Frontal and parietal metabolic disturbances in unipolar depression

Biver, Françoise; Goldman, Serge; Delvenne, Véronique; Luxen, André; Maertelaer, Viviane De; Hubain, Philippe; Mendlewicz, Julien; Lotstra, Françoise

doi:10.1016/0006-3223(94)91213-0

Cited by 287 publications

(137 citation statements)

References 18 publications

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“…Several studies have reported abnormally increased CBF/metabolism bilaterally in the posterior orbital cortex as well as in the left ventrolateral prefrontal cortex (VLPFC) and the anterior insula in unmedicated subjects with primary MDD. 16,17,[32][33][34][35] This finding is not specific for mood disorders, as it has been reported in various anxiety disorders as well as in experimentally induced sadness and anxiety. 36 Although CBF/ metabolism seems to consistently be decreased in the remitted phase as compared with the depressed phase of MDD, 17,[37][38][39] an inverse relationship between depression severity and CBF/metabolism during the depressed phase of the illness has been reported.…”

Section: Functional Anatomy Of Mood Disordersmentioning

confidence: 83%

Neural circuitry and neuroplasticity in mood disorders: Insights for novel therapeutic targets

Carlson¹,

Singh²,

Zarate³

et al. 2006

NeuroRX

132

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Summary:Major depressive disorder and bipolar disorder are severe mood disorders that affect the lives and functioning of millions each year. The majority of previous neurobiological research and standard pharmacotherapy regimens have approached these illnesses as purely neurochemical disorders, with particular focus on the monoaminergic neurotransmitter systems. Not altogether surprisingly, these treatments are inadequate for many individuals afflicted with these devastating illnesses. Recent advances in functional brain imaging have identified critical neural circuits involving the amygdala and other limbic structures, prefrontal cortical regions, thalamus, and basal ganglia that modulate emotional behavior and are disturbed in primary and secondary mood disorders. Growing evidence suggests that mechanisms of neural plasticity and cellular resilience, including impairments of neurotrophic signaling cascades as well as altered glutamatergic and glucocorticoid signaling, underlie the dysregulation in these circuits. The increasing ability to monitor and modulate activity in these circuits is beginning to yield greater insight into the neurobiological basis of mood disorders. Modulation of dysregulated activity in these affective circuits via pharmacological agents that enhance neuronal resilience and plasticity, and possibly via emerging nonpharmacologic, circuitry-based modalities (for example, deep brain stimulation, magnetic stimulation, or vagus nerve stimulation) offers promising targets for novel experimental therapeutics in the treatment of mood disorders.

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Section: Functional Anatomy Of Mood Disordersmentioning

confidence: 83%

Neural circuitry and neuroplasticity in mood disorders: Insights for novel therapeutic targets

Carlson¹,

Singh²,

Zarate³

et al. 2006

NeuroRX

132

View full text Add to dashboard Cite

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“…Multiple positron emission tomography (PET) and single photon emission computed tomography (SPECT) studies have shown low metabolism and/or blood flow at baseline in depressed subjects in the left (32)(33)(34)(35) and bilateral (36-43) dorsolateral prefrontal cortex and medial prefrontal cortex/anterior cingulate (34,38,(41)(42)(43)(44)(45)(46)(47)(48) or blunted activation with cognitive tasks in the anterior cingulate (49,50). Other PET and SPECT studies of patients with unipolar depression showed low metabolism and/or blood flow in the caudate (36-41, 51, 52), thalamus (37), temporal cortex (37,38,51,53,54), parietal cortex (34,40,51), and left putamen (37). Experimental induction of depression resulted in a specific decrease in metabolism in the orbitofrontal cortex (part of the prefrontal cortex) (55,56).…”

Section: Isotretinoin and Brain Functioningmentioning

confidence: 98%

Functional Brain Imaging Alterations in Acne Patients Treated With Isotretinoin

Bremner

Fani²,

Ashraf³

et al. 2005

AJP

105

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Objective: Although there have been case reports suggesting a relationship between treatment with the acne medication isotretinoin and the development of depression and suicide, this topic remains controversial. In order for isotretinoin to cause depression, it must have an effect on the brain; however, the effects of isotretinoin on brain functioning in acne patients have not been established. The purpose of this study was to assess the effects of isotretinoin on brain functioning in acne patients. Results: Isotretinoin but not antibiotic treatment was associated with decreased brain metabolism in the orbitofrontal cortex (-21% change versus 2% change for antibiotic), a brain area known to mediate symptoms of depression. There were no differences in the severity of depressive symptoms between the isotretinoin and antibiotic treatment groups before or after treatment. Conclusions:This study suggests that isotretinoin treatment is associated with changes in brain functioning.

