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Приложение 1

Международная классификация болезней 10-го пересмотра
The ICD-10 Classification of Mental and Behavioural Disorders
World Health Organization, Geneva, 1992

МКБ-10 определяет расстройство поведения как повторяющийся и постоянный парттерн асоциального, агрессивного или дерзкого и вызывающего поведения, - открытого неповиновения. Поведение оценивают сравнительно с ровесниками, которые ведут себя соответственно социальным ожиданиям и выходит за рамки детского озорства или подросткового бунтарства. Однократные асоциальные поступки или правонарушения не являются основанием для диагноза. Для диагностики необходимо систематическое поведение любой из нижеследующих категорий:
- крайняя степень задиристости или запугивание других, - жестокость по отношению к животным или к другим, - серьёзное причинение вреда имуществу, - поджоги, - воровство, - лживость, - прогулы школьных занятий, - побеги из дома, - необычно частые и серьёзные вспышки гнева, - дерзкое, провокативное поведение, - стойкое серьёзное неповиновение. Нарушения поведения могут быть симптомами и других психиатрических расстройств, и в этом случае кодируется основной диагноз.
Полностью на английском языке:
F91 Conduct Disorders
Conduct disorders are characterized by a repetitive and persistent pattern of dissocial, aggressive, or defiant сonduct. Such behaviour, when at its most extreme for the individual, should amount to major violations of age-appropriate social expectations, and is therefore more severe than ordinary childish mischief or adolescent rebelliousness. Isolated dissocial or criminal acts are not in themselves grounds for the diagnosis, which implies an enduring pattern of behaviour.
Features of conduct disorder can also be symptomatic of other psychiatric conditions, in which case the underlying diagnosis should be coded.
Disorders of conduct may in some cases proceed to dissocial personality disorder (F60.2). Conduct disorder is frequently associated with adverse psychosocial environments, including unsatisfactory family relationships and failure at school, and is more commonly noted in boys. Its distinction from emotional disorder is well validated; its separation from hyperactivity is less clear and there is often overlap.
Diagnostic Guidelines
Judgements concerning the presence of conduct disorder should take into account the child's developmental level. Temper tantrums, for example, are a normal part of a 3-year-old's development and their mere presence would not be grounds for diagnosis. Equally, the violation of other people's civic rights (as by violent crime) is not within the capacity of most 7-year-olds and so is not a necessary diagnostic criterion for that age group.
Examples of the behaviours on which the diagnosis is based include the following: excessive levels of fighting or bullying; cruelty to animals or other people; severe destructiveness to property; firesetting; stealing; repeated lying; truancy from school and running away from home; unusually frequent and severe temper tantrums; defiant provocative behaviour; and persistent severe disobedience. Any one of these categories, if marked, is sufficient for the diagnosis, but isolated dissocial acts are not.
Exclusion criteria include uncommon but serious underlying conditions such as schizophrenia, mania, pervasive developmental disorder, hyperkinetic disorder, and depression.
This diagnosis is not recommended unless the duration of the behaviour described above has been 6 months or longer.
Differential diagnosis. Conduct disorder overlaps with other conditions. The coexistence of emotional disorders of childhood (F93.-) should lead to a diagnosis of mixed disorder of conduct and emotions (F92.-). If a case also meets the criteria for hyperkinetic disorder (F90.-), that condition should be diagnosed instead. However, milder or more situation-specific levels of overactivity and inattentiveness are common in children with conduct disorder, as are low self-esteem and minor emotional upsets; neither excludes the diagnosis.
* conduct disorders associated with emotional disorders (F92.-) or hyperkinetic disorders (F90.-)
* mood [affective] disorders (F30-F39)
* pervasive developmental disorders (F84.-)
* schizophrenia (F20.-)

