Prepared by Dr. Kathryn Chung and Susan O'Connor, Northwest PADRECC
Telephone-based cognitive-behavioral therapy for depression in Parkinson disease.
Depression is relatively common in Parkinson disease and effective treatment options including face to face cognitive behavioral therapy (CBT) are available. Unfortunately, many barriers can impede access to face to face therapy, including geographical restriction, or special transportation needs. With the advent of telemedicine, it is worthwhile determining if telephone-based CBT could recapitulate the successes of face to face psychotherapy. In this pilot trial, 21 depressed PD patients (with a Clinical Impression Scale of ≥ 4, meaning moderately severe, or worse) participated in a 10 week trial of telephone-based CBT. The primary outcome measured was the change in score in the Hamilton Rating Scale for Depression (HAM-D17), with a substantial number of secondary outcomes (10) including change in Beck Depression Inventory Scales, a Clinical Global Impression of Improvement Scale (CGI-I), and quality of life (Short Form-36). Results showed a mean change in HAM-D17 of 7.91 points (P<0.001) and at 4 weeks after CBT concluded, 52% of subjects were classified as responders (>50% improvement on HAM-D17 or much improved or very much improved on CGI-I). Feasibility was considered quite high, as 95% of subjects completed all 10 CBT sessions. Overall, results were similar to this groups prior findings of the benefits of face to face CBT. The authors acknowledge the limits of a small pilot trial and its uncontrolled design. This work is important, as it provides evidence that a more feasible solution to a common problem in PD may not sacrifice efficacy.
Journal of Geriatric Psychiatry and Neurology 24 (4); http://www.ncbi.nlm.nih.gov/pubmed/22228827
Beyond Nine Years of Continuous Subthalamic Nucleus Deep Brain Stimulation in Parkinson’s Disease
Previous studies have demonstrated that deep brain stimulation (DBS ) of the subthalamic nucleus (STN) and the globus pallidus pars interior (Gpi) is superior to medical management for the treatment of levodopa induced motor complications in advanced parkinson’s disease (PD). In this study, Zibetti et al evaluated 14 patients treated with STN stimulation for at least 9 years. All subjects were assessed prior to surgery, at 1, 5 and > 9 years. The researchers found that SNT-DBS significantly improved the motor Unified Parkinson’s Disease Rating Scale (UPDRS) score at all follow up visits with 42% improvement at 9 years. In addition, there was a 39% reduction in the dosage of dopaminergic drugs. Off period duration and time spent with dyskinesia was reduced by 64% and 65% respectively. At 9 years, patients did, however, report an overall decline in activities of daily living and neuropsychological assessment showed that 29% of patients developed significant cognitive dysfunction. The results of this study indicate a long-term effect of DBS of the STN on the cardinal motor symptoms and motor complications in advanced PD. Worsening of disability due to disease progression and emergence of cognitive impairment was observed. To date, this is the longest reported study of outcomes following STN-DBS in PD.
Zibetti et al. Beyond Nine Years of Continuous Subthalamic Nucleus Deep Brain Stimulation in Parkinson’s Disease. Movement Disorders 2011; 26: 2327-2334.
Neuropathy and Levodopa: A Review of Neuropathy in Parkinson Disease: Prevalence and Determinants
In the November volume of Neurology, Y.A. Rajabally and J. Martey reported on a possible association between levodopa use in individuals with Parkinson’s disease (PD) and neuropathy. The goal of this study was to establish the prevalence of neuropathy in patients with PD and to evaluate for possible associations between neuropathy, vitamin B12 levels and levodopa exposure. In this study 37 consecutive patients with PD were compared to age matched controls. The diagnosis of neuropathy was based off a neuropathy screening scale. They found an increase in neuropathy in the PD group compared to the control group, 37.8% to 8.1%. Next they compared the prevalence of B12 deficiency in the group of PD patients with neuropathy to a control group of consecutive neuropathy patients without PD. Here they found that B12 deficiency is significantly more common in PD patients with neuropathy than a control group with neuropathy without PD. Finally they determined if cumulative levodopa exposure resulted in B12 deficiency. Here they found that cumulative levodopa exposure does correlate to lower B12 levels only in PD individuals with neuropathy. In the PD group as a single cohort, there was no significant correlation between cumulative levodopa exposure and neuropathy. This study highlights that neuropathy is prevalent in the PD population, and that if neuropathy is suspected, checking B12 levels may be warranted. This neuropathy may be related to levodopa exposure, however more studies are needed to determine how significant a role levodopa plays in the development of neuropathy.
Neurology 2011 Nov 29;77(22):1947-50