Abstract

Patients with schizophrenia elicit several clinical features, such as psychotic symptoms, cognitive impairment, and subtle decline of intelligence. The latter two features become evident around the onset of the illness, although they may exist even before the disease onset in a substantial proportion of cases. Here, we review the literature concerning intelligence decline (ID) during the progression of schizophrenia. ID can be estimated by comparing premorbid and current intellectual quotient (IQ) by means of the Adult Reading Test and Wechsler Adult Intelligence Scale (WAIS), respectively. For the purpose of brief assessment, we have recently developed the WAIS-Short Form, which consists of Similarities and Symbol Search and well reflects functional outcomes. According to the degree of ID, patients were classified into three distinct subgroups; deteriorated, preserved, and compromised groups. Patients who show deteriorated IQ (deteriorated group) elicit ID from a premorbid level (≥10-point difference between current and premorbid IQ), while patients who show preserved or compromised IQ do not show such decline (<10-point difference). Furthermore, the latter patients were divided into patients with preserved and compromised IQ based on an estimated premorbid IQ score >90 or below 90, respectively. We have recently shown the distribution of ID in a large cohort of schizophrenia patients. Consistent with previous studies, approximately 30% of schizophrenia patients had a decline of less than 10 points, i.e., normal intellectual performance. In contrast, approximately 70% of patients showed deterioration of IQ. These results indicate that there is a subgroup of schizophrenia patients who have mild or minimal intellectual deficits, following the onset of the disorder. Therefore, a careful assessment of ID is important in identifying appropriate interventions, including medications, cognitive remediation, and social/community services.

Highlights

  • Specialty section: This article was submitted to Psychopathology, a section of the journal Frontiers in Psychiatry

  • We suggest that genetic variants related to cognitive impairments including intelligence decline (ID) might be associated with the N-methyld-aspartate (NMDA) glutamate network [7] or in delta[4]desaturase, sphingolipid 2 (DEGS2) gene expression [17, 83]

  • Similar to our proposal regarding the composition of drug trials, we suggest that patients without ID should be initially detected and excluded from clinical trials to develop cognitive remediation programs for patients with schizophrenia

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Summary

ID in Schizophrenia

Schizophrenia is a common and complex psychiatric disorder with clinical and genetic heterogeneity [1]. Cognitive impairments in numerous and diverse domains, including attention, working, verbal and visual memories, processing speed, social cognition, and general intelligence (i.e., a 1- to 2-SD decline in performance on neuropsychological tests compared with healthy individuals), are a core feature of the disorder and a reasonable target for treatment [3,4,5,6,7,8,9]. These deficits contribute to social or occupational dysfunction and poor life outcomes [10,11,12]. (iii) Compromised IQ: patients with less than a 10-point difference between estimated premorbid and current IQ and with an estimated premorbid IQ below 90

DISTRIBUTION OF ID IN SCHIZOPHRENIA
WRAT NART WRAT WRAT WTAR
PATHOPHYSIOLOGY OF COGNITIVE IMPAIRMENTS IN SCHIZOPHRENIA
EFFECTS OF ANTIPSYCHOTICS ON ID IN SCHIZOPHRENIA
COGNITIVE REMEDIATION
CONCLUSION
Findings
AUTHOR CONTRIBUTIONS
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