Depression is frequent in Parkinson's disease, but its pathophysiology remains unclear. Two recent studies have investigated the role of serotonergic system at the presynaptic level. The objective of the present study was to use positron emission tomography and [(18)F]MPPF to investigate the role of postsynaptic serotonergic system dysfunction in the pathophysiology of depression in Parkinson's disease. Four parkinsonian patients with depression and 8 parkinsonian patients without depression were enrolled. Each patient underwent a scan using [(18)F]MPPF, a selective serotonin 1A receptor antagonist. Voxel-by-voxel statistical comparison of [(18)F]MPPF uptake of the 2 groups of parkinsonian patients and with 7 matched normal subjects was made using statistical parametric mapping (P uncorrected < .001). Compared with nondepressed parkinsonian patients, depressed patients exhibited reduced tracer uptake in the left hippocampus, the right insula, the left superior temporal cortex, and the orbitofrontal cortex. Compared with controls, nondepressed parkinsonian patients presented reduced [(18)F]MPPF uptake bilaterally in the inferior frontal cortex as well as in the right ventral striatum and insula. Compared with controls, [(18)F]MPPF uptake was decreased in depressed parkinsonian patients in the left dorsal anterior cingulate and orbitofrontal cortices, in the right hippocampic region, and in the temporal cortex. The present imaging study suggests that abnormalities in serotonin 1A receptor neurotransmission in the limbic system may be involved in the neural mechanisms underlying depression in patients with Parkinson's disease.

Objectives: Repetitive transcranial magnetic stimulation (rTMS) seems to be effective as an antidepressant, however, some confusion remains about the best parameters to apply and the efficacy of its association with pharmacological antidepressant treatments. Method: In a single blind randomized study 14 patients with unipolar resistant depression to one antidepressant treatment were enrolled to receive, in combination with venlafaxine (150 mg), either 20 sessions of 10 Hz rTMS (2000 pulses per session) applied over the left dorsolateral prefrontal cortex (DLPFC) or 20 sessions of 1 Hz rTMS (120 stimulations per sessions) applied over the right DLPFC. Results: A similar antidepressant effect was observed in both groups with a comparable antidepressant delay of action (2 weeks) and a comparable number of responders (MADRS < 15) after 4 weeks of daily rTMS sessions (66 vs 50%). Conclusion: Low- and high- frequency rTMS seems to be effective as an add-on treatment to venlafaxine as monotherapy in pharmacological refractory major depression (stage 1). Due to its short duration (one session of 1 Hz rTMS lasts 4 min vs 16 for 10 Hz rTMS) and its safety, low frequency rTMS may be a useful alternative treatment for patients with refractory depression.

No abstract

No abstract

No abstract