing hypertension in middle-aged women and men: the Farmingham Heart Study. JAMA 2002; 287:1003-1010.
· Wells KB, Burnam AM, Rogers W, et al. The course of depression in adult outpatients: results from the Medical Outcomes Study. Arch Gen Psychiatry 1992; 49:788-794.
· Widiger TA. Categorical versus dimensional classification: implications from and for research. J Pers Disord 1992; 6:287–300.
· Widiger TA, Samuel DB. Diagnostic categories or dimensions? A question for the Diagnostic and Statistical Manual of Mental Disorders—Fifth Edition. J Abnormal Psychol 2005; 114:494–504.
· Wittchen HU. What is comorbdity-fact or artefact? Br J Psychiatry 1996; 168 (Suppl 30): 7-8.
· Wolchik SA, West SG, Sandler IN, et al. An experimental evaluation of theory-based mother and mother-child programs for children of divorce. J Consult Clin Psychol 2000; 68:843-856.
· World Health Organization. International Classification of Impairments, Disabilities and Handicaps. Geneva: WHO 1980.
· World Health Organization. The ICD-10 Classification of Mental and Behavioural Disorders: Clinical Descriptions and Diagnostic Guidelines. Geneva: WHO 1992.
· World Health Organization. Diagnostic and Management Guidelines for Mental Disorders in Primary Care, ICD-10 Chapter V Primary Care Version. Seattle: Hogrefe and Huber Publishers 1996.
· World Health Organization. (WHO document: Fact sheet N° 220, November 2001). Geneva: WHO 2001a.
· World Health Organization. International Classification of Functioning, Disability and Health. Geneva: WHO 2001b.
· World Health Organization. The World Health Report 2002: Reducing Risks, Promoting Healthy Life. Geneva: WHO 2002.
· Zenere FJ, Lazarus PJ. The decline of youth suicidal behavior in an urban, multicultural public school system following the introduction of a prevention and intervention program. Suicide Threatening Behav 1997; 27:387-403.
ICD-11: DRAFT PROPOSAL FOR CHANGES IN THE ORGANIC, INCLUDING SYMPTOMATIC, MENTAL DISORDERS SECTION
Prof. S. K. Khandelwal, MD, MRCPsych, Dr. Kumar R. Maji, MD
1. Changing the name of the F00-F09 category from – ‘organic, including symptomatic, mental disorders’ to ‘neuropsychiatric disorders including symptomatic, mental disorders’.
2. To place tic disorder under F00-F09 from its current place under F95 (F90 - F98: behavioural and emotional disorders with onset usually occurring in childhood and adolescence).
3. To exclude organic dissociative disorder
Supporting Evidence for the Proposed Changes
The essence of classification system is to arrange something in an ordered fashion instead of placing it haphazardly. From ancient to recent times, various efforts have been made to classify mental disorders, with gradual refinement of the concept of mental disorders and their classifications. ICD-10 (International Classification of Disease - 10th edition) and DSM-IV (Diagnostic and Statistical Manual of Mental Disorders - 4th edition) are the two widely accepted classificatory systems for mental disorders, though certain others country specific classificatory systems do exist.
Mental disorders classificatory system is not only used by psychiatrist, it is also used by other physicians, psychologists, social workers, nurses, occupational and rehabilitation therapists, counselors and other health and mental health professionals. Efforts should be made to make the ICD-11 more clinically useful and acceptable to those who apply it, should have few differences with DSM-V and at the same time, it should keep the layout of existing coding system intact.
Great strides have been made over the past few decades in the field of clinical neuroscience, including functional and structural brain imaging, electrophysiology and electro-diagnosis, cellular and molecular biology, genetics and neuropsychopharmacology. Despite these developments in the field of neuroscience, the understanding of the pathophysiology of mental disorders is still in a nascent state. Therefore, the seminal article by Robins and Guze (1970) is still relevant to the process of revision of classification of mental disorders.
I. Replacing the term organic mental disorder by neuropsychiatric disorders
This rubric in ICD-10 covers a range of mental disorders with a common theme of demonstrable etiology in cerebral disease, brain injury, or other insult leading to cerebral dysfunction which may be primary (where the causative factors affect the brain directly) or secondary (where systemic diseases involve brain like other multiple organs). The term ‘organic’ used here means that disorders or syndrome in this category can be attributed to an independently diagnosable cerebral or systemic disease or disorder and the term ‘symptomatic’ is used where the cerebral involvement is secondary to systemic illness (ICD-10, Clinical Descriptions and Diagnostic Guidelines).
The use of the term ‘organcity’ in psychiatric classification is attended with controversy. DSM-II (1968), categorized organic mental disorders as organic brain syndrome (OBS), caused by diffuse brain dysfunction that lead to deficits in orientation and intellectual functioning (e.g. memory, judgement, comprehension) and to changes in affective modulation (lability or shallowness). Subsequently, OBS was replaced by the term organic mental disorders (OMD) in DSM-III (1980), which further made a fundamental distinction between OBS and OMD with reference to absence or presence of etiological factors. In DSM-III-R (1987), all these disorder were placed under the section of ‘Organic Mental Syndromes and Disorders’ which was eventually deleted in the DSM-IV (1994).
In ICD-8 (1969) all organic psychotic conditions were placed along with functional psychoses under the rubric of ‘psychosis’ (290-299). Code 290 to 294 in ICD-8 (290: senile and pre-senile dementia, 291: alcoholic psychosis, 292: psychosis associated with intracranial infection, 293: psychosis associated with other cerebral condition, 294: psychosis associated with other physical condition) underwent mild modifications and were included in ICD-9 under a new term: ‘organic psychotic conditions (290-294). The latest revision ICD-10 (1992) retained the term ‘organic’ for this group of disorders.
The term organic is very difficult to define and moreover, it incorrectly implies non-biological basis for non-organic (functional) psychiatric illnesses. In addition, merely placing ‘organic’ in front of a variety of symptom or syndromes (hallucinosis, catatonic disorder, delusional disorder, mood disorder, anxiety disorder, dissociative disorder, emotionally labile disorder), does not advance classification keeping in view the future development in neurosciences (Kopelman et al 2002). The term ‘neuropsychiatric disorder’ is probably the appropriate substitute for organic mental disorder, owing to its broad spectrum coverage. For example, head-injury, within neuropsychiatric disorders, would include (besides dementia due to head trauma and post-concussional syndrome) confusional states, memory disorders, executive and personality changes, head-injury related mood changes, etc. Epilepsy is another disorder where a number of specific neuropsychiatric syndromes could be incorporated.
Code F06 in ICD-10, uses the term ‘other mental disorders due to brain damage and dysfunction and to physical disease,’ while DSM-IV uses the term ‘mental disorders due to general medical condition.’ In the ICD-10 code, the word ‘organic’ has been placed before psychiatric disorders which often manifest in certain medical conditions. More clarity and specificity is required in describing these conditions or subtypes to avoid confusion among other health professionals who often witness such conditions, which is probably not possible by mere presence of the term ‘organic’ before such entity. Example of more appropriate description would be – catatonic disorder in Vit-B12 deficiency, delusional (schizophrenia – like) disorder in epilepsy etc. (Kopelman et al 2002). However, this type of description is reminiscent of ‘combination categories’ of ICD-8. Therefore, more accurate and appropriate description of these conditions requires utilization of separate independent axes.
II. Inclusion of tic disorder
Tic disorders comprise a group of disorders, such as, transient tic disorder, chronic motor or vocal tic disorder, combined vocal and multiple motor tic disorder (de la Tourette’s syndrome), other tic disorder and tic disorder unspecified. Currently, ‘tic disorder’ has been placed in the category of ‘behavioural and emotional disorders with onset usually occurring in childhood and adolescence’ (F90-F98; F95) of ICD-10. Tic disorder has also found a place under G-25 [diseases of nervous system, other extrapyramidal and movement disorders] of ICD-10, as an inclusion term. Though the onset predominantly occurs during childhood and adolescence, onset has been reported in adult age group also (Burd et al, 1986a, b).
Tic disorders have a substantial genetic basis; with first degree relatives having up to ten fold increased risk (Tourette Syndrome Association International Consortium for Genetics 1999). It also has high concordance rate in monozygotic twin (53%) in comparison to dizygotic twins (8%) (Leckman et al 1995b). Compelling indirect evidence from pharmacological studies indicates involvement of basal ganglia (Leckman et al 1995b). Electrical stimulation of the amygdala produces motor and vocal responses resembling tics (Jadresic 1992). Though the definite pathophysiology of tic disorders is not known but internationally a research consensus has been reached which suggest that the basal ganglia and the related thalamo-cortical circuitry is involved.
We proposes that tic disorder should be placed under ‘Neuropsychiatric disorder’ currently ‘F00-F09’, instead of its placement under ‘F90-F98’ as in ICD-10. Further information about the onset of illness could well be coded using a fifth character code.
III. Exclusion of organic dissociative disorder
The term ‘dissociative’ has replaced the older term ‘hysteria’ in current ICD-10. The basic theme in dissociative disorder is disruption (partial or complete) in the usually integrated function of consciousness, memory, identity, perception and motor control, in the absence of any physical disorder that might explain the symptoms. The evidence for psychological causation has been presumed in the form of clear or unclear (if patient denies) stressful events or problems or disturbed relationship with onset. ICD-10 has given preference of plausible mechanism for causation by using the term ‘dissociation’ instead of older term ‘psychogenic’ for this condition to avoid etiological assumptions.
‘Organic dissociative disorder’ has been placed in category of F06 (other mental disorders due to brain damage and dysfunction and to physical disease) of current ICD-10 whereas in DSM–IV, no such entity exists.
The term ‘organic dissociative disorder’ is paradoxical. The mere presence of organic lesion somewhere in the brain of an individual, which is unrelated with dissociative symptoms can’t make him/her a patient with organic dissociative disorder. If the lesion is related with the symptoms then the diagnosis cannot remain dissociative, and in that situation diagnoses like organic amnestic syndrome would be a more appropriate as per the current ICD-10 classificatory system. Moreover, there is dearth of literature on this issue, raising questions about its diagnostic validity.
We propose that such a paradoxical term should be excluded from ICD-11.
OTHER ISSUES THAT WERE DISCUSSED (CONSENSUS NOT REACHED)
1. Recording ‘dementia’ – as a single code using the third character of the alphanumeric system (including substance induced dementia)
2. Inclusion of psychotropic induced neuropsychiatric conditions.
3. Exclusion of ‘Mild cognitive disorder’.
IV. Placing dementia under a single code – including substance induced dementia
As per the coding conventions of ICD-10, each of the categories has a code composed of four characters. The first character is a letter which designates the chapter – a group of diseases of particular specificity. The second character – a digit describes a subgroup of disorders, e.g. organic, including symptomatic, mental disorder. The third character, also a digit, describes the disease or disorder and the fourth character – a digit, details the condition more elaborately e.g. describing its course and other characteristics. A further fifth, sixth and seventh character could be used as a specifier to have more accurate descriptions.
The ICD-10 chapter F categorizes dementia utilizing four different codes (F00 -dementia in Alzheimer’s disease, F01 - vascular dementia, F02 – dementia in other diseases classified elsewhere, F03 - unspecified dementia), whereas DSM-IV places different types of etiologically based dementias under a single section (dementia), because dementias share common symptoms and presentation.
Placement of dementia in ICD-10, utilizing four different codes invites criticism regarding the diagnostic validity and reliability of each code for dementia. Dementia, characterized by the development of multiple cognitive deficits (including memory impairment) that are due to the multiple etiologies (e.g. Alzheimer’s disease, cerebrovascular disease or combination of both), or due to direct physiological effects of general medical conditions or to the persisting effects of substance, is a clinical diagnosis (Boise et al 1999). Having four different codes for dementia in ICD-10 is anomalous with respect to the basic coding convention of ICD-10, as all of these apparently separate disorders have common symptomatology. Placing dementia as a single code (as is the case with DSM-IV) would likely improve its diagnostic stability and probably would improve its applicability and usefulness in clinical practice and research.
Therefore, we propose that dementia should have a single code with further sub typing, based on probable etiological factor (fourth character). Further specification could be achieved with fifth and sixth characters. An example is given below:
F - Mental health chapter
0 - Neuropsychiatric disorder
0 - Dementia
0 - Alzheimer’s disease
0 - Early onset
However, some members of the Department suggested caution with this recommendation based on the argument that classification was not only meant to code disorders but also to assist in research related to aetiology, outcome and prognosis; and also that such a change would require shifting of conditions from their current places, e.g. alcohol and other substance induced dementia.
V. Inclusion of psychotropic medication induced neuropsychiatric condition
In clinical practice of psychiatry, we often notice psychotropic induced psychiatric conditions which would require urgent attention and proper management, e.g. lithium toxicity, valproate toxicity, neuroleptic malignant syndrome (NMS), acute dystonia, tardive dyskinesia, serotonin syndrome etc.
Currently these conditions are placed in ICD-10 either in the chapter of nervous system disease [G21 (secondary Parkinsonism), G24 (dystonia), G25 (other extrapyramidal and movement disorder)] or in the chapter of Y40-Y59 (Drugs, medicaments and biological substances causing adverse effects in therapeutic use).
DSM-IV placed these conditions under the rubric of ‘other conditions that may be a focus of clinical attention’.
In the coming years, more developments are expected in the field of neuropsycho-pharmacology with newer pharmacological molecules to treat psychiatric disorder. In clinical psychiatric practice, medication induced problems are very common and some of the conditions have poor prognosis which often require clinical attention. Proper management of these conditions would require an understanding and adequate knowledge about these conditions. These conditions fulfil features of ‘organicity’ with temporal association, clear and consistent clinical descriptions, possible explainable pathophysiology and good diagnostic reliability and validity; hence, they deserve a place in F00-F09.
The house, however, felt that their placement within codes for physical disorders was adequate if they did not cause specific mental syndromes.
VI. Exclusion of Mild Cognitive Disorder
The characteristic feature of this disorder is a decline in cognitive performance (memory, learning, or concentration) to an extent that is insufficient to make a diagnosis of dementia, delirium or organic amnestic disorder. However, the objective tests indicate deficits and the individual experiences distress or difficulty in carrying out usual activities. The disorder has been placed under the code F06 (other mental disorder due to brain damage and dysfunction and to physical disease). DSM-IV does not have such a diagnostic entity. However, DSM-IV includes mild neurocognitive disorder in the category of cognitive disorder not otherwise specified.
The ICD-10 (Clinical Descriptions and Diagnostic Guidelines) mentions that the boundaries of this category (mild cognitive disorder) are still to be firmly confirmed. Mild cognitive disorder as a diagnostic entity fails to differentiate between age related cognitive change, old age specific cognitive problems, and the presence of psychopathology (depression, anxiety) with genuine mild cognitive deficiency. Various outcome studies have failed to demonstrate its diagnostic stability or utility as a predictor of dementia (Christensen et al. 1995, Christensen et al. 1997, Schroder et al. 1998, Ritchie et al. 2001, Larrieu et al. 2002, Kumar et al. 2005). Therefore, it was proposed that this entity should not be included as a separate category in ICD-11. If included, it should be kept in the unspecified category of mental disorders.
However, the house wished to retain this category because it was felt that it is a common condition and more studies are required before it is excluded.
· American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 3rd Edn-Revised (DSM-III-R). Washington DC: APA, 1987.
· American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th Edn.–Text Revision, (DSM-IV-TR). Washington DC: APA, 2000.
· Boise L, Camicioli R, Morgan DL, et al. Diagnosing dementia: perspective of primary care physicians. Gerontologist 1999; 39:457-464.
· Burd L, Kerbeshian L, Wickenheiser M, et al (1986). A prevalence study of Gilles de la Tourette’s syndrome in North Dakota school children. J Am Acad Child Adolesc Psychiatry 1986; 25:552.
· Burd L, Kerbeshian L, Wickenheiser M, et al. Prevalence of Gilles de la Tourette’s syndrome in North Dakota adults. Am J Psychiatry 1986; 143:787-788.
· Christensen H, Henderson AS, Jorm AF, et al. ICD-10 mild cognitive disorder: epidemiological evidence on its validity. Psychol Med 1995; 25:105-120.
· Christensen H, Henderson AS, Korten AE, et al. ICD-10 mild cognitive disorder: its outcome three years later. Int J Geriatr Psychiatry 1997; 12:581-586
· Jadresic D. The role of the amygdaloid complex in Gilles de la Tourette’s syndrome. Br J Psychiatry 1992; 161: 532-534.
· Kopelman MD, Fleminger S. Experience and perspectives on the classification of organic mental disorders. Psychopathology 2002; 35:76-81.
· Kumar R, Dear KB, Christensen H, et al. Prevalence of mild cognitive impairment in 60 to 64 year old community dwelling individuals: the personality and total health through life 60+ study. Dement Geriatr Cogn Disorder 2005; 19:67-74
· Larrieu S, Letteneur L, Orgogozo JM, et al. Incidence and outcome of mild cognitive impairment in a population-based prospective cohort. Neurology 2005; 59:1594–1599
· Leckman JF, Cohen DJ. Tic Disorders. In Rutter M, Taylor E, Hersov L (Eds). Child and Adolescent Psychiatry – Modern Approaches. Oxford: Blackwell Scientific Publications 1994; pp 455-466.
· Leckman JF, Pauls DL, Cohen DJ. Tic Disorders. In Bloom FE, Kupfer DJ (Eds). Psychopharmacology: The Fourth Generation of Progress. New York: Raven 1995; pp 1665-1674.
· Ritchie K, Artero S, Touchon J, et al. Classification criteria for mild cognitive impairment: a population based validation study. Neurology 2001; 56:37-42.
· Robins E, Guze SB. Establishment of diagnostic validity in psychiatric illness: its application to schizophrenia. Am J Psychiatry 1970; 126:983-987.
· Rutter M, Taylor E. Child and Adolescent Psychiatry -Modern Approaches. 4th Edn. Oxford: Blackwell Scientific Publications, 2005.
· Sartorius N. Understanding the ICD-10 Classification of Mental Disorders – A Pocket Reference. 2nd Edn. London: Science Press Limited, 2002.
· Schroder J, Kratz B, Pantel J, et al. Prevalence of mild cognitive impairment in an elderly community sample. J Neural Transm 1998 (Suppl.); 54:51-59.
· Taylor MA. DSM-III organic mental disorders. In Diagnosis and Classification in Psychiatry: A Critical Appraisal of DSM-III. Tischler GL (Ed.). Cambridge: Cambridge University Press 1987; pp 147-174.
· World Health Organization. ICD-10 Classification of Mental and Behavioural Disorders (Clinical Description and Diagnostic Guideline). Geneva: WHO, 2002.
· Yudofsky SC, Hales RE. Textbook of Neuropsychiatry and Clinical Neurosciences. 4th Edn. Washington DC: American Psychiatric Publishing Inc. 2002.
Address for Correspondence: Dr. S. K. Khandelwal, Professor, Department of Psychiatry and National Drug Dependence Treatment Centre, All India Institute of Medical Sciences, New Delhi-110029, India. Fax: +91 11 26588663. E-mail:
ICD-11: DRAFT PROPOSAL FOR CHANGES IN THE ‘MENTAL AND EHAVIOURAL DISORDERS DUE TO PSYCHOACTIVE SUBSTANCE USE’ SECTION
Tripathi BM, MD, MRCPsy; Jhanjee S, MD, DNB; Kattimani S, MD
1. F1x.07-Pathological intoxication
Suggestion: removal from diagnostic system
Currently, this diagnosis is applicable to alcohol use only and the clinical utility and diagnostic validity of this category has not been established. Hence, this category needs to be removed from the classificatory system.
2. F15-Mental and behavioral disorders due to use of other stimulants, including caffeine Suggestion: removal of caffeine from this rubric to Z category.
Caffeine is a commonly used psychoactive substance and its use is socially sanctioned across cultures. Current categorization of caffeine with stimulants suggests that caffeine is a drug of potentially abuse. This has treatment and policy implications, hence, caffeine should be removed from this category. However, since coding inappropriate use of caffeine has some clinical utility, it may be coded in the Z category.
3. F1x.1 Harmful use
Suggestion: Replacement of the term ‘harmful use’ by the term ‘misuse’ and proposal for new diagnostic criteria.
Proposed diagnostic criteria for ‘misuse of psychoactive substance’ are as under:
This diagnosis requires that at least one of the criteria mentioned below is met, but the criteria for dependence syndrome are not fulfilled.
- Persistent use despite evidence of damage to mental or physical health of the user.
- Persistent use despite awareness of its likely effect on physical or psychological health.
- Persistent uses despite awareness of possible impairment in functioning like operating delicate instruments.
· Persistent use despite change in behavior that includes neglect of studies, neglect of family or repeated absenteeism from work.
· Persistent use despite social problems due to drug use (this will exclude social or traditional use of psychoactive substance).
4. Creation of single subcategory-F1x.21 supported abstinence’
Suggestion: The current subcategories, F1x.21, F1x.22, and F1x.23 should be subsumed under a single subcategory named ‘F1x.21 supported abstinence’.
In order to simplify and make room for growing evidence in favour of non-pharmacological interventions in maintaining abstinence, the currently existing subcategories like F1x.21-currently abstinent but in a protected environment, F1x.22-currently abstinent on a clinically supervised maintenance or replacement regime and F1x.23- currently abstinent but receiving treatment with aversive or blocking drugs, should be subsumed under a single subcategory of ‘supported abstinence’.
5. Creation of new subcategories: F1x.8x Sleep disorders due to psychoactive substance use, and F1x.8x Sexual dysfunction due to psychoactive substance use
In view of their clinical utility these two subcategories should be incorporated in the classificatory system.
6. Recognition of importance of injectible drug use
Suggestion: Injecting drug use should be included in the classification either as a specifier or in the Z Category.
In view of clinical and public health implications of using drugs via parenteral route, this needs to be documented either as a specifier in this chapter or needs to be placed under the Z category.
Supporting evidence for proposed changes
I. F1x.07-Pathological intoxication
There is no Indian or International literature supporting the clinical utility and validity of this diagnostic category. The inter-rater reliability of this condition is poor and other factors may be responsible for such a presentation, e.g. personality traits, metabolic changes and the social context under which alcohol is consumed. An example of the pragmatic difficulties associated with its use is the forensic situation, where it may be difficult to defend the diagnosis due to lack of scientific evidence, and lack of expert consensus (Winckler 1999). Hence, it would be better to remove from this category from the classificatory system.
II. F15-Mental and behavioral disorders due to use of other stimulants, including caffeine
Caffeine has been placed in F15 along with other stimulants. The ‘other stimulants’ are psychoactive substances with known abuse liability and potential to produce dependence. Current categorization suggests that caffeine is a potentially abusive drug. This implies that a large population consuming caffeine has a psychiatric problem (with potential for stigmatization) and is in need of treatment intervention. Placing it along with other stimulants in this category does not do justice to such a widely used substance. Hence, caffeine should be removed from this category. Since, the presence of this category may still retain some clinical utility as a condition meriting health attention in specific situations, inappropriate use of caffeine may be coded in the Z category.
III. F1x.1 Harmful use: Change in title and criteria for diagnosis
Current diagnostic criteria for ‘harmful use of psychoactive substance’ require that actual damage should have been caused to the mental or physical health of the user. The diagnosis is arrived at by assessment of retrospective damage done to the subject and it does not consider the potential harm by use of the psychoactive substance in the future. This makes the diagnosis ‘harmful use’ very restrictive, as it cannot be applied to many individuals who may benefit from clinical intervention. Further, many studies have documented poor inter-rater reliability for this diagnostic category (Pull et al, 1997) and the concordance between ‘abuse’ in DSM-IV and ‘harmful use’ in ICD-10 is low (Hasin 2003). To obviate these shortcomings a change in current diagnostic criteria are proposed, as above.
The term ‘harmful use’ may be replaced by the term ‘misuse of psychoactive substance.’ Other terms like ‘abuse’ of psychoactive substance was not considered because of the derogatory connotation attached with the word while the term ‘hazardous use of psychoactive substance’ may highlight the dangerousness involved in the substance use, which may not be universal for all psychoactive substances. The term ‘dysfunctional use’ was considered but the house felt that ‘misuse’ had greater acceptability in current scientific discourse.
IV. Consolidation of subcategories F1x.21, F1x.22, F1x.23 under a single subcategory named ‘F1x.21 supported abstinence’
The current subcategories, F1x.21, F1x.22, and F1x.23 are:
§ F1x.21-currently abstinent, but in a protected environment
§ F1x.22-currently abstinent on a clinically supervised maintenance or replacement regime
§ F1x.23- currently abstinent but receiving treatment with aversive or blocking drugs
These subcategories can be brought together under a single subcategory F1x.21- ‘supported abstinence’, to make the coding system more uniform and simple, in light of the fact that abstinence states may be supported by methods other than those mentioned in the existing subcategories such as by involvement in self-help groups like Alcoholic Anonymous(AA), cognitive behavior therapy and other non-pharmacological interventions.
V. Creation of new subcategories F1x.8x Sleep disorders due to psychoactive substance use’ and F1x.8x Sexual dysfunction due to psychoactive substance use
Patients using psychoactive substance commonly report sleep disorders and sexual dysfunction. These conditions act as risk factors for relapse if they are not addressed properly. Kumar and Muthulagan (2004) have documented the presence of sleep disorders in patients abstaining from alcohol and many studies have reported that sexual dysfunctions are common in various disorders related to psychoactive substance use (Kumar et al, 1997; Gupta and Jiloha 1998; Singh 1998).
