Thalamic and amygdala-hippocampal volume reductions in first-degree relatives of patients with schizophrenia: An MRI-based morphometric analysis

Citation
Lj. Seidman et al., Thalamic and amygdala-hippocampal volume reductions in first-degree relatives of patients with schizophrenia: An MRI-based morphometric analysis, BIOL PSYCHI, 46(7), 1999, pp. 941-954
Citations number
91
Categorie Soggetti
Neurosciences & Behavoir
Journal title
BIOLOGICAL PSYCHIATRY
ISSN journal
00063223 → ACNP
Volume
46
Issue
7
Year of publication
1999
Pages
941 - 954
Database
ISI
SICI code
0006-3223(19991001)46:7<941:TAAVRI>2.0.ZU;2-2
Abstract
Background: Schizophrenia is characterized by subcortical and cortical brai n abnormalities. Evidence indicates that some nonpsychotic relatives of sch izophrenic patients manifest biobehavioral abnormalities, Including brain a bnormalities. The goal of this study was to determine whether amygdala-hipp ocampal and thalamic abnormalities are present in relatives of schizophreni c patients. Methods: Subjects were 28 nonpsychotic, and nonschizotypal, first-degree ad ult relatives of schizophrenics and 26 normal control subjects. Sixty conti guous 3 mm coronal, T1-weighted 3D magnetic resonance images of the brain w ere acquired on a 1.5 Tesla magnet. Cortical and subcortical gray and white matter and cerebrospinal fluid (CSF) were segmented using a semi-automated intensity contour mapping algorithm. Analyses of covariance of the volumes of brain regions, controlling for expected intellectual (i.e., reading) ab ility and diagnosis, were used to compare groups. Results: The main findings were that relatives had significant volume reduc tions bilaterally in the amygdala-hippocampal region and thalamus compared to control subjects. Marginal differences were noted in the pallidum, putam en, cerebellum and third and fourth ventricles. Conclusions: Results support the hypothesis that core components of the vul nerability to schizophrenia include structural abnormalities in the thalamu s and amygdala-hippocampus. These findings require further work to determin e if the abnormalities are an expression of the genetic liability to schizo phrenia. Biol Psychiatry 1999; 46:941-954 (C) 1999 Society of Biological ps ychiatry.