Failures of individuation and communication disorders in children.
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OBJECTIVES: To review current literature on population, cytogenetic and molecular studies of specific language disorders (SLD) and pervasive developmental disorders (PDD). DEVELOPMENT: Clinical concordance studies in twins and in vertical familial groups suggest polygenic multifactorial modes of inheritance, but in some families an autosomal dominant model may be present. The data favour not a modular, but rather a molar model of the relationship between genes and neural abilities for communicative behaviors. Several extensive genome screenings have demonstrated linkage to specific markers on 7q for SLD, and on 7q and 2q for PDD. The strong evidence of linkage on 7q for both disorders has led to the hypothesis that this region contains several separate quantitative trait loci (QTL) related to different communicative abilities. Mutations in different QTL would facilitate the different disabilities and stereotyped behaviors associated with the phenotypic spectrum of PDD. There are other candidate regions for QTLs but the linkage is weaker and there is little agreement between studies; due, in part, to over extensive inclusion criteria and small sizes of familial groups. CONCLUSIONS: To enhance linkage research in further molecular genetic studies, clinicians must refine behavioral target traits when selecting familial groups and enlarge the size of familial groups by including non handicapped members with related behavioral traits. At present, a chromosome region in 7q shows the strongest evidence for communication related QTL, but other QTL need to be identified elsewhere in the genome in order to explain the genetic contribution to the large spectrum of language and autistic disorders.
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A continuing interest in clarity of reporting generated a change in our reporting format from the traditional report to the problem-oriented structure. This article discusses the differences and the advantages and disadvantages of each.
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An early childhood language analysis and intervention program, based on two models of pragmatics, is described. The theoretical constructs of each pragmatics model are described first, followed by a discussion of how the clinicians in the program translate these constructs into procedures for the analysis of and intervention with language disorders in preschool-aged children. Mention is made in conclusion of the limitations within which the program operates.
In a setting in which somatic symptoms without obvious organic causes are prevalent and in which doctors do not have very convincing explanations to offer, people in prolonged contact with such patients may appear to develop similar symptoms but claim the original patient as the source of their symptoms. At times, it is the original patient that detects the similarity and raises the question of contagion. Based on a study of four Nigerian patients, the author proposes the possible existence of a shared somatic disorder, comparable in many ways to induced psychotic disorder (DSM-III-R) and reopens the discussion on the whole concept of sharing/communication of psychiatric symptoms.
This study demonstrates the effectiveness of a modified Double ABCX or FAAR model in predicting successful adaptation--good marital adjustment, few maternal depressive symptoms, and an in-home rating of family functioning--in 45 families of autistic and communication-impaired children. The model consisted of severity of the handicap and other family stresses, family resources of cohesion and social support, family definition of the handicap, and adequacy of coping patterns. Canonical correlation and subsequent multiple regression procedures demonstrated that family adaptation was positively predicted by adequacy of social support and active coping patterns. Poorer adaptation was predicted by other family stresses, unwarranted maternal self-blame for the handicap, and maternal definition of the handicap as a family catastrophe. Findings for cohesion were mixed. Resources and beliefs were more predictive of adaptation than severity of the child's handicap.