VI. Inclusion of specifier or new subcategory: injectible drug use (IDU)
In addition to the obvious health risks associated with injection drug use, experts opine that this form of drug use gives rise to a severe form of dependence. Results from the National Household Survey, India (NHS, India), show that 0.1% of the sample reported ‘ever’ -injecting drug use (Ray 2004). Common reasons for shifting to injecting route cited by the sample were - better high, and peer pressure due to association with other IDU users. About 97% reported having shared syringes and 74.2% reported having shared needles (Ray, 2004). Needle sharing and unsafe sexual practices as part of drug use subculture can lead to HIV infection and AIDS in this population of drug users. The rate of HIV seroconversion seems to be significantly more rapid in India than that observed in Western countries (Agarwal et al, 1998; Birla Singh and Sharma 1998). Due to the obvious public health and clinical implications of injection drug use, it merits an inclusion as a specifier in the psychoactive substance use section or a placement in the Z category.
OTHER ISSUES THAT WERE DISCUSSED (CONSENSUS NOT REACHED)
1. Creation of a new category: mental and behavioral disorders due to psychoactive substance use of mixed properties
2. Inclusion of psychoactive substances like antidepressants and antihistamines with known abuse and dependence producing capability under the category of substance use disorders
3. Change of title from ‘psychoactive substance induced psychotic disorders’ to ‘behavioral and psychological manifestations due to psychoactive substance use’ for better representation of wide array of specific behavioral and psychiatric manifestations due to psychoactive substance use
4. Creation of separate category of ‘cannabis induced psychosis’
5. Sub typing alcohol use disorders
6. Sub typing of opioid dependence into early onset and late onset opioid dependence
7. Inclusion of protracted withdrawal as specifier
VII. Creation of a new category: Mental and behavioral disorders due to psychoactive substance use of mixed properties
Current classificatory systems categorize psychoactive substances based on their psychoactive properties, viz. hallucinogens, sedatives or stimulants while at the same time some psychoactive substances have been placed under the their respective generic drug classes like opioids, cannabinoids, nicotine, cocaine, etc. There should be uniformity in categorizing psychoactive substances either based on the class of substances they belong to or based on their main psychoactive property. There are psychoactive substances having both stimulant and hallucinogenic properties like MDMA. There may be difficulty in categorizing such substances, and to overcome this, a suggestion to introduce a separate category named ‘mental and behavioral disorders due to psychoactive substance use of mixed properties’ was made. This did not find consensus in the group discussion and hence was dropped from the final proposal.
VIII. To include psychoactive substances like antidepressants and antihistamines with known abuse and dependence producing capability under the category of substance use disorders
There was a suggestion to include other psychoactive substances with proven dependence and withdrawal producing capability like
antidepressants, monoamine oxidase inhibitors (Ananath et al, 1995) and antihistamines (Pal et al, 2005), under the ‘mental and behavioural disorders due to psychoactive substance use’ category, moving them from the existing category of F55.0 (abuse of non-dependence producing substances) in ICD-10. The house felt that in the absence of strong evidence, it would be inappropriate to consider these drugs as psychoactive substances with abuse liability. Hence the suggestion was dropped from the final draft.
IX. To change the title from ‘Psychoactive substance induced psychotic disorders’ to ‘Behavioral and psychological manifestations due to psychoactive substance use’ for better representation of wide array of specific behavioral and psychiatric manifestations due to psychoactive substance use
Subcategories under ‘Psychoactive substance induced psychotic disorders’ may be changed to include a broad array of behavioral and psychological symptoms and syndromes like depressive disorder, panic attacks, obsessive-compulsive disorder, agoraphobia etc. Hence it was proposed to change psychotic disorders to ‘Psychiatric and behavioral changes due to psychoactive substance use’ or ‘Behavioral and psychological manifestations due to psychoactive substance use’. Since any change in the title was likely to replicate the main title ‘Mental and behavioral disorders due to psychoactive substance use’ of this chapter, this suggestion was withheld.
X. Creation of separate category of ‘cannabis induced psychosis’
Cannabis induced psychosis has been extensively described in Indian literature. It was argued that cannabis induced psychosis be considered as a separate independent category under F12.5. It differs from other psychiatric disorders in terms of psychopathology that consists of both psychotic (paranoid delusions) and affective symptoms, and is characterized by rapid changes in symptomatology. Such a presentation cannot be easily categorized into either affective or psychotic disorder (Sarkar et al, 2003; Mallik et al, 2004) and has course and treatment implications. A specific rubric will also draw increased research attention to this condition. The house felt that sufficient literature had not yet accrued to support a separate category of cannabis induced psychosis, so this suggestion was dropped from the final draft.
XI. Sub typing alcohol use disorders
A descriptive study showed that patients with primary alcoholism differ from patients with secondary alcoholism on severity of dependence, presence of interpersonal problems, in their compliance to treatment and in maintaining abstinence in the follow-up period (Ramesh et al, 1996).Some authors have tried to study drinking pattern using multivariate techniques. Based on factor analysis of their data, one group of authors proposed that alcohol use was of 3 types - alcohol abuse, alcohol dependence and social drinking (Mathrubootham et al, 1997). Alcohol dependence could be further classified into low and moderate dependence.Such studies support the exclusion of social drinking from diagnostic categorization, and can help in reduction of false positives for alcohol abuse or dependence. However some authors have used the term ‘problems drinkers’ to identify those who do not fulfilling criteria for alcohol dependence but still require some form of intervention for their alcohol use (Satesh and Sengupta 1997). The house agreed with the onclusions reached by Gupta and Basu (1999) that alcohol subtyping would merit further study before inclusion in the classificatory system.
XII. Sub typing of opioid dependence into early onset and late onset opioid dependence
Some authors have suggested the differentiation between opioid dependence of early onset defined as age less than 20 years at the initiation of opioids and late onset defined as age more than 20 years at the initiation of opioids. There appears to be significant difference between the two groups regarding substance use pattern and presence of psychopathology, which might need to be considered in treatment planning (De et al, 1998).However, the house felt that the evidence for the use of this specifier was not compelling as yet.
XIII. Inclusion of protracted withdrawal as specifier
There was suggestion to consider ‘protracted withdrawal state’ as a specifier besides the existing F1x.3 withdrawal state, which is an acute physiological state due to sudden cessation or decrease in the quantity of psychoactive substance on which an individual is dependent. It has been well established that protracted withdrawal is one of the risk factor for relapse in cases of psychoactive substance use disorders (Satel et al, 1993).However, the house felt that there was not enough evidence to support the separation of acute and protracted withdrawal states.
ICD revision process should also consider the identification of risk factors for relapse and factors that alter prognosis and intervention strategies. The multiaxial system similar to that suggested by WPA workgroup in 1994 may be used with some alteration (Kastrup 2002). It needs to be established whether diagnostic criteria needs to be changed in order to make its applicable in special populations like women (Selvaraj et al, 1997; Prasad et al, 2000; Irpati et al, 2005), elderly (Grover et al, 2005), and adolescents (Tripathi and Lal 1999). While revising existing classification, available research evidence should be considered carefully, and proposed changes should be evaluated for their utility in treatment decisions and in prognostication, for forensic purposes, for potential benefits to special groups like children. Also, issues related to third parties like reimbursement providers, public opinion and implication for government policies should be carefully considered during the revision process.
§ Agarwal AK, Yaima Singh N, Bijaya Devi L, et al. Clinical Features and HIV progression as observed longitudinally in a cohort of injecting drug users in Manipur. Indian J Med Res 1998; 108:51-57.
§ Ananath J, Swartz JR, Gadasall R, Borogoyne K. Abuse of monoamine oxidase inhibitors. Indian J Psychiatry 1995; 37:145.
§ Babu S, Sengupta SN. A study of problem drinkers in a general hospital. Indian J Psychiatry 1997; 39:13.
§ Birla Singh M, Sharma SG. AIDS in follow-up study of 76 injecting heroin users. Indian J Psychiatry 1998; 40 (Suppl):85-86.
§ De B, Mattoo SK, Basu D. A comparative study of early onset versus late onset opioid dependence. Indian J Psychiatry 1998; 40 (Suppl):19.
§ Ganguly KK, Sharma HK, Krishnamachari KA. An ethnographic account of opium consumers of Rajasthan (India): socio-medical perspective. Addiction 1995; 90:9-12.
§ Grover S, Irpati AS, Saluja BS, Mattoo SK, Basu D. Substance dependence in the elderly: a study from a de-addiction centre in north India. Indian J Psychiatry 2003; 45:244-246.
§ Gupta N, Basu D. The ongoing quest for sub typing substance abuse: current status. Indian J Psychiatry 1999; 41:289-299.
§ Gupta V, Jiloha RC. Psychological evaluation of male alcoholics. Indian J Psychiatry 1998; 20 (Suppl):82.
§ Hasin D. Classification of alcohol use disorders. Alc Res Health 2003, 27:5-17.
§ Irpati AS, Saluja BS, Grover S, Mattoo SK, Basu D.Socio-demographic and clinical profile of substance dependence in women attending a de-addiction centre in north India. Indian J Psychiatry 2005; 47 (Suppl):41.
§ Kastrup M. Experience with current multiaxial diagnostic systems: a critical review. Psychopathology 2002; 35:122–126.
§ Kumar A, Muthulagan. Sleep disturbances in Alcohol abstinent individual. Indian J Psychiatry 2004; 46 (Suppl):23-24.
§ Kumar HP, Shet PS, Singh S, Benegal V (1997). Prevalence of sexual dysfunction in male alcoholics. Indian J Psychiatry 1997; 39 (Suppl):52.
§ Mallik A, Dutta P, Chatterjee J. Physical and psychiatric comorbidity in patients with cannabis abuse. Indian J Psychiatry 2004; 46 (Suppl):41.
§ Mathrubootham N, Bashyam VSP, Shahjahan. Multivariate analysis of drinking behavior in a rural population. Indian J Psychiatry 1997; 39:212.
§ Pal H, Kumar R, Bhushan S, Berry N. Psychiatric co-morbidity associated with pheniramine abuse and dependence: a case report. Indian J Psychiatry 2005; 47:60-62.
§ Prasad S, Murthy P, Mallika R, Vandana, Gopinath PS. Alcohol dependence in women: a preliminary profile. NIMHANS Journal, 1998; 2:87-91.
§ Pull CB, Saunders JB, Mavreas V, et al. Concordance between ICD-10 alcohol and drug use disorder criteria and diagnoses as measured by the AUDADIS-ADR, CIDI and SCAN: results of a cross-national study. Drug Alcohol Depend 1997; 47:207-216.
§ Ramesh R, Sengupta SN, Sharma PSVN. Primary and secondary alcoholism. Indian J Psychiatry 1996; 38 (Suppl):54.
§ Ray R (Ed). The Extent, Pattern and Trends of Drug Abuse in India, National Survey, Monograph, New Delhi: United Nations Office on Drugs and Crime, Regional Office for Southeast Asia and Ministry of Social Justice and Empowerment, Government of India 2004.
§ Sarkar J, Murthy P, Katiaperumal VG, Channabasavanna SM. Psychiatric morbidity in cannabis. Indian J Psychiatry 1996; 38 (Suppl):83.
§ Satel SL, Kosten TR, Schuckit MA, Fischman MW.Should protracted withdrawal from drugs be included in DSM-IV? Am J Psychiatry 1993; 150:695-704.
§ Selvaraj V, Prasad S, Ashok MV, Appaya MP. Women alcoholics: are they different from men alcoholics? Indian J Psychiatry 1997, 39:288.
§ Singh SD. Addictive substances and sexuality. Indian J Psychiatry 1998; 40 (Suppl):84.
§ Tripathi BM, Lal R. Substance abuse in children and adolescents. Indian J Pediatrics 1999, 66:569-575.
§ Winckler P. "Pathological intoxication.” Diagnostic artefact or a reliable psychiatric diagnosis? [Article in German]. Nervenarzt 1999; 70:803-809.
ICD-11: DRAFT PROPOSAL FOR CHANGES IN THE ‘SCHIZOPHRENIA, SCHIZOTYPAL AND DELUSIONAL DISORDERS’ SECTION
Rakesh Lal, MD, Mamta Sood, MD, DPM, Amardeep Kumar, MD
Schizophrenia (F 20)
1. Higher weight should be given to negative symptoms of schizophrenia
2. Pattern of course in schizophrenia needs to be redefined/simplified to: (a) single episode, (b) episodic-remitting course with full remission, (c) episodic-remitting course with partial remission, and (d) chronic
3. Age of onset in schizophrenia should be specified
4. Removal of catatonic schizophrenia (F20.2) as a subgroup of schizophrenia; placing catatonia as clinical course specifier of schizophrenia.
5. Removal of post-schizophrenic depression as a subtype; depressive symptoms to be included as phase specifier: (a) prodromal, (b) active psychotic phase, (c) post psychotic phase <12 months, (d) post psychotic phase >12 months
6. Dimensions for schizophrenia to be included
7. Schizo-obsessive subtype to be included under the categories meriting further study
8. Induced delusional disorder to be included under delusional disorders (F24 [induced delusional disorder] should be shifted under F22)
9. “Persistent” to be removed from persistent delusional disorder
10. Course specifier for ATPD to be included: (a) single episode and (b) recurrent (specify the number of episodes)
11. Schizoaffective disorder, concurrent and sequential types to be included
Thus, we propose the draft for this section should read as follows:
Type of schizophrenia – x
F20.0 Paranoid schizophrenia
F20.1 Hebephrenic schizophrenia
F20.2 Undifferentiated schizophrenia
F20.3 Residual Schizophrenia
F20.4 Simple schizophrenia
F20.8 Other schizophrenia
F20.9 Schizophrenia, unspecified
Course – a
Age at onset – b
Catatonic symptoms – c
Depressive symptoms - d
Delusional disorders (F22)
F22: Delusional disorders
F22.0 Delusional disorder
F22.1 Induced delusional disorder
F22.8 Other delusional disorder
F22.9 Delusional disorder, unspecified
Acute and transient psychotic disorders (F23)
x – subtype
a – course which may be: 0 - single episode, 1- recurrent, current episode
Schizoaffective disorders (F25)
x – subtype
a – course which may be: 0 - concurrent, 1- sequential
Supportive Evidence for Proposed Changes
Schizophrenia, schizotypal and delusional disorders (F20-F29) section in ICD10 include non-affective psychiatric disorders conceptualized to be broadly related to each other. The classification of these disorders in ICD-10 has achieved fairly good reliability, ensuring the international comparability of research, clinical work and education. While, these categories have not achieved expected nosological validity based on criteria given by Robin and Guze (1970), the past decade has witnessed research into specific areas that has elucidated and questioned many already existing issues and has thrown up several new issues for consideration.
I. Higher weight should be given to negative symptoms of schizophrenia
There is an emphasis on positive symptoms for diagnosing schizophrenia in ICD10. Presence of only one SFRS is enough to make the diagnosis whereas two of the negative, catatonic, formal thought disorder or persistent hallucinations with accompanying delusions/overvalued ideas are required to make the diagnosis of schizophrenia. Inclusion of Schneider’s first rank symptoms (SFRS)/positive symptoms in the diagnostic guidelines has increased reliability of diagnosis of schizophrenia in ICD10. However, it is now well established that SFRS are present in other psychiatric conditions as well (Taylor et al, 1973; Brockington et al, 1980). Also, current research recognizes that negative symptoms are defining features of schizophrenia.
- Reliability: studies show that it is possible to distinguish schizophrenia from other non-affective psychotic disorders as patients with schizophrenia are characterized by more pronounced negative symptoms (Jager et al, 2003). Negative symptoms are useful to differentiate between schizophrenia and schizoaffective disorders from mood-incongruent psychotic mania or mixed mania (Pini et al, 2004).
- Internal validity: negative symptoms constitute an indicator of severity of schizophrenia (Rocca et al, 2005).
- External validity: the literature search focused on the following questions-
- Are negative symptoms common enough?
Negative symptoms have been reported frequently in patients with schizophrenia.
- Are negative symptoms more liable for familial aggregation and genetic transmission?
Patients of schizophrenia with affected relatives are reportedto have a high magnitude of negative symptoms that are relativelytreatment resistant. Twin studies and other data show that relativesof probands with greater negative symptoms have higher morbid risks for illness than the relatives of probands who have greaterpositive symptoms. Negative symptoms are also presentin some nonschizophrenic relatives of patients with schizophrenia,as in those with schizotypal personality disorders (Malaspina et al, 2000).
o Is there any evidence to support different response to treatment and clinical course and outcome?
Typical antipsychotics cause relatively more improvement in positive symptoms as compared to negative symptoms. Moreover, typical antipsychotics cause extra pyramidal side effects which may mimic some of the negative symptoms. Atypical antipsychotics have been proven in placebo-controlled trials to be effective in treating negative symptoms of acute schizophrenic episodes (Moller et al, 2003). Negative symptoms are widely suspected to reflect frontal lobe dysfunction and are associated with poor outcome (Potkin et al, 2002).
· Boundary problems: negative symptoms in schizophrenia may be either primary or secondary to positive symptoms, antipsychotic side effects, dysphoric affect and environmental deprivation. Boundary problems exist between these.
Discussion: The literature suggests that negative symptoms are increasingly recognized as defining features of schizophrenia but it is not clear how they can be used in differentiating schizophrenia from other conditions. Some studies report that negative feature like apathy may be useful in this regard. Studies are needed to identify pattern and type of primary negative symptoms in schizophrenia. Increasing the weight age of negative symptoms in making diagnosis of schizophrenia can be achieved by adding another criteria that records negative symptoms not currently included under (h) like avolition, loss of drive, aimless behaviour, empty speech.
II. Addition of early onset (onset before 18 years of age) as age of onset specifier
Awareness about early onset schizophrenia is increasing. Premorbid developmental impairments, including language, motor and social deficits; insidious onset in at least 75% of children; elementary auditory hallucinations; less complex delusions related to childhood themes; and negative symptoms namely flat or inappropriate affect; are more frequent and pronounced in earlier, than in later-onset schizophrenia.. A marked deterioration from the previous level of functioning is also present in these children, and an impaired outcome is reported in approximately 50-60% of cases.
· Internal validity: Remschmidt et al (2006) reported that the early onset schizophrenia (childhood onset) has diagnostic stability in 91% of cases in a 42-years follow up study.
· External validity: The literature search focused on the following questions:
o Is schizophrenia with early onset common enough?
The frequency of childhood schizophrenia is less than 1 in 10,000 children, but there is a remarkable increase in frequency between 13 and 18 years of age (Remschmidt et al, 2005).
o Is schizophrenia with early onset more liable for familial aggregation and genetic transmission?
There is strong evidence for the importance of genetic factors in schizophrenia in children and adolescents (Remschmidt et al, 2005).
o Does schizophrenia with early onset have a different profile of neuropsychological deficits, treatment response, and course and outcome?
Early onset schizophrenia has greater neuropsychological deficits than adult onset schizophrenia (Biswas et al, 2006; White et al, 2006). Early onset schizophrenia is also more severe and is frequently treatment-resistant (Shaw et al, 2006). The long-term course of childhood- and adolescent-onset schizophrenia is worse than in adult-onset schizophrenia, and the patients with manifestation of the disorder below the age of 14 have a very poor prognosis (Remschmidt et al, 2005).
· Boundary problems: Boundary problem exists with autism, disintegrative disorder, multiplex complex developmental disorder (MCDD), multiple developmental impairment (MDI), affective psychoses, Asperger syndrome, drug-induced psychosis and psychotic states caused by organic disorders.
Discussion: Early onset schizophrenia (onset before 18 years) has good internal and external validity. Thus, the group proposed its (age of onset) inclusion as a specifier ‘b’.
III. Pattern of course needs to be simplified
The review of literature did not support the complex pattern included under the current course specifier in ICD-10. It is tedious for use in clinical practice as well as research, hence it is rarely used. Provision of a simpler pattern of course specifier would increase its clinical utility without compromising on its validity. The group proposed the following pattern for course specifier:
· single episode
· episodic - remitting course with full remission.
· episodic - remitting course with partial remission.
IV. Removal of catatonic schizophrenia F20.2 as a subgroup of schizophrenia and placing it as clinical course specifier of schizophrenia
Kraepelin recognized catatonia as a form of dementia praecox and Bleuler included it within his wide group of schizophrenias. Catatonia as a subtype of schizophrenia has been included in all classificatory systems. Recent research shows that catatonia is a syndrome which is characterized by association with neurological and general medical conditions, mood disorders; use of effective therapeutics and development of reliable instruments.
· Reliability: catatonic features are well-defined and can be reliably ascertained (Taylor et al 2003, Pommepuy et al, 2001)
· Internal validity: symptoms of catatonia appear to be independent of the key symptoms of schizophrenia on correlation analysis (Cernovsky et al, 1998). The subtype shows limited stability over time changing from one group to other (McGlashan et al, 1994).
· External validity: The literature search focused on the following questions-
o Is the catatonic syndrome common enough?
Catatonic presentations are common in acute in-patient psychiatric settings (Banerjee et al, 1995; Chalasani et al, 2005). The prevalence of catatonia among psychiatricpatients is reported to range from 7.6% to 38 % (Taylor et al, 2003).
o Is the catatonic syndrome specific to schizophrenia?
Catatonic presentation is more common in mood disorder than in schizophrenia. It is also found in many other conditions (Taylor et al, 2003).
o Does the catatonic syndrome have a different response to treatment in various disorders?
Catatonia responds to specific treatments like lorazepam and ECT irrespective of the disorder (Taylor et al 2003).
Discussion: Customary clinical practice continues to overvalue the idea that presence of catatonia is diagnostic of schizophrenia. The reliability of catatonic features is good; however the internal and external validity of catatonic schizophrenia is questionable. This type of presentation appears in the course of schizophrenia at various stages with limited stability. Further, it is recommended that at the time of presentation, if catatonic features are present, these are treated symptomatically with lorazepam or ECT; final management, course and prognosis are decided by the underlying condition that is uncovered after patient recovers from catatonia. So, catatonia can be conceptualized mainly as a clinical specifier. Thus, the group proposes its placement as a clinical course specifier ‘c’.
V. Removal of post-schizophrenic depression as a subtype; depressive symptoms to be included as a phase specifier.
Depression occurs frequently in schizophrenia. Occurrence of depression in schizophrenia has often been associated with worse outcome , impaired functioning, personal suffering , higher rates of relapse or rehospitalization and suicide. In ICD 10, depressive features are included under schizophrenia as ‘mild degree of depression’ preceding psychotic symptoms and as ‘post psychotic depression subtype’. In the former situation, it is a symptom and in the latter situation, a syndrome. A depressive episode present concurrently with schizophrenia is diagnosed as a schizoaffective disorder. The confusion attending the term depression in schizophrenia is attributable to three questions viz., whether it is the symptom or syndrome of depression that is being considered; the phase of schizophrenia in which it is occurring; and its causation (whether it is integral part of schizophrenic process, a de-novo phenomenon or a reaction to stress).
· Reliability: Depressive features like diminished interest, pleasure, energy, or motivation and psychomotor retardation and impaired ability to concentrate, are difficult to differentiate from the negative symptoms. Also, these are difficult to distinguish from antipsychotic induced side effects (Siris, 2000).
· Internal validity: The diagnosis of post-schizophrenic depression according to ICD-10 classification requires that the general criteria of schizophrenic illness be met within the last 12 months and that some schizophrenic symptoms should be present concurrently with the depressive episode. It tries to make this subtype specific to schizophrenia by putting a duration limit to this subtype without looking into phenomenological and course patterns of depressive symptoms. The study done by Bressan et al (2003) suggests that depressive episode in schizophrenia is not restricted to the first year following the psychotic episode. Such episodes were found during prodrome, acute psychotic phase, during first year following the psychotic episode and thereafter with no significant difference in incidence occurring during the first year and thereafter. Depressive episodes accompanying the active psychotic phase remit along with the psychosis, and post-psychotic depression can occur de novo without concomitant change in positive or negative symptoms (Birchwood et al, 2000).
· External validity: The literature search focused on the following questions:
o Are depressive symptoms common enough?
Depressive symptoms in schizophrenia are often severe but are poorly recognized by psychiatrists (Bressan et al, 2003). The prevalence varies from 7%-75% according to the approach used for their identification (Micallef et al, 2006). Depressive symptoms of substantial severity are often found in 50% of newly diagnosed cases of schizophrenia and 33% of cases of chronic schizophrenia that have relapsed (Whitehead et al, 2002).
o Is the response to treatment of depressive symptoms similar in different phases of schizophrenia?
A Cochrane systematic data review found no convincing evidence to support or refute the use of antidepressants in treating depression in people with schizophrenia (Whitehead et al, 2002). However, a study done by Birchwood et al (2000) found that depression accompanying acute psychotic phase remits with psychosis.
· Boundary problems: A major problem exists concerning the boundary between depressive symptoms in schizophrenia, schizoaffective disorder (depressive type) and depressive episode per se.
Discussion: Post-schizophrenic depression as a subtype of schizophrenia has questionable reliability and validity. Depression in schizophrenia is common and it occurs during prodrome, active psychotic phase, within first year and thereafter. The efficacy of antidepressants is equivocal. The boundary problem exists with schizoaffective disorder (depressive type) and depressive episode (F32.-). Thus, the group proposes removal of post-schizophrenic depression as a subtype; depressive symptoms should be included as a course specifier‘d’. Depressive symptoms fulfilling diagnostic criteria for depressive episode (F32.-) occurring could be diagnosed independently as a co morbid condition.
