Parkinson’s disease and depression: evidence for an alteration of the basal limbic system detected by transcranial sonography
Identifieur interne : 002005 ( Main/Exploration ); précédent : 002004; suivant : 002006Parkinson’s disease and depression: evidence for an alteration of the basal limbic system detected by transcranial sonography
Auteurs : Thomas Becker ; Georg Becker ; Jochen Seufert ; Erich Hofmann ; Klaus W. Lange ; Markus Naumann ; Alfred Lindner ; Heinz Reichmann ; Peter Riederer ; Helmut Beckmann ; Karlheinz ReinersSource :
- Journal of Neurology, Neurosurgery & Psychiatry [ 0022-3050 ] ; 1997-11-01.
Abstract
OBJECTIVES Depression is a frequent symptom in Parkinson’s disease. Compelling evidence suggests a role of the brainstem in the control of mood and cognition. In patients with unipolar depression transcranial sonography (TS) studies have shown structural alteration of the mesencephalic brainstem raphe which could suggest an involvement of the basal limbic system in the pathogenesis of primary mood disorders. The objective of the present study was to evaluate whether a similar alteration could be found in depressed patients with Parkinson’s disease using TS. METHODS Thirty patients with Parkinson’s disease and 30 age and sex adjusted controls were examined by TS. Raphe echogenicity was rated semiquantitatively. The severity of motor symptoms and depression was rated using standard research instruments. RESULTS Raphe echogenicity was significantly reduced in depressed patients with Parkinson’s disease compared with non-depressed patients with Parkinson’s disease and control subjects. Raphe echogenicity correlated negatively with degree of motor impairment, and differences in raphe echo between depressed and non-depressed patients with Parkinson’s disease were upheld when motor impairment was controlled for. CONCLUSION These preliminary findings suggest that, as in unipolar depression, a morphological alteration of the brainstem raphe might be involved in the pathogenesis of depression in Parkinson’s disease. This raphe alteration may reflect involvement in the basal limbic system in the pathogenesis of secondary depression. This concept is in line with current knowledge on the pathogenesis of both depression in Parkinson’s disease and primary depressive disorders.
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DOI: 10.1136/jnnp.63.5.590
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Compelling evidence suggests a role of the brainstem in the control of mood and cognition. In patients with unipolar depression transcranial sonography (TS) studies have shown structural alteration of the mesencephalic brainstem raphe which could suggest an involvement of the basal limbic system in the pathogenesis of primary mood disorders. The objective of the present study was to evaluate whether a similar alteration could be found in depressed patients with Parkinson’s disease using TS. METHODS Thirty patients with Parkinson’s disease and 30 age and sex adjusted controls were examined by TS. Raphe echogenicity was rated semiquantitatively. The severity of motor symptoms and depression was rated using standard research instruments. RESULTS Raphe echogenicity was significantly reduced in depressed patients with Parkinson’s disease compared with non-depressed patients with Parkinson’s disease and control subjects. Raphe echogenicity correlated negatively with degree of motor impairment, and differences in raphe echo between depressed and non-depressed patients with Parkinson’s disease were upheld when motor impairment was controlled for. CONCLUSION These preliminary findings suggest that, as in unipolar depression, a morphological alteration of the brainstem raphe might be involved in the pathogenesis of depression in Parkinson’s disease. This raphe alteration may reflect involvement in the basal limbic system in the pathogenesis of secondary depression. This concept is in line with current knowledge on the pathogenesis of both depression in Parkinson’s disease and primary depressive disorders.</div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Becker, Georg" sort="Becker, Georg" uniqKey="Becker G" first="Georg" last="Becker">Georg Becker</name><name sortKey="Becker, Thomas" sort="Becker, Thomas" uniqKey="Becker T" first="Thomas" last="Becker">Thomas Becker</name><name sortKey="Beckmann, Helmut" sort="Beckmann, Helmut" uniqKey="Beckmann H" first="Helmut" last="Beckmann">Helmut Beckmann</name><name sortKey="Hofmann, Erich" sort="Hofmann, Erich" uniqKey="Hofmann E" first="Erich" last="Hofmann">Erich Hofmann</name><name sortKey="Lange, Klaus W" sort="Lange, Klaus W" uniqKey="Lange K" first="Klaus W" last="Lange">Klaus W. Lange</name><name sortKey="Lindner, Alfred" sort="Lindner, Alfred" uniqKey="Lindner A" first="Alfred" last="Lindner">Alfred Lindner</name><name sortKey="Naumann, Markus" sort="Naumann, Markus" uniqKey="Naumann M" first="Markus" last="Naumann">Markus Naumann</name><name sortKey="Reichmann, Heinz" sort="Reichmann, Heinz" uniqKey="Reichmann H" first="Heinz" last="Reichmann">Heinz Reichmann</name><name sortKey="Reiners, Karlheinz" sort="Reiners, Karlheinz" uniqKey="Reiners K" first="Karlheinz" last="Reiners">Karlheinz Reiners</name><name sortKey="Riederer, Peter" sort="Riederer, Peter" uniqKey="Riederer P" first="Peter" last="Riederer">Peter Riederer</name><name sortKey="Seufert, Jochen" sort="Seufert, Jochen" uniqKey="Seufert J" first="Jochen" last="Seufert">Jochen Seufert</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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