Though relatively modest in size, this is the largest placebo-controlled trial done to date in patients with Parkinson disease (PD) and depression. Nortriptyline was efficacious in the treatment of depression and paroxetine CR was not. When compared directly, nortriptyline produced significantly more responders than did paroxetine CR. The trial suggests that depression in patients with PD is responsive to treatment and raises questions about the relative efficacy of dual reuptake inhibitors and selective serotonin reuptake inhibitors.

Objective Despite the negative effects of depression in Parkinson’s disease, there is currently no evidence-based standard of care. The purpose of this study was to examine the efficacy of individually-administered Cognitive Behavior Therapy (CBT) versus clinical monitoring (with no new treatment) for depression in this medical population. Methods Eighty depressed (DSM-IV criteria) patients with Parkinson’s disease participated in an NIH-sponsored randomized-controlled trial of CBT vs. clinical monitoring (1:1 ratio) in an academic medical center from April 2007 to July 2010. All patients concurrently continued under the care of their personal physicians on stable medication regimens. The Hamilton Depression Rating Scale (HAM-D 17) was the primary outcome. CBT was modified to meet the unique needs of the Parkinson’s population and provided for 10 weeks. Assessments were completed at baseline and 5 (midpoint), 10 (end of treatment), and 14 weeks (follow-up) post-randomization by blind raters. Results The CBT group reported greater reductions in depression (HAM-D 17) vs. clinical monitoring (P<.0001). At week 10, mean HAM-D change was 7.35 for CBT vs. 0.05 for clinical monitoring (P<.0001). CBT was also superior to clinical monitoring on several secondary outcomes (i.e., Beck Depression Inventory, anxiety, quality of life, coping, Parkinson’s disease symptom ratings). There were more treatment responders in the CBT group (56% vs. 8%, P<.0001). Conclusions CBT may be a viable approach for the treatment of depression in Parkinson’s disease. Further research is needed to replicate and extend these findings.

Sleep disturbances are very common in patients with PD and are associated with a variety of negative outcomes. The evaluation of sleep disturbances in these patients is complex, as sleep may be affected by a host of primary sleep disorders, other primary medical or psychiatric conditions, reactions to medications, aging or the neuropathophysiology of PD itself. In this article we review the evaluation of the common disturbances of sleep seen in PD. This includes the primary sleep disorders, the interaction of depression and insomnia, the impact that medications for PD have on sleep, as well as the role of factors such as nocturia, pain, dystonia, akinesia, difficulty turning in bed and vivid dreaming. The treatment of sleep disturbances in PD is largely unstudied but recommendations based on clinical experience in PD and research studies in other geriatric populations can be made. Important principles include, diagnosis, treating the specific sleep disorder or co-occurring disorder, and control of the motor aspects of PD.

Background Although face-to-face cognitive-behavioral therapy was found to be beneficial for the treatment of depression in Parkinson’s disease (PD) in a recent randomized-controlled trial, access to care was identified as a critical issue that needs to be addressed in order to improve the management of this non-motor complication in PD. The purpose of this study was to examine the feasibility and effect of telephone-based cognitive-behavioral therapy for depression in Parkinson’s disease. Methods Twenty-one depressed people with Parkinson’s disease participated in an NIH-sponsored uncontrolled pilot trial of telephone-based cognitive-behavioral therapy in an academic medical center from October 2009 to February 2011. The Hamilton Depression Rating Scale was the primary outcome. Treatment was provided to people with Parkinson’s disease for 10 weeks, modified for delivery over the phone, and supplemented with 4 separate phone-based caregiver educational sessions. Assessments were completed at baseline and 5 (midpoint), 10 (end-of-treatment), and 14 weeks (follow-up) post-enrollment. Results Twenty (95%) people with Parkinson’s disease completed the study treatment. Phone-based cognitive-behavioral therapy was associated with significant improvements in depression, anxiety, negative thoughts, and coping. Mean Hamilton Depression Rating Scale change from baseline to week 10 was 7.91 points (P<.001, Cohen’s d=1.21). Conclusions Telephone-based cognitive-behavioral therapy may be a feasible and helpful approach for treating depression in Parkinson’s disease and warrants further exploration in randomized-controlled trials. Results were comparable to those observed in the few in-person cognitive-behavioral treatment studies for depression in Parkinson’s disease conducted to date.