VI. Dimensions of schizophrenia to be introduced
Over the last decade many studies have highlighted the dimensions of schizophrenia. In eighties, the negative–positive distinction was extensively studied. Van der Does et al (1995) investigated the stability of an earlier reported four-dimensional symptom model (positive symptoms, negative symptoms, disorganization, and depression) and found a stable four-dimensional structure that closely resembled the factor structure of their first assessment. The symptom dimensions were uncorrelated, except for disorganization and depression. The results of a cluster analysis suggest the existence of at least four subtypes of schizophrenia: positive, negative, mixed, and disorganized. A fifth subtype included patients with few symptoms and suggested the occurrence of simple schizophrenia (Dollfus et al, 1996; Lykouras et al, 2001). Klingberg et al (2006) reported the occurrence of five factors viz., negative, impulsive, positive, disorganization, and depression.
Discussion: While the search of literature suggests the occurrence of many dimensions underlying schizophrenia, the evidence for reliability and validity of different dimensions is variable. Issues pertaining to dimensional classification will be covered under the general section.
VII. Introduction of schizo-obsessive subtype of schizophrenia under ‘Conditions meriting further study’
Co-occurrence of obsessive compulsive (OC) symptoms and psychotic illness was first recognized over a century ago. Interest in this area has been revived recently because of increased recognition of higher-than-expected co morbidity rates. There is growing evidence that patients with schizophrenia and obsessive compulsive disorder, termed schizo-obsessive may represent a special category of schizophrenia population.
· Reliability: The reliability of OC symptoms in schizophrenia is yet to be established. When obsessive-compulsive symptoms occur without insight, it becomes difficult to distinguish them from delusions.
· Internal validity: Assessment of internal validity for this entity should distinguish among the following possibilities: (a) OC symptoms that occur only in the context of psychosis, and that may overlap with psychotic phenomenology, are part of psychosis; (b) OC symptoms occurring only in the prodromal phase of schizophrenia; (c) Neuroleptic-induced OC symptoms; and (d) OC or frank obsessive-compulsive disorder (OCD) occurring concurrently with schizophrenia.
- External validity: the literature search focused on the following questions:
- Are OC common enough in schizophrenia?
Recent studies have revealed much higher co-morbidity rates for OCD in the schizophrenia than previously recognized. Investigators have reported prevalence rates of clinically significant OC symptoms in schizophrenia population to be 10%-52% and of OCD in schizophrenia population to be 7.8%-26% (Berman et al, 1995; Kruger et al, 2000; Tibbo et al, 2000; Craig et al, 2002; Thomas et al 2005). Comparisons of current co-morbidity figures with individual lifetime prevalence rates for each disorder (2%-3% for OCD and 1% for schizophrenia) suggests that there exists greater than chance rate of co-occurrence between the two conditions (Bottas et al, 2005).
- b) Does schizophrenia with OC symptoms have a different clinical profile?
Schizophrenia with OC symptoms possess a distinct clinical and neuropsychological profile that differs from that of schizophrenia without OC symptoms. This profile includes a worse clinical course with poor treatment response, lower functioning levels, and greater impairment of functions primarily subserved by the frontal lobes. In addition, the former patients showed a higher level of negative symptoms and worse overall psychopathology (Hwang, 2000).
- Are the underlying biological bases for schizophrenia with or without OC symptoms same?
There is significant overlap in the proposed circuits of OCD and schizophrenia, which may lead to co-expression of symptoms. Although there is overlap in neurotransmitter dysfunction, the interactions are complex, especially in regard to the serotonin and dopamine systems (Tibbo et al 1999, Gross-Isseroff et al 2003).
- Boundary problems: a major problem would be to separate schizo-obsessive subtype from OCD with poor insight particularly given that it has traditionally been distinguished from psychotic disorders on the basis of the individual recognizing the compulsions or obsessions as ego-dystonic, implying the presence of insight.
Discussion: at present the epidemiological and biological evidence suggests that schizo-obsessive disorder as a subtype of schizophrenia deserves attention as it may be sufficiently distinct in terms of aetiology, treatment and outcome. The group proposes that schizo-obsessive subtype of schizophrenia should be introduced as a conditions meriting further study.
F22: Persistent delusional disorder
VIII. Deletion of the term ‘persistent’
ICD-10 mentions the word ‘persistent’ to mean that these disorders are ‘usually persistent and sometimes lifelong’. The global outcome of delusional disorders is shown to be better than that for schizophrenia. Kendler and Walsh (1995) reported the duration of illness for delusional disorders (38±26 months) to be shorter than that for schizophrenia (159±134 months). It is argued that to bring this category closer to that of DSM-IV the term ‘persistent’ should be dropped.
IX. Shifting of F24 (induced delusional disorder) under F22
The underlying assumption behind placing F24 as a separate diagnostic category in ICD-10 appears to be presence of a definite cause and spontaneous resolution of symptoms after removal of the cause. Literature review suggests that this category has not been adequately validated. The occurrence of its four subtypes viz., folie imposee, folie simultanee, folie communiqué and folie induite is largely based on the resistance offered and time of appearance of psychotic symptoms in the secondary cases. Except for folie imposee, these disorders in secondary cases do not have a clear onset and offset with the primary case (Wehmeier et al, 2003). Management of these patients requires multiple treatments including removal of etiologic agent, antipsychotics, individual and group psychotherapy, and family therapy (Kumar et al, 2005). As these conditions are phenomenologically similar to cases with delusional disorders, the group proposes that this category can be shifted under F22 as F22.1 for better understanding of etiology and long term course and outcome.
F23: Acute and transient psychotic disorders
X. Introduction of course specifier for acute and transient psychotic disorders
Acute and transient psychotic disorders get re-diagnosed as other non-organic psychotic disorder if they recur. Studies have suggested that these cases recur and recurrent acute remitting psychotic states are 10 times more common in developing than in industrialized countries; are two times more common in females than males; exhibit long term benign course and have lesser negative symptoms (Susser et al,1995; Sajith et al, 2002). Better delineation of non-affective acute remitting psychosis in current diagnostic systems could lead to better understanding of this condition and improve the applicability of diagnostic systems in developing countries, where these conditions are more common than in industrialized countries. To better understand the course and outcome of acute and transient psychotic disorders, the group proposed the introduction of a course specifier for this group of disorders. A fifth character may be used to classify the course e.g. F23.x.a
x – subtype
a – course which may be 0 - single episode, and 1 - recurrent, current episode
F25: Schizoaffective disorders
XI. Introduction of concurrent and sequential subtypes as course specifier
In ICD-10, the schizoaffective disorder is defined as the concurrent occurrence of schizophrenic symptoms with a major affective disorder. Longitudinal aspects of course are npt reflected well in the current classification. There is little evidence to support a chronological distinction regarding the co-existence of schizophrenic and affective symptomatology. Thus two types of schizoaffective disorder must be distinguished: the 'concurrent' and the 'sequential' type (Marneros 2003). The first includes conditions with coincident schizophrenic and affective symptoms and the latter is defined as the schizoaffective disorder under a longitudinal aspect subsuming disorders with a symptom change between different episodes. The group felt that this change will improve the reliability and validity of schizoaffective disorders. A fifth character may be used to classify course e.g. F25.x.a
x – subtype
a – course which may be 0 – concurrent, and 1 - sequential
In the coming decades, efforts to explore simpler clues like endo-phenotypes to genetic underpinnings of disorders covered under this section will continue. It is being conceptualized that both genes and brain circuits they regulate may underlie symptom complexes across many diagnostic categories. The dimensional approach to psychiatric diagnosis will probably help in better segregating these symptom complexes. Also, there is issue of sub-threshold symptoms seen in primary care. Besides reliability and validity, issues of clinical utility are important. The changes proposed in the present classification of these disorders need to synthesize these issues.
1. Banerjee A, Sharma LN. Catatonia incidence in acute psychiatric admissions. Indian J Psychiatry 1995; 37:35-40.
2. Berman I, Kalinowski SM, Berman SM, et al. Obsessive and compulsive symptoms in chronic schizophrenia. Compr Psychiatry 1995; 36: 6-10.
3. Bertelson A. Schizophrenia and related disorders: experience with current diagnostic systems. Psychopathology 2002; 35:89-93.
4. Birchwood M, Iqbal Z, Chadwick P, et al. Cognitive approach to depression and suicidal thinking in psychosis. 1. Ontogeny of post-psychotic depression. Br J Psychiatry 2000; 177:516-521.
5. Biswas P, Malhotra S, Malhotra A, et al. Comparative study of neuropsychological correlates in schizophrenia with onset in childhood, adolescent and adulthood. Eur Child Adolesc Psychiatry 2006; 15:360-366.
6. Bottas A, Cooke RG, Richter MA. Comorbidity and pathophysiology of obsessive-compulsive disorder in schizophrenia: Is there evidence for a schizo-obsessive subtype of schizophrenia? J Psychiatry Neurosci 2005, 30, 187-193.
7. Bressan RA, Chaves AC, Pilowsky LS, et al. Depressive episode in stable schizophrenia: critical evaluation of DSM-IV and ICD-10 criteria. Psychiatry Res 2003; 117:47-56.
8. Brockington IF, Wainwright S, Kendell RE. Manic patients with schizophrenia or paranoid symptoms. Psychol Med 1980; 10:73-83
9. Cernovsky ZZ, Landmark JA, Mersky H, et al. The relationship of catatonia symptoms to symptoms of schizophrenia. Can J Psychiatry 1998; 43:1031-1035.
10. Chalasani P, Healy D, Morriss R. Presentation and frequency of catatonia in new admissions to two acute psychiatric admission units in India and Wales. Psychol Med 2005; 35:1667-1675.
11. Craig T, Hwang M, Bromet E. Obsessive-compulsive and panic symptoms in patients with first admission psychosis. Am J Psychiatry 2002; 159: 592-598.
12. Dollfus S, Everitt B, Ribeyre JM, et al. Identifying subtypes of schizophrenia by cluster analyses. Schizophr Bull 1996; 22: 545-555
13. Gross-Isseroff R, Hermesh H, Zohar J, et al. Neuroimaging communality between schizophrenia and obsessive-compulsive disorder: a putative basis for schizo-obsessive disorder? World J Biol Psychiatry 2003; 4: 129-134.
14. Jager M, Bottlender R, Strauss A, et al. On the descriptive validity of ICD-10 schizophrenia: empirical analyses in the spectrum of non-affective functional psychoses. Psychopathology 2003; 36:152-159.
15. Klingberg S, Wittorf A, Wiedemann G. Disorganization and cognitive impairment in schizophrenia: independent symptom dimensions? Eur Arch Psychiatry Clin Neurosci 2006; 8: 532-540
16. Kruger S, Braunig P, Hoffler J, et al. Prevalence of obsessive-compulsive disorder in schizophrenia and significance of motor symptoms. J Neuropsychiatry Clin Neurosci 2000; 12:16-24.
17. Kumar PNS, Subramanyam N, Thomas B, et al. Folie a deux. Indian J Psychiatry 2005; 47:164-166.
18. Lykouras L, Oulis P, Daskalopoulou E, et al. Clinical subtypes of schizophrenic disorders: a cluster analytic study. Psychopathology 2001; 34:23-28
20. Marneros A. The schizoaffective phenomenon: the state of the art. Acta Psychiatr Scand 2003; 418:29-33.
21. McGlashan TH, Fenton WS. Classical subtypes for schizophrenia. In Widiger TA, Frances AJ, Pincus HA, et al. (Eds.). DSM-IV Sourcebook. Vol I. Washington: American Psychiatric Association 1994: pp. 419-440.
22. Moller HJ. Management of the negative symptoms of schizophrenia: new treatment options. CNS Drugs 2003; 17:793-823.
23. Micallef G, Fakra E, Blin O. Use of antidepressant drugs in schizophrenia patient with depression. Encephale 2006; 32:263-269.
24. Potkin SG, Alva G, Fleming K, et al. A PET study of the pathophysiology of negative symptoms in schizophrenia. Am J Psychiatry 2002; 159:227-237.
25. Pini S, de Queiroz V, Dell'Osso L, et al. Cross-sectional similarities and differences between schizophrenia, schizoaffective disorder and mania or mixed mania with mood-incongruent psychotic features. Eur Psychiatry 2004; 19:8-14.
27. Remschmidt H, Theisen FM. Schizophrenia and related disorders in children and adolescents. J Neural Transm 2005 (Suppl); 69:121-141.
28. Remschmidt H, Martin M, Fleischhaker C, et al. Forty-two-years later: the outcome of childhood onset schizophrenia. J Neural Transm 2007, 114: 505-512.
30. Sajith SG, Chandrasekaran R, Sadanandan Unni KE, et al. Acute polymorphic psychotic disorder: diagnostic stability over three years. Acta Psychiatr Scand 2002; 105:104-109.
31. Siris SG. Depression in schizophrenia: perspective in the era of “atypical” antipsychotic agents. Am J Psychiatry 2000; 157:1379-1389
32. Susser E, Varma VK, Malhotra S, et al. Delineation of acute and transient psychotic disorders in a developing country setting. Br J Psychiatry 1995; 167:216-219.
33. Taylor MA, Abrams R. The phenomenology of mania: A new look at some old patients. Arch General Psychiatry 1973; 29:520-522
34. Taylor MA, Fink M. Catatonia in psychiatric classification: A home of its own. Am J Psychiatry 2003; 160: 1233-1241.
35. Thomas N, Tharyan P. Prevalence of obsessive-compulsive symptoms in drug-free patients with schizophrenia. Indian J Psychiatry 2005; 47 (Suppl):37-43.
36. Tibbo P, Kroetsch M, Chue P, et al. Obsessive-compulsive disorder in schizophrenia. J Psychiatr Res 2000; 34:139-146.
37. Tibbo P, Warneke L. Obsessive-compulsive disorder in schizophrenia: epidemiologic and biologic overlap. J Psychiatry Neurosci 1999; 24: 15-24.
39. Wehmeier PM, Barth N, Remschmidt H. Induced delusional disorder. A review of the concept and an unusual case of folie a famille. Psychopathology 2003; 36:37-45
40. White T, Ho BC, Ward J, et al. Neuropsychological performance in first episode adolescents with schizophrenia: a comparison with first episode adults and adolescent control subjects. Biol Psychiatry 2006; 60:463-471.
41. Whitehead C, Moss S, Cardno A, et al. Antidepressants for people with both schizophrenia and depression. Cochrane Database Syst Rev 2000; 2:CD002305
42. Willem Van der Does AJ, Dingemans PM, Linszen DH, et al. Dimensions and subtypes of recent-onset schizophrenia. A longitudinal analysis. J Nerv Ment Dis 1995; 183:681-687
ICD-11: DRAFT PROPOSAL FOR CHANGES IN THE ‘MOOD DISORDERS SECTION
Atul Ambekar, MD, Raman Deep MD, Rajat Ray, MD
1. Addition of following specifiers to an episode of the disorder to describe the onset, clinical features and course:
1.1. Chronic – if the duration exceeds two years
1.2. In Partial/ Full remission
1.3. With Post-partum onset
1.4. With Melancholic symptoms
1.5. With Catatonic Symptoms
1.6. With Onset in childhood and adolescence
2. Addition of following specifiers for the course of recurrent episodes:
2.1. With / without complete inter-episodic recovery
2.2. With Seasonal Pattern
2.3. With Rapid cycling
2.4. With Onset in childhood and adolescence
3. The term ‘somatic syndrome’ to describe a depressive episode should be replaced by the term ‘melancholic symptoms.’
4. Since, as per ICD-10, “…the term mood is given preference over affective as mood represents a more enduring mood state…” the term ‘Bipolar affective disorders’ should be replaced by the term ‘Bipolar Mood disorders.’
5. The presence of following symptoms should be acknowledged to be a part of presentation of depressive disorders in the text description in a more detailed and lucid manner:
5.1. Somatic (i.e. physical or somatoform) symptoms, at times, have been reported to be the only presenting symptom of depression (i.e. ‘somatised depression’) rather than the more common psychological symptoms.
5.2. Anger attacks can also be a part of presenting symptoms of depression.
6. There seems to be a requirement for separate coding of recurrent mania under bipolar disorders rather than classifying it as an inclusion term in ‘Other bipolar affective disorders’ (F31.8).
7. Depressive episode(s) with hypomania (i.e. Bipolar-II disorder) merits a separate code rather than classifying it as an inclusion term in ‘Other bipolar affective disorders’ (F31.8).
Supporting evidence for proposed changes
We began by conducting a comprehensive search (comprising both electronic and manual search) of the studies on mood disorders published in the Indian psychiatric/mental health journals. Attempt was also made to include the psychiatric research published in Indian medical/social journals (i.e. journals not dedicated to psychiatry/mental health alone). This review of the available Indian literature was conducted focusing on studies published between years 1992 (i.e. when ICD-10 was published) till date. We could locate 190 articles on mood disorders of which 161 had been published in Indian journals and 29 in International journals.
All the research articles were color-coded and divided into five broad categories for diagnostic validity as per Robins and Guze criteria (i.e. clinical description, family studies, laboratory studies, follow-up studies, and delimitation from other disorders: Table 1).
TABLE 1: Number of publications according to categories for diagnostic validity
ICD-10 sub category
from other disorders*
Bipolar affective disorder
Recurrent depressive disorder
Persistent mood disorder
Publications include: Original research articles/reviews/case reports/letter to editors/posters
*As per Robin and Guze Criteria (loosely applied) - ‘’Best fit’’
#Total is more than 100 % (i.e. 190 articles) as some articles could be classified in more than 1 category
The evidence was weighed for and against the diagnostic validity of a particular entity in mood disorders category and discussed among the members of team. We conducted a more diligent search in Indian and international literature for the following areas: (1) data inadequately represented in the Indian literature; (2) entities that were controversial in terms of their nosological status; (3) new categories/criteria/specifiers which could be potential candidate for inclusion: and (4) of interest as reflected in recent literature. References to publications from other countries have been made in the following situations: (1) as a primary reference where Indian studies were non-existent; (2) as supplement to the available Indian studies; and (3) to provide for an international perspective on controversial/debatable areas.
I. Addition of following specifiers to an episode of the disorder to describe the onset, clinical features and course:
Chronic mania: Clinical description of chronic mania dates back to the 19th century when Kraepelin routinely described such cases in his presentations. More recently, chronic mania has been defined as presence of symptoms in excess of 2 years (Perugi et al, 1998). Prolonged continuation of manic episode has been reported from India as well, mainly in the form of case-reports. A manic episode lasting approximately five decades has been reported (Mendhekar et al, 2004). In the international literature, the prevalence of chronic mania is estimated to be around 6-13%, due to the variable criteria sets chosen to describe the condition(Perugi et al,1998; Malhi et al, 2001). Chronic mania differs partially in its psychopathological presentation from acute mania. While, disturbances in the biological functions such as sleep and appetite are hallmark of an acute episode, chronic mania is devoid of the psychomotor and vegetative symptoms seen in the acute episode. Though, schizophrenia is a potential differential diagnosis in such cases, the absence of the flattening of affect and gross thought abnormality differentiates chronic mania from schizophrenia. At times, it becomes very difficult to diagnose a case of mania because of “personality style of the patient superimposed on a cyclothymic or hyperthymic temperament” (Mendhekar et al, 2004). Though not many follow-up studies are available, experts suggest that chronic mania is a poor responder to the conventional treatment for the mood disorders namely the mood stabilizers and neuroleptics.
Chronic depression: Studies examining depressive disorders have reported a relatively high frequency of cases with a chronic course. This is especially true for elderly patients, females, and those with comorbid illnesses (medical/psychiatric/substance use) (McIntyre and O'Donovan, 2004).
1.2 In Partial/ Full remission
Mania in partial remission: Generally a manic episode is short lasting and its mean duration is reported to be three months. However, a few case reports from India suggest that some episode do not remit completely. For instance, Chawla and colleagues (2006) reported the case with five episodes over past 22 years with persistent mood congruent delusion in the inter-episodic period. Characterization of the ‘inter-episodic’ period in such cases by the specifier “in partial remission” would benefit communication between professionals as well as management of the case.
Depression in partial remission: Incomplete remission from depression is quite common, with approximately one third of patients continuing to have residual depression (Burt, 2004). The presence of residual symptomatology after an episode of depression is associated with an increased risk of short-term relapse and a chronic course; a higher risk of suicide attempts; poor social functioning; higher comorbidity and poor outcome of comorbid illnesses; and increased social and economic costs (Kennedy and Paykel, 2004).
1.3 With post-partum onset
The Satra Bruk classification workshop held in Sweden in 1999 proposed the introduction of a specifier for post partum onset (defined as onset within three months of delivery) (Elliott, 2000).
Depression with post-partum onset: An average general populationprevalence figure of 13% has been reported for postpartum depression (O’Hara and Swain,1996).In the Indian context, Patel et al (2002) reported prevalence of postpartum depression in 23% of mothers at 6-8 weeks of childbirth; 78% of these patientshad had clinically substantial psychological morbidity duringthe antenatal period. More than one-half of the patients remainedill at 6 months after delivery. Incidence has been found to be 16% and 10% in early and late post-partum period, respectively, in another study (Sood and Sood, 2003). Economic deprivation and poor marital relationships were important risk factors for occurrence and chronicity of depression. The gender of child was also found to be a determinant of postnatal depression, a reflection of the cultural preference for a male child over a female one (Patel et al, 2002). In developedcountries, the risk factors for postnatal depression are pasthistory of psychological disorder, psychological disorder duringpregnancy, low socioeconomic status, complicated delivery, andpoor marital relationship. Additionally, post-partum depression has been found to have a substantial risk of recurrence in subsequent post-partum periods (30%-50%). Women in developing countries whosepopulations have low incomes face considerable inequalities,ranging from fewer opportunities in education and employmentto less control over personal decisions, such as the use ofcontraception to plan pregnancies. Thus women in developing countries have all the risk-factors for post-natal depression in abundance, making the specification of ‘onset during postpartum period’ even more important in such contexts.
Post-partum mania: Despite diverse presentations, there is strong evidence fromclinical, outcome, and genetic studies for a close relationship between puerperal psychosis and bipolar disorder (Dorothy et al, 2006). Women who have suffered an episode of puerperal psychosis remainat high risk of developing further affective episodes (Davidson and Robertson,1985),and puerperal episodes of illness follow 20% to 30% of birthsto women with a history of bipolar disorder or affective psychosis(Kendell,1987). Family studies of puerperal psychosis consistently demonstratefamilial aggregation of psychiatric (predominantly affective)disorder, with morbidity risks for first-degree relatives inthe range of 10% to 50% (Platz and Kendell, 1988; Dean, 1989). The findingof higher rates of affective disorder in relatives of puerperalprobands suggests a major overlap in the familial factors predisposingto puerperal psychosis and bipolar disorder.
1.4 With melancholic symptoms
A number of attempts have been made by various researchers to define a "biological symptomatic profile" of depression by means of genetic, biological and therapeutic studies (Staner, 1988; Rush and Weissenburger, 1994; Schotte, 1997; Parker, 2000; Hill and Gorzalka, 2005). Psychomotor and appetite disturbances, early awakening, anhedonia and psychotic symptoms seem more likely to reflect this biological dysfunction in depression (Staner, 1988). Studies have supported the construct validity of the DSM-III melancholic subtype of major depression. Schotte (1997) has proposed the integrated threshold model:
(i) Melancholic and non-melancholic depression may be regarded as continuous classes in terms of overall severity of depression; and
(ii) Both groups form discrete categories with regard to the melancholic symptoms, which emerge as the severity of depression increases.
Melancholic symptom features are predictive of a positive response to ECT and to tricyclic antidepressants in the severely ill. Key features include psychomotor retardation, unreactive mood, pervasive anhedonia, and distinct quality of mood. Melancholic features are associated with shorter REM latency and/or nonsuppression of cortisol during the dexamethasone suppression test. Depressive episodes that are not melancholic may take on melancholic features with repetition and passage of time in some individuals. Once melancholic features are present, it is unclear whether they repeat across subsequent episodes. Melancholic features are not uniquely associated with a positive family history of depression per se, but they may be especially associated with a family history of severe depression (Rush and Weissenburger, 1994). Bipolar depression appears to be more likely to be 'melancholic' in type, thus providing an indirect strategy for the clinical definition of melancholia (Parker, 2000)
A recent study has pointed towards some similarities between melancholic depression and an endocannabinoid deficiency state. Interestingly, endocannabinoid activity is down-regulated by chronic stress and possibly increased by some antidepressant regimens. It has been proposed that an endocannabinoid deficiency may underlie some of the symptoms of melancholic depression, and that enhancement of this system may ultimately be a novel form of pharmacotherapy for treatment-resistant depression (Hill and Gorzalka, 2005).
While, the validity of the specification of melancholic symptoms in a depressive episode has been largely established (Rush and Weissenburger, 1994), we are raising a semantic issue here. In the current system (ICD-10) the symptoms historically regarded as ‘melancholic’ are called ‘somatic’. We propose that the term ‘melancholic' should be preferred as it is specific to depression, while the term ‘somatic’ leads to confusion with ‘somatoform symptoms / disorders.’
1.5 With catatonic symptoms
Approximately 8-14% of patients with psychiatric illness have catatonia as a presenting feature (Pommepuy and Januel, 2002).
Depression with catatonia: Depressed patients with catatonia have been found to be older, to have a significantly higher frequency of major depression, to have more severe cognitive impairments and more severe deficits in activities of daily living than depressed non-catatonic patients (Starkstein et al, 1996).
Mania with catatonia: Manic patients with catatonia are reported to have more mixed episodes, more severe manic symptoms, more general psychopathology, higher co-morbidity, longer hospitalization, and lower Global Assessment of Functioning (GAF) scores than the noncatatonic patients. Thus, the presence of catatonic symptoms in mania is regarded as a marker of a worse course and outcome (Braunig et al, 1998).
