Abstract

ABSTRACT Depression is common in certain neurological diseases and is clinically indistinguishable from mood symptoms characteristic of primary affective illness. The association of depression with diseases involving the basal ganglia is particularly well recognized. While the specific mechanisms of mood disorders in these neurological patients are unknown, selective neural pathways affected directly and indirectly by basal ganglia injury provide a strategy for examining these patients with functional imaging techniques. Glucose metabolism has been measured with p 18 F-fluoro-deoxy-glucose (FDG) and positron emission tomography (PET) in depressed and nondepressed patients with Parkinson's disease, Huntington's disease, and caudate strokes. These studies have demonstrated bilateral hypometabolism of orbital-inferior prefrontal cortex and anterior temporal cortex in depressed subjects, independent of disease etiology. This pattern is similar to that seen in patients with primary unipolar depression studied using comparable acquisition and analysis strategies. These findings suggest that disruption of paralimbic pathways linking frontal cortex, temporal cortex, and striatum may contribute to depression in patients with both primary depression and depression associated with basal ganglia disease, and support the concept of a neuroanatomical locus for mood regulation.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.