The ICD-10 Classification of Mental and Behavioural Disorders
World Health Organization, Geneva, 1992
F91.3 Oppositional Defiant Disorder
This type of conduct disorder is characteristically seen in children below the age of 9 or 10 years. It is defined by the presence of markedly defiant, disobedient, provocative behaviour and by the absence of more severe dissocial or aggressive acts that violate the law or the rights of others. The disorder requires that the overall criteria for F91 be met: even severely mischievous or naughty behaviour is not in itself sufficient for diagnosis. Many authorities consider that oppositional defiant patterns of behaviour represent a less severe type of conduct disorder, rather than a qualitatively distinct type. Research evidence is lacking on whether the distinction is qualitative or quantitative. However, findings suggest that, in so far as it is distinctive, this is true mainly or only in younger children. Caution should be employed in using this category, especially in the case of older children. Clinically significant conduct disorders in older children are usually accompanied by dissocial or aggressive behaviour that go beyond defiance, disobedience, or disruptiveness, although, not infrequently, they are preceded by oppositional defiant disorders at an earlier age. The category is included to reflect common diagnostic practice and to facilitate the classification of disorders occurring in young children.
Diagnostic Guidelines
The essential feature of this disorder is a pattern of persistently negativistic, hostile, defiant, provocative, and disruptive behaviour, which is clearly outside the normal range of behaviour for a child of the same age in the same sociocultural context, and which does not include the more serious violations of the rights of others as reflected in the aggressive and dissocial behaviour specified for categories F91.0 and F91.2. Children with this disorder tend frequently and actively to defy adult requests or rules and deliberately to annoy other people. Usually they tend to be angry, resentful, and easily annoyed by other people whom they blame for their own mistakes or difficulties. They generally have a low frustration tolerance and readily lose their temper. Typically, their defiance has a provocative quality, so that they initiate confrontations and generally exhibit excessive levels of rudeness, uncooperativeness, and resistance to authority.
Frequently, this behaviour is most evident in interactions with adults or peers whom the child knows well, and signs of the disorder may not be evident during a clinical interview.
The key distinction from other types of conduct disorder is the absence of behaviour that violates the law and the basic rights of others, such as theft, cruelty, bullying, assault, and destructiveness. The definite presence of any of the above would exclude the diagnosis. However, oppositional defiant behaviour, as outlined in the paragraph above, is often found in other types of conduct disorder. If another type (F91.0-F91.2) is present, it should be coded in preference to oppositional defiant disorder.
* conduct disorders including overtly dissocial or aggressive behaviour (F91.0-F91.2)

Приложение 2
10.1177/1087054708324551 http://jad.sagepub.com hosted at http://online.sagepub.com

Journal of Attention Disorders
Volume 12 Number 3
November 2008 284-285
© 2008 Sage Publications

Request for Secondary Data Analyses Related to Diagnostic Criteria for DSM-V Disruptive Disorders

The ADHD and Disruptive Behavior Disorders Work Group for the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V), published by the American Psychiatric Association, is in the process of evaluating the existing criteria for ADHD, Oppositional Defiant Disorder (ODD), Conduct Disorder (CD), and Antisocial Personality Disorder (APD). It has identified several key issues that need to be addressed empirically in considering revisions. The key issues are summarized below. Most of these issues focus on the cross-sectional and longitudinal predictive validity of the diagnostic criteria with respect to impairment, course (both short term and long term), treatment response, family history, neurocognitive correlates, and other clinically important validators.

Investigators with data, published or unpublished, that could address any of these issues are encouraged to make their reports or results available to the Work Group by submitting them to DSM5@psych.org. Reporting requirements, full Work Group membership, and additional information about how these questions were developed can also be requested from DSM5@psych.org. Data reports will be used and cited internally by the Work Group but not published independently; thus, submission of reports using unpublished data would not preclude later publication and investigators will retain control of publication options. Investigators who submit data analyses used by the Work Group will be designated Advisors to the DSM-V ADHD and Disruptive Behavior Disorders Work Group.

A. Research Questions Related to the Disruptive Behavior Disorders (DBDs)

DBD 1. Childhood- and adolescent-onset subtypes of CD:
(a) Do variations in the age of onset criterion influence the predictive validity of the subtypes?
(b) Can additional criterion information (such as callous-unemotional traits or biomarkers) improve the predictive validity?