1.6 With onset in childhood and adolescence
An increasing amount of research has challenged the traditional view that juvenile-onset bipolar disorder is a rare condition. The cumulative incidence of bipolar disorder in childhood and adolescence may equal the 1% rate in adults (Lewinsohn et al, 1995). Available Western studies suggest that childhood/ adolescent onset bipolar disorder have a greater prevalence of chronicity, psychosis, mixed and atypical features, high incidence of rapid cycling, and poor response to mood stabilizers (Geller et al, 2004; Wozniak, 2005). However, studies from India report a high rate of recovery and low chronicity (Rajeev et al, 2003; Jairam, 2004).
We support the continued inclusion of mood disorders within ‘general psychiatric’ disorder categories rather than among F90-F98 (…disorders with onset usually occurring in childhood and adolescence). However, we recommend that onset in childhood and adolescence be specified to ensure required clinical and research attention towards these conditions.
II. Addition of following specifiers for the course of recurrent episodes:
2.1 Those with / without complete inter-episodic recovery
Traditionally, bipolar disorder has been considered as an episodic disorder with good inter-episode recovery. More recent studies have shown that in some cases complete recovery may not be achieved and subsyndromal symptoms persist in the inter-episodic period. The notion of complete interepisodic recovery is challenged further by studies documenting that certain patients demonstrate social, marital, occupational and cognitive dysfunction, even when euthymic (Watson and Young, 2001).
In line with our earlier recommendation for a specifier for complete/ incomplete remission of single ‘episode,’ we suggest that a provision should be made to specify whether the lifetime course of a recurrent disorder is characterised by complete/incomplete interepisodic recovery.
2.2. With seasonal pattern
There are a few studies on seasonal pattern of mood disorders from India. The available evidence suggests that:
- Certain mood disorder patients do exhibit seasonal pattern in terms of onset of their mood episodes
- Seasonality of mood episodes among Indian patients may exhibit a ‘reverse pattern’ to that suggested by western studies (i.e. summer depression and/or winter mania)
A significant proportion (22%) of bipolar affective disorder patients has been found to have seasonal pattern (Avasthi et al, 1996). Further, patients with seasonal pattern have been reported to have episodes mostly in summer and winter, longer episode duration and more psychotic features as compared to patients with no seasonal pattern. There also appears to be a genetic propensity present to mood variations in relation to environmental temperature (Fernandes et al, 1996).
The studies on seasonal pattern of mood disorders from India have been mainly limited to one group of authors. If, indeed, the concept of seasonal pattern (more so, the reverse seasonal pattern) of mood disorders is to be validated, there is a need to replicate these findings in other centres of India. A provision in the classificatory system for separately coding the specifier of seasonal pattern will stimulate further research in this area.
2.3 With rapid cycling
Rapid cycling among patients with bipolar affective disorders is important because of its implications for long-term prognosis and for the use of antidepressants. Indian literature about rapid cycling is mainly restricted to case-reports (Garg et al, 1998). International literature (Bauer et al, 1994) suggests that about 15-20% of bipolar disorders have a course which could be characterised as ‘rapid cycling’ (defined as four or more mood episodes in a year). Rapid cycling is associated with female gender, substantial depressive morbidity, high risk for serious suicide attempts, poor response to lithium and fair response to calcium channel blockers (Frye and Altshuler, 1997; Coryell et al, 2003). Some studies suggest that rapid cycling (spontaneous or induced) once established, becomes for many years a stable rhythm in a substantial proportion of patients (Koukopoulos A, et al, 2003). However, other studies examining data related to phenomenology, family history, and long-term outcome do not support rapid cycling as a separate entity but as a temporary complicated clinical state (Kilzieh and Akiskal, 1999)
We propose that patients with a course characterized by four or more episodes in a year for at least two consecutive years should be specified as having ‘rapid cycling.’ The duration criterion (two years) is in line with that currently employed for other chronic disorders such as dysthymia and cyclothymia as suggested by certain authors (Koukopoulos et al, 2003).
III. The term ‘somatic syndrome’ should be replaced by ‘melancholic symptoms’.
As discussed in the recommendation number 1.4, the term ‘somatic syndrome’ does not include somatic (i.e. physical) symptoms of depression. The symptoms described are more commonly referred to as melancholic symptoms in the existing literature. In order to avoid confusion with somatic symptoms and in line with the available research, we recommend the change of terminology from ‘somatic’ to ‘melancholic’.
IV. Since, “the term mood is given preference over affective in ICD-10 as mood represents a more enduring mood state”, the term ‘bipolar affective disorders’ can be replaced by ‘bipolar mood disorders’.
The ICD prefers the use of the term mood over affective as mood represents a more enduring emotional state in contrast to affect which represents a feeling tone in response to present events. The F30-39 category has been named mood disorders in ICD-10. Following the same rationale, the term bipolar affective disorder can be replaced by bipolar mood disorder.
V. The presence of following symptoms should be acknowledged to be a part of presentation of depressive disorders in the text description in a more detailed and lucid manner:
5.1 Somatic (i.e. physical or somatoform) symptoms, at times, have been reported to be the only presenting symptom of depression (i.e. ‘somatised depression’) rather than the more common psychological symptoms.
Somatic (i.e. physical or somatoform) symptoms of depression are common in manycountries, but their frequency varies depending on how somatizationis defined. In part, this variation may also reflect characteristics of physiciansand health care systems, as well as cultural differences amongpatients.
In some Western as well as Indian studies, a majority of patients with depression present with somatic (i.e. physical or somatoform) symptoms but acknowledgepsychological symptoms (such as depressed mood or guilt) when they were specifically asked about them (Goldberg & Bridges, 1988; Raguram et al, 2001). Even more importantly, the largest study to examine the relation between somatic symptoms and depression (which utilized data from World Health Organization's studyof psychological problems in general health care - 25, 916 patients from 15 primarycare centres in 14 countries in 5 continents) found that somatic symptoms are often the only or predominant presenting complaints in some patients with depressive illnesses (Simon et al, 1999). In this study, of the 5447patients who underwent a structured assessment for depressive and somatoform disorders, 1146 met the criteria for major depression. Among them, 69% reported only somatic symptoms (Simon et al, 1999).
The personal significance and meaning of the symptoms are shaped by cultural notions concerning the human body in health and in sickness. Although both depressive and somatic symptoms were distressing to Indian patients, qualitative analysis showed that depressive symptoms, unlike somatic symptoms, were construed as socially disadvantageous (Raguram et al, 2001).
5.2 Anger attacks can also be a part of presenting symptoms of depression.
Anger attacks have been proposed as a specific form of anger in depression. They are characterized by a rapid onset of intense anger and a crescendo of autonomic arousal occurring in response to trivial provocations. They resemble panic attacks but lack the predominant affects of fear and anxiety associated with panic attacks. They typically occur in situations in which an individual feels emotionally trapped and experiences outbursts of anger that are later described by the patient as being uncharacteristic and inappropriate to the situation at hand. The prevalence of anger attacks in depressed patients is approximately 30% to 40 % (Fava and Rosenbaum, 1999). Though the presence or absence of hostility, anger and aggression in depression has been a matter of controversy, anger attacks have been found to occur more often in depressed patients in comparison to healthy controls. Some studies have reported that depressed patients with anger attacks differ from those without such attacks in terms of clinical profile, comorbid personality disorders and certain biological variables. Serotonergic dysfunction may characterize this distinct subtype of depression - depression with anger attacks (Painuly et al, 2005). Fraquas et al (2006) reported that serum levels of homocysteine were positively correlated with length of current major depressive episode in patients with anger attacks but not in those without anger attacks. The attacks have been found to disappear in 53% to 71% of depressed patients treated with fluoxetine, sertraline, or imipramine (Fava and Rosenbaum, 1999). Significance of aggression as a gender-specific diagnostic criterion for depression has been proposed as ‘male depressive syndrome’ (Winkler, 2005).
VI. There seems to be a requirement for separate coding of recurrent mania under bipolar disorders rather than classifying it as an inclusion term in ‘other bipolar affective disorders’ (F31.8).
In the current edition of ICD, recurrent mania finds mention as an inclusion term under other bipolar affective disorders (31.8). The previous edition, ICD-9, had a separate category called recurrent mania. However, there has been persistent debate about the same. Avasthi et al (1996) reported that recurrent mania was by no means uncommon in India (6.5%). A recent review examining the nosological status and validity of recurrent unipolar mania (Harish et al 2005) also concluded that unipolar or recurrent mania occurs in sizeable number of patients (5%-25%). Unipolar mania exhibit consistent differences from bipolar mania in clinical, course and outcome, laboratory and family studies.
We recommend that, recurrent mania should be coded separately under the broad category of bipolar affective disorders rather than as an inclusion term with ‘other bipolar disorders’.
VII. Depressive episode(s) with hypomania (i.e. bipolar-II disorder) merits a separate code rather than being classified as an inclusion term in ‘other bipolar affective disorders’ (F31.8)
There are few Indian data on depressive episode(s) with hypomania. Klerman (1989) and Akiskal (1999) labelled recurrent depression with hypomania as Bipolar affective disorder (BPAD)-II in their classifications of bipolar spectrum disorders. Bipolar II disorder is also recognized as adistinct subtype in the DSM-IV (1994) classification. The life-time prevalence rates of both bipolar I and bipolarII disorders have been estimated at 0.6%, giving a combinedfigure of 1.2% (Weissman and Myers, 1978). A number of recent studies have helped in establishing bipolar-II disorder as a separate entity from BPAD-I disorder as well as recurrent depressive disorder. The summary of these studies is presented below:
Clinical description: Goodwin and Jamison (1990) have suggested that sub-syndromal bipolarity appears at a meanage of 14 years, while the initial episode of bipolar I disorder occurs at a median age of 18 years and bipolar II disorderat a median age of 21 years. Majority of available studies conclude that bipolar II disorder has an intermediate age of onset as compared to bipolar I or unipolar disorder.
The gender ratio of bipolar II patients tended to favour women having this disorder as compared to bipolar I patients where the gender ratio was fairly equal (Dunner, 1993). Clinical differences have been found in some studies comparing females and males suffering from BPAD-II. Females, as opposed to males, had significantly lower age at onset, more axis I co-morbidity, atypical depressions, intra–depression hypomanic symptoms (i.e., mixed depression), and family history of suicidal behavior. Females had more sadness, loss of energy, loss of interest, and suicidal ideas (Benazzi, 2005). Differences were found mainly on the depressive pole of the disorder and not of great magnitude but the authors concluded that these findings merit further attention.
When compared with Bipolar-I and unipolar disorders, researchhas found certain distinct differences in rates of recovery, clinical features and number of episodes. Rapid cycling was noted among bipolar I and bipolar II (but not unipolar) patients. Patients with seasonal affective disorder were more likely to be bipolar II than unipolar. Clinically depressed bipolar I patients evidenced psychomotor retardation; whereas, depressed bipolar II and unipolar patients either had psychomotor agitation or psychomotor retardation. One clinical feature that has consistently appeared to differentiate patients with bipolar II disorder from those with bipolar Idisorder or unipolar depression is the risk of suicide, whichappears to be elevated in this group (Bourgeois 1997). A history of suicide attempt was highest among bipolar II as compared to bipolar I and unipolar depressed patients (Dunner 1993). This may be related to the fact that the diagnosisis often missed, and consequently patients are ineffectivelytreated (MacQueen and Young, 2001). Also, high rates of comorbid disorders have been reported among patientswith bipolar II disorder (Savino et al, 1993; Pini et al, 1997), including substance abuseor dependence, anxiety disorders, and personality disorders.
Family studies: distinct familial inheritancefor bipolar II disorder has been suggested (Cassano et al, 1999). A tendencytowards a mild expression of mania may run in families (Kato et al, 2000). A summation of the large-scale studies where relatives of bipolar I, bipolar II, and unipolar patients were interviewed to determine their diagnosis revealed an elevated morbid risk for mania (bipolar I disorder) in relatives of bipolar I patients and bipolar II patients, as compared to relatives of unipolar patients and an elevated morbid risk for bipolar II disorder in relatives of bipolar II probands. These latter data suggested that bipolar II might "breed true." The family study data supported the notion that bipolar II was more similar to bipolar I than unipolar disorder but that bipolar II may be (on a familial basis) somewhat distinct from both bipolar I and unipolar disorder.
Laboratory studies: Preliminary imaging (Altshuler et al, 1995) and biochemical(Kato et al, 2000) studies that have separately examined subjects with bipolarI and bipolar II disorders have found differences in these groupsthat further support the view of bipolar II disorder as a discretediagnostic entity. Periventricular hyperintensities were found to be more common in bipolar I patients (62%) than in bipolar II patients (38%) and normal comparison subjects (30%; Altshuler et al, 1995). The rate of 5178C genotype was significantly higher in patients with bipolar disorder (64.8%, P < 0.05) compared with controls (53.2%) when paternally transmitted cases were excluded. This effect was more prominent in patients with bipolar II disorder (75.6%, P < 0.02 to controls). Bipolar II patients with 5178A genotype without family history had significantly later age at onset (56.0 ±14.7 years, P < 0.05) than other bipolar patients (Kato et al 2000). The major difficulty in assessing the review of the biological studies was the fact that no biological study consistently predicted discrimination of bipolar from unipolar patients, and many of the studies suffered from small sample size and lack of replication.
Some studies have found differences betweenbipolar I and bipolar II disorders on magnetic resonance imaging (MRI)and on the presence of vascular abnormalities, includingRaynaud's phenomenon, migraine and ‘migraine equivalents’(Altshuler et al, 1995).
Delimitation from other disorders: the conceptof a trichotomy of mood disorders—bipolar I, bipolar II,and unipolar major depression—has been supported by studies that found distinct patterns of symptoms (as discussed above) and distinct familial inheritancefor bipolar II disorder (Cassano et al, 1999). Researchhas found distinct differences in rates of recovery,clinical features, and number of episodes. Preliminary imaging (Altshuler et al, 1995) and biochemical (Kato, 2000) studies that have separately examined subjects with bipolarI and bipolar II disorders have found differences in these groupsthat further support the view of bipolar II disorder as a discretediagnostic entity. The results of some studies support the notion that bipolarII disorder is intermediate between unipolar depression andbipolar I disorder with respect to illness course.
Follow-up studies: bipolar II disorder appears to be diagnostically stable (Angst, 1986; Coryell, 1996).A variety of studies suggest that the probability of patients with bipolar II disorderdeveloping a manic episode was about 4% to 17% over up to 40 years of follow-up, with many of the studies supporting low rates of diagnostic conversion from bipolar II to bipolar I (Dunner and Tay, 1993; Coryell et al, 1995). Studies suggest that the number of episodes of depression maybe a stronger predictor of psychosocial outcome than mania in Bipolar II disorder (MacQueen et al, 2000). Preliminary studies suggest that the newer anticonvulsants maybe of benefit for this group.
There seems to be overwhelming evidence for existence of a valid diagnostic entity, characterised by depressive episode(s) with hypomania, which has been labelled “Bipolar-II disorder” in research studies as well as in DSM-IV. The ICD-10 at present mentions it as an inclusion term under ‘other bipolar disorders’ (F31.8). Over past one-and-half decades since the current version of ICD came into being, even more research evidence has been generated pointing towards diagnostic validity of this entity. Hence, in our opinion it is now time that this entity be accorded a distinct status of its own.
For the purpose of proposing modifications to the classification of mood disorders in the ICD-11, we have restricted ourselves to only those recommendations, (a) which have some evidence of validity in the existing literature, and (b) which have potential utility for the clinicians and researchers if incorporated. While the strength of the evidence-base varies from one recommendation to another, in terms of utility, we believe all of them to be quite useful. For many of our recommendations, we have deliberately not gone into details of definition / criteria. We believe that these definitions and criteria could only be refined, once the system provides for coding them. Till this consensus about definitions is achieved, we suggest that drafters for ICD-11 incorporate these recommendations with the most likely acceptable and/or flexible criteria, leaving some room for clinicians and researchers.
· Akiskal HS, Pinto O. The evolving bipolar spectrum. Prototypes I, II, III, and IV. Psychiatr Clin North Am 1999; 22:517-534.
· Altshuler LL, Curran JG, Hauser P, et al. T2 hyper intensities in bipolar disorder: magnetic resonance imaging comparison and literature meta-analysis. Am J Psychiatry 1995; 152:1139-1144.
· Angst J. The course of major depression, atypical bipolar disorder, and bipolar disorder, in Hippius H (Ed): New Results in Depression Research. Berlin: Springer-Verlag 1986.
· American Psychiatric Association. DSM IV: Diagnostic and Statistical - Manual, 4th Edition. Washington DC: APA 1994.
· Avasthi A, Sharma A, Gupta N Seasonality and unipolar recurrent mania: preliminary findings from a retrospective study. Indian J Psychiatry 1996; 38: 236-239.
· Bauer MS, Calabrese JR, Dunner DL, et al. Multi-site data reanalysis: validity of rapid cycling as a course modifier for bipolar disorder in DSM-IV. Am J Psychiatry 1994; 151, 506 -515.
· Benazzi, F. A comparison of the age of onset of bipolar I and bipolar II outpatients. J Affect Disord 1999; 54:249-253.
· Benazzi F. Gender differences in bipolar–II disorder. Eur Arch Psychiatr Neurosci 2005; 256: 67-71
· Bourgeois ML, Hantouche E, Akiskal HS. The EPIMAN and EPIDEP French studies of bipolarity: preliminary results. J Bipolar Disord 1997; 1:13-19.
· Braunig P, Kruger S, Shugar G, et al. Prevalence and clinical significance of catatonic symptoms in mania. Compr Psychiatry 1998; 39(1):35-46.
· Burt VK. Plotting the course to remission: the search for better outcomes in the treatment of depression. J Clin Psychiatry 2004; 65: S12-S20.
· Cassano GB, Dell' Osso L, Frank E, et al. The bipolar spectrum: a clinical reality in search of diagnostic criteria and an assessment methodology. J Affect Disord 1999; 54:319-328.
· Chawla JM, Balhara YS, Mohan I, Sagar R. Chronic mania: an unexpectedly long episode? Indian J Med Sci 2006, 60:199-201.
· Coryell W. Bipolar II disorder: a progress report. J Affect Disord 1996; 41:159 -162.
· Coryell W, Solomon D, Turvey C. The long-term course of rapid-cycling bipolar disorder. Arch Gen Psychiatry 2003; 60:914-924.
· Davidson J, Robertson E. A follow-up study of postpartum illness, 1946–1978. Acta Psychiatr Scand 1985; 71:451–457.
· Dorothy S, Anthony JR, Wisner LW, et al. A review of post-partum psychosis. J Women Health 2006; 15:352-364.
· Dunner DL. A review of the diagnostic status of "bipolar II" for the DSM-IV work group on mood disorders. Depression 1993; 1:2-10.
· Dunner DL, Fieve RR. Clinical factors in lithium carbonate prophylaxis failure. Arch Gen Psychiatry 1974; 30:229-231.
· Dunner DL, Tay LK. Diagnostic reliability of the history of hypomania in bipolar II patients and patients with major depression. Compr Psychiatry 1993; 34:303-307.
· Elliott SA. Report on the Satra Bruk workshop on classification of postnatal mental disorders. Arch Women Ment Health 2000; 3:27–33.
· Fernandes P, Avasthi A., Santosh PJ. Familial reverse seasonal affective disorder: a case report. Indian J Psychiatry 1996; 38: ,257-259
· Fraquas RJ, Papakoustas GI, Mischoulon D, et al. Anger attacks in major depressive disorder and serum levels of homocysteine. Biol Psychiatry 2006; 60:270-274
· Frye MA, Altshuler LL. Selection of initial treatment for bipolar disorder manic phase, In Rush AJ, (Ed.): Mood Disorder, Systemic Medication management, Karger: Basel, Switzerland. (Reprinted : Panther publication private limited, Bangalore), 1997.
· Garg PD, Singh P, Kumar N, et al. Classic ultra-rapid cycler bipolar disorder: a case report. Indian J Psychiatry 1998; 40:389-391.
· Geller B,Tillman R, Craney JL, et al..Four year prospective outcome and natural history of mania in children with a prepubertal and early adolescent bipolar disorder phenotype. Arch Gen Psychiatry 2004; 61:459-467.
· Goldberg DP, Bridges K. Somatic presentations of psychiatric illness in primary care setting. J Psychosom Res 1988; 32:137-144.
· Goodwin FK, Jamison KR. Manic Depressive Illness. New York: Oxford University Press 1990.
· Harish T, Grover S, Basu D. Recurrent unipolar mania: does it warrant a separate nosological status? German J Psychiatry 2005; 8:8-15.
· Hill MN, Gorzalka BB. Is there a role for the endocannabinoid system in the etiology and treatment of melancholic depression? Behav Pharmacol 2005; 16:333-352.
· Jairam R, Srinath S, Girimaji S, et al. A prospective 4-5 year follow-up of juvenile onset bipolar disorder. Bipolar Disord 2004; 6:386-394.
· Kato T, Kunugi H, Nanko S, et al. Association of bipolar disorder with the 5178 polymorphism in mitochondrial DNA. Am J Med Genetics 2000; 96:182-186.
· Kendell RE, Chalmers JC, Platz C. Epidemiology of puerperal psychoses. Br J Psychiatry 1987; 150:662-673.
· Kennedy N, Paykel ES. Residual symptoms at remission from depression: impact on long-term outcome. J Affective Disorders 2004; 80:135-144.
· Kilzieh N, Akiskal HS. Rapid-cycling bipolar disorder. An overview of research and clinical experience. Psychiatr Clin North Am 1999; 22:585-607.
· Klerman GL. The spectrum of mania. Compr Psychiatry 1981; 22:11-20.
· Koukopoulos A, Sani G, Koukopoulos AE, et al. Duration and stability of the rapid-cycling course: a long-term personal follow-up of 109 patients. J Affective Disord 2003; 73:75-85.
· Lewinsohn PM., Klein DN, Seeley JR. Bipolar Disorders in a community sample of older adolescents: Prevalence, phenomenology, comorbidity and course. J Am Acad Child Adolesc Psychiatry 1995; 34:454-463.
· MacQueen GM, Young TL. Bipolar II disorder: symptoms, course, and response to treatment. Psychiatr Serv 2001; 52:358-361.
· MacQueen GM, Young LT, Joffe RT. Effect of number of episodes on well-being and functioning with bipolar disorder. Acta Psychiatr Scand 2000; 101:374-381.
· Malhi GS, Mitchell PB, Parker GB. Rediscovering chronic mania. Acta Psychiatr Scand 2001; 104:153-156.
· Mendhekar DN, Srivastav PK, Jiloha RC, et al. Chronic but not resistant mania: a case report. Acta Psychiatr Scand 2004; 109:147-149.
· O’Hara MW, Swain AM. Rates and risk of postpartum depression - a meta-analysis. Int Rev Psychiatry 1996; 8:37-54.
· Parker G. The nature of bipolar depression: implications for the definition of melancholia. J Affective Disord 2000; 59:217-224.
· Patel V, Rodrigues M, De Souza N. Gender, poverty and post natal depression: a study of mothers in Goa, India. Am J Psychiatry 2002; 159:43-47.
· Perugi G., Akiskal HS, Rossi L, et al. Chronic mania. Family history, prior course, clinical picture and social consequences. Br J Psychiatry 1998; 173:514-518.
· Pini S, Cassano GB, Simonini E, et al. Prevalence of anxiety disorders comorbidity in bipolar depression, unipolar depression, and dysthymia. J Affect Disord 1997; 42:145-153.
· Platz C, Kendell RE. A matched-control follow-up and family study of "puerperal psychosis." Br J Psychiatry 1988; 153:90–94.
· Pommepuy N, Januel D. Catatonia: resurgence of a concept. A review of the international literature. Encephale 2002; 28:481-492.
· Raguram R, Weiss MG, Keval H, et al. Cultural dimensions of clinical depression in Bangalore, India. Anthropol Med 2001; 8: 31-46.
· Rajeev J, Srinath S, Reddy YC, et al. The index manic episode in juvenile onset bipolar disorder. The pattern of recovery. Can J Psychiatry 2003; 48:42-45.
Robins E, Guze SB. Establishment of diagnostic validity in psychiatric illness: its application to schizophrenia. Am J Psychiatry 1970; 126:983–987.
· Rush AJ, Weissenburger JE. Melancholic symptom features and DSM-IV. Am J Psychiatry 1994; 151:489-498.
· Savino M, Perugi G, Simonini E, et al. Affective comorbidity in panic disorder: is there a bipolar connection? J Affect Disord 1993; 28:155-163.
· Schotte CK, Maes M, Cluydts R, et al. Cluster analytic validation of the DSM melancholic depression. The threshold model: integration of quantitative and qualitative distinctions between unipolar depressive subtypes. Psychiatr Res 1997; 71:181-19.5.
· Simon GE, VonKorff M, Piccinell M, et al. An international study of the relation between somatic symptoms and depression. NEJM 1999; 18:1329-1335.
· Sood M, Sood AK. Depression in pregnancy and postpartum period. Indian J Psychiatry 2003; 45:48-51.
· Staner L. Reevaluation of melancholic depression. Acta Psychiatr Bel 1988; 88: 313-340.
· Starkstein SE, Petracca A, Teson E, et al. Catatonia in depression: prevalence, clinical correlates, and validation of a scale. J Neurol Neurosurg Psychiatry 1996; 60:326-332.
