The structural neuroimaging of bipolar disorder

Abstract

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.

Volume and shape analysis of subcortical brain structures and ventricles in euthymic bipolar I disorder

“…Structural MRI studies of amygdala volumes in BD have also produced inconsistent findings, with increased, decreased and no amygdala volume change being reported (Emsell and McDonald, 2009). Amygdala changes reported in the recent international mega-analysis parallel the reported hippocampal findings, that is, significantly increased amygdala volumes in lithium-treated BD patients compared with BD patients not treated with lithium and HC (Hallahan et al, 2011).…”

“…Previous studies investigating amygdala volumes in BD yielded no overall consensus (Emsell and McDonald, 2009). One issue is the actual definition of the hippocampus/amygdala boundary, particularly in older studies (Boccardi et al, 2011).…”

“…The present study focused on euthymic individuals diagnosed with BP-I disorder. Existing magnetic resonance imaging (MRI) studies investigating morphological changes in the illness are difficult to compare due to the small, heterogeneous samples used (Emsell and McDonald, 2009). Therefore, a large-scale sample of euthymic BD-I individuals is required to investigate volume and shape abnormalities.…”

MR Spectroscopic Studies of the Brain in Psychiatric Disorders

“…Mood stabilizers in general, and lithium in particular, have been shown to have neurotrophic effects and to promote neuroplasticity (Manji et al 2000;Quiroz et al 2010). The use of lithium by bipolar patients has consistently been associated with increased volume of the anterior cingulate cortex and the hippocampus (Emsell and McDonald 2009). These brain morphometry differences and the neurotrophic effects of mood stabilizing medications should be kept in mind when interpreting the 1H-MRS findings in bipolar disorder.…”

Does body shaping influence brain shape? Habitual physical activity is linked to brain morphology independent of age

“…Structural brain alterations, mostly in terms of reduced gray matter (GM) volumes and densities, were commonly observed in major mental disorders associated with both cognitive and emotional impairments (Emsell and McDonald 2009;Eker and Gonul 2010;Rigucci et al 2010). Smaller hippocampal volume has been reported after repeated episodes of major depression (Videbech and Ravnkilde 2004;Egger et al 2008;Vasic et al 2008;Bergouignan et al 2009;McKinnon et al 2009) and chronic schizophrenia (Henn and Braus, 1999;Honea et 2010.…”