DBD 2. Development of lifespan criteria for CD and APD:
(a) Can developmentally sensitive criteria be identified that link both CD and APD in one antisocial disorder across the lifespan?
(b) How could psychopathic/callous-unemotional traits be integrated into such criteria?

DBD 3. Usefulness of ODD as a separate diagnostic category:
(a) Does the diagnosis of ODD have independent predictive validity when comorbid disorders are controlled?
(b) Does comorbid ODD add incremental predictive utility to other diagnoses (e.g., ADHD)?

DBD 4. Diagnostic criteria for ODD:
(a) Does requiring a pervasiveness criterion improve the predictive validity of ODD?
(b) Do the emotional (e.g., spiteful, angry) versus behavioral (e.g., argues, defies) symptoms of ODD show relatively greater continuity with CD/APD or with emotional disorders?

B. Research Questions Related to ADHD

ADHD 1. Defining ADHD subtypes:
(a) Can alternative methods for defining ADHD subtypes identify subgroups with greater predictive validity than the current DSM-IV definition?
(b) Are these subtypes best thought of as subtypes of the same disorder or as distinct disorders?

ADHD 2. ADHD diagnostic criteria in adults:
(a) Which existing symptoms are most diagnostically informative in adults?
(b) Which are redundant or expendable when making an ADHD diagnosis in adults with regard to predictive validity?

C. Cross-Cutting Research Questions

ADHD/DBD 1. Validity of disorders across groups:
(a) Do the existing criteria for ADHD, ODD, and CD show acceptable predictive validity across different genders, ethnic groups, and developmental stages?
(b) Can the predictive validity of these disorders be improved by including criteria that are specific to the child’s gender, ethnic group, or developmental stage without masking real etiological effects across groups?

ADHD/DBD 2. Comorbidity among disorders:
(a) Does consideration of aggression and/or CD identify an important subgroup of youth with ADHD with respect to predictive validity?
(b) Is this group best thought of as a subtype of CD, a subtype of ADHD, or a third disorder? "

Приложение 3

The ICD-10 Classification of Mental and Behavioural Disorders
World Health Organization, Geneva, 1992

F84.5 Asperger's syndrome

A. A lack of any clinically significant general delay in spoken or receptive language or cognitive development. Diagnosis requires that single words should have developed by two years of age or earlier and that communicative phrases be used by three years of age or earlier. Self-help skills, adaptive behaviour and curiosity about the environment during the first three years should be at a level consistent with normal intellectual development. However, motor milestones may be somewhat delayed and motor clumsiness is usual (although not a necessary diagnostic feature). Isolated special skills, often related to abnormal preoccupations, are common, but are not required for diagnosis.
B. Qualitative abnormalities in reciprocal social interaction (criteria as for autism).
C. An unusually intense circumscribed interest or restricted, repetitive, and stereotyped patterns of behaviour, interests and activities (criteria as for autism; however it would be less usual for these to include either motor mannerisms or preoccupations with part- objects or non-functional elements of play materials).
D. The disorder is not attributable to the other varieties of pervasive developmental disorder; schizotypal disorder (F21); simple schizophrenia (F20.6); reactive and disinhibited attachment disorder of childhood (F94.1 and .2); obsessional personality disorder (F60.5); obsessive-сompulsive disorder (F42).

Michael Fitzgerald and Mark A. Bellgrove (2006) The Overlap Between Alexithymia And Asperger’s Syndrome. J Autism Dev Disord. 2006 May; 36(4): 573–576.

