Subcortical and temporal structures in affective disorder and schizophrenia: A magnetic resonance imaging study

Swayze, Victor W.; Andreasen, Nancy C.; Alliger, Randall; Yuh, William T. C.; Ehrhardt, James C.

doi:10.1016/0006-3223(92)90046-3

Cited by 381 publications

(253 citation statements)

References 85 publications

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“…In our present study, the effect was not lateralized to either hemisphere. Some studies have not found any differences in this region (e.g., Swayze et al, 1992;Becker et al, 1996;Staal et al, 2000). Mixed findings may be due to methodological differences such as different segmentation and measurement techniques, and different slice thicknesses, as well as differing symptom profiles of patients.…”

Section: Discussionmentioning

confidence: 98%

An MRI study of temporal lobe abnormalities and negative symptoms in chronic schizophrenia

Anderson

Wible

McCarley

et al. 2002

Schizophrenia Research

100

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Previous magnetic resonance imaging (MRI) studies have reported various subtle brain abnormalities in schizophrenic patients, including temporal lobe abnormalities, which are of particular interest given the role of this brain region in auditory and language processing, and the characteristic deficits in these processes in schizophrenia. Subjects in this study were 16 male patients diagnosed with chronic schizophrenia and 15 healthy male comparison subjects. These patients were characterized by negative symptoms. High spatial resolution coronal MRI 1.5-mm-thick slices were used to measure the gray matter volume of the superior temporal gyrus, anterior and posterior amygdala/ hippocampal complex, and parahippocampal gyrus. Patients, relative to normal comparison subjects, evinced a reduction of gray matter volume in bilateral superior temporal gyri and anterior amygdala/ hippocampal complex. The reduction in gray matter of the superior temporal gyrus in patients with schizophrenia is consistent with previous findings, and is noteworthy in that it was found in this group of patients with predominantly negative symptoms. The reduction in the anterior amygdala/ hippocampal complex was an additional temporal lobe finding. These results underscore the role of temporal lobe structures in the pathophysiology of schizophrenia.

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Section: Discussionmentioning

confidence: 98%

An MRI study of temporal lobe abnormalities and negative symptoms in chronic schizophrenia

Anderson

Wible

McCarley

et al. 2002

Schizophrenia Research

100

View full text Add to dashboard Cite

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“…While the importance of the amygdala in mood disorders is undisputed, volumetric studies of the amygdala in bipolar disorder have yielded contradictory findings (summarized in Table 1). In an early study of 48 patients, Swayze et al (1992) found no significant difference in amygdala volume between bipolar patients and controls. However, this study had poor spatial resolution, having been conducted at 0.5 Tesla using 1-cm thick slices.…”

Section: Introductionmentioning

confidence: 93%

“…Subsequent studies have reported either greater (Altshuler et al, ,2000Strakowski et al, 1999;Brambilla et al, 2003) or smaller (Pearlson et al, 1997;Blumberg et al, 2003;DelBello et al, 2004;Chen et al, 2004;Chang et al, 2005) amygdala volumes with bipolar disorder. These latter experiments had improved structural imaging techniques over Swayze et al (1992), but also had smaller sample sizes and varying anatomic boundary definitions. The majority of studies that reported amygdala enlargement used a method described by Bartzokis et al (1998), whereas the other studies did not.…”

Section: Introductionmentioning

confidence: 99%

Age-dependent reduction of amygdala volume in bipolar disorder

Doty

Payne

Steffens

et al. 2008

Psychiatry Research: Neuroimaging

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The amygdala is hypothesized to play a critical role in mood regulation, yet its involvement in bipolar disorder remains unclear. The aim of the present study was to compare measurements of amygdala volumes in a relatively large sample of bipolar disorder patients and healthy controls ranging in age from 18 to 49 yrs. Fifty-four adult patients meeting DSM-IV criteria for bipolar disorder and 41 healthy controls matched for age, sex, and education underwent structural 1.5 Tesla MRI scanning. Volumetric measurements of the amygdala were obtained using a manual region-of-interest tracing method with software that allowed simultaneous visualization of the amygdala in three orthogonal planes. The anterior head of the hippocampus was removed in the sagittal plane prior to amygdala volumetry measurement. Multiple regression analysis was computed on amygdala volume measurements as a function of diagnosis, age, sex, and cerebral volume. Bipolar patients showed an age-related reduction of amygdala volume but controls did not. Among bipolar subjects, amygdala volume was unrelated to medication history. There were no significant hemispheric or sex interactions with the main effects. Results support a role for amygdala dysfunction in bipolar disorder which appears most robustly in older relative to younger adult patients. Differential aging effects in bipolar disorder may compromise amygdala integrity and contribute to mood dysregulation.

