Basal ganglia volumetric studies in affective disorder: what did we learn in the last 15 years?

Bonelli, Raphael M.; Kapfhammer, Hans-Peter; Pillay, Srinivasan S.; Yurgelun‐Todd, Deborah

doi:10.1007/s00702-005-0372-7

Cited by 36 publications

(13 citation statements)

References 87 publications

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“…We also found that reduced pallidal volume was associated with more depressive symptomatology, which agrees with prior work [14,28]. Existing models of depression indicate that the globus pallidus and other basal ganglia regions are components of prefrontal and limbic circuits important for goal-directed behaviors and executive cognitive control processes that support emotion and mood regulation [74].…”

Section: Discussionsupporting

confidence: 90%

“…In support of this possibility, reduced tissue volumes within the basal ganglia have been associated with major depression in postmortem samples [23,24]. Moreover, previous magnetic resonance imaging (MRI) studies on patients with major depressive disorder (MDD) have reported volumetric reductions in striatal and pallidal regions [21,25–28]. Secondly, case study evidence indicates that selective bilateral lesions to the globus pallidus result in depressive symptoms and concurrent weight gain [29].…”

Section: Introductionmentioning

confidence: 99%

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Basal ganglia morphology links the metabolic syndrome and depressive symptoms

Onyewuenyi

Muldoon

Christie

et al. 2014

Physiology & Behavior

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The metabolic syndrome (MetS) is a clustering of cardiovascular and cerebrovascular risk factors that are often comorbid with depressive symptoms. Individual components of the MetS also covary with the morphology of basal ganglia regions that are altered by depression. However, it remains unknown whether the covariation between the MetS and depressive symptomatology can be accounted for in part by morphological changes in the basal ganglia. Accordingly, we tested the hypothesis that increased depressive symptoms among individuals with the MetS might be statistically mediated by reduced grey matter volume in basal ganglia regions. The presence of the MetS was determined in 147 middle-aged adults using the criteria of the National Cholesterol Education Program, Adult Treatment Panel III. Basal ganglia volumes were determined on an a priori basis by automated segmentation of high-resolution magnetic resonance images. Depressive symptoms were assessed using the Patient Health Questionnaire. Even after controlling for demographic and other confounding factors, having the MetS and meeting more MetS criteria covaried with reduced globus pallidus volume. Meeting more MetS criteria and reduced pallidal volume were also related to depressive symptoms. Moreover, the MetS-depression association was statistically mediated by pallidal volume. In summary, reduced globus pallidus volume is a neural correlate of the MetS that may partly account for its association with depressive symptoms.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Basal ganglia morphology links the metabolic syndrome and depressive symptoms

Onyewuenyi

Muldoon

Christie

et al. 2014

Physiology & Behavior

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“…There are widespread limbic connections with both cortex and the nucleus accumbens/ ventral striatal region. 54 The dorsolateral prefrontal cortex, associated with executive function, has a similar circuit structure projecting to the head of the caudate nucleus, globus pallidus, and mediodorsal nucleus. This circuit mediates executive function.…”

Section: Anatomic Circuits Of Frontal-subcortical Dementiamentioning

confidence: 99%

Frontal-Subcortical Dementias

Bonelli¹,

Cummings²

2008

The Neurologist

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Frontal-subcortical dementias are a heterogeneous group of disorders that share primary pathology in subcortical structure and a characteristic pattern of neuropsychologic impairment. Their clinical presentation is characterized by memory disorders, an impaired ability to manipulate acquired knowledge, important changes of personality (apathy, inertia, or depression), and slowed thought processes (or bradyphrenia). It also has marked frontal dysfunction. Classic frontal-subcortical dementias include Huntington chorea, Parkinson disease dementia, progressive supranuclear palsy, thalamic degeneration, subcortical vascular dementia, multiple sclerosis, the acquired immunodeficiency syndrome dementia complex, depressive pseudodementia, and some other rare dementias like spinocerebellar degenerative syndromes, Hallervorden-Spatz disease, choreoacanthocytosis, idiopathic basal ganglia calcification, Guamanian parkinsonism-dementia complex, corticobasal degeneration multiple system atrophy, Wilson disease, metachromatic leukodystrophy, adrenoleukodystrophy, hypoparathyroidism, sarcoidosis, and other CNS inflammatory disorders. Anatomic data suggest that the frontal signs result from a disconnection of the frontal cortex from the basal ganglia. However, most frontal-subcortical dementias show cortical atrophy in later stages, and cortical dementias have subcortical pathology at some point. In fact, the concept might be seen as a continuum, and only the 2 extremes would be represented by pure cortical or subcortical pathology. Anyway, subcortical disorders may still be more similar to one another than they are to AD. Possibly, frontal-subcortical and cortical dementias are the description of the prior main target of the disease process, ending up in both cases in a global dementia. Although the dichotomy cortical versus frontal-subcortical dementia is not strict, the 2 concepts still seem to have advantages.

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“…Dysfunction has been implicated in schizophrenia, OCD and anxiety disorders; and both major depression and mania can arise from neurological lesions in the BG, e.g. in stroke, Huntington's disease (Bonelli, Kapfhammer, Pillay, & YurgelunTodd, 2006).…”

Section: Basal Gangliamentioning

confidence: 99%

The structural neuroimaging of bipolar disorder

Emsell

McDonald

2009

International Review of Psychiatry

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There is an increasing body of literature fuelled by advances in high-resolution structural MRI acquisition and image processing techniques which implicates subtle neuroanatomical abnormalities in the aetiopathogenesis of bipolar disorder. This account reviews the main findings from structural neuroimaging research into regional brain abnormalities, the impact of genetic liability and mood stabilizing medication on brain structure in bipolar disorder, and the overlapping structural deviations found in the allied disorders of schizophrenia and depression. The manifold challenges extant within neuroimaging research are highlighted with accompanying recommendations for future studies. The most consistent findings include preservation of total cerebral volume with regional grey and white matter structural changes in prefrontal, midline and anterior limbic networks, non-contingent ventriculomegaly and increased rates of white matter hyperintensities, with more pronounced deficits in juveniles suffering from the illness. There is increasing evidence that medication has observable effects on brain structure, whereby lithium status is associated with volumetric increase in the medial temporal lobe and anterior cingulate gyrus. However, research continues to be confounded by the use of highly heterogeneous methodology and clinical populations, in studies employing small scale, low-powered, cross-sectional designs. Future work should investigate larger, clinically homogenous groups of patients and unaffected relatives, combining both categorical and dimensional approaches to illness classification in cross-sectional and longitudinal designs in order to elucidate trait versus state mechanisms, genetic effects and medication/illness progression effects over time.

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Basal ganglia volumetric studies in affective disorder: what did we learn in the last 15 years?

Cited by 36 publications

References 87 publications

Basal ganglia morphology links the metabolic syndrome and depressive symptoms

Basal ganglia morphology links the metabolic syndrome and depressive symptoms

Frontal-Subcortical Dementias

The structural neuroimaging of bipolar disorder

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