Alexithymia is characterised by an inability to express emotions verbally and by improvished fantasy and imaginal life. Individuals so affected may also experience difficulty in distinguishing emotional states from bodily sensations. Alexithymia is thought of as a psychosomatic disorder since the inability to identify and verbalise feelings may predispose to somatization. The term was coined by Sifneos (1972) but descriptions of conditions with alexithymic features predate this work. Aetiological theories of the disorder have variously emphasised genetic, neuropshysiological, developmental and psychodynamic factors (Krystal, 1998; Parker & Taylor, 1997). Like Alexithymia, Asperger's disorder is also characterised by core disturbances in speech and language and social relationships. Here we aim to demonstrate that there is considerable overlap in the clinical presentation of persons with a diagnosis of Alexithymia and Asperger's syndrome.
As John Nemiah (1996) points out there is now a large literature devoted to the construction of standardised Alexithymia rating scales and their applications to clinical research. Alexithymia may now be measured as a valid and reliable clinical phenomenon (Nemiah, 1996, 1977). It is interesting that the description of Alexithymia focusing on aetiology and treatment all are similar to the literature on Asperger's syndrome. Taylor, Bagby and Parker (1997) describes persons with Alexithymia as having difficulty in describing feelings and having difficulty in distinguishing between feelings and bodily sensations. He also points out their difficulties with affective self-regulation. Thus sufferers may have difficulties in the appraisal and expression of emotion and in the ability to use feelings to guide behaviour. Indeed Taylor et al. (1997) state that persons with Alexithymia “know very little about their own feelings and, in most instances, are unable to link them with memories, fantasies, and higher level effects, or specific situations” (page 29). It is argued that the inability of the patient with Alexithymia to express and modulate feelings, may lead to a discharge of tension through, for example, impulsive acts or compulsive behaviour such as binge eating (Bagby & Taylor, 1997).
Cognitive Problems In Alexithymia / Asperger’s Syndrome
Taylor et al. (1997) notes that individuals with Alexithymia have problems with introspection, poor capacity for fantasy, and that they show a stimulus bound, externally orientated cognitive style. Indeed James Grotstein (in Disorders of Affect Regulation by Taylor et al., 1997) describes Alexithymia as “an affect processing disorder that interrupts or seriously interferes with the organisms self-organising and reorganising processes” (page 12). This means that they have a diffuse sense of self. Indeed there is an earlier disorder called Pensee Operatoire (operative thinking) described by Marty and de M'Uzan (1963) where there is a similar utilitarian thinking style to that seen in Alexithymia and indeed Asperger's disorder. Krystal (1998) has described patients with La Pensee Operatoire as showing a “dull, mundane, unimaginative, utilitarian, and sequential recitation of concrete facts” (page 246). He also notes that these patients show a cognitive style where there is an “absence of the human quality (which) contributes to making these patients thoughts “operative” or thing orientated” (page 247). Such patients may often be described as dull, colourless and boring even when they are intellectual and clever (Taylor, 1984). Of course many persons with Alexithymia or Asperger's syndrome or La Pensee Operatoire can operate very well or indeed at superior levels in their work as mathematicians, engineers, etc. (Baron-Cohen, Wheelwright, Skinner, Martin, & Clubley, 2001).
Problems With Social Relationships In Alexithymia and Asperger’s Syndrome
Taylor et al. (1997) noted that Alexithymic individuals are “unable to identify accurately their own subjective feelings, verbally communicate emotional distress to other people very poorly, thereby failing to enlist others as sources of aid and comfort” (page 30). In addition they note that persons with Alexithymia have a preference to be alone or avoid people altogether. Krystal (1998) notes their tendency “to be like a rock or an island” and that “the degree of detachment in relation to others and their attitudes towards themselves is sometimes so flat that they feel psychotic to the interviewer and give the impression that the patient has deadened his object and self-representations or at least sapped it of all humanity” (page 246). Wing's (1981) criteria for Asperger's disorder (Asperger, 1944) emphasise a lack of normal interest and pleasure in people around them and a significant reduction in shared interests. Thus difficulties with social relationships are common to both Alexithymia and Asperger's disorder. Krystal notes the tendency of Alexithymic individuals to treat people as if they were machines. McDougall (1984) notes their great fear in intimacy situations and the problems experienced by these individuals in understanding social groups. Persons with Asperger's syndrome have similar problems. They have problems with social “know-how,” have empathy deficit and are often very over controlling, and have difficulty reading the non-verbal cues other people demonstrate in social interaction.