· Watson S, Young AH. Bipolar disorders: new approaches to therapy. Expert Opin Pharmacotherapeutics 2001; 2:601-612.
· Weissman MM, Myers JK. Epidemiology of mental disorders: emerging trends in the United States. Arch Gen Psychiatry 1978; 35:705 -712.
· Winkler D, Pjrek E, Kasper S. Anger attacks in depression--evidence for a male depressive syndrome. Psychother Psychosom 2005; 74:303-307.
· Wozniak J. Recognizing and managing bipolar in children. J Clin.Psychiatry 2005; 66:18-23
Address for Correspondence: Dr. Atul Ambekar M.D., Assistant Professor, National Drug Dependence Treatment Centre, All India Institute of Medical Sciences.
ICD-11: DRAFT PROPOSAL FOR CHANGES IN THE ‘NEUROTIC, STRESS RELATED AND SOMATOFORM DISORDERS’ SECTION
R K Chadda, MD, Nand Kumar, MD
1. The generalized anxiety disorder category of ICD 11 should mentioned specific duration of the anxiety symptoms (preferably 3 months) to qualify for the diagnosis. .
2. The cases of OCD presenting with poor insight should be specified in the ICD-11.
3. Dhat syndrome should be excluded from culture bound syndromes and suitably be placed as a subtype of somatoform disorder and as a specifier for anxiety and depressive disorders.
Supporting evidence for proposed changes
We were assigned with the task of possible modifications in the classification and categorisation of the Neurotic, Stress related and Somatoform disorders grouped under the codes F 40 to F 49 in the ICD-10 (International Classification of Diseases, 10th revision) for proposed ICD 11. Our recommendations were formulated on the basis of a comprehensive search (both electronic and manual search) of Indian and international literature pertaining to anxiety, somatoform and stress related disorder. The literature search of Indian studies was focused on studies published since 1990 onwards. The collected evidence was presented to an expert-panel comprising of Faculty of Department of Psychiatry, All India Institute of Medical Sciences, New Delhi for thorough discussion. This final draft of the recommendations has been prepared based on the consensus of the expert panel. We have made an attempt to examine the validity of our recommendations in the light of Robins and Guze (1970) criteria viz. clinical description, family studies, follow-up studies, laboratory studies and delimitation from other disorders.
I. The generalized anxiety disorder category of ICD 11 should mention specific duration of the anxiety symptoms (preferably 3 months of duration) to qualify for the diagnosis.
In ICD 10, the essential feature of generalized anxiety disorder(GAD) is anxiety that is generalized and persistent and not restricted to any particular environmental circumstances. In addition the sufferer must have primary symptoms of anxiety on most days for at least several weeks at a time and usually for several months. The ICD 10 does not mention the exact duration of clinical features to diagnose the anxiety disorder.
The current diagnostic threshold for GAD raises questions about diagnostic requirements, such as whether 6-month duration and other psycho-physiological symptoms are needed for optimal identification of individuals who suffer from a clinically significant condition. Flint (2005) highlighted that in the community, period-prevalence of co morbidity of GAD with another psychiatric disorder is 4%, while the prevalence of pure GAD is only 1%. Early recognition of GAD is of paramount importance considering the co morbidity between GAD and other (especially depressive) disorders (Kessler 2001). Temporally primary GAD significantly predicts the subsequent onset of depression and other secondary disorders highlighting the importance of early intervention and treatment of primary GAD to prevent the subsequent onset of secondary anxiety and depression. Unfortunately, little is known about this possibility because, few people with pure GAD seek treatment. Specification of a duration criterion (preferably for 3 months) could help in early identification of the disorder (before the onset of co morbidity) and paving the way for collection of epidemiological data on pure GAD and also to develop outreach strategies that may correct this situation of low help-seeking in such cases.
Recent data from the US National Co morbidity Survey Replication (NCS-R), carried out during 2001-2003 also focused on the duration requirement for diagnosis of GAD using WHO Composite International Diagnostic Interview as assessment tool (Kessler 2005, Ruscio et al 2007). The report suggests that a large number of people suffer from a GAD-like syndrome with less than six months duration. The study also pointed out that cases of GAD with episodes of 1-5 months did not differ greatly from those with episodes of six or more months in onset, persistence, impairment, co-morbidity, parental GAD, or sociodemographic correlates.
II. The cases of OCD presenting with poor insight should be specified in the ICD 11
The past decade has seen tremendous strides in the knowledge about the cause, epidemiology, and treatment of obsessive compulsive disorder. Research on clinical characteristics of the disorder have focused on several areas, including identification of subtypes, the role of insight, and patterns of co morbidity (Aigner et al 2005, Bellino et al 2005).
Poor insight identifies a group of OCD patients with distinct clinical characteristics. InOCD with poor insight, patients generally fail to recognize that the obsessions or compulsions are excessive or unreasonable. In a study from India, Ravi Kishore et al (2004) evaluated 100 subjects with OCD (DSM-IV), who had received adequate drug treatment. They observed that 25% of the subjects had poor insight. Poor insight was associated with poor response to drug treatment, earlier age-at-onset, longer duration of illness, a greater number of obsessive-compulsive symptoms, more severe illness and higher co morbidity rate, particularly with major depression. In a study conducted in Bangalore (India), it was observed that poor insight was an important clinical predictor of poor response to treatment with SSRI (seen in 40% to 60% of the sample); (Shetti et al 2005). Similarly, Erzegovesi (2001) evaluated clinical variables that might influence the antiobsessional response to proserotonergic drugs in a sample of 159 patients with obsessive-compulsive disorder (OCD). It was observed that non responders (43.4%) had an earlier onset and a higher frequency of "poor insight" subtype and somatic obsessions in comparison to treatment responders.
Several studies have shown significant brain abnormalities in OCD patients (Aigner et al, 2005). A recent MRI study has shown that there are significantly more features suggestive of structural brain abnormalities in OCD patients with poor insight in comparison to OCD patients with good insight (Aigner et al 2005).
Literature on clinical and psychobiological distinctiveness of hoarding behaviour in OCD (Bellino 2005; Lochner at al 2005) also supports the need for a specifier related to insight in OCD. In OCD, hoarding is associated with poor insight, lack of resistance to the compulsion to hoard, poor treatment motivation, poor response to SSRIs in comparison to other OCD symptom dimensions. Further, at the level of biological and psychosocial determinants, pathological hoarding could be associated with schizophrenia, OCD, and tic disorders, possibly through dopaminergic mechanisms (Damecour & Charron 1998).
Co morbidity between OCD and schizophrenia is an area of emerging interest. Evidence shows that obsessions and compulsions are more common in patients with schizophrenia than was previously thought (Matsunaga et al 2000). Matsunaga et al (2000) further observed that OCD patients are less likely to have poor insight (PI), compared to patients with OCD and schizophrenia; however, OCD patients with poor insight showed a similar degree of functional impairment to that observed in patients with OCD and schizophrenia, pointing towards different outcomes in the two subgroups of OCD. The authors compared 78 OCD patients (primary interest [PI] group: 36% of the sample based on insight question of the Yale-Brown Obsessive-Compulsive Scale) with 20 schizophrenics with OCD (OCD+S). After a 6-month combination of clomipramine and cognitive-behavioral treatment, 14 of 25 OCD PI patients no longer fell in the PI category, which was associated with reduced OCD severity and depressive status. Schizotypal personality disorder (SPD) was more common in patients whose insight remained poor even after the treatment. Co morbid SPD in PI patients may be associated with worse prognosis.
III. Dhat syndrome should be excluded from culture bound syndromes and suitably be placed as a subtype of somatoform disorder and as a specifier for anxiety and depressive disorders.
The current classification systems ICD–10 (World Health Organization, 1992) does not give clear operational guidelines for the diagnosis of Dhat syndrome, possibly because it is considered a culture-bound syndrome. Once we label a clinical entity as culture bound, it runs the risk of exclusion from mainstream psychiatric classification with resultant lack of research and understanding (Chadda & Ahuja 1990; Bhatia & Malik 1991; Sumathipala et al 2004).
Dhat syndrome, originally described in India based on cultural beliefs of people, has been found to be highly prevalent in countries neighboring India such as Pakistan, Nepal, Myanmar, Sri Lanka and others (Sumathipala 2004). The patients of Dhat syndrome present with multiple somatic and psychological symptoms in the background of perceived loss of semen. This causal belief is not culture bound - male preoccupation with semen loss is universal and has been frequently associated with depression and anxiety. Similarly, in patients presenting with ‘Dhat syndrome,’ it is not uncommon on clinical exploration to find underlying neurotic and depressive disorders. Several authors have commented that Dhat syndrome should be considered as a culturally determined symptom of (or syndrome within) common disorders like depression, anxiety and somatisation rather than as a culture bound syndrome (Wig 1994). Various experts have questioned the validity of Dhat syndrome being viewed as a single neurotic disorder in ICD–10, where it is included under ‘other specific neurotic disorders’ (F48.8). Indeed, it is difficult to classify a high proportion of these cases as ‘pure’ Dhat (Chadda & Ahuja 1990; Chadda 1995; Bhatia & Malik 1991). Several Indian studies have recommended that Dhat syndrome should be integrated into existing rubrics of psychiatric classification in appropriate places (Chadda & Ahuja 1990; Bhatia & Malik 1991; Wig 1994). This might help to formulate the management of Dhat syndrome comprehensively on a biopsychosocial model depending upon its clinical presentation.
Fatigue is a common symptom in Dhat syndrome. Disorders with fatigue as the main symptom are often grouped together as functional somatic syndromes (Bhatia & Malik 1991; Barsky & Borus 1999). The basic cognitive formulation offered to explain these disorders is based on somatosensory amplification, misattribution and abnormal illness behaviour. These mechanisms seem to operate in patients with Dhat syndrome, who frequently make their first contact with departments other than psychiatry, for example urology, dermatology and general medicine, and are then referred to psychiatry. Also, partly as a result of arbitrary diagnostic guidelines, but also due to their own expectations and characteristics, patients are often dissatisfied with their treatment or causal explanations offered (Chadda & Ahuja 1990). These features suggest that patients without anxiety and depression should be placed within somatoform disorders.
· Robins E, Guze SB. Establishment of diagnostic validity in psychiatric illness: its application to schizophrenia. Am J Psychiatry 1970; 126:983-987.
· Malhotra HK, Wig NN. Dhat syndrome: a culture-bound sex neurosis of the orient. Arch Sexual Behav 1975; 4:519 -528.
· Chadda RK, Ahuja N. Dhat syndrome: a sex neurosis of the Indian subcontinent. Br J Psychiatry 1990; 156: 577-579
· Bhatia MS, Malik SC. Dhat syndrome: a useful diagnostic entity in Indian culture. Br J Psychiatry 1991; 159:691-695.
· World Health Organization. ICD-10 Classification of Mental and Behavioral Disorders. Geneva: WHO, 1992.
· Wig NN. An overview of cross-cultural and national issues in psychiatric classification. In Mezzich J, Honda Y, Kastrup M (Eds.). Psychiatric Diagnosis. NewYork: Springer1994: pp 3-10.
· Chadda RK. Dhat syndrome: is it a distinct clinical entity? A study of illness behavior characteristic. Acta Psychiatr Scand 1995; 91:136-139
· Mumford DB. The ‘Dhat syndrome’: a culturally determined symptom of depression? Acta Psychiatr Scand 1996; 94: 163-167.
· Damecour CL, Charron M Hoarding: a symptom, not a syndrome. J Clin Psychiatry 1998; 59: 267-272
· Kessler RC, Keller MB, Wittchen HU. The epidemiology of generalized anxiety disorder. Psychiatr Clin North Am 2001; 24:19-39.
· Erzegovesi S, Cavallini MC, Cavedini P, et al. Clinical predictors of drug response in obsessive-compulsive disorder. J Clin Psychopharmacology 2001; 21:488-492.
· Matsunaga H, Kiriike N, Matsui T, et al. Obsessive-compulsive disorder with poor insight. Compr Psychiatry 2002; 43: 150-157.
· Ravi Kishore V, Samar R, Janardhan Reddy YC, et al. Clinical characteristics and treatment response in poor and good insight obsessive-compulsive disorder. Eur Psychiatry 2004; 19: 202-208
· Sumathipala A, Siribaddana S, Bhugra D (2004) Culture bound syndromes: the story of dhat syndrome. Br J Psychiatry 2004; 184:200-209
· Aigner M, Zitterl W, Prayer D, et al. Magnetic resonance imaging in patients with obsessive-compulsive disorder with good versus poor insight. Psychiatry Res 2005; 140:173-179.
· Bellino S, Patria L, Ziero S, et al Clinical picture of obsessive-compulsive disorder with poor insight: a regression model. Psychiatry Res 2005; 136:223-231.
· Flint AJ. Generalized anxiety disorder in elderly patients: epidemiology, diagnosis and treatment options. Drugs Aging 2005; 22:101-114.
· Kessler RC, Brandenburg N, Lane M, et al. (2005) Re-thinking the duration requirement for generalized anxiety disorder: evidence from the national co morbidity survey replication. Psychol Med 2005; 35:1073-1082.
· Lochner C, Kinnear CJ, Hemmings SM, et al Hoarding in obsessive-compulsive disorder: clinical and genetic correlates. J Clin Psychiatry 2005; 66:1155-1160.
· Shetti CN, Reddy YC, Kandavel T, et al. Clinical predictors of drug nonresponse in obsessive-compulsive disorder. J Clin Psychiatry 2005; 66:1517-1523.
· Ruscio AM, Chiu WT, Roy Byrne P, et al. Broadening the definition of generalized anxiety disorder: effects on prevalence and association with other disorders in the national co morbidity survey replication. J Anxiety Disord 2007; 21:662-676
ICD-11: DRAFT PROPOSAL FOR CHANGES IN THE ‘BEHAVIOURAL SYNDROMES ASSOCIATED WITH PHYSIOLOGICAL DISTURBANCES AND PHYSICAL FACTORS’ SECTION
Anju Dhawan, MD, Tina Lal, MD
Proposals for the Category F50: Eating Disorders
1. Fat phobia may be used as a specifier of Anorexia Nervosa and Bulimia Nervosa, rather than as an essential criterion for these diagnoses as evidence suggests that fat phobia or dread for fat may not be the core psychopathology of anorexia nervosa and bulimia nervosa across cultures.
2. Amenorrhea may be used as a specifier of Anorexia Nervosa rather than as an essential criterion for this diagnosis as amenorrhea may not be present in all cases of Anorexia Nervosa at presentation. Anorexia Nervosa may be identified on the basis of substantial self-induced starvation to the extent of producing significant medical morbidity including amenorrhea.
3. Age and sex standardized BMI should be used as a criterion for anorexia nervosa.
Proposals for the Category F53: Mental and Behavioral Disorders associated with Perinatal Period
4. The title of the category should be changed from “mental and behavioral disorders associated with puerperium not elsewhere classified” to “mental and behavioral disorders associated with perinatal period not elsewhere classified” where the perinatal period is defined from conception till 3 months postpartum.
5. A specifier for onset in the perinatal period should be added to all disorders in mood, psychotic and adjustment disorder sections of ICD i.e, F20-29, F30-39, and F43.
6. The text description of ICD11 should mention the unique features that occur during the perinatal period like delusions involving the baby, risk of infanticide, disinterest in the infant, guilt because of dissonance between the mother's mood and society's expectation of happiness, and less than optimum development of a mother/infant relationship.
7. A rubric for disorders of mother-infant relationship should be created.
Measuring the validity of psychiatric diagnoses is still anunsolved problem. Yet, revisions of the Diagnostic and StatisticalManual of Mental Disorders and of chapter V of the InternationalClassification of Diseases are now under way, with the hopeof improving the validity of the current systems. In this article we present few proposals for changes in the section F50-59 of the ICD 10, on the basis of available Indian data, Western data and clinical experience with due emphasis on criteria laid down by Robins and Guze and Kendell.
Evidence for the Proposed Changes
F50: EATING DISORDERS
Recent years have seen increasing dissatisfaction with the criteria for eating disorders as they currently stand, which combined with good evidence that a large number of patients of all ages presenting for treatment fall into the ‘not otherwise specified’ or ‘atypical’ category, has resulted in lively debate and suggestions for improvement.
Anorexia nervosa (AN) and bulimia nervosa (BN) are currently considered as disorders confined to the Western culture. Although many influences have been noted as formative in the development of eating disorders, slimness has received most attention in recent years. The recent identification of eating disorders in non-Western societies and different subcultures within the Western world has led to suggestions that Western cultural ideals of slimness and beauty have infiltrated these societies (Nasser, 1994; Shroff & Thompson, 2004). The biomedical definition of anorexia nervosa and bulimia nervosa emphasizes fat phobia in the presentation of these disorders. However, evidence exists that suggests anorexia nervosa and bulimia nervosa can exist without the Western fear of fatness and that this culturally biased view may obscure health care professionals’ understanding of a patient’s own cultural reasons for self-starvation, and even hinder their recovery Khandelwal et al, 1995).
I. Fat phobia may be used as a specifier of Anorexia Nervosa and Bulimia Nervosa, rather than as an essential criterion for these diagnoses.
Anorexia nervosa was earlier believed to be limited to the white Caucasian population in the West. But, in the last two decades it has been identified with increasing frequency in non western societies (including Hong Kong, Taiwan, China, Malaysia, India, Pakistan and Singapore) as well as ethnic groups in the West.
Current diagnostic criteria for anorexia nervosa are largely influenced by western cultural concept of dread of fat and drive for thinness. The diagnostic criteria for anorexia nervosa as outlined by the ICD 10 include: ‘A body image distortion in the form of specific psychopathology whereby a dread of fatness persists as an intrusive overvalued idea and the patient imposes a low weight threshold on himself or herself’. The contemporary diagnostic criteria therefore de-emphasize ‘emaciation’ and emphasize ‘fat-phobia’. Nasser (1994) attributed the transculturality of anorexia nervosa to a globalization of ‘fat-phobia’ because of the emergence of a culturally shrunken world due to mass communication technology. Thus, Western researchers presume that incidences of anorexia nervosa in non-Western societies are replicas of the West. As a result, fat-phobia still remains the ‘core’ psychopathology underlying anorexia nervosa despite its presence in non-Western societies. Indeed, in the current diagnostic systems cases that do not meet the criterion of fat-phobia are labeled as atypical (eating disorder not otherwise specified (EDNOS) in DSM IV or atypical in ICD 10).
Dread of fatness as the core psychopathology does not explain all cases of anorexia nervosa especially in the non western societies. Several cases of anorexia nervosa without accompanying fat-phobia have been reported in different societies and cultures (China: Lee 1995, Lee 2001; India: Khandelwal and Saxena 1990, Khandelwal et al, 1995). Lee et al (2001) evaluated 48 consecutive patients with broadly defined anorexia nervosa with a self-report rationale for food refusal questionnaire. Two-thirds (32) of the patients expressed fat-phobia but one third (16) did not. Sensation of abdominal bloating and low appetite were among the other rationales given by patients for refusal to eat. Based on a qualitative analysis of 70 Chinese anorexia nervosa patients (who had all been examined by an experienced psychiatrist over a period of 12 years), Lee (1995) reported that 59% of patients did not express any fat-phobia throughout their illness. They differed from their fat-phobic counterparts only in that they were premorbidly slimmer and demonstrated no signs of bulimia, often considered a sign of fat phobia.
Khandelwal & Saxena (1990) and Khandelwal et al (1995) asserted that the presentation of eating disorders in India varied from the typical description of anorexia nervosa. Their female anorexic patients typically showed decreased appetite, excessive weight loss and amenorrhea but no fat-phobia or body image disturbance. Though finally diagnosed and treated as cases of eating disorder, they presented considerable difficulty in diagnosis according to current classification systems. They suggested that this variation was due to sociocultural factors, as Indian culture does not dictate slimness as a beauty ideal, and that there was not as much concern with body image as in the West.
Banks (1992) studied the case of two anorectic women from the Minneapolis–St Paul area of Minnesota. Both women were from conservative religious fundamentalist backgrounds and expressed their desire to reduce food intake through religious understanding about food, the body and sexuality, provided by their religious culture.
The western version of fat phobic anorexia nervosa has neglected the full metaphorical significance of self-starvation and, when applied in a cross-cultural context, may constitute a category fallacy. Most non-Western patients will fall into the atypical group by not fulfilling criteria of dread of fat. Lee (1995) suggested the use of more culturally sensitive diagnostic criteria. One of the diagnostic criterions suggested by Lee (1995) states that, ‘the patients use complaints (such as abdominal bloating or pain, loss of appetite, no hunger, distaste for food, fear of fatness, and/or “don’t know”) to resist attempts to make them increase food intake.’ Due to its seeming ubiquity in Western anorexics and the relative lack of cross-cultural studies on anorexia nervosa it may be too early to shed the concept of fat phobia entirely. Hence, fat phobia should be retained as a specifier of anorexia nervosa, rather than as an essential criterion.
II. Amenorrhea may be used as a specifier of Anorexia Nervosa rather than as an essential criterion for this diagnosis. Anorexia Nervosa may be identified on the basis of substantial self-induced starvation to the extent of producing significant medical morbidity including amenorrhea.
The criterion of amenorrhea was not required for the diagnosis of AN or BN by DSM-III although it was typically associated with anorexia nervosa. Amenorrhea was initially introduced as a criterion for several reasons (Garfinkel et al, 1996; Falk & Halmi, 1982). It was mentioned in historical reports of cases of anorexia nervosa in females. Also, it was hypothesized in more recent decades that anorexia was due to a primary impairment of hypothalamic functioning. Since then, however, it has been observed that amenorrhea generally follows loss of body weight and body fat. While, amenorrhea can occur is a minority of women before substantial weight loss (Theander, 1970), women with all the behavioral and psychopathological symptoms characteristics of anorexia nervosa including weight below the current diagnostic criterion may continue to menstruate. Also, there is no parallel criterion for males (Watson & Andersen, 2003). In a large community epidemiological survey, amenorrhoea did not discriminate between women with anorexia nervosa and women with all the features except amenorrhoea, across a number of relevant variables (Garfinkel et al, 1996).
ICD-10 differs from DSM-IV in being less stringent about the duration of amenorrhea and including some reference to change in male reproductive hormone function. There are some inherent limitations however in both of these diagnostic systems, as they impose a historically appreciated but perhaps overly specific medical criterion of amenorrhea. Current ICD-10 and DSM-IV anorexia nervosa category excludes substantial numbers of individuals who do not fulfill the monotheitic diagnostic criteria, because of the absence of amenorrhea, or because their final weight does not reach the required threshold, despite having clinically significant psychopathologies gravitating around preoccupation with body weight, food, and eating (Mitrany, 1992; Williamson et al 1992; Thaw et al, 2001). A diagnosis of eating disorder not otherwise specified (EDNOS), which is typically regarded as residual, is often misinterpreted as indicating problems of lesser clinical significance (Mitchell, 2005). Levels of distress, behavioral abnormalities, and cognitions similar to those associated with a full syndrome eating disorder often accompany EDNOS (Herzog et al, 1993; Thaw et al, 2001). In an effort to develop homogenous diagnostic groups that can have implications for treatment and course, care must be taken not to exclude people because of small variability in the symptom picture (Dancyger & Garfinkel, 1995).
It is therefore suggested that amenorrhea may be retained as a specifier of anorexia nervosa rather than as an essential criteria. Anorexia Nervosa may be identified on the basis of substantial self induced starvation to the extent of producing significant medical morbidity, which may include amenorrhea.
III. Age and sex standardized BMI should be used as a criterion for anorexia nervosa
The weight criterion for anorexia nervosa has also varied over the years. Regardless of the degree of actual weight loss, patients with anorexia nervosa - like symptoms appear to experience a high degree of physiological and psychological distress similar to full anorexia nervosa. For example, a patient may begin dieting at a healthy personal weight of 115% (of ideal) and loses to 90% of this weight, with significant functional medical consequences, but never reach the 85% criterion. In fact partial-syndrome anorexia appears to be more common than anorexia nervosa (King, 1989; Walters & Kendler, 1995). About 1.5% of young women have an eating disorder in full form (Dancyger & Garfinkel, 1995; Ghaderi & Scott, 2001) and another 7%–10% have some, but not all of the features of an eating disorder (Dancyger & Garfinkel, 1995). There is controversy as to whether eating disorders are qualitatively distinct or whether they exist along a continuum of dieting and weight concerns. Herzog et al (1993) followed up a group of 33 women with partial syndrome AN, BN, or both for an average of 41 months. At follow-up, 45% of the subjects had gone on to develop a full-criteria eating disorder, and as many as 82% had met full criteria for an eating disorder at least once during the course of their illness. Similarly, King (1989) observed a spectrum of eating disorder severities with some movement between diagnostic groupings over the 12–18 month follow-up in his study of women in a general practice. These findings suggest that a continuum of pathology may exist in which partial syndromes may reflect an earlier phase in the disorder and thus an artifact of the particular timing of the intake interview or assessment.
The primary weight criterion for a diagnosis of anorexia nervosa is a weight less than 85% of what is considered normal for that person’s age and height (DSM-IV). A body mass index (BMI) less than or equal to 17.5 kg/m2, which originated from the ICD-10 diagnostic criteria for research is not adjusted for age and sex. It should be realized that a body mass index of 17.5 is a strict weight cutoff only for individuals over age 20. For children, and to a lesser extent for adolescents, the body mass index cutoff is less strict than the primary DSM-IV weight criterion.
In keeping with the categorical approach to diagnosis, a cutoff may be specified on the dimension of body size/weight. If ICD persists with BMI, at the minimum, it would require a better specification with regard to age and sex.