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“…Right caudate volume was larger only in affected monozygotic twins. 206 Imaging studies of caudate in adults with BD have been ambiguous, with some studies also showing an increased volume, 207 but other suggesting either a difference in the opposite direction-decreased caudate in older bipolar patients, particularly those with illness onset after 45 years of age 208 -or no differences in patients with minimal exposure to antipsychotics, 209 hospitalized manic patients, 210 bipolar patients, 211 or first-episode manic patients. 212 The heritability of caudate volume is unknown, but enlarged caudate volumes are associated with both genetic 213,214 and environmental factors, 215 including antipsychotic use.…”

Section: Basal Gangliamentioning

confidence: 99%

The phenotypes of bipolar disorder: relevance for genetic investigations

2005

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The search for susceptibility genes for bipolar disorder (BD) depends on appropriate definitions of the phenotype. In this paper, we review data on diagnosis and clinical features of BD that could be used in genetic studies to better characterize patients or to define homogeneous subgroups. Clinical symptoms, long-term course, comorbid conditions, and response to prophylactic treatment may define groups associated with more or less specific loci. One such group is characterized by symptoms of psychosis and linkage to 13q and 22q. A second group includes mainly bipolar II patients with comorbid panic disorder, rapid mood switching, and evidence of chromosome 18 linkage. A third group comprises typical BD with an episodic course and favourable response to lithium prophylaxis. Reproducibility of cognitive deficits across studies raises the possibility of using cognitive profiles as endophenotypes of BD, with deficits in verbal explicit memory and executive function commonly reported. Brain imaging provides a more ambiguous data set consistent with heterogeneity of the illness. Keywords: bipolar disorder; genetics; endophenotype; neurocognitive function; brain imaging Bipolar disorder (BD) has a genetic basis with heritability of at least 80%. 1 A number of studies have attempted to map the susceptibility loci giving evidence of linkage in multiple genomic regions. In particular, findings in 4p, 4q, 8q, 10p, 12q24, 13q, 18p, 18q, 21q, and 22q have been supported by more than one study. [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19] However, these studies have not identified any specific genes, and a recent metaanalysis of available genome scans showed no regions with a conclusive evidence of linkage. 20 The relatively slow progress of gene-mapping efforts is often explained by the 'complex' nature of the illness and of the genotype-phenotype relation. The complexity most likely includes heterogeneity, interactions of multiple loci, incomplete penetrance, as well as phenotypes resulting from environmental effects-either alone or in interaction with the genetic predisposition. The goal of psychiatric genetic research is identification of (heritable) variations in DNA sequence or function that influence behaviour or give rise to mental illness. By definition, in complex (multifactorial) traits, this link is not unique and specific. That is, a particular change in gene sequence does not necessarily lead to a specific behaviour, and similar behaviours (symptoms) may be due to distinct (sets of) genes. Moreover, we must consider the possibility that the path between the genotype and behaviour is not unidirectional. Emerging examples point not only to general effects of environment, for instance stress, on behaviour, but also to specific behaviours influencing gene function that can be transmitted onto the next generation. 21 No single method is considered clearly superior in identifying susceptibility genes for complex traits such as BD. Most researchers agree that a combination of strategies is most lik...

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Subcortical and temporal structures in affective disorder and schizophrenia: A magnetic resonance imaging study

Cited by 381 publications

References 85 publications

An MRI study of temporal lobe abnormalities and negative symptoms in chronic schizophrenia

An MRI study of temporal lobe abnormalities and negative symptoms in chronic schizophrenia

Age-dependent reduction of amygdala volume in bipolar disorder

The phenotypes of bipolar disorder: relevance for genetic investigations

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