Speech and Language Problems In Alexithymia and Asperger’s Syndrome
Taylor et al. (1997) describes persons with Alexithymia as showing speech which is deficient in nuance, meagre in the use of metaphor and lacking affect, which of course is typical of the kind of speech that persons with Asperger's syndrome produce. He also notes that their language is characterised by flatness, banality and is fact based. Krystal (1998) notes that “the associations of these patients are characterised by an almost complete absence of thoughts relating to inner attitudes, feelings, wishes, or drives; and a recounting in great and often boring detail, of events in their external environment and their own actions in this setting” (page 248) and they also show a decreased use of the pronoun I. They show clear impairment in symbolic function. Indeed McDougall (1978) observed that Alexithymic patients use speech as “an act rather than a symbolic means of communication of ideas or affect” (page 45). Krystal noted that these patients with Alexithymia showed a “poorness and flatness of the contents of their communication” (page 246) as shown by their prosody and their monotone tone of voice. They can learn approximately socially appropriate responses but these are often excessively formal but these expressions lack nuance, lack proper prosody, are often very formal, and pedantic. They strike the listener as being somewhat unusual or overly formal. Speech and prosodic abnormalities are widely reported in autism spectrum disorders, including Asperger's disorder (Shriberg et al., 2001). Such abnormalities are perhaps indicative of dysfunction to the right hemisphere (see below) in these disorders. Krystal also observes that patients with Alexithymia “give a boring recital of information with a mentality approaching that of mental retardation” (page 272). This description is again very similar to Asperger's syndrome. In our own clinical experience (M.F.) we have noted that it is not uncommon to under estimate the IQ of some persons with Asperger's syndrome. Indeed, the opposite can also happen because of the great knowledge apparent in a single narrow area.
Non-verbal behavior In Alexithymia and Asperger’s Syndrome
Bagby and Taylor (1997) note “a somewhat stiff wooden posture, and a prosody of facial emotional expression” (page 29) in patients with Alexithymia. They also note their problems in identifying non-verbal facial emotion. Difficulties in the perception of facial emotions expressed by others is a cardinal feature of autism spectrum disorders. Damasio and Maurer (1978) suggested that autism is accompanied by dysfunction within mesolimbic brain circuits, including the ventromedial prefrontal cortex, medial temporal lobe, striatum and limbic thalamus. Damage to these areas causes deficits in social and emotional functioning, stereotype and obsessionality that also characterise autism spectrum disorders. Indeed, functional imaging studies have reported aberrant activation patterns within the above defined circuitry when autistic individuals perform tasks requiring the recognition of facial expressions (e.g., happy, sad, disgust) (Ogai et al., 2003).
It appears from this discussion that there is considerable overlap between Asperger's syndrome and Alexithymia with social interactional difficulties, unusual language, problems in non-verbal behaviour, problems with affective interaction, and a rather factual based thinking style. In addition Alexithymia like Asperger's syndrome, presents as a dimensional, rather than categorical, construct, suggesting multiple aetiological routes.
Aetiology of Alexithymia ETIOLOGY OF ALEXITHYMIA