F53: Mental and Behavioral Disorders associated with Puerperium Not Elsewhere Classified
Recently delivered mothers are vulnerable to the whole spectrum of general psychiatric disorders, as well as those resulting from the physical and psychological changes of childbirth. Nearly 30% of women have adjustment problems and 15%-20% have minor to major depression. Maternal suicide and infanticide are rare but the more common and yet less recognized risks are those of maternal illness – beginning in utero – on the infant. Considering the high risk of maternal and infant morbidity and mortality (Appleby, 1991; Patel et al, 2003; Anoop et al, 2004; Buist, 2006) associated with post partum disorders it is essential to fabricate a diagnostic system with adequate sensitivity for identification of these disorders.
The rubric of postpartum disorders may be particularly important for developing countries. Indian studies have found high rates of post partum depression (16% to 23%) and have highlighted the importance of social factors, specifically poverty and female gender of the infant as risk factors for the same (Patel et al 2002; Chandran et al 2002).
Current status of postpartum disorder in ICD 10: The ICD-10, permits the classification of mental and behavioural disorders associated with the puerperium (F53) only if they have an onset within six weeks of delivery and if they cannot be classified elsewhere in the ICD 10 either because insufficient information is available or because it is considered that special additional clinical features are present that make classification elsewhere inappropriate. It will usually be possible to classify mental disorders associated with puerperium by using two other codes: the first is elsewhere in chapter V (F) and indicates the specific type of mental disorder (usually affective F30-F39), and the second is O99.3 (mental diseases and diseases of the nervous system complicating the puerperium) of ICD 10. The DSM-IV, with an even shorter onset specifier of four weeks, is restricted to four diagnoses only, and likewise is rarely used. In the light of available evidence that post partum disorders can occur for periods up to 1 year post delivery and that symptoms may have onset during the last trimester of pregnancy the current “6 weeks post partum onset” diagnostic criteria in ICD 10 is too restrictive.
Specific features of postnatal mood disorder are acknowledged in the text of DSM IV (e.g., fluctuating course and mood lability, delusions including the baby, risk of infanticide, disinterest in the infant, guilt because of dissonance between the mother's mood and society's expectation of happiness, and less than optimum development of a mother/infant relationship). These features are not described in the ICD 10.
IV. The title of the category should be changed from “mental and behavioral disorders associated with puerperium not elsewhere classified” to “mental and behavioral disorders associated with perinatal period not elsewhere classified” where the perinatal period is defined from conception till 3 months postpartum.
Recent literature shows a growing focus on the entire perinatal period for mental health of the mother as this period significantly influences the healthy development of the fetus and the newborn. The perinatal mental health period spans conception to two years after childbirth according to some experts (Kowalenko et al 2000; Currid, 2004). It is the time when women are most likely to be admitted to a psychiatric hospital (Dean and Kendell, 1981), are at increased risk of experiencing an affective mental illness, and those with a pre-existing mental illness are more prone to relapse or recurrence of the condition (R C Psych 2000; Pritchard & Harris, 1996). A meta-analysis of 59 studies (including 12,810 women, mainly from developed countries) found an average prevalence rate of non-psychotic postnatal depression (PND) of 13% (95% CI - 12.3%-13.4%) (O' Hara et al, 1996). Most cases develop within the first 3 months, with a peak incidence at 4-6 weeks. Although one study showed that most cases last around 3 months and resolve spontaneously without treatment, another study showed that 50% of cases lasted over 6 months and some persisted at 4 years. Two prospective studies from Goa and Tamil Nadu detected depressive disorder in 23% and 16% respectively, with depression persisting six months after child birth in 11%-14% of women (Chandran et al 2002; Patel et al 2002). Depression and anxiety often begin in pregnancy, particularly in the third trimester, and so ‘perinatal’ rather than postnatal depression might be a better term.
However, the evidence for familial aggregationwas significant for narrowly defined postpartum depression (onsetwithin 4-8 weeks of delivery) but not for a broader definition(onset within 6 months of delivery) that is perhaps more typicalof the way the diagnosis is used as a lay term and applied inclinical practice (Forty et al, 2006). Based on such evidence, the Satra Bruk classification workshop held in Sweden in 1999, proposed to add a postnatal onset specifier of 3 months (Elliot, 2000).
Balancing available scientific evidence with common clinical usage a proposal for ICD 11 is to replace the duration of onset in the puerperium by onset from conception to 3 months post delivery i.e., the perinatal period.
V. A specifier for onset in the perinatal period should be added to all disorders in mood, psychotic and adjustment disorder sections of ICD i.e. F20-29, F30-39, and F43.
Recently delivered mothers are vulnerable to the entire spectrum of general psychiatric disorders, as well as those resulting from the physical and psychological changes of childbirth. The postpartum “blues” can be part of the normative postpartum adjustment and affect up to 80% of women (Robin, 1962; Pitt, 1968). The mild symptoms of the blues differ qualitatively and quantitatively from postpartum major depression and do not interfere with maternal role functioning (Miller, 1999).
The prevalence of major or minor depression in pregnant women ranges from 7% to 26% (Chandran et al 2002; Patel et al 2002; Moses-Kolko & Roth, 2004). Depression during pregnancy is a strong predictor of postpartum depression and is associated with adverse effects on fetal development (Graff et al, 1991; Chandran et al 2002; Patel et al 2002). The reported rate of recurrence of postnatal depression (PND) after a subsequent childbirth is 30% and the rate is higher for women in whom the first episode of PND is the first-ever depressive episode, compared with the rate in women who have had previous non-puerperal depression (41% vs. 18%) (Cooper & Murray, 1995).
Most cases of post-partum psychosis are manic-depressive in form, and there is much evidence for a close connection between puerperal and bipolar disorders. Nearly half of women with bipolar disorder experience childbearing-related episodes (Blehar et al, 1998), predominantly depression. Another literature links post-partum and 'cycloid' (acute polymorphic) psychoses.
Post-partum anxiety disorders are underemphasized and may be more common than depression (Matthey et al, 2003). A review of eight studies of 'panic disorder' showed that 44% anxious women had an exacerbation and 10% a new onset, in the puerperium (Hertzberg, 1999). The focus of anxiety is also important, because it may indicate specific psychological treatment. Since the pioneering study of Bydlowski and Raoul-Duval (1978), over 40 papers have appeared on PTSD resulting from stressful parturition. There have been eight quantitative studies, showing rates up to 5.6% (Creedy et al, 2000). Obsessions of infanticide were among the first post-partum disorders to be described (Chapman, 1959; Button, 1972). Other morbid phenomena can also become a problem for some mothers. A disorder akin to dysmorphophobia, based on the bodily changes resulting from pregnancy and childbirth, is common.
The available evidence regarding etiology, familiality and course of postpartum mental illness especially postpartum depression and postpartum psychosis, the two most studied disorders do not support post partum disorders as a distinct diagnostic entity. Though the exact etiology is unknown, childbirth seems to act as a specific trigger for many mental disorders in line with the stress diathesis model. As nearly the entire spectrum of mood disorders, psychotic disorders and anxiety and stress related conditions are seen in the perinatal period we propose that the specifier ‘onset within perinatal period’ should be added to all diagnoses in mood disorder, psychosis and adjustment disorder sections (ICD-10 F20-29, F30-39, F43 ).
VI. The text description of ICD11 should mention the unique features that occur during the perinatal period like delusions involving the baby, risk of infanticide, disinterest in the infant, guilt because of dissonance between the mother's mood and society's expectation of happiness, and less than optimum development of a mother/infant relationship.
Psychiatric disorders occurring in the postpartum period have many unique features. Chandran et al (2002) assessed 50 Indian women admitted to a psychiatric hospital for severe mental illness occurring in the postpartum period. Nearly half (43%) of the mothers reported infanticidal ideas, 36% reported infanticidal behavior, and 34% reported both infanticidal ideas and behavior. Logistic regression analyses indicated that presence of depression and psychotic ideas predicted infanticidal ideas, whereas presence of psychotic ideas toward the infant predicted infanticidal behavior.
Many mothers are excessively anxious about the health and safety of their children or they may fear the awesome responsibility of infant care. Most mothers are shielded from this by family support, but it can be a problem in isolated nuclear families. A mother with infant-focused anxiety may develop a phobia for the infant (Sved-Williams, 1992). Fear of cot death can reach pathological proportions (Weightman et al, 1999). Its main manifestation is nocturnal vigilance – the mother lying awake listening to the infant's breathing, with frequent checks that lead to exhausting sleep deprivation. As mentioned earlier, obsessions of infanticide were among the first post-partum disorders to be described (Chapman, 1959; Button, 1972) and a disorder akin to dysmorphophobia, based on the bodily changes resulting from pregnancy and childbirth is common.
Specific features of postnatal mood disorder are not acknowledged in the ICD 10 though they appear in the text of DSM IV (e.g., fluctuating course and mood lability, etc.). It is recommended that the text description of various disorders should highlight features specific to the perinatal period.
VII. A rubric for disorders of mother-infant relationship should be created
Developing a relationship with the newborn is the central and most important psychological process of the puerperium. A disturbed mother infant relationship is phenomenon distinct from depression. On one hand, mothers’ aversion to her infant is often disproportionate to depression and can occur without it; on the other hand, only a minority of depressed mothers has a relationship problem with their infants. This has led to proposals for a distinct ‘disorder of impaired mother-infant interaction’ (Brockington, 2004). Disorders of the mother-infant relationship are prominent in 10-25% of mothers referred to psychiatrists after childbirth. The etiology is probably different from post-partum depression, with more emphasis on unwanted pregnancy and challenging infant behaviour.
The main reason for the neglect of these disorders is their absence from ICD-10 and DSM-IV. In ICD-10, attachment disorders of childhood (reactive 94.1 and disinhibited 94.2) and 'Z codes' that include hostility towards the child, and scapegoating, address issues related only to the child's psychiatric state. One of the challenges for ICD-11 and DSM-V is to find a place for these disorders, so that they can be recognized by practitioners, and referred for expert treatment (Ainsworth et al, 1972; Salariya et al,1984; Hipwell & Kumar, 1996; Nagata et al, 2000; Brockington et al, 2001).
Though research in this area is lacking, the identification of this concept will sharpen the focus of studies aimed at preventing child abuse and neglect. Disorders of mother infant interaction may be included in the category F 53.
· Ainsworth MDS, Bell SM, Stayton DJ. Individual differences in the development of some attachment behaviours. Merrill Palmer Q 1972; 18:123-143.
· Anoop S, Saravanan B, Joseph A, Cherian A, Jacob KS. Maternal depression and low maternal intelligence as risk factors for malnutrition in children: a community based case-control study from South India. Arch Dis Child 2004; 89:325-329.
· Appleby L. Suicide during pregnancy and in the first postnatal year. BMJ 1991; 302:137-40.
· Banks CJ. ‘Culture’ in culture–bound syndromes: the case of anorexia nervosa. Soc Sci Med 1992; 34, 867-884.
· Blehar MC, DePaulo JR, Gershon ES, et al. Women with bipolar disorder: findings from the NIMG Genetics initiative sample. Psychopharmacol Bull 1998; 34:239-243.
· Brockington I. Diagnosis and management of post-partum disorders: a review. World Psychiatry 2004; 3:89-95.
· Brockington IF, Oates J, George S, et al. A screening questionnaire for mother-infant bonding disorders. Arch Women Ment Health 2001; 3:133-140.
· Buist A. Perinatal depression - assessment and management. Aust Fam Physician 2006; 35:670-673.
· Button JH, Reivich RS. Obsessions of infanticide. A review of 42 cases. Arch Gen Psychiatry 1972; 27:235-240.
· Bydlowski M, Raoul-Duval A. Un avatar psychique méconnu de la puerpéralité: la névrose traumatique post-obstétricale. Perspectives Psychiatriques 1978; 4:321-328.
· Chandran M, Tharyan P, Muliyil J, et al. Post-partum depression in a cohort of women from a rural area of Tamil Nadu, India. Incidence and risk factors. Br J Psychiatry 2002; 181:499-504.
· Chapman AH. Obsessions of infanticide. Arch Gen Psychiatry 1959; 1:12-16.
· Cooper P, Murray L. Course and recurrence of postnatal depression: evidence for the specificity of the diagnostic concept. Br J Psychiatry 1995; 166:191-195.
· Creedy DK, Shochet IM, Horsfall J. Childbirth and the development of acute trauma symptoms: incidence and contributing factors. Birth 2000; 27:104-111.
· Currid T. Improving perinatal mental health care. Nursing Standard 2004; 19:40-43.
· Dancyger IF, Garfinkel PE. The relationship of partial syndrome eating disorders to anorexia nervosa and bulimia nervosa. Psychol Med 1995, 25:1019-1025.
· Dean C, Kendell R The symptomatology of puerperal illnesses. Br J Psychiatry 1981; 139:128-133.
· Elliott SA. Report on the Satra Bruk workshop on classification of postnatal mental disorders. Arch Women Ment Health 2000; 3:27-33.
· Falk JR, Halmi KA. Amenorrhea in anorexia nervosa: examination of the critical body weight hypothesis. Biol Psychiatry 1982; 17:799-806.
· Forty L, Jones L, Macgregor S, et al. Familiality of postpartum depression in unipolar disorder: results of a family study. Am J Psychiatry 2006, 163:1549-1553.
· Garfinkel PE, Lin E, Goering P, et al. Should amenorrhea be necessary for the diagnosis of anorexia nervosa? Evidence from a Canadian community sample. Br J Psychiatry 2006, 168:500-506.
· Ghaderi A, Scott B. Prevalence, incidence and prospective risk factors for eating disorders. Acta Psychiatr Scand 2001, 104:122-130.
· Graff LA, Dyck DG, Schallow JR. Predicting postpartum depressive symptoms and structural modeling analysis. Percept Mot Skills 1991, 73:1137-1138.
· Hertzberg T, Wahlbeck K. The impact of pregnancy and puerperium on panic disorder: a review. J Psychosom Obst Gynaecol 1999; 20:59-64.
· Herzog DB, Hopkins JD, Burns CD. A follow-up study of 33 subdiagnostic eating disordered women. Int J Eat Disord 1993; 14:261-267.
· Hipwell AE, Kumar R. Maternal psychopathology and prediction of outcome based on mother-infant interaction ratings. Br J Psychiatry 1996; 169:655-661.
· Khandelwal SK, Saxena S. Anorexia nervosa in people of Asian extraction. Br J Psychiatry 1990; 157:784.
· Khandelwal SK, Sharan P, Saxena S. Eating disorders: an Indian perspective. Int J Soc Psychiatry 1995; 41:132-146.
· King MB. Eating disorders in a general practice population. Prevalence, characteristics and follow-up at 12 to 18 months. Psychol Med 1989; 14(Suppl):1-34.
· Kowalenko N. The perinatal period, early interventions for mental health. In Kosky R (Ed): Clinical Approaches to Early Intervention in Child and Adolescent Mental Health. Adelaide: Australian Early Intervention Network for Mental Health in Young People 2000.
· Lee S. Self-starvation in context. Towards a culturally sensitive understanding of anorexia nervosa. Soc Sci Med 1995; 41:23-36.
· Lee S., Lee AM, Ngai E, et al. Rationales for food refusal in Chinese patients with anorexia nervosa. Int J Eat Disord 2001; 29:224-229.
· Matthey S, Barnett B, Howie P, et al. Diagnosing postpartum depression in mothers and fathers: whatever happened to anxiety? J Affect Disord 2003; 74:139-147.
· Miller L. Beyond the blues. In: Miller L (Ed.): Postpartum Mood Disorders. Washington DC: American Psychiatric Press 1999.
· Mitchell JE, Cook-Myers T, Wonderlich SA. Diagnostic criteria for anorexia nervosa: looking ahead to DSM-V. Int J Eat Disord 2005; 37 (Suppl):S95-S97
· Mitrany E. Atypical eating disorders. J Adolesc Health 1992; 13(2 Suppl 1):400-402.
· Moses-Kolko EL, Roth EK. Antepartum and postpartum depression: healthy mom, healthy baby. J Am Med Womens Assoc 2004; 59:181-191.
· Nagata M, Nagai Y, Sobajima H, et al. Maternity blues and attachment to children in mothers of full-term normal infants. Acta Psychiatr Scand 2000; 101:209-217.
· Nonacs R, Cohen LS. Depression during pregnancy: aiagnosis and treatment options. J Clin Psychiatry 2002, 63(Suppl 7):24-30.
· Nasser M. Screening for abnormal eating attitudes in a population of Egyptian secondary school girls. In: Lee S (Ed.): Reconsidering the Status of Anorexia Nervosa as a Western Culture–Bound Syndrome. Soc Sci Med 1994; 42: 21-34.
· O’Hara MW, Swain AM. Rates and risk of postpartum depression: a meta analysis. Int Rev Psychiatry 1996; 8:37-54.
· Patel V, Rodrigues M, DeSouza N. Gender, poverty, and postnatal depression: a study of mothers in Goa, India. Am J Psychiatry 2002; 159:43-47.
· Patel V, DeSouza N, Rodrigues M. Postnatal depression and infant growth and development in low income countries: a cohort study from Goa, India. Arch Dis Child 2003; 88:34-37.
· Pitt B. “Atypical” depression following childbirth. Br J Psychiatry 1968; 114:1325-1335.
· Pritchard DB, Harris B. Aspects of perinatal psychiatric illness. Br J Psychiatry 1996; 169:555-562.
· Robin AA. Psychological changes of normal parturition. Psychiatr Q 1962; 36:129.
· Royal College of Psychiatrists. Perinatal Maternal Mental Health Services. Council Report CR 88. London: R C Psych 2000.
· Salariya EM, Cater JI. Mother-child relationship - FIRST score. J Advanced Nursing 1984; 9:589-595.
· Shroff H, Thompson JK. Body image and eating disturbance in India: media and interpersonal influences. Int J Eat Disord 2004; 35:198-203.
· Sved-Williams AE. Phobic reactions of mothers to their own babies. Aust N Zeal J Psychiatry 1992; 26:631-638.
· Thaw JM, Williamson DA, Martin CK. Impact of altering DSM-IV criteria for anorexia and bulimia nervosa on the base rates of eating disorder diagnoses. Eat Weight Disord 2001; 6:121-129.
· Theander S. Anorexia nervosa: a psychiatric investigation of 94 female patients. Acta Psychiatr Scand 1970, 214 (Suppl):1-194.
· Walters EE, Kendler KS. Anorexia nervosa and anorexic like symptoms in a population-based female twin study. Am J Psychiatry 1995; 152: 64-71.
· Watson TL, Andersen AE. A critical examination of the amenorrhea and weight criteria for diagnosing anorexia nervosa. Acta Psychiatr Scand 2003; 108:175-182.
· Williamson DA, Gleaves DH, Savin SS. Empirical classification of eating disorder not otherwise specified: support for DSM-IV changes. J Psychopathology Behav Assess 1992; 14: 201-216.
· Weightman J, Dalal BM, Brockington IF. Pathological fear of cot death. Psychopathology 1999; 167:246–249
ICD-11: DRAFT PROPOSAL FOR CHANGES IN THE “PERSONALITY DISORDERS” SECTION
Pratap Sharan, MD, PhD, Nanaji Kaw, MD, Sabish Balan, MD, Kushal Jain, MD
1. Both categorical and dimensional approaches should be used to define personality disorders
2. Trait and behavioural exemplars should be included together in each criterion
3. Some PDs like Dependent PD, Histrionic PD & Anxious (avoidant) PD require substantial modification for cross-cultural use
4. Each personality disorder (PD) should list more traits
5. Some PDs like Emotionally Unstable PD-Impulsive Type, Mixed PD, Troublesome Personality Change, Enduring Personality Change should be shifted to PD: others
6. Controlling/dominating PD requires to be added to category requiring further study
Supporting evidence for proposed changes
Many South Asian psychiatrists would question the relevance of diagnosing and studying personality disorders. A major reason for the lack of interest in these conditions is their apparent rarity. A meta-analysis of general population studies carried out in India puts the prevalence figure for personality disorders at 0.6 per 1000 (Reddy and Chandrashekhar 1998). Very low rates have also been reported from Sri Lanka (Wijesinghe et al 1978). However, there are several shortcomings in the surveys conducted in developing countries (de Girolamo and Reich 1993).
Since the publication of the Diagnostic and Statistical Manual (DSM-III) in 1980 and its creation of a separate diagnostic axis (i.e. Axis II) for personality disorders, interest in the description and classification of personality disorders has expanded dramatically in the West. Between 20% and 40% of outpatients and more than 50% of inpatients in the western psychiatric set-up are reported to have comorbid personality disorders (Tyrer et al 1991). Comorbidity studies in India also suggest that personality disorders are common. In recent Indian studies, rates as high as 37.5% in patients with bipolar disorder, 40.8% in those with major depressive disorder (Naidu et al 1998) and 25.6% in those with substance use disorder (Kishore et al 1994) have been reported.
If personality disorders were a common but benign condition, there would still be no pragmatic reason to study them. However, they lead to a disturbance in functioning as great as that in most major mental disorders (Nakao et al 1992). Personality disorders are associated with high rates of separation and divorce; unemployment and inefficiency; and poor quality of life for the individual and his/her family. Patients with personality' disorders have an increased risk of mortality through suicide, homicide and accidents. Also, when a personality disorder is present, treatment of other coexisting psychiatric or medical conditions is frequently more complicated, lengthier, or less successful; a pattern that may at times be due to lack of recognition of the personality disorder (Oldham 1994).
Differences between ICD 10 and DSM IV Classificatory Systems
The ICD-10 and DSM-IV are different but overlapping classification systems. Both have adopted polythetic diagnosis criterion a polythetic approach as against a monothetic approach. There are some differences in the nomenclatures such as anankastic in ICD-10 is obsessive-compulsive in DSM-IV, anxious in ICD-10 is avoidant in DSM-IV, and dissocial in ICD-10 is antisocial in DSM-IV. In ICD-10, borderline and impulsive personality disorders are viewed as subtypes of emotionally unstable personality disorder. In ICD-10, schizotypal disorder is considered to be an attenuated manifestation of schizophrenia and is categorized with the psychotic disorders; narcissistic, depressive and passive aggressive personality disorders do not find a mention.
There are also several marked differences in the criteria of the two systems and some minor variation in wording. The ICD-10 form of paranoid personality disorder includes excessive self-importance and self-reference as criteria, while in DSM-IV excessive self-importance forms a central part of narcissistic personality disorders. DSM-IV's schizoid personality disorder omits preoccupation with fantasy and introspection as criteria, though these are required in ICD-10.On the other hand, DSM-IV's antisocial personality disorder requires features of childhood conduct disorder, and emphasizes on law-breaking and criminal acts, while ICD-10's dissocial personality disorder does not mention childhood conduct symptoms in its set of criteria and is more concerned with generic concepts such as lack of empathy, inability to profit from experience and inability to maintain enduring relationships. In general, ICD-10 maintains a division between personality and mental state less clearly; for example, allowing the inclusion of persistent feelings of anxiety as a criterion in anxious personality disorder, and of obsessions in anankastic personality disorder.
ICD-10 requires the presence of three of the seven criteria to make a diagnosis (except for emotionally unstable personality disorder), while DSM-IV requires four or five from a list that varies from seven to nine (with the exception of antisocial personality disorder) (Sara et al 1996).
I. Both categorical and dimensional approaches should be used to define personality disorders
Current classification systems employ a categorical model for classifying personality disorders. However, there is considerable overlap among personality disorders. The dimensional model of classification has been proposed as a means to overcome these problems, as it can provide flexible, comprehensive and reliable information on subjects. However, much of the external validity research that is available currently has been conducted using categorical concepts, even though data on dimensional conceptualization of personality disorders is fast accumulating. Data support sometimes categorical, sometimes dimensional and sometimes both types of concepts.
Epidemiology: The prevalence of personality disorders defined in categorical terms range from 10.3% to 13.5% in community samples when assessment instruments specific to these disorders are used. The rate varied with age, with some decrease in older age groups. Urban populations and lower socioeconomic groups showed higher rates. The sex ratio was different for specific types of personality disorders, though the overall rate of prevalence was roughly equal for the two sexes (Reich and de Girolamo 1997). Prevalence rates of personality disorders may be lower in developing countries but methodological shortcomings in surveys done in these countries preclude direct comparisons. In the International Pilot Study of Personality Disorders (IPSPD), the following personality disorders were frequently diagnosed in a clinical sample at Bangalore (India): schizotypal (19.1 %) and borderline (14.7%) according to the DSM-III-R system; and emotionally unstable (8.6%) according to the ICD-I0 system (Loranger et al1997).
Reliability: The overlap between personality disorders defined in categorical terms is a reason forthe modest reliability seen in diagnosis, when different categorical conceptualizations of the same personality disorder (Hirshfield and Holzer 1994), different diagnostic systems (Sara et al 1996), or even different instruments operationalizing the same diagnostic system (Zimmerman 1994) are used.
Face validity: The face validity of the criteria sets for categorical definitions is low forboth the DSM-IIIR (Blashfield and Breen 1989) and ICD10 (Blashfield 1990) personality disorders.
Biological studies: There is some genetic support to categorical conceptualization of cluster A personality disorders, which are seen as existing in a genetic spectrum with psychotic disorders (Siever 1994, Siever, 2005). Antisocial personality disorder also appears to be heritable (Cadoret et al1995), but the specificity of a familial/genetic relationship of other personality disorders is suspect (Reich 1989; Torgersen 1994). On the other hand, Livesley and coworkers (Livesley et al 1992; Livesley 2005) demonstrated that 15 of the 18 personality disorder dimensions thought to underlie the DSM-III-R personality disorders had heritability in the range of 30%-60%. The results were similar to those reported for normal personalities and suggested a continuity between the normal and disordered personality.
