Depression in Parkinson's disease: biogenic amines in CSF of ?de novo? patients

Kühn, Wilfried; Müller, Tobias; Gerlach, Manfred; Sofić, E.; Fuchs, Gerd; Heye, N.; Prautsch, R.; Przuntek, H.

doi:10.1007/bf01271258

Cited by 52 publications

(30 citation statements)

References 15 publications

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“…Lower concentrations of the serotonin metabolite 5-hydroxyindole acetic acid (5-HIAA) have been found in the cerebrospinal fluid (CSF) of depressed compared with nondepressed PD patients in some studies 18,36 but not all. 37 Patients with major depression tend to have lower CSF 5-HIAA levels than those with milder affective disturbance, although poor sensitivity and specificity limit the usefulness of this measurement as a biological marker. 38 Recent reports relating to mood disturbance resulting from deep brain stimulation of the subthalamic nucleus (STN) have further highlighted the complex pathophysiology of depression in PD.…”

Section: 25mentioning

confidence: 99%

Beyond the iron mask: Towards better recognition and treatment of depression associated with Parkinson's disease

2002

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This review examines the frequency of depression complicating Parkinson's disease (PD), its aetiology and clinical features, and also how it may be recognised and treated. Studies investigating the frequency of depression in PD have yielded figures ranging between 2.7% and 70%. Methodological differences account for much of the disparity. The aetiology of depression in PD is complex, and probably relates to both biological and exogenous factors. Dysfunction of multiple neurotransmitter systems, including the serotonergic system, may be involved. Mood disturbances resulting from deep brain stimulation of the subthalamic nucleus may provide a fruitful area for future research, and assist our understanding of the neural networks involved in mediating depression. Several recent studies have confirmed that depression in the PD patient is a major determinant of quality of life and that this is closely related to dysfunction in other clinically important health areas. The validity for many existing scales in the screening, diagnosis, and monitoring of depression in the PD patient has not been established. The Montgomery-Asberg Depression Rating Scale and the Hamilton Rating Scale for Depression appear to have good diagnostic sensitivity and specificity when compared with DSM-IV criteria. Recommendations for the optimal drug treatment of depression in PD are difficult to give, due to an inexplicable dearth of sizeable, placebo-controlled studies. A majority of physicians would probably now opt for a selective serotonin reuptake inhibitor in the depressed PD patient. There is no good evidence that these drugs are associated with a worsening of motor features, but they should probably not be coprescribed with selegiline, because of the risk of causing a potentially serious serotonin syndrome. Several studies have suggested that depression in the PD patient is associated with a more rapid deterioration in cognitive and motor functions, perhaps as a surrogate marker for more extensive brainstem cell loss.

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Section: 25mentioning

confidence: 99%

Beyond the iron mask: Towards better recognition and treatment of depression associated with Parkinson's disease

2002

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“…However, the occurrence of depression before the onset of motor symptoms, the association of depression with hereditary forms of PD, and lack of association with the severity of motor symptoms in PD all argue for a significant biological component (Tandberg et al, 1997). PD related disturbances in various neurotransmitter systems, such as the dopaminergic, serotonergic, and noradrenergic pathways, are probably linked to specific neurobehavioral features and may contribute to the high occurrence of depression in PD (Mayeux et al, 1986;Chan-Palay, 1993;Kuhn et al, 1996;Leentjens, 2004). However, there is yet no convincing evidence to suggest that the aetiology of depression in PD is different from that in patients without PD, and it has been claimed that depression in PD and depression in primary affective disorders share many common pathogenic factors (Sano et al, 1990;Leentjens et al, 2002).…”

Section: Introductionmentioning

confidence: 97%

Depressive symptom profile in Parkinson's disease: a comparison with depression in elderly patients without Parkinson's disease

Ehrt

Brønnick

Leentjens

et al. 2006

Int J Geriat Psychiatry

105

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“…Indeed, degeneration of serotonergic nerve cells, decreased brain serotonin content, and alterations in the activities of various types of serotonin receptors, have all been demonstrated in post-mortem studies using neurochemical and autoradiographic techniques (Jellinger, 1991) (Scatton et al, 1983;Chen et al, 1998). Moreover, in vivo studies have consistently demonstrated reduced levels of 5-hydroxyindoleacetic acid (5-HIAA), a breakdown product of serotonin, in the cerebrospinal fluid (CSF) of PD patients (Johanson and Roos, 1967;Kuhn et al, 1996), with some studies reporting an additional reduction of 5-HIAA in depressed PD patients (Mayeux et al, 1984;Kostic et al, 1987). These findings show the involvement of serotonin in PD.…”

Section: Introductionmentioning

confidence: 99%

The Serotonergic Hypothesis for Depression in Parkinson's Disease: an Experimental Approach

Leentjens

Scholtissen

Vreeling

et al. 2005

Neuropsychopharmacol

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The serotonergic hypothesis for depression in Parkinson's disease (PD) states that the reduced cerebral serotonergic activity that occurs in PD constitutes a biological risk factor for depression. The aim of our study was to assess the serotonergic hypothesis of depression in PD patients using an experimental approach. In a double-blind, randomized order, placebo-controlled crossover design, the response on the Profile of Mood States (POMS) questionnaire to acute tryptophan depletion (ATD) was studied in 15 PD nondepressed patients and 15 control subjects, without a prior personal or family history of depression. PD patients had lower (worse) baseline scores on the sadness, fatigue and vigor subscales of the POMS, in both ATD and the placebo condition, but not on the tension and anger subscales. There was however neither a significe between group effect, nor significe within-group effect due to ATD. We could find no evidence of a specific serotonergic vulnerability of PD patients for depression. Therefore, our results do not support the serotonergic hypothesis for depression in PD.

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Depression in Parkinson's disease: biogenic amines in CSF of ?de novo? patients

Cited by 52 publications

References 15 publications

Beyond the iron mask: Towards better recognition and treatment of depression associated with Parkinson's disease

Beyond the iron mask: Towards better recognition and treatment of depression associated with Parkinson's disease

Depressive symptom profile in Parkinson's disease: a comparison with depression in elderly patients without Parkinson's disease

The Serotonergic Hypothesis for Depression in Parkinson's Disease: an Experimental Approach

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