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.In the 1962 [2] model, anhedonia washypothesized to represent a fundamental and aetiologically importantfactor in the development of schizotypy, actually falling somewhat  between  the genetic defect hypokrisia and the other schizotypic sign/symptoms interpersonal aversiveness, cognitive slippage, and ambivalence.As of 1990, Meehl de-emphasized anhedonia (termed hypohedonia; but seealso [10]) as a fundamental aetiologic factor in the development ofschizotypy and schizophrenia.Hypohedonia was now viewed as playingan aetiologic role in the development of schizotypy by functioning as anontaxonic (i.e.dimensional) polygenic potentiator (i.e.not deriving fromthe core genetically determined schizophrenia diathesis).The reconfigura-tion of hypohedonia s role in the 1990 [5] model was rather major and wasdiscussed further elsewhere [6,11].Meehl [5] noted that many schizotypesindeed display what he termed   secondary  hypohedonia, namelyclinically observable symptoms of a low hedonic capacity that derivefrom either a primary hedonic deficit or aversive drift.He noted [11] thatthe schizotypy taxon (i.e.core, true schizotypy)   will generate hypohedonictaxonicity in the adult population .Furthermore, in the 1990 [5] revision,Meehl strongly suggested associative loosening and aversive drift are thoseCLUSTER A PERSONALITY DISORDERS: COMMENTARIES ___________________________ 79psychological processes (deriving from hypokrisia) that genuinely deter-mine the behavioural and psychological characteristics of the schizotype.What does the schizotype look like? The answer to this question is   itdepends on the level of compensation that characterizes the individual .Amost important assumption in Meehl s model is that schizotypy, as apersonality organization reflective of a latent liability (i.e.not directlyobservable) for schizophrenia, can manifest itself phenotypically (i.e.behaviourally and psychologically) in various degrees of clinical compen-sation.This personality organization gives rise to schizotypic psychologicaland behavioural manifestations [2,5,10], such as subtle thought disorder(cognitive slippage) or excessive interpersonal fear, yet it may bemanifested relatively   quietly  , so to speak, through deviance detectableonly on laboratory measures as endophenotypes (e.g.eye trackingdysfunction, sustained attention deficits, psychomotor impairment, somato-sensory dysfunction).In short, the schizotype may be highly compensated(showing minimal signs and symptoms of schizotypic functioning), or mayreveal transient failures in compensation, or may be diagnosably schizo-phrenic.A crucial implication of this assumption is that not all schizotypesdevelop diagnosable schizophrenia (i.e.one could genuinely be at risk yetnever develop a psychotic illness), however all schizotypes will displaysome evidence of their underlying liability in the form of aberrantpsychobiologic and/or psychological functioning.This particular implica-tion of the model has guided nearly 40 years of research directed atdeveloping methods for the valid and efficient detection of schizotypyendophenotypes (through clinical, psychometric, or other means) and itarticulated the heart of the   diathesis-stressor  model/approach forpsychopathology.In discussing Meehl s model of schizotypy, it is important to point outseveral misconceptions of the model and the resultant fallacies which oftenunderlie the misunderstandings:Fallacy #1: Schizotypy is the same as DSM-IV schizotypal personality disorder.Meehl was quite clear that his conceptualization of schizotypy was notsynonymous with the DSM-IV diagnosis of schizotypal personality disorder(see [5]).Although there is some degree of phenomenologic similaritybetween schizotypic symptoms and signs and the diagnostic criteria forDSM-IV schizotypal personality disorder, important differences existbetween the two concepts [ Pobierz całość w formacie PDF ]