Neuroimaging studies have provided some evidence for categorically defined personality disorders, e.g. increased ventricular-to-brain ratio and inefficient prefrontal cerebral processing in schizotypal subjects (Siever 1994). Positron emission tomography (PET) studies have also demonstrated some abnormalities in patients with antisocial personality disorder and metabolite borderline personality disorder (Doaln 1994; De la Fuente et al 1998; Pidimore et al 2005; Schmahl and Bremner 2006).
Neurochemical studies on the other hand have mainly provided evidence for dimensional conceptualization of personality features. E.g. schizotypal patients who display features of the deficit dimension have low cerebrospinal fluid (CSF) levels of the dopamine metabolite homovanillic acid (HVA) and those who have features of psychotic dimension have high CSF HVA levels (Siever 1994). In patients with duster B personality disorders (antisocial and borderline), 5-hydroxyindole acetic acid (5-HIAA) (a metabolite of serotonin) levels in the CSF and parameters of 5-HT (serotonin) functioning have been found to be inversely related to dimensions of impulsive aggression and negative affect. Also, platelet monoamine oxidase (MAO) levels are inversely related to dimensions of sensation-seeking and impulsivity (Dolan 1994; Coccarro et al 1997; Lara and Akiskal 2006, Lyons-Ruth et al, 2007).
Electrophysiological studies provide some evidence for categorically defined concepts. Abnormalities in relation to eye-movement and information processing have been reported to occur in patients with schizotypal personality disorder (Cadenhead et al 1993; Siever 1994; Evans et al 2007). Patients with borderline personality disorder have a decreased latency and increased density of rapid eye movements (REM) during sleep EEG recording. Some studies have also reported eye movement dysfunction and auditory evoked potential abnormalities in these patients (Lahmeyer et al1989; De la Fuente et al 1998; Boutros et al 2003; Howard and McCullagh, 2007). Evoked potential studies done under distraction conditions in patients with antisocial personality disorder reveal abnormalities in the P300 wave, suggesting deficits in information processing.
Treatment Studies: These studies have largely supported dimensional concepts. In general, pharmacotherapy aims at the correction of target symptoms such as aggression and behavioural dyscontrol, anxiety and mood dysregulation, and psychotic symptoms (including cognitive distortions) (Stein 1992; Cloninger et al 1997; Mohan 2002; Lara and Akiskal 2006). The limited data available on analytic psychotherapy (Bateman and Fonagy 1999) also do not support a diagnosis-based approach However, some data on other forms of psychotherapy have shown promise for specific categories of personality disorders, e.g. cognitive-behavioural therapy in avoidant personality disorder (Alden 1989) and dialectical behaviour therapy for borderline personality disorder (Linehan et al 1991).
Course and outcome: The literature regarding the long-term outcome of personality disorders is sparse (Skodol et al 2007). Most attention has been paid to formerly institutionalized patients with borderline, antisocial and schizotypal personality disorders. Borderline patients at 10-25 years follow up have a wide range of outcomes, from clinical recovery (50%-60%) to suicide (3%-9%). Suicide is particularly common in patients who have co-morbid depression or a history of substance abuse. If psychopathic traits are prominent, the long-term outcome in antisocial persons is bleak, though a substantial proportion of persons who exhibit a pattern of antisocial behaviour alone, recovers by the fourthdecade of life (Stone 1993). Schizotypal patients tend to remain isolated and lead marginal lives.
Boundary problems: within categorically defined personality disorders: Even though moderate internal consistency may exist forDSM-IIIR criteria sets of individual personality disorders, the correlation with other personality disorders is fairly high (Nunberger et al 1994; Widiger 2003). Consequently, there is a high rate of comorbidity (1.3 to 6.0) between personality disorders (Dolan et al 1995). Studies using multivariate statistical techniques have found that dimensions derived empirically bear a resemblance to some DSM-IIIR diagnoses but the correspondence between them is not close. In general, these studies have partially supported the cluster concept of the DSM system, with usually four superordinate factors corresponding to clusters I, II, III and obsessive-compulsive personality disorder emerging across many but not all studies (Hyler and Lyons 1988; Schroeder and Livesley 1991; Mulder and Joyce 1997; Skodol et al, 2007). The current classification systems have been criticized for either making over-refined descriptive distinctions, or forwrongly conceptualizing personality disorders as categories when they might be more properly described as trait dimensions.
Boundary problems: between personality disorders (Axis II) and symptom (state) disorders (Axis I): Although the distinction between Axes I and II disorders is valuable from the clinical point of view, the differentiation between the two sets of disorders is often problematic and at times even illusory. Particular problems exist in relation to differentiation between schizotypal personality disorder and schizophrenia spectrum disorders; borderline personality disorder and mood disorders; antisocial personality disorder and substance use disorders; and avoidant personality disorder and social phobia (Widiger and Shea 1991).
Boundary problems: between normal personality and personality disorder: Supporters of dimensional approach view personality disorders as extremes of temperamental traits found in the normal population (Schroeder and Livesley 1991; Costa and Widiger 1994; Paris 1997). The main reservations against this approach have been that (i) it has not been shown whether the three to five major dimensions found to describe normal personality (Digman 1990) also continuously underlie personality disorders; and (ii) some of the symptoms of personality disorders e.g. suicidal behaviour, self-mutilation do not have normative personality counterparts (Lenzwenger and Clarkin 1996). However, Livesley et al. (1992) showed that trait dimensions of personality disorders underlying DSM-III-R personality disorders in patient and general population samples are continuously distributed. They also demonstrated considerable similarity between the second-order factors (four) of personality pathology traits and four of the 'big five' factors of normal personality (Schroeder and Livesley 1991).
Authors who have used dimensional scaling techniques (Widiger et al 1987; Schroeder and Livesley 1991; Livesley et al 1992) and some who have carried out biological investigations in the area of personality disorders (Livesley et al 1993; Coccarro et al 1997) feel that the dimensional model fits the data on personality pathology in a better way. However, there are problems with this approach. It is not clear how personality pathology is actually organized at the latent level. The limited empirical evidence available suggests that schizotypy (Lenzwenger and Korfine 1992), borderline pathology (Trull et al 1990) and psychopathy (Harris et al 1994) may be organized as categories at the latent level. Further, biologists such as Kagan et al. (1987) and Magnusson (1986) noted that at least some personality traits may be dealt with in terms of physiobehavioural composites that are qualitatively distinct (categorical) rather than continuous (dimensional). In defence of the dimensional model, it may be said that the categorical criteria sets of schizotypal, borderline and antisocial personality disorders have been criticized for being saturated with items conveying the presence of symptomatic acts rather than personality traits (Stone 1993). Thus, they may have been more liable to show discreteness. The matter has not been adequately explored up to now for exclusive reliance on one or the other type of concepts.
Apart from the categories of personality disorders, ICD 11 should provide for agreed upon dimensions of personality and personality disorders. Evidence based candidates may be:
Dimensional models of personality:
· Interpersonal circumplex models (Wiggins 1979; Benjamin 1996)
· 3-factor models (Eysenck and Eysenk 1968),
· 5-factor models (Goldberg 1992; Costa & McCrae 1985; Zuckerman et al 1993)
· 7-factor models (Cloninger 1987; Cloniger et al, 1993; Tellegen et al 1991)
Dimensional models of PDs:
· 4-factor model (Livesley et al 1992)
· 5-factor model (Clark 1993)
II. Traits and behavioral exemplars should be included together in each criterion
Livesley and Jackson (1992) suggest ways to improve the classification of personality disorders by changing the way the classification is developed, evaluated, and modified so that it successively approximates a valid system. They argue that the first step in developing a classification is to ensure the content validity of diagnostic concepts because this is a prerequisite for other components of validity. Using trait and behavioural exemplars together in personality disorder criterion is a way to improve the content validity of personality disorders as it helps in tying the criterion to the concept and structure of the personality disorder, and in clarifying the nature of diagnostic items and the model for organizing diagnostic decisions. An example of using trait and behavioural exemplars together is given below:
· Gross and persistent attitude of irresponsibility and disregard for social norms, rules and obligations, e.g. leaving a child less than 3 years of age alone at home for an hour to go and buy alcohol, dring at high speed around a blind corner, takes bribes, etc.
Specification of trait and behaviour exemplars would reduce the discrepancy between DSM-IV's antisocial personality disorder, which emphasizes law-breaking and criminal acts; and ICD-10's dissocial personality disorder, which is more concerned with generic concepts such as lack of empathy, inability to profit from experience and inability to maintain enduring relationships.
Defining the trait underlying the behaviour will also clarify the differentiation between Axis I and Axis II disorders. The differentiation between Axes I and II disorders parallels to some extent the distinction between personality traits and emotional states. Neuroticism, for example, involves the disposition to experience negative affects (McCrae and Costa 1990), and a correlation with mood states supports rather than questions its validity (Watson and Clark 1984). States and traits may best be conceptualized under prototypal concepts that provide meaningful distinction, but merge into each other at the boundaries (coaxial syndrome). It is useful to retain the differentiation because it has been shown that states affect personality domains differently, with relatively large parts of personality and behaviour (e.g. novelty-seeking, reward dependence) remaining unaffected by current states such as anxiety or depression (Svrakic et al 1992). Efforts to increase the distinction between state and trait disorders by adding or deleting existing criteria might change the meaning of the construct under study, e.g. borderline personality disorder would not remain the same if affective instability were to be removed from its description (Widiger and Shea 1991). On the other hand, defining the trait features consistently will improve reliability without compromising on validity.
III. Some personality disorders like Dependent PD, Histrionic PD and Anxious (avoidant) PD require substantial modification for cross-cultural use
The International Pilot Study for Personality Disorders (IPSPD) (Loranger et al 1997) demonstrated that personality disorders, as presently defined, could be identified at all sites (multinational, multilingual, multicultural). Similarly, cross-national studies suggest that the Three Factor Model of Eysenck (Eysenck 1982) and Five Factor Model (Costa and Widiger 1994) were invariant across cultures. However, these studies do not confirm the cross-cultural validity or usefulness of western diagnostic categories or personality dimensions, as they may have identified ethnic artefacts rather then culturally meaningful configurations (Lewis-Fernandez and Kleinman 1994). The five factors that emerged on the use of a lexicon of Chinese trait descriptors were different from the factors extracted from the Chinese translation of English words from an established five-factor questionnaire (Yang and Bond 1990). It has been hypothesized that culture can influence: the genetic selection of specific temperamental characteristics in highly inbred groups, learning inside and outside the family, the threshold when personality vulnerability cannot be compensated by the person, and the social threshold when such decompensations are labeled pathological (Neki 1970; Paris 1997).
From a cultural constructionist perspective, personality disorders are based on Anglo-American concepts of personhood and codes of appropriate bahaviour and owe their existence to the medicalization of disvalued social behaviour. Anxious (avoidant) and dependent personality disorders were excluded from the Chinese classificatory system because of the apparent rarity of these disorders and because it was felt that some of the defining features (e.g. subordination of one’s own needs to those of others on whom one is dependent) were normative in the Chinese culture which defines personhood not by autonomy and assertiveness but by intergenerational interdependence and self-effacement (Mezzich et al 2000).
In a similar way histrionic and dependent personality disorder may not be very useful in the Indian context. An observation of 290 cases (two thirds randomly selected and one third selected because of evidence of personality pathology) in a North-Western Indian clinical sample drawn from a general hospital setting (Sharan 2001) revealed only two case of histrionic personality disorder (0.7%) and 1 case of dependent personality disorder (0.3%). These disorders were not reported in the Bangalore centre (sample drawn from mental hospital setting) of the IPSPD also (Loranger et al1997). Histrionic behaviour may not be reported (histrionic personality disorder dimension had a moderately negative correlation with the lie/social desirability scale) or may be suppressed due to social disapproval, while dependent behaviour may be culturally normative. Specific problems with the criteria sets found in the Indian context were:
· Dependent PD (DPD)
o Some criteria difficult to apply to women in non western setting especially regarding those regarding life decisions, subordination of needs
· Avoidant PD (APD) (Dropped from Chinese classification)
o Some criteria difficult to apply, e.g. unwillingness to become involved with people unless certain of being liked, avoidance of social or occupational activities that involve significant interpersonal contact
· Histrionic PD (HPD)
o Criteria often not observed in the formal clinical setting, e.g. seductiveness, over concern with physical attractiveness
o Some criteria difficult to apply to women in non western setting, e.g. suggestibility, continual seeking of excitement
Experience with collectivistic cultures suggests that some personality disorders like Dependent PD, Histrionic PD and Anxious (avoidant) PD require substantial modification for cross-cultural use. Till more evidence accrues in these cultures, these personality disorders should be shifted to PD: Other category.
IV. Each personality disorder should list more traits
ICD-10 requires the presence of three of the seven criteria to make a diagnosis (except for emotionally unstable personality disorder), while DSM-IV requires four or five from a list that varies from seven to nine (with the exception of antisocial personality disorder) (Sara et al1996). Livesley et al (1987) developed reliable scales to assess more than 50 traits thought to underlie each of the DSM III personality disorders.
The larger number of traits for each personality disorder would improve content coverage for personality disorders ensuring that they are not too narrowly defined. This expansion would also make it possible to include more culture-specific traits in the criterion set without reducing the possibility of making the diagnosis cross-culturally - with the help of other (less culture-specific) criteria.
V. Some personality disorders like Emotionally Unstable PD – Impulsive Type, Mixed PD, Troublesome Personality Change, Enduring Personality Change should be shifted to PD: Others category
ICD-10 requires the presence of three of the seven criteria to make a diagnosis for all personality disorders, except for emotionally unstable PD – impulsive type, in which only 2 of 5 criteria suffice. Three criteria of this disorder have overlapping behavioural referrants, hence the diagnosis can be made very easily. This is reflected in Indian studies. Emotionally unstable PD – impulsive type was the commonest diagnosis in an enriched clinical sample (two thirds randomly selected, one third selected for personality pathology) from Chandiagrh (4.1% definite diagnosis, 6.6% probable diagnosis) (Sharan, 2001); and also in the Bangalore sample of the IPSPD (4.3%) (Loranger et al 1997). However, clinicians rarely use the diagnosis owing perhaps to the unfamiliarity of the concept or because they think that it is only a part syndrome (Sharan, 2001).
Specification of mixed PD does not mention the number criteria required and the number of types of PD from which these criteria should be selected. Further, the mixed category may have no added advantage in a situation where all personality disorders have a lot of overlap and comorbid diagnosis is the norm.
No substantial empirical data have accrued to substantiate the validity of the following entities:
· F61.1 Troublesome personality changes
· F62 Enduring personality changes (EPC), not attributable to brain damage and disease
o F62.0 Enduring personality change after catastrophic experience
o F62.1 Enduring personality change after psychiatric illness
o F62.8 Other enduring personality changes
o F62.9 Enduring personality change, unspecified
Hence, giving them a status above better established entities like narcissistic personality disorder appears anomalous.
VI. Controlling/dominating PD requires to be added to category requiring further study
Sharan (2001) found unexpectedly large (>0.4) correlation between the dimensional scores of ICD 10 paranoid and dissocial and emotionally unstable personality disorders. This is reflected in clinical experience (Sharan, paper submitted for publication) where a constellation of traits which can be tentatively termed as controlling/dominating personality disorder, present often for treatment. They seem to share features of emotionally unstable, paranoid (with narcissistic elements) and anankastic personality disorders. Studies of normal personality dimensions carried out in eastern cultures have noted rotational differences in structure, e.g. rotation of extraversion and agreeableness axes towards dominance and affiliation (Kagitbak et al 1996). Kagitbak et al (1996) feel that cultural nuances like an emphasis on smooth interpersonal relationships in Asia may be responsible for this shift of axes. It is understandable that conflicted dominance may show up (be labelled as) a personality disorder in cultures that emphasize subservience to hierarchy. In a similar way, while anxious (avoidant) personality was excluded from the Chinese classificatory system, Shinkeisitsu and Tajin Kyoufu (avoiding/rejecting due to interpersonal sensitivity) personality were described in Japan (Ono et al 1996). Shinkeisitsu and Tajin Kyoufu may reflect conflicts along the dimension of affiliation.
Controlling/dominating personality disorder and Tajin Kyoufu have parallels in the Structural Analysis of Social Behaviour (SASB) model (Benjamin 1996) where interpersonal behaviours as conceptualized as constituted by inputs from two primary dimensions - interdependence (dominance/submission versus independence) and affiliation (aggression versus sexuality).
Kernberg (1996) regards affects to be instinctive components of human behavior that emerge in the earliest stages of development and are gradually organized as part of early object relations into gratifying, rewarding, pleasurable affects or libido as an overarching drive, and into painful, aversive, negative affects which are organized into aggression as an overarching drive. Rage represents the basic affect of aggression as a drive, and its vicissitudes explain the origins of hatred and envy, as well as of anger and irritability as moods. He suggests that the earliest function of rage is the effort to eliminate a source of irritation or pain. A second function of rage is to eliminate an obstacle or barrier toward gratification. The third, developmentally a higher level function of rage is the elimination of a bad object that is intra psychically perceived as a willful source of frustration standing between the self and the gratification of a need. At a more advanced level, the wish is no longer to destroy the bad object, but to make it suffer. At a further level of development, the wish to make the bad object suffer shifts into the wish to dominate and control the bad object in order to avoid fears of persecution from it; as obsessive mechanisms attempt to regulate the suppression or repression of aggression. Finally, the original self-affirmative implications of rage may be seen in sublimatory aspects of the aggressive response in the search for autonomy and self-affirmation, and for freedom from external control. We feel that the controlling/dominating personality disorder person probably operates at the level where the wish to make the bad object suffer shifts into the wish to dominate and control the bad object as obsessive mechanisms attempt to regulate the suppression or repression of aggression but often fail to do so.
Proposed criteria for controlling/dominating PD
- Makes unreasonable demands on significant others
- Expects significant others to always comply with his/her needs and wishes
- Tries to take important life decisions for significant others
- Uses coercion to make others submit to exactly his/her way of doing things
- Marked tendency to quarrelsome behaviour and anger outbursts if things are not done in the way he/she wants
- Uses coercion/manipulative efforts to prevent significant others from leaving the relationship
- Suspiciousness and distortion of experience during situations of interpersonal conflict
- Depends on significant others to carry out activities and help make decision, but finds faults with actions and rejects ideas given by them
- Rigidity and stubbornness
· Alden L. Short term structured treatment for avoidant personality disorder. J Consult Clin Psychol 1989; 57:765-774.
· Bateman A, Fonagy P. Effectiveness of partial hospitalization in the treatment of borderline personality disorder: A randomized controlled trial. Am J Psychiatry 1999; 156:1563-1569.
· Benjamin LS. An interpersonal theory of personality disorders. In: Clarkin JF, Lenzwenger MF (Eds.): Major theories of personality disorder. New York: Guildford Press 1996; pp. 142-220.
· BIashfield RK. An American view of the ICD-l0 personality disorders. Acta Psychiatr Scand 1990; 82:250-256.
· BIashfield RK, Breen MJ. Face validity of the DSM - IIIR personality disorders. Am J Psychiatry 1989; 146:1575-1579.
· Boutros NN, Torello M, McGlashan TH. Electrophysiological aberrations in borderline personality disorder: state of the evidence. J Neuropsychiatry Clin Neurosci 2003; 15:145-154.
· Cadenhead KS, Geyer MA, Braff DL. (1993). Impaired startle prepulse inhibition and habituation in patients with schizotypal personality disorder. Am J Psychiatry 1993; 150:1862-1867.
· Cadoret RJ, Yates WR, Troughton E, et al. Genetic-environmental interaction in the genesis of aggressivity and conduct disorders. Arch Gen Psychiatry 1995; 52:916-924.
· Clark LA. Manual of the Schedule for Nonadaptive and Adaptive Personality. Minneapolis, University of Minnesota Press 1993.
· Cloninger CR. A systematic method for clinical description and classification of personality variants: A proposal. Arch Gen Psychiatry 1987; 44:573-588.
· Cloninger CR, Svrakic DM, Przybeck TR. A psychobiological model of temperament and character. Arch Gen Psychiatry 1993; 50:975-990.
· Coccarro EF, Kavoussi RJ, Hauger RL. Serotonin function and antiaggressive response to fluoxetine: A pilot study. Biol Psychiatry 1997; 42:546-552.
· Costa PT, Widiger TA. Personality disorders and the five factor model of personality. Washington DC: American Psychological Association 1994.
· Costa PT, McCrae RR. The NEO Personality Inventory. Odessa, FL: Psychological Assessment Resources 1985.
· de Girolamo G, Reich JH. Personality disorders (epidemiology of mental disorders and psychosocial problems). Geneva: World Health Organization 1993.
· De la Fuente JM, Tugendhaft P, Mavroudakis N. Electroencephalographic abnormalities in borderline personality disorder. Psychiatr Res 1998; 77:131-138.
· Digman JM. Personality structure: emergence of the five factor model. Annu Rev Psychol 1990; 41:417-440.
· Dolan B, Evans C, Norton K Multiple axis-II diagnoses of personality disorder. Br J Psychiatry 1995; 166:107-112.
· Dolan M. Psychopathy: a neurobiological perspective. Br J Psychiatry 1994; 165:151-159.
· Evans LH, Gray NS, Snowden RJ. Reduced P50 suppression is associated with the cognitive disorganisation dimension of schizotypy. Schizophr Res 2007; 97:152-162.
· Eysenck HJ. Culture and personality abnormality. In: AI-Issa I. (Ed.): Culture and psychopathology. Baltimore: University Park Press 1982; pp 277-308.
· Eysenck, HJ, Eysenck SBG. Manual for the Eyseck Personality Inventory. San Diego, CA: Educational and Industrial Testing Service 1968.
· Goldberg LR. The development of markers of the Big-Five factor structure. Psychol Assess 1992; 4:26-42.
· Harris GT, Rice ME, Quinsey VL. Psychopathy as a taxon: evidence that psychopaths are a discrete class. J Consult Clin Psychol 1994; 62:387-397.
· Hirschfield RMA, Holzer CE. Depressive personality disorder: Clinical implications. J Clin Psychiatry 1994; 55 (Suppl 4):10-17.
· Howard R, McCullagh P. Neuroaffective processing in criminal psychopaths: brain event-related potentials reveal task-specific anomalies. Personal Disord 2007; 21:322-339.
· Hyler SE, Lyons M. Factor analysis of the DSM III personality disorders clusters: A replication? Compr Psychiatry 1988; 29:304-308.
· Kagan J, Reznick JS, Snidman N. The physiology and psychology of behavioural inhibition in children. Child Dev 1987; 58:1459-1473.
· Kajitbak MS, Church AT, Akamine TX. Cross-cultural generalizability of personality dimensions: relating indigenous and imported dimensions in two cultures. J Pers Soc Psychol 1996; 70:99-114.
· Kernberg DF. (1996). A psychoanalytic theory of personality disorders. In: Clarkin JF, Lenzwenger MF (Eds.): Major theories of personality disorder. New York: Guildford Press 1996; pp. 106-141.
· Kishore P, Lal N, Trivedi JK, et al. A study of comorbidity in psychoactive substance dependence patients. Indian J Psychiatry 1994; 36:133-137.
· Lahmeyer HW, Reynolds CF, Kupfer DJ, et al. Biologic markers in borderline personality disorder: a review. J Clin Psychiatry 1989; 50:217-225.
· Lara DR, Akiskal HS. Toward an integrative model of the spectrum of mood, behavioral and personality disorders based on fear and anger traits: II. Implications for neurobiology, genetics and psychopharmacological treatment. J Affect Disord 2006; 94:89-103.
· Lenzwenger MF, Clarkin JF. The personality disorders: history, classification and research issues. In: Clarkin JF, Lenzwenger MF (Eds.): Major theories of personality disorder. New York: Guildford Press 1996; pp. 1-35.
· Lenzwenger MF, Korfine L. Confirming the latent structure and base rate of schizotypy: a taxometric approach. J Abnormal Psychol 1992; 101:576-581.
· Lewis-Ferernandez R, Kleinman A. Culture, personality and psychopathology. J Abnormal Psychol 1994; 103:67-7l.
· Linehan MM, Armstrong HE, Suarez A, et al Cognitive-behavioural treatment of chronically parasuicidal borderline patients. Arch Gen Psychiatry 1991; 48:1060-1064.
· Livesley WJ, Jackson DN. Guidelines for developing, evaluating, and revising the classification of personality disorders. J Nerv Ment Dis 1992; 180:609-618.
· Livesley WJ, Reiffer LI, Sheldon AE, et al. Prototypicality ratings of DSM-III criteria for personality disorders. J Nerv Ment Dis 1987; 175:395-401.
· Livesley WJ. Behavioral and molecular genetic contributions to a dimensional classification of personality disorder. J Pers Disord 2005; 19:131-155.
· Livesley WJ, Jackson DN, Schroeder ML. Factorial structure of traits delineating personality disorders in clinical and general population samples. J Abnormal Psychol 1992; 101:432-440.
· Livesley WJ, Jang KL, Jackson DN, et al. Genetic and environmental contributions to dimensional assessment of personality disorder. Am J Psychiatry 1993; 150:1826-183l.
· Loranger AW, Janca A, Sartorius N. Assessment and diagnosis of personality disorders. The ICD-10 International Personality Disorder Examination (IPDE). Cambridge: Cambridge University Press 1997.
