Frontal lobe dysfunction in secondary depression
1994; American Psychiatric Association Publishing; Volume: 6; Issue: 4 Linguagem: Inglês
10.1176/jnp.6.4.428
ISSN1545-7222
Autores Tópico(s)Genetic Neurodegenerative Diseases
ResumoBack to table of contents Previous article Next article No AccessFrontal lobe dysfunction in secondary depressionPublished Online:1 Apr 2006https://doi.org/10.1176/jnp.6.4.428AboutSectionsView articleAbstractPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail View articleAbstractDepression is common in patients with neurological disease, particularly with diseases involving the basal ganglia. Although the mechanisms of mood disorders in these patients are poorly understood, selective neural pathways affected directly and indirectly by basal ganglia injury provide a strategy for examining these patients with functional imaging techniques. Studies of regional cerebral glucose metabolism by use of positron-emission tomography are reviewed. These studies demonstrate 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. These findings suggest that disruption of paralimbic pathways linking frontal cortex, temporal cortex, and striatum may contribute to both primary depression and depression associated with basal ganglia disease. The findings support the evolving concept of a neuroanatomical locus for mood regulation. Access content To read the fulltext, please use one of the options below to sign in or purchase access. Personal login Institutional Login Sign in via OpenAthens Purchase Save for later Item saved, go to cart PPV Articles - Journal of Neuropsychiatry and Clinical Neurosciences $35.00 Add to cart PPV Articles - Journal of Neuropsychiatry and Clinical Neurosciences Checkout Please login/register if you wish to pair your device and check access availability. Not a subscriber? 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