The course and outcome of SD is highly variable; male gender and prevalent tonic phenotype predict a poor outcome.

Based on several open-label and case studies, repetitive transcranial magnetic stimulation (rTMS) seems to have an antidepressive effect on patients with Parkinson's disease (PD). However, this hypothesis requires further confirmation. We conducted a randomized, double-blind placebo-controlled study to evaluate the effect of rTMS over the left dorsolateral prefrontal cortex (DLPFC) on depression and various motor and nonmotor features of PD. Twenty-two PD patients with mild or moderate depressive episodes were assigned into two groups, one receiving real-rTMS (90% of resting motor threshold, 5 Hz, 600 pulses-a-day for 10 days) over the left DLPFC, and another group receiving sham-rTMS. An investigator blinded to the treatment performed three video-taped examinations on each patient: before stimulation (baseline), 1 day (short term), and 30 days after treatment session ended (long-term effect). Mini-Mental State Examination, Unified Parkinson's Disease Rating Scale (UPDRS), Hoehn-Yahr, Epworth Sleepiness, Visual Analog and Montgomery-Asberg Depression Rating Scales (MADRS), Beck Depression Inventory (BDI), and Trail making and Stroop tests were applied. In the actively treated group, not only depression rating scales showed significant improvement 30 days after treatment ended (BDI by 44.4% and MADRS by 26.1%), but also the accuracy of Stroop test (by 16%). We could also demonstrate an insignificant improvement in UPDRS-III by 7.5 points (31.9%, P = 0.06). In the sham-treated group none of the examined tests and scales improved significantly after sham stimulation. Our study demonstrated the beneficial effect of the left DLPFC rTMS on depression in PD lasting at least 30 days after treatment. However, this result should be confirmed in patients with severe depression by further clinical trials.

Abstract:The origin of the high rate of depression in idiopathic Parkinson's disease (PD) is unknown. We applied voxelbased morphometry (VBM), as a sensitive tool in detection of gray matter MR density alterations, to find differences in depressed and nondepressed PD patients. Patients with idiopathic PD were classified into depressed (DPD) and nondepressed (NDPD) groups based on the Montgomery-Åsberg Depression Rating Scale (MADRS). Subsequently, a group comparisons were performed between depressed PD (n ϭ 23), nondepressed PD (n ϭ 27) and normal healthy controls (NC, n ϭ 16). There was no difference in gray matter density comparing healthy controls to any PD groups. However, when NDPD and DPD cohorts were compared, density alteration of the bilateral orbitofrontal, bilateral rectal gyrus, and also the right superior temporal pole was detected in the depressed subgroup. Exploratory analyses revealed an inverse correlation of MADRS scores and severity of VBM alteration in these regions beside the right medial temporal gyrus, anterior and medial cingular gyrus, and parahippocampal gyrus. These results suggest that depression in PD is related to gray matter decrease in the bilateral orbitofrontal and right temporal regions as well as the limbic system.

Background: Minimal clinically important difference (MCID) is the smallest change in an outcome, which a patient identifies as meaningful. Although the 2 most frequently applied Parkinson's disease (PD) “quality of life” questionnaires (the PDQ-39 and PDQ-8) provide encouragingly similar results, their MCID thresholds appear to be vastly different. Our aim was to calculate the MCID estimates for both PDQ-39 and PDQ-8 Summary Indices (PDQ-39-SI and PDQ-8-SI) by the utilization of both anchor- and distribution-based techniques. Methods: Nine hundred eighty-five paired investigations of 365 patients were included. Three different techniques were used simultaneously to calculate the MCID values. Results: First, we replicated the previously published results demonstrating how both PDQ-39-SI and PDQ-8-SI provide similar values and respond in a similar way to changes. Subsequently, we calculated the MCID thresholds. The most optimal estimates for MCID thresholds for PDQ-39-SI were -4.72 and +4.22 for detecting minimal clinically important improvement and worsening. For PDQ-8-SI, these estimates were -5.94 and +4.91 points for detecting minimal clinically important improvement and worsening respectively. Conclusions: Our study is the first one that directly compared the MCID estimates for both PDQ-39-SI and PDQ-8-SI on a large pool of patients including all disease severity stages. These MICD estimates varied across PD severity.

Characteristics considered to be typical of IA (focal, left temporal seizures appearing on grounds of a long-lasting, intractable epilepsy) seem only partially legitimate. We suggest that in new-onset IA, female gender and a preexisting heart condition could serve as predispositions in an otherwise benign epilepsy. We speculate that in late-onset IA, male-predominant changes in neuronal networks in chronic, intractable epilepsy and an accompanying autonomic dysregulation serve as facilitating factors.