· Lyons-Ruth K, Holmes BM, Sasvari-Szekely M, et al. Serotonin transporter polymorphism and borderline or antisocial traits among low-income young adults. Psychiatr Genet 2007; 17:339-343.
· Magnusson D. Individual development in an interactional perspective, Vol. 1. In: Magnusson D. (Ed.): Series: Paths through life. Hillsdale, NJ: Lawrence Erlbaum 1986.
· McCrae RR, Costa PT. Personality in adulthood. New York: Guilford 1990.
· Mezzich JE, Otero-Ojeda AA, Lee SS. International psychiatric diagnosis. In: Sadock BJ, Sadock VA (Eds.): Comprehensive Textbook of Psychiatry. Ed 7. Philadelphia: Lippincott, Williams & Wilkins, 2000; pp 839-853.
· Mohan R. Treatments for borderline personality disorder: integrating evidence into practice. Int Rev Psychiatry 2002; 14:42-51.
· Mulder RT, Joyce PR. Temperament and the structure of personality disorder symptoms. Psychol Med 1997; 27:99-106.
· Naidu H, Thacore AS, Issac S. Personality disorders in mood disorders: coexistence, diagnosis, stability and implication. Indian J Psychiatry 1998; 40 (Suppl.):38.
· Nakao K, Gunderson JG, Phillips KA. Functional impairment in personality disorders. J Pers Disord 1992; 6:24-33.
· Neki JS. Personality disorders: some problems of nosology and classification. In: Neki JS, Prabhu GG (Eds.): Personality Development and Personal Illness. New Delhi: All India Institute of Medical Sciences 1970; pp. 117-127.
· Nunberger HG, Marlin GA, Pollack S. An empirical method to refine personality disorder classification using stepwise logistic regression modelling to develop diagnostic criteria and thresholds. Compr Psychiatry 1994; 35:409-419.
· Oldham JM. Personality disorders: current perspectives. JAMA 1994; 272:1770-1776.
· Ono Y, Yoshimura K, Sueoka R, et al. Avoidant personality disorder and Tajin Kyoufu: sociocultural implications of the WHO/ADAMHA international study of personality disorders in Japan. Acta Psychiatr Scand 1996; 93:172-176.
· Paris J. Social factors in the personality disorders. Transcult Psychiatry 1997; 34:421-52.
· Pridmore S, Chambers A, McArthur M. Neuroimaging in psychopathy. Aust N Z J Psychiatry 2005; 39:856-865.
· Reddy MV, Chandrashekhar CR. Prevalence of mental and behavioural disorders in India: A metaanalysis. Indian J Psychiatry 1998; 40:149-157.
· Reich JH, de Girolamo G. Epidemiology of DSM-III personality disorders in the community and in clinical populations. In: Loranger AW, Janca A, Sartorius N (Eds.):Assessment and diagnosis of personality disorders. The ICD-10 International Personality Disorder Examination (IPDE). Cambridge: Cambridge University Press 1997; pp. 18-42.
· Reich JH. Familiality of DSM-III dramatic and anxious personality clusters. J Nerv Ment Dis 1989; 177:96-100.
· Sara G, Raven P, Mann A. A comparison of DSM-IIIR and ICD-10 personality disorder criteria in an outpatient population. Psychol Med 1996; 26:151-160.
· Schmahl C, Bremner JD. Neuroimaging in borderline personality disorder. J Psychiatr Res 2006; 40:419-427.
· Schroeder ML, Livesley WJ. An evaluation of DSM-IIIR personality disorders. Acta Psychiatr Scand 1991; 84:512-519.
· Sharan P. Structure of Personality and Personality Disorders in the Indian Context (Unpublished Ph D thesis). Chandigarh: Postgraduate Institute of Medical Education and Research 2001.
· Siever LJ. Endophenotypes in the personality disorders. J Psychiatry Neurosci 2007; 32:162-173.
· Siever LJ. Biological factors in schizotypal personality disorders. Acta Psychiatr Scand 1994; 90 (Suppl 384):45-50.
· Skodol AW, Johnson JG, Cohen P, et al. Personality disorder and impaired functioning from adolescence to adulthood. Br J Psychiatry 2007; 190:415-420.
· Stein G. Drug treatment of the personality disorders. Br J Psychiatry 1992; 161:167-184.
· Stone MH. Long-term outcome in personality disorders. Br J Psychiatry 1993; 162:299-313.
· Svrakic DM, Przrbeck TR, Cloninger CR. Mood states and personality traits. J Affect Disord 1992; 24:217-226.
· Tellegen A, Grove WM, Waller NG. Inventory of Personal Characteristics #7 (IPC). Unpublished materials, University of Minnesota 1991.
· Torgersen S. Genetics in borderline conditions. Acta Psychiatr Scand 1994; 89 (Suppl 379):19-25.
· Trull T, Widiger T, Guthrie P. Categorical versus dimensional status of borderline personality disorder. J Abnormal Psychol 1990; 99:40-8.
· Tyrer P, Casey P, Fergison B. Personality disorders in perspective. Br J Psychiatry 1991; 159:463-471.
· Watson D, Clark LA. Negative affectivity: the disposition to experience aversive emotional states. Psychol Bull 1984; 38:465-490.
· Widiger TA. Personality disorder and Axis I psychopathology: the problematic boundary of Axis I and Axis II. J Personal Disord 2003; 17:90-108.
· Widiger TA, Trull TJ, Hurt SW, et al. A multidimensional scaling of the DSM-III personality disorders. Arch Gen Psychiatry 1987; 44:557-563.
· Widiger TJ, Shea T. Differentiation of Axis I and Axis II disorders. J Abnormal Psychol 1991; 100:399-406.
· Wiggins JS. A psychological taxonomy of trait descriptive terms: the interpersonal domain. J Pers Soc Psychol 1979; 37:395-412.
· Wijesinghe CP, Dissanayake SAW, Dassanayake PVLN. Survey of psychiatric morbidity in a semi-urban population in Sri Lanka. Results of a census survey. Acta Psychiatrica Scandinavica 1978; 58:413-441.
· Yang KS, Bond MH. Exploring implicit personality theories with indigenous or imported constructs: the Chinese case. J Pers Soc Psychol 1990; 58:1087-1095.
· Zimmerman M. Diagnosing personality disorders. A review of issues and research methods. Arch Gen Psychiatry 1994; 51:225-245.
· Zuckerman M, Kuhlman DM, Joireman J, et al. A comparison of three structural models of personality: the big three, the big five and the alternate five. J Pers Soc Psychol 1993; 65:757-768.
Address for Correspondence: Professor Pratap Sharan, Department of Psychiatry, All India Institute of Medical Sciences, Ansari Nagar, New Delhi – 110029.
ICD-11: DRAFT PROPOSAL FOR CHANGES IN THE CATEGORIES ‘F70 – F98’
Manju Mehta, PhD; Rajesh Sagar, MD; Ravindra Rao, MD.
1. Change in the diagnostic criteria of hyperkinetic disorders
The diagnostic criteria for Attention Deficit Hyperactivity Disorder (ADHD) followed by the Diagnostic and Statistical Manual (DSM – IV) should be incorporated as it is in the ICD 11 edition. Thus, the criteria should be as follows:
I. Either A or B:
A. Six or more of the following symptoms of inattention have been present for at least 6 months to a point that is disruptive and inappropriate for the developmental level:
1. Often does not give close attention to details or makes careless mistakes in schoolwork, work, or other activities.
2. Often has trouble keeping attention on tasks or play activities.
3. Often does not seem to listen when spoken to directly.
4. Often does not follow instructions and fails to finish schoolwork, chores, or duties in the workplace (not due to oppositional behavior or failure to understand instructions).
5. Often has trouble organizing activities.
6. Often avoids, dislikes, or doesn't want to do things that take a lot of mental effort for a long period of time (such as schoolwork or homework).
7. Often loses things needed for tasks and activities (e.g. toys, school assignments, pencils, books, or tools).
8. Is often easily distracted.
9. Is often forgetful in daily activities.
B. Six or more of the following symptoms of hyperactivity-impulsivity have been present for at least 6 months to an extent that is disruptive and inappropriate for developmental level:
1. Often fidgets with hands or feet or squirms in seat.
2. Often gets up from seat when remaining in seat is expected.
3. Often runs about or climbs when and where it is not appropriate (adolescents or adults may feel very restless).
4. Often has trouble playing or enjoying leisure activities quietly.
5. Is often "on the go" or often acts as if "driven by a motor".
6. Often talks excessively.
1. Often blurts out answers before questions have been finished.
2. Often has trouble waiting one's turn.
3. Often interrupts or intrudes on others (e.g., butts into conversations or games).
II.Some symptoms that cause impairment were present before age 7 years.
III.Some impairment from the symptoms is present in two or more settings (e.g. at school/work and at home).
IV.There must be clear evidence of significant impairment in social, school, or work functioning.
V.The symptoms do not happen only during the course of a pervasive developmental disorder, schizophrenia, or other psychotic disorder. The symptoms are not better accounted for by another mental disorder (e.g. mood disorder, anxiety disorder, dissociative disorder, or a personality disorder).
2. Change in the subcategories of hyperkinetic disorder
The following categories for hyperkinetic disorder should be used in ICD 11.
1. ADHD, combined type
2. ADHD, predominantly inattention type
3. ADHD, predominantly hyperactive-impulsive type
4. Hyperkinetic conduct disorder
5. Other ADHD
6. ADHD, unspecified
3. Inclusion of borderline intelligence in the ‘Z’ category (factors influencing health status and contact with health services)
1. An intelligence quotient level of 70 to 84 using a standardized intelligence test (for which local cultural norms have been determined).
2. The reduced level of intellectual functioning should result in diminished ability to manage the daily demands of the normal social environment
3. The onset should be before 18 years of age
Evidence for the Proposed Changes
I. Change in the diagnostic criteria of hyperkinetic disorders
The current diagnostic criteria for hyperkinetic disorder in the ICD 10 differ from the diagnostic criteria incorporated in DSM IV in the following ways:
§ ICD 10 has divided the symptoms of hyperkinetic disorder into 3 main clusters – inattention, hyperactivity and impulsivity; DSM IV, on the other hand, has combined the hyperactivity and impulsivity clusters.
§ ICD 10 requires that the child should meet the criteria in more than one situation, whereas DSM IV requires the child has impairment in more than one situation (rather than meeting the entire criteria in more than one situation).
For ADHD/ hyperkinetic disorder, DSM IV criteria are better researched, while ICD 10 descriptions are used more often in clinics. Consequently, much of the published articles work relate to DSM IV criteria of ADHD.
Epidemiological studies: Malhi and Singhi (2000) reported that 8.1% of a consecutive sample of 245 children referred for evaluation to the Psychology outpatient services of the Department of Pediatrics of a tertiary care teaching hospital had ADHD. In a similar study, Mukhopadhyay et al (2003) found that 15.5% of children presenting to a child guidance clinic in a pediatric hospital over a one year period had ADHD. These studies demonstrated the utility of the ADHD diagnosis and the ease of applicability of DSM IV criteria in the Indian pediatric population.
Phenomenology: A factor analysis of symptoms of the disorder showed that a two-factor model had the best fit to the data – inattention and hyperactivity/ impulsivity (Hudziak et al, 1998). This supports the DSM IV proposal of two subtypes of ADHD rather than the three subtypes proposed by ICD 10. Studies have shown that while ADHD is a broad, heterogeneous category, the subgroup of children diagnosed as hyperkinetic disorder (the subtype in ICD 10) fit in the severe ADHD combined subtype of DSM IV criteria (El-Sayed et al, 2003).
Course and prognosis: A study that compared the predictive validity of ADHD according to ICD 10 and DSM IV criteria (Lahey et al. 2006) concluded that while both ICD-10 hyperkinetic disorder and DSM-IV ADHD exhibit predictive validity over 6 years, ICD-10 hyperkinetic disorder appears to under-identify children with persistent ADHD symptoms and related impairment. Children who met criteria for DSM-IV ADHD but not hyperkinetic disorder exhibited at least as much functional impairment over time as hyperkinetic children. A review by El-Sayed et al (2003) concluded that children showing symptoms above the threshold for a diagnosis of ADHD according to DSM IV are at risk of developing co morbid conditions and increasing stress in both parents and teachers. Theses reports suggest that children with features of ADHD, who cannot be diagnosed by ICD 10, but receive such a diagnosis according to DSM IV criteria need to be identified and managed appropriately.
II. Change in the subcategories of hyperkinetic disorder
The hyperkinetic disorder (ADHD) in ICD 10 and DSM IV is currently sub classified as follows (Table 1):
Table 1: Subcategory of Attention Deficit Hyperactivity Disorder (Hyperkinetic Disorder) in current classificatory system
F90.0 Disturbance of activity and attention
314.01 ADHD, combined type (ADHD-C)
314.02 ADHD, predominantly inattention type (ADHD-I)
314.03 ADHD, predominantly hyperactive-impulsive type (ADHD-HI)
F98.8 Inclusion term in other specified behavioral and emotional disorders
F90.1 Hyperkinetic conduct disorder
F90.8 Other hyperkinetic disorder
F90.9 Hyperkinetic disorder, unspecified
ICD: International Classification of Disease; DSM: Diagnostic and Statistical Manual
ADHD: Attention Deficit Hyperactivity Disorder
The authors propose the following categories to be used for hyperkinetic disorder/ADHD in ICD 11:
1. ADHD, combined type
2. ADHD, predominantly inattention type
3. ADHD, predominantly hyperactive-impulsive type
4. Hyperkinetic Conduct disorder
5. Other ADHD
6. ADHD, unspecified
Epidemiological studies: Studies using the DSM IV criteria show that ADHD – inattentive subtype is the most common one followed by ADHD – combined subtype (2nd most common) and ADHD – hyperactive impulsive subtype (Graetz et al, 2001; Ford et al, 2003). The study by Malhi and Singhi (2000) confirmed that all the 3 subtypes of ADHD (according to DSM IV criteria) were common in India – 50% of the children had hyperactive-impulsive subtype, 35% had the inattentive subtype and 15% had the combined subtype.
Sociodemographic profile: Studies have shown that ADHD-hyperactive impulsive subtype is more frequent in the younger age group as compared to the ADHD-inattention subtype (Nolan et al. 1999, Malhi and Singhi, 2000). It also has been seen that ADHD-inattention subtype is more common among females than males (Biederman et al. 2002).
Comorbidity: Studies have shown differences in the comorbidity between the three subtypes of ADHD. Thus, higher rates of anxiety and depression were seen in those with ADHD-combined subtype and ADHD-inattention subtype compared to those with ADHD-hyperactive impulsive subtype (MTA Cooperative Group, 1999). One study has found higher rates of bipolar disorder and tic disorder in those with ADHD-combined subtype (Faraone et al, 1998). Oppositional defiant and conduct disorders are most commonly seen in children with ADHD-combined subtype, followed by ADHD-hyperactive impulsive and ADHD-inattention subtypes (Morgan et al, 1996). An Indian study (Malhi and Singhi, 2000) found differences between the 3 subtypes with respect to intelligence, academic difficulties, relationship with peers and behavioral problems.
Family studies: Though some studies have shown increased rates of a particular subtype in the relatives of the affected children (Faraone et al. 2000), other studies have not found such increased rates (Smalley et al, 2000). Thus the family studies have been inconclusive.
Treatment response: Studies on differential stimulant treatment response among various subtypes of hyperkinetic disorder/ADHD are not available as most of the trials have only recruited children with combined ADHD (MTA Cooperative Group, 1999). Studies that have employed other subtypes, have not reported treatment response separately (Kratochvil et al, 2002).
Course and prognosis: The degree and type of impairment have been shown to be different among different subtypes of ADHD. Lahey et al (2006) have shown that ADHD-combined and ADHD-hyperactive impulsive subtypes have greater impairment than ADHD-inattention subtype. It is also seen that ADHD-inattention subtype is associated with more academic problems, whereas ADHD-hyperactive impulsive subtype is associated with more social and behavioral problems (Gadow et al, 2000; Graetz et al, 2001).
Thus, studies have shown that there are several differences between the subtypes of ADHD, thereby making it important to recognize these subtypes.
II a. Retaining the Hyperkinetic Conduct disorder subtype of ADHD
Co-occurrence: While most children who meet the criteria for conduct disorder also meet the criteria for ADHD; only about one third of adolescents with conduct disorder meet the criteria for ADHD (Reeves et al, 1987; Szatmari et al, 1989).
Impairment: In terms of academic achievement, children with combined ADHD/conduct disorder have higher rates of reading disorders than ADHD and controls (McGee et al, 1984). Children with combined ADHD/conduct disorder were found to be more impaired in verbal skill, visual motor integration and visuospatial skills as compared to children with ADHD and controls (Moffitt and Silva, 1988). An Indian study (Malhotra et al, 1999) compared hyperkinetic conduct disorder (HCD) with conduct disorder and found that the HCD children had lower intelligence, more perinatal complications and delayed milestones.
Family history: Biederman et al (1992) examined the rates of psychiatric diagnosis among relatives of a large sample of ADHD and ADHD/conduct disorder. While the rates of ADHD was the same in both group of relatives, conduct disorder was more common among relatives of combined ADHD/conduct disorder than among ADHD disorder alone. Furthermore, relatives with conduct disorder also tended to have ADHD. This means that the two disorders co-segregated, indicating that ADHD/conduct disorder is a distinct familial subtype.
Course and prognosis: Studies have shown differences in the long term outcomes of both subgroups of children. The ADHD/conduct disorder subgroup showed more antisocial and defiant behaviors (August et al, 1983). Also this group showed a higher rate of substance use. Studies have also concluded that while ADHD itself conveys some risk for adult antisocial behavior, the combined ADHD/conduct disorder group had sharp rise in the risk of adult antisocial personality and criminal conviction (Mannuzza et al, 1989). The Indian study (Malhotra et al, 1999) that compared hyperkinetic conduct disorder (HCD) with conduct disorder also found that the HCD group had an younger age of onset, more gradual development of conduct symptoms and a longer duration of conduct symptoms.
Treatment response: Studies do not show any difference in the response to stimulant treatment between the ADHD/conduct disorder and ADHD group alone (Klonman et al, 1989).
Available evidence suggests that there is a need to have a separate diagnostic subgroup of hyperkinetic disorder.
III. Inclusion of borderline intelligence in the ‘Z’ category (factors influencing health status and contact with health services)
The group of F70 – F79 consists of mental retardation, which includes the mild, moderate and severe types. Most of the intelligence tests used have a separate category for borderline intelligence. The DSM IV, too, places borderline intelligence in the group of ‘additional conditions that may be a focus of clinical attention’.
Borderline intellectual functioning, has received little attention to date. However, some studies on prevalence of this condition show that it is present in up to 7%–18% of the population (Hassiotis et al, 1999; Ninivaggi, 2001).
In a study by Chen et al (2006), it was seen that children with subaverage cognitive abilities were more likely to develop mental health problems than their counterparts with IQs above 80 in later life. Another study by Hassiotis et al (1999) which have also shown that those with comorbid borderline intelligence and psychotic illness had greater disability and were more likely to suffer extrapyramidal side-effects and show evidence of negative symptoms than those with psychotic illness with normal intelligence. This may lead to difficulties in other domains of adaptive functioning. Thus, studies have shown that individuals with borderline intelligence may require a separate category.
Hence, borderline intelligence should be included in the ‘Z’ category to provide recognition to this condition in the international classificatory system.
· American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Ed 4, Text Revision, Washington DC: APA, 2000.
· August GJ, Stewart MA, Holmes CS. A four-year follow-up of hyperactive boys with and without conduct disorder. Br J Psychiatry 1983; 143:192-198.
· Biederman J, Faraone SV, Keenan K, et al. Further evidence for family-genetic risk factors in attention deficit hyperactivity disorder: patterns of comorbidity in probands and relatives in psychiatrically and pediatrically referred samples. Arch Gen Psychiatry 1992; 49:728–738.
· Biederman J, Mick E, Faraone SV, et al. Influence of gender on attention- deficit/hyperactivity disorder in children referred to a psychiatric clinic. Am J Psychiatry 2002; 159:36–42.
· Chen CY, Lawlor JP, Duggan AK, et al. Mild cognitive impairment in early life and mental health problems in adulthood. Am J Public Health. 2006; 96:1772-1778.
· El-Sayed E, Larsson JO, Persson HE, et al. "Maturational lag" hypothesis of attention deficit hyperactivity disorder: an update. Acta Paediatr 2003; 92:776-784.
· Faraone SV, Biederman J, Friedman D. Validity of DSM-IV subtypes of attention- deficit/hyperactivity disorder: a family study perspective. J Am Acad Child Adolesc Psychiatry 2000; 39:300–307.
· Faraone SV, Biederman J, Weber W, et al. Psychiatric, neuropsychological and psychosocial features of DSM-IV subtypes of attention-deficit/hyperactivity disorder: results from a clinically referred sample. J Am Acad Child Adolesc Psychiatry 1998; 37:185–193.
· Ford T, Goodman R, Meltzer H. The British child and adolescent mental health survey 1999: the prevalence of DSM-IV disorders. J Am Acad Child Adolesc Psychiatry 2003; 42:1203–1211.
· Gadow KD, Nolan EE, Litcher L et al. Comparison of attention-deficit hyperactivity disorder symptom subtypes in Ukrainian schoolchildren. J Am Acad Child Adolesc Psychiatry 2000; 39:1520-1527.
· Graetz BW, Sawyer MG, Hazell PL, et al. Validity of DSM-IV ADHD subtypes in a nationally representative sample of Australian children and adolescents. J Am Acad Child Adolesc Psychiatry 2001;40: 1410–1417.
· Hassiotis A, Ukoumunne O, Tyrer P, et al. Prevalence and characteristics of patients with severe mental illness and borderline intellectual functioning. Report from the UK700 randomised controlled trial of case management. Br J Psychiatry. 1999; 175:135-140.
· Hudziak JJ, Heath AC, Madden PF, et al. Latent class and factor analysis of DSM-IV ADHD: a twin study of female adolescents. J Am Acad Child Adolesc Psychiatry 1998; 37:848–857.
· Klonman R, Brumaghim JT, Salzman LF, et al. Comparative effects of methylphenidate on attention-deficit hyperactivity disorder with and without aggressive/noncompliant features. Psychopharmacol Bull 1989; 25:109-113.
· Kratochvil CJ, Heiligenstein JH, Dittmann R, et al. Atomoxetine and methylphenidate treatment in children with ADHD: a prospective, randomised, open-label trial. J Am Acad Child Adolesc Psychiatry 2002; 41:776–784.
· Lahey BB, Pelham WE, Chronis A, et al. Predictive validity of ICD-10 hyperkinetic disorder relative to DSM-IV attention-deficit/hyperactivity disorder among younger children. J Child Psychol Psychiatry. 2006; 47:472-479.
· Malhi P, Singhi P. Spectrum of attention deficit hyperactivity disorders in children among referrals to psychology services. Indian Pediatr 2000; 37:1256-1260.
· Malhotra S, Aga VM, Balraj, et al. Comparison of conduct disorder and hyperkinetic disorder: a retrospective clinical study from north India. Indian J Psychiatry 1999; 41:111-121.
· Mannuzza S, Klein RG, Konig PH, et al. Hyperactive boys almost grown up, IV: criminality and its relationship to psychiatric status. Arch Gen Psychiatry 1989; 46:1073–1079.
· McGee R, Williams S, Silva PA. Behavioral and developmental characteristics of aggressive, hyperactive, and aggressive-hyperactive boys. J Am Acad Child Adolesc Psychiatry 1984; 23:270–279.
· Moffitt TE, Silva PA. Self-reported delinquency, neuropsychological deficit, and history of attention deficit disorder. J Abnorm Child Psychol 1988; 16:553–569.
· Morgan A, Hynd G, Riccio C, Hall J. Validity of DSM-IV ADHD predominantly inattentive and combined types: relationship to previous DSM diagnoses/subtype differences. J Am Acad Child Adolesc Psychiatry 1996; 35:325–333.
· MTA Cooperative Group. Moderators and mediators of treatment response for children with attention-deficit/ hyperactivity disorder. Arch Gen Psychiatry 1999; 56:1088–1096.
· Mukhopadhyay M, Misra S, Mitra T, et al. Attention deficit hyperactivity disorder. Indian J Pediatr 2003; 70:789-792.
· Ninivaggi FJ. Borderline intellectual functioning in children and adolescents: reexamining an underrecognized yet prevalent clinical comorbidity. Conn Med 2001; 65:7-11.
· Nolan EE, Gadow KD, Sprafkin J. Teacher reports of DSM-IV ADHD, ODD and CD symptoms in schoolchildren. J Am Acad Child Adolesc Psychiatry 1999; 40:241–249.
· Reeves JC, Werry JS, Elkind GS, et al. Attention deficit, conduct, oppositional, and anxiety disorders in children, II: clinical characteristics. J Am Acad Child Adolesc Psychiatry 1987; 26:144–155.
· Smalley SL, McGough JJ, Del’Homme M, et al. Familial clustering of symptoms and disruptive behaviours in multiplex families with attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry 2000; 39:1135–1143.
· Szatmari P, Boyle M, Offord DR. ADHD and conduct disorder: degree of diagnostic overlap and differences among correlates. J Am Acad Child Adolesc Psychiatry 1989; 28:865–872.
· World Health Organization. The ICD 10 Classification of Mental and Behavioral Disorders. Clinical Descriptions and Diagnostic Guidelines. Geneva: WHO, 1992.