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“…One report noted that in mildly depressed unmedicated predominantly rapid cycling bipolar inpatients with treatment resistance compared to healthy controls relative metabolic activity was increased in left prefrontal cortex, including ventrolateral structures such as the inferior frontal gyrus (Ketter et al, 2001). Increased prefrontal metabolism has also been reported in some studies of unmedicated depressed patients with major depressive disorder imaged in the resting condition (Baxter et al, 1987;Cohen et al, 1992;Drevets et al, 1992;Biver et al, 1994;Ketter and Drevets, 2002;Drevets et al, 2002).…”

Section: Introductionmentioning

confidence: 94%

Decreased prefrontal, anterior cingulate, insula, and ventral striatal metabolism in medication-free depressed outpatients with bipolar disorder

Brooks

Wang

Bonner

et al. 2009

Journal of Psychiatric Research

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This study explored whether cerebral metabolic changes seen in treatment resistant and rapid cycling bipolar depression inpatients are also found in an outpatient sample not specifically selected for treatment resistance or rapid cycling. We assessed 15 depressed outpatients with bipolar disorder (six type I and nine type II) who were medication-free for at least 2 weeks and were not predominantly rapid cycling. The average 28-item Hamilton Depression Scale (HAM-D) total score was 33.9. The healthy control group comprised 19 agematched subjects. All participants received a resting quantitative 18 F-fluoro-deoxyglucose positron emission tomography scan. Data analyses were performed with Statistical Parametric Mapping (SPM5). Analyses revealed that depressed patients exhibited similar global metabolism, but decreased absolute regional metabolism in the left much more than right dorsolateral prefrontal cortex, bilateral (left Contributions Dr. Brooks conceived the study, performed the analyses and drafted the manuscript. Dr. Wang collected data and edited the manuscript. Dr. Bonner collected data, assisted with data analyses, and edited the manuscript. Dr. Rosen assisted with data analyses and edited the manuscript. Dr. Hoblyn assisted with the literature search and edited the manuscript. Ms. Hill collected data and assisted with editing the manuscript. Dr. Ketter collected data, contributed to study design, and edited the manuscript. All authors contributed to and have approved the final manuscript. Conflict of interest Role of funding sourceNo sponsor had any role in study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the paper for publication. greater than right) insula, bilateral subgenual prefrontal cortex, anterior cingulate, medial prefrontal cortex, ventral striatum, and right precuneus. No region exhibited absolute hypermetabolism. Moreover, HAM-D scores inversely correlated with absolute global metabolism and regional metabolism in the bilateral medial prefrontal gyrus, postcentral gyrus, and middle temporal gyrus. Analysis of relative cerebral metabolism yielded a similar, but less robust pattern of findings. Our findings confirm prefrontal and anterior paralimbic metabolic decreases in cerebral metabolism outside of inpatients specifically selected for treatment resistant and rapid cycling bipolar disorder. Prefrontal metabolic rates were inversely related to severity of depression. There was no evidence of regional hypermetabolism, perhaps because this phenomenon is less robust or more variable than prefrontal hypometabolism. NIH Public Access

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Frontal and parietal metabolic disturbances in unipolar depression

Cited by 287 publications

References 18 publications

Neural circuitry and neuroplasticity in mood disorders: Insights for novel therapeutic targets

Neural circuitry and neuroplasticity in mood disorders: Insights for novel therapeutic targets

Functional Brain Imaging Alterations in Acne Patients Treated With Isotretinoin

Decreased prefrontal, anterior cingulate, insula, and ventral striatal metabolism in medication-free depressed outpatients with bipolar disorder

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