Structural brain abnormalities in first-episode mania

Strakowski, Stephen M.; Wilson, Daniel R.; Tohen, Mauricio; Woods, Bryan T.; Douglass, Andrew; Stoll, Andrew L.

doi:10.1016/0006-3223(93)90098-x

Cited by 191 publications

(162 citation statements)

References 21 publications

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“…246 First-episode manic patients exhibited a trend towards reduced total cerebral white matter and significantly larger ratios of grey and white matter relative to healthy controls. 212 Other studies, including a meta-analysis of available data, reported no change in total or prefrontal white matter, however. [193][194][195][247][248][249] Anterior cingulate In a recent study of patients with BD, schizophrenia, and their first-degree relatives, McDonald et al 245 examined associations between genetic liability and variations in grey or white matter volumes.…”

Section: Basal Gangliamentioning

confidence: 99%

“…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. No association between antipsychotics or mood-stabilizing medications and caudate volume was reported in the above reviewed studies of BD, however.…”

Section: Basal Gangliamentioning

confidence: 99%

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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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Section: Basal Gangliamentioning

confidence: 99%

Section: Basal Gangliamentioning

confidence: 99%

The phenotypes of bipolar disorder: relevance for genetic investigations

2005

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“…1 MRI Analysis of Cerebellum in Bipolar Disorder 65 medullare were included. The ROI was then measured using a thresholding technique (Strakowski et al 1993.…”

Section: Mri Proceduresmentioning

confidence: 99%

“…1 MRI Analysis of Cerebellum in Bipolar Disorder 65 medullare were included. The ROI was then measured using a thresholding technique (Strakowski et al 1993.The vermis was divided into three ROIs (Courchesne et al 1988): V1 ϭ lobules I-V, V2 ϭ lobules VI-VII, and V3 ϭ lobules VIII-X. The cerebellar tonsils were not included in measurements as they are not part of the vermis.…”

mentioning

confidence: 99%

“…The areas of V1, V2, and V3 were measured on the realigned midsagittal slice by tracing the ROI and then using a thresholding technique. Total cerebral volumes were measured to control for differences in brain size when making comparisons (Strakowski et al 1993(Strakowski et al , 1998. Interrater reliability was established for each structure by having two raters independently measure each ROI from 10 subjects.…”

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confidence: 99%

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MRI Analysis of the Cerebellum in Bipolar Disorder A Pilot Study

DelBello

Strakowski

Zimmerman

et al. 1999

Neuropsychopharmacology

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Since qualitative CT studies have suggested decreased cerebellar size in patients with bipolar disorder, we performed a quantitative analysis of the cerebellum in patients with bipolar disorder to determine whether highresolution, thin slice magnetic resonance imaging (MRI) morphometry would reveal similar results. Bipolar patients hospitalized for a first manic episode ( n ϭ 16), bipolar patients with prior manic episodes hospitalized for a manic episode ( n ϭ 14), and normal volunteers ( n ϭ15Although traditionally regarded as a regulator of motor function, the cerebellum has also been found to project to regions of the brain that modulate mood (Anand et al. 1959;Heath et al. 1978;Courchesne et al. 1989). Several case reports have identified cerebellar atrophy in patients with mood dysregulation and in patients with bipolar disorder (Cutting 1976;Hamilton et al. 1983;Joseph et al. 1985;Yadalam et al. 1985;Jurjus et al. 1994).Moreover, several studies have found abnormal cerebellar anatomy in patients with affective disorders (reviewed in Soares and Mann 1997). Two studies reported a greater rate of cerebellar atrophy in manic patients than in patients with schizophrenia or normal controls (Nasrallah et al. 1981(Nasrallah et al. , 1982. Additionally, Yates et al. (1987) found a greater rate of cerebellar atrophy in patients with bipolar disorder who were over fifty years old, but not in younger bipolar patients compared with healthy volunteers. Lippmann et al. (1982) found bipolar patients with co-occurring alcohol abuse had increased rates of both vermal atrophy and cerebellar hemisphere atrophy compared with normal healthy volunteers, suggesting that alcohol abuse may contribute to abnormal cerebellar anatomy in bipolar patients. Rieder et al. (1983) found no difference in cerebellar size among patients with bipolar disorder, schizophrenia, and schizoaffective disorder. Results of these contradic- Despite numerous studies suggesting an association between cerebellar atrophy and bipolar disorder, there are no quantitative analyses of the cerebellum in patients with mania using MRI morphometry (Soares and Mann 1997). The aim of this study was to morphometrically assess the cerebellum of patients with bipolar disorder using high-resolution, thin slice, MRI, which allows for superior visualization of cerebellar anatomy.Previous investigators have found that lithium toxicity (Donaldson and Cuningham 1983;Kores and Lader 1997), depression (Shah et al. 1992;Escalona et al. 1993), and alcohol use (Lippmann et al. 1982) are associated with smaller cerebellar size. Therefore, cerebellar size may be associated with chronic affective illness or confounding variables associated with chronicity, such as number of previous episodes of depression, substance use, and medication effects. Yates et al. (1987) found that multiple-episode bipolar patients had a greater rate of cerebellar atrophy that healthy volunteers. Studying bipolar patients at the onset of their illnesses may eliminate confounding variables associated with ch...

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