Neuroanatomy of comorbid schizophrenia and learning disability: a controlled study

Citation
Tl. Sanderson et al., Neuroanatomy of comorbid schizophrenia and learning disability: a controlled study, LANCET, 354(9193), 1999, pp. 1867-1871
Citations number
32
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Journal title
LANCET
ISSN journal
01406736 → ACNP
Volume
354
Issue
9193
Year of publication
1999
Pages
1867 - 1871
Database
ISI
SICI code
0140-6736(19991127)354:9193<1867:NOCSAL>2.0.ZU;2-V
Abstract
Background Reasons for the higher frequency of schizophrenia in learning-di sabled populations are uncertain. We investigated the neuroanatomical basis for this phenomenon by structural magnetic resonance imaging (MRI) in pati ents with learning disability and schizophrenia, learning-disabled patients , and patients with schizophrenia. Methods Age-matched and sex-matched patients with learning disability (20 c ases), schizophrenia (25), and both disorders (23) underwent MRI scans of t he brain. Whole brain areas and specific regions of interest were examined. 29 normal controls were also scanned. Findings The scans of the group with both disorders were closely similar to those of the schizophrenic group, in terms of both general structures and the structure of the amygdalahippocampus. However, the amygdala-hippocampus was significantly smaller on both sides than that of normal controls (left 4.1 vs 4.5 cm(3), p=0.011; right 4.2 vs 4.99 cm(3), p<0.0001). The brains of learning-disabled patients were generally smaller than those of the othe r three groups, but the amygdalohippocampal complexes were larger. Interpretation In terms of brain structure, patients with comorbid learning disability and schizophrenia resemble patients with schizophrenia and not those with learning disability. We suggest that the higher frequency of sch izophrenia in learning-disabled patients is due to a greater tendency of sc hizophrenic patients to develop cognitive deficits, and that within the lea rning-disabled population there may be individuals whose deficits result fr om undiagnosed schizophrenia.