Quantitative proton magnetic resonance spectroscopy of the basal ganglia in patients with affective disorders

Hamakawa, Hiroshi; Kato, Takeshi; Murashita, Jun; Kato, Nobuo

doi:10.1007/s004060050017

Cited by 145 publications

(87 citation statements)

References 11 publications

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“…This would suggest that Cr may not be a stable resonance to be used as an internal standard or reference ratio in bipolar depression research. This certainly warrants further investigation as the current literature in bipolar disorder, although different in methodology, mood state, and brain region, has reported increased creatine (Deicken et al, 2001;Michael et al, 2003Ftrend, Hamakawa et al, 1999Fmen only), decreased creatine (Deicken et al, 2003), or no change in creatine (Hamakawa et al, 1998;Friedman et al, 2004;Cecil et al, 2002;Brambilla et al, 2005;Frey et al, 2005).…”

Section: Discussionmentioning

confidence: 88%

Increased Anterior Cingulate/Medial Prefrontal Cortical Glutamate and Creatine in Bipolar Depression

Frye

Watzl

Banakar

et al. 2007

Neuropsychopharmacol

202

127

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Proton magnetic resonance spectroscopy ( 1 HMRS) is an in vivo brain imaging method that can be used to investigate psychotropic drug mechanism of action. This study evaluated baseline 1 HMRS spectra of bipolar depressed patients and whether the level of cerebral metabolites changed after an open trial of lamotrigine, an anti-glutamatergic mood stabilizer. Twenty-three bipolar depressed and 12 control subjects underwent a MRS scan of the anterior cingulate/medial prefrontal cortex. The scan was performed on a GE whole-body 1.5 T MRI scanner using single-voxel PRESS (TE/TR ¼ 30/3000 ms, 3 Â 3 Â 3 cm 3 and post-processed offline with LCModel. Baseline CSF-corrected absolute concentrations of glutamate + glutamine ([Glx]), glutamate ([Glu]), and creatine + phosphocreatine ([Cr]) were significantly higher in bipolar depressed subjects vs healthy controls. The non-melancholic subtype had significantly higher baseline [Glx] and [Glu] levels than the melancholic subtype. Remission with lamotrigine was associated with significantly lower post-treatment glutamine ([Gln]) in comparison to non-remission. These data suggest that non-melancholic bipolar depression is characterized by increased glutamate coupled with increased energy expenditure. Lamotrigine appears to reduce glutamine levels associated with treatment remission. Further study is encouraged to determine if these MR spectroscopic markers can delineate drug mechanism of action and subsequent treatment response.

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Section: Discussionmentioning

confidence: 88%

Increased Anterior Cingulate/Medial Prefrontal Cortical Glutamate and Creatine in Bipolar Depression

Frye

Watzl

Banakar

et al. 2007

Neuropsychopharmacol

202

127

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“…Charles et al (12) reported that elevated choline/creatine ratios decreased after antidepressant treatment, whereas a later study by Renshaw et al (13) yielded opposite results. Hamakawa et al (14) found higher choline levels and choline/creatine ratios in bipolar patients during a depressive episode. Vythilingam et al (15) reported lower caudate Nacetylaspartate/creatine ratios and increased choline/creatine ratios in the putamen in major depression.…”

mentioning

confidence: 97%

Lateralized Caudate Metabolic Abnormalities in Adolescent Major Depressive Disorder: A Proton MR Spectroscopy Study

