cognitive model of hallucinations
   A generic term referring to a group of explanatory models that emphasize the role of cognitive rather than biological mechanisms in the mediation of hallucinations. As these cognitive mechanisms are generally understood in the wider context of a neuropsychological framework that incorporates relevant biological factors, the term cognitive model should not be interpreted here as referring to an explanatory model focusing exclusively on mental processes. Traditionally, cognitive models of hallucinations have focused predominantly on the group of * auditory hallucinations. The major psychological mechanisms addressed by these models are an unusual vividness of auditory images in hallucination-prone individuals, the quality of their *inner speech, and default source monitoring of inner speech. However, many cognitive models are multifactorial in nature, incorporating a wide range of mechanisms and coping strategies in their explanatory theses. The American psychoanalyst and founder of cognitive therapy Aaron T. Beck (b. 1921) and the Canadian psychologist Neil A. Rector summarize their cognitive model of auditory hallucinations (designed with reference to individuals with a clinical diagnosis of * schizophrenia) as follows. "The formation, fixation, and maintenance of hallucinations are dependent on multiple determinants: Hypervalent ('hot') cognitions of sufficient energy to exceed perceptual threshold and consequently to be transformed into hallucinations, a low threshold for auditory perceptual-ization exacerbated by stress, isolation, or fatigue, an externalizing bias that reinforces the purported external origin of the voices and resource-sparingstrategiesthathelptofixbeliefinexter-nal origin and diminished reality-testing... The maintenance of hallucinations is, in turn, determined by a range of beliefs: delusions regarding an external agent, underlying core beliefs, and the perceived 'relationship' with the voices. Specific coping responses and safety-seeking behaviors are also implicated." In addition to these cognitive mechanisms, Beck and Rector acknowledge the contribution of biological factors such as neuronal hypoconnectivity, an excessive priming of neurons during adolescence, and "cerebral flooding" with dopamine. Crucial to cognitive models such as those of Beck and Rector is the assumption that cognitions can be transformed into percepts, whereas biomedical models of hallucinatory experience tend to grant cognitions no more than a pathoplastic or shaping role with reference to the content of hallucinations.
   References
   Beck, A.T., Rector, N.A. (2003). A cognitive model of hallucinations. Cognitive Therapy and Research, 27, 19-52. Van der Gaag, M., Hageman, M.C., Birchwood, M. (2003). Evidence for a cognitive model of auditory hallucinations. Journal of Nervous and Mental Disease, 191, 542-545.

Dictionary of Hallucinations. . 2010.

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