At an aetiological level there also appears to be overlap between Alexithymia and Asperger's disorder, in terms of the brain circuitry that is thought dysfunctional in these conditions. One source of information regarding the cerebral localisation of affective function has come from patients who have undergone commissurectomies. Hoppe and Bogen (1977) reported on 12 commissurectomized patients who experienced, among other difficulties, Alexithymia. Cerebral commissurectomies also result in impoverishment of dreams and fantasies, and difficulty in describing feelings, as well as a pronounced operative style of thinking. A similar clinical presentation has also been reported in a case of agenesis of the corpus callousm. Hoppe and Bogen (1977) has postulated that Alexithymia may involve interruption of the normal flow of information between the two hemispheres. An alternative hypothesis to a deficit in inter-hemispheric communication is that the right-hemisphere itself may be dysfunctional in Alexithymia (Krystal, 1998). Supporting evidence for this proposition comes from lesion studies that demonstrate abnormal prosody in right-hemisphere patients. Prosodic abnormalities are a feature of both Alexithymia and Asperger's disorder. The right-hemisphere may also be specialised for processing the whole, rather than the detail. Patients with right-hemisphere lesions show deficits on visual-perceptual tasks where they are required to process the whole at the expense of the detail (Robertson, Lamb, & Knight, 1988). Influential cognitive theories of autism, such as weak central coherence, propose an alternative information processing style such that affected individuals show detailed-focussed processing that occurs at the expense of the global form (Happe, 1999). This processing style may extend to the semantic domain where for example, people with autism spectrum disorder do not show the usual advantage for recalling sentences better than unconnected word strings (Hermelin & O'Connor, 1967). It would be interesting to investigate whether individuals with Alexithymia demonstrate similar behavioural profiles in verbal and perceptual tasks. Persons with Alexithymia have greater tendencies to alcohol abuse, “psychosomatic complaints,” and have a tendency to social conformity. Alexithymia has been seen as a response to chronic illness. Clearly however differences exist between aetiological accounts of the disorders. Whereas Asperger's syndrome is a neurodevelopmental disorder, Alexithymia may be more of a personality trait.
Despite the apparent overlap between the disorders, aetiological differences may exist. One point of difference may lie in the genetic and neurochemical underpinnings of the disorders. Although not conclusive, a number of studies have indicated an association between polymorphisms of the Serotonin transporter gene and Autism Spectrum Disorder (Cook et al., 1997; Kim et al., 2002). By contrast associations with polymorphisms of the dopamine system have not been reliably identified in Autism Spectrum Disorders. In a recent study Ham et al. (2005) reported an association between the catechol-O-methyltransferase Val 108/158Met polymorphism and Alexithymia. Interestingly, an association was reported with the Valine allele which is associated with lowered prefrontal dopamine tone and is also thought to confer a small amount of risk to schizophrenia (Egan et al., 2001). In contrast to Autism Spectrum Disorders, Ham et al. did not report any association between Alexithymia and polymorphisms of the Serotonin transporter gene. These very preliminary findings suggest a greater involvement of the dopamine system in Alexithymia and the Serotonin system in Autism Spectrum Disorders. Other points of difference between the disorder lie in the greater tendency on the part of persons with Alexithymia, relative to those with Asperger's disorder, to alcohol abuse, psychosomatic complaints and social conformity. Alexithymia has also been seen as a response to chronic illness.
Treatment of Alexithymia TREATMENT OF ALEXITHYMIA
Not surprisingly, persons with Alexithymia, like persons with Asperger's syndrome, show a very poor response to psychoanalytic psychotherapy (Freyberger, 1977; McDougall, 1982). Alexithymic patients need a more cognitive behavioural therapy like patients with Asperger's syndrome. Krystal (1998) described patients with Alexithymia as being “antianalytic.” The same could be said of persons with Asperger's syndrome. Formal psychoanalytic psychotherapy is an impediment with patients with Alexithymia (Task Force Report of American Psychiatric Association, 1989) and Asperger's syndrome (Klin & Volkmar, 2000a, b).
Ego psychological approaches which is similar to cognitive behavioural therapy are helpful. These work better with patients who have problems working with feelings and phantasies.
It is important that psychiatrists making a diagnosis of Alexithymia consider Asperger's syndrome in the differential diagnosis.
*Dr. Bellgrove is supported in part by a Wellcome Trust (UK) International Biomedical Research Collaboration Grant on Autism.

Office remark:
Time budget 10 hours:
Study of previous tests results 1 hour
Observation+testing 2 hours
Processing Rorschach-test results 2 hours
Participation in the discussion 1 hour
Report writing 3 hours
Feedback & parental guidance 1 hour
Invoice # 414, 415 

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