Gabbay

Hess

Liu

et al. 2007

AJP

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Objective-Proton magnetic resonance spectroscopy ( 1 H-MRS) has been increasingly used to examine striatal neurochemistry in adult major depressive disorder. This study extends the use of this modality to pediatric major depression to test the hypothesis that adolescents with major depression have elevated concentrations of striatal choline and creatine and lower concentrations of N-acetylaspartate.Method-Fourteen adolescents (ages 12-19 years, eight female) who had major depressive disorder for at least 8 weeks and a severity score of 40 or higher on the Children's Depression Rating Scale -Revised and 10 healthy comparison adolescents (six female) group-matched for gender, age, and handedness were enrolled. All underwent three-dimensional 3-T 1 H-MRS at high spatial resolution (0.75-cm 3 voxels). Relative levels of choline, creatine, and N-acetylaspartate in the left and right caudate, putamen, and thalamus were scaled into concentrations using phantom replacement, and levels were compared for the two cohorts.Results-Relative to comparison subjects, adolescents with major depressive disorder had significantly elevated concentrations of choline (2.11 mM versus 1.56 mM) and creatine (6.65 mM versus 5.26 mM) in the left caudate. No other neurochemical differences were observed between the groups.Conclusions-These findings most likely reflect accelerated membrane turnover and impaired metabolism in the left caudate. The results are consistent with prior imaging reports of focal and lateralized abnormalities in the caudate in adult major depression.Rates of major depressive disorder rise dramatically in adolescence, with an estimated lifetime prevalence of 15% in adolescents by ages 15-18. Major depression is associated with significant morbidity, including deterioration in academic functioning, increased risk of substance use, and attempted and completed suicides (1,2). Furthermore, adolescent major depression is a strong predictor of major depression in adulthood, which carries its own burden of disadvantage (3). These findings highlight the need for specific neurobiological research in adolescent major depression.Converging lines of evidence suggest that the pathophysiology of depression entails impairment of cellular resilience and neuroplasticity in specific cortical, subcortical, and limbic brain regions. The relationship between the basal ganglia and depression has been inferred from the high comorbidity between depression and Parkinson's disease as well as Huntington's NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript disease, both basal ganglia-related disorders. In addition, morphometric studies (but not all) and functional neuroimaging studies have documented smaller caudate, putamen, and thalamus as well as impaired metabolism and blood flow in the striatum and thalamus in depression (4-10).Proton magnetic resonance spectroscopy ( 1 H-MRS) has provided additional evidence for the involvement of the striatum in adult major depression. 1 H-MRS provides metabolic assay of ne...

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“…In addition, increased choline/NAA ratios were also found in the basal ganglia in both the depressive and euthymic states (Hamakawa et al, 1998). As discussed above, these findings may be the expression of underlying changes in ATP expenditure and availability, oxygen consumption, and/or glutamatergic activity in BPD.…”

Section: Could Impairments Of Cellular Plasticity and Resilience Be Amentioning

confidence: 78%

Mitochondrially Mediated Plasticity in the Pathophysiology and Treatment of Bipolar Disorder

Quiróz

Gray

Kato

et al. 2008

Neuropsychopharmacol

Self Cite

150

102

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Bipolar disorder (BPD) has traditionally been conceptualized as a neurochemical disorder, but there is mounting evidence for impairments of cellular plasticity and resilience. Here, we review and synthesize the evidence that critical aspects of mitochondrial function may play an integral role in the pathophysiology and treatment of BPD. Retrospective database searches were performed, including MEDLINE, abstract booklets, and conference proceedings. Articles were also obtained from references therein and personal communications, including original scientific work, reviews, and meta-analyses of the literature. Material regarding the potential role of mitochondrial function included genetic studies, microarray studies, studies of intracellular calcium regulation, neuroimaging studies, postmortem brain studies, and preclinical and clinical studies of cellular plasticity and resilience. We review these data and discuss their implications not only in the context of changing existing conceptualizations regarding the pathophysiology of BPD, but also for the strategic development of improved therapeutics. We have focused on specific aspects of mitochondrial dysfunction that may have major relevance for the pathophysiology and treatment of BPD. Notably, we discuss calcium dysregulation, oxidative phosphorylation abnormalities, and abnormalities in cellular resilience and synaptic plasticity. Accumulating evidence from microarray studies, biochemical studies, neuroimaging, and postmortem brain studies all support the role of mitochondrial dysfunction in the pathophysiology of BPD. We propose that although BPD is not a classic mitochondrial disease, subtle deficits in mitochondrial function likely play an important role in various facets of BPD, and that enhancing mitochondrial function may represent a critical component for the optimal long-term treatment of the disorder.

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Quantitative proton magnetic resonance spectroscopy of the basal ganglia in patients with affective disorders

Cited by 145 publications

References 11 publications

Increased Anterior Cingulate/Medial Prefrontal Cortical Glutamate and Creatine in Bipolar Depression

Increased Anterior Cingulate/Medial Prefrontal Cortical Glutamate and Creatine in Bipolar Depression

Lateralized Caudate Metabolic Abnormalities in Adolescent Major Depressive Disorder: A Proton MR Spectroscopy Study

Mitochondrially Mediated Plasticity in the Pathophysiology and Treatment of Bipolar Disorder

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