Parkinson’s disease and depression: evidence for an alteration of the basal limbic system detected by transcranial sonography
- Thomas Beckera,
- Georg Beckerb,
- Jochen Seufertb,
- Erich Hofmannc,
- Klaus W Langed,
- Markus Naumannb,
- Alfred Lindnerb,
- Heinz Reichmannb,
- Peter Riederera,
- Helmut Beckmanna,
- Karlheinz Reinersb
- aDepartment of Psychiatry, University of Würzburg, Füchsleinstrasse 15, D-97080 Würzburg, Germany, bDepartment of Neurology, University of Würzburg, Josef-Schneider-Strasse 11, D-97080 Würzburg, Germany, cDepartment of Neuroradiology, University of Würzburg, Josef-Schneider-Strasse 11, D-97080 Würzburg, Germany, dSection of Neuropsychology, Department of Psychology, University of Freiburg, Postfach, D-79085 Freiburg, Germany
- Dr Thomas Becker, Institute of Psychiatry, De Crespigny Park, Denmark Hill, London SE5 8AF.
- Received 10 July 1997
- Revised 8 May 1997
- Accepted 15 May 1997
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.
