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Schizophrenia — progressive and massive decline in response readiness by episodes
Author(s) -
Levander S.,
Jensen J.,
Gråwe R.,
Tuninger E.
Publication year - 2001
Publication title -
acta psychiatrica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.849
H-Index - 146
eISSN - 1600-0447
pISSN - 0001-690X
DOI - 10.1034/j.1600-0447.2001.104s408065.x
Subject(s) - neuropsychology , psychology , schizophrenia (object oriented programming) , neurocognitive , confounding , neuropsychological test , psychiatry , cognition , psychosis , clinical psychology , medicine , pathology
Objective: To relate the pattern of neuropsychological impairments among schizophrenic patients to case history data and disease characteristics in a cross‐sectional study of unselected patients, and to integrate these data with two previous longitudinal studies of neuropsychological impairments among schizophrenic patients. Method: One hundred consecutive schizophrenic patients were studied with respect to clinical case history and current symptoms, medication and neuropsychological impairment using a comprehensive computerized test battery. Results: The most salient finding was a marked slowing of response readiness, linearly related to the number of previous acute episodes. The resulting deficit was far beyond what has been obtained in any other group of subjects (average −6 SD for >five episode patients). The impairments in many of the other neuropsychological parameters could to some extent be explained with reference to response slowing, with one exception — verbal short‐term memory. Adjustment for important confounding factors (age, duration of illness, medication) did not change the strong negative association between response readiness and number of previous episodes. Conclusion: These findings, together with findings of our two previous longitudinal studies and a recent replication, prompted us to suggest that each acute schizophrenic episode inflicts damage to a set of hypothetical structures, cognitive pattern generators. We assume that these structures translate intentions to logistic programs. When damaged, delays are introduced into executive functions and corollary discharge processes will run out of phase with intentions. This model implicates new ways of looking at the generative mechanisms of the illness, and on treatment strategies.