Parkinson's disease (PD) is a common neurodegenerative disease affecting up to one million individuals in the United States. Depression is found in 40 to 50% of these patients and is associated with a variety of poor outcomes for both patients and their families. Despite this, there are few evidence-based data to guide clinical care. This was an NIH-funded, randomized, controlled trial of paroxetine, nortriptyline, and placebo. It included an 8 week acute phase and a 16 week blind extension phase. This report details the impact of depression treatment on quality of life (QoL) and disability in the acute and extension phase of this study. Secondary outcomes included relapse, tolerability, safety, and the impact of depression treatment on PD physical functioning. Patients who had improvement in depression, compared with those who did not, had significant gains in measures of QoL and disability (PDQ-8, P = 0.0001; SF-36, P = 0.0001) at 8 weeks and maintained their gains in the extension phase. Patients who were on active drug were significantly less likely to relapse in the extension phase than those on placebo (P = 0.041). Though relatively modest in size, this trial provides the first controlled data on the impact of treatment of depression on QoL and disability in PD. It suggests that successfully treating depression in PD leads to important, sustained improvements in these outcomes and that patients who improve on antidepressants are less likely to relapse than are patients who initially improve on placebo.

Parkinson’s disease (PD) is a common neurodegenerative disease affecting up to one million individuals in the US. Sleep disturbances, typically in sleep maintenance, are found in up to 88% of these individuals and are associated with a variety of poor outcomes. Despite being common and important, there are few data to guide clinical care. We conducted a six week, randomized, controlled trial of eszopiclone and placebo in thirty patients with PD and insomnia. Patients with other primary sleep disorders (PSG defined) were excluded. The primary outcome was total sleep time (TST) and secondary measures included wake after sleep onset (WASO), number of awakenings and quality of sleep, among others. The groups did not significantly differ on TST, but significant differences, favoring eszopiclone, did emerge in number of awakenings (p=.035), quality of sleep (p=.018) and in physician rated CGI improvement (p=.035). There was also a trend towards significance in WASO (p=.071). There were no significant differences between groups in measures of daytime functioning. The drug was well tolerated, with 33% of patients on eszopiclone and 27% of patients on placebo reporting adverse events. Though modest in size, this is the first controlled study of the treatment of insomnia in patients with PD. Eszopiclone did not increase total sleep time significantly but was superior to placebo in improving quality of sleep and some measures of sleep maintenance which is the most common sleep difficulty experienced by patients with PD. Definitive trials of the treatment of sleep disorders in this population are warranted.

Objective-Parkinson's disease is frequently complicated by depression (dPD) and there is a paucity of controlled research that can inform the management of this disabling non-motor complaint. A randomized controlled trial of nortriptyline, paroxetine, and placebo for the treatment of dPD was recently completed. The purpose of this paper is to describe the baseline pattern of depressive symptom presentation in PD, the specific symptoms of dPD that improve with pharmacotherapy, and the residual symptoms which remain in patients who meet a priori criteria for response or remission after acute treatment (8-weeks). Design/Intervention-A randomized controlled trial of nortriptyline, paroxetine, and placebo. Setting-TheMeasurement-The four subscales (core mood, anxiety, insomnia, somatic) and individual items from the Hamilton Rating Scale for Depression were the focus of the current study. These measures were assessed at baseline and week 8. Results-Baseline depressive symptoms were unrelated to motor functioning. Treatment response was associated with significant improvements in the core mood, anxiety, insomnia, and somatic symptoms seen in dPD. Residual symptoms, like sadness and loss of interest, persisted in treatment responders in a milder form than was initially present.Conclusions-Antidepressants may influence all symptoms of dPD, including those which share great overlap with the physical disease process. Additional research regarding adjunctive interventions is needed to help optimize the management of dPD.

Depression is very common in PD and linked with a faster progression of physical symptoms, greater cognitive decline, and poorer quality of life. Non-pharmacological approaches, like cognitivebehavioral therapy (CBT), for the treatment of depression in Parkinson's disease (dPD) have received little experimental attention despite strong demonstrated efficacy in other geriatric and medical populations. Depressed PD patients often differ from the depressed non-PD elderly in that they present with increased rates of both executive dysfunction and co-morbid psychiatric diagnoses, may differ in their depressive symptom presentation, and typically have caregivers who are highly involved in their treatment. Therefore, it is not possible to conclude that empirically validated treatments in the depressed aged will generalize to those with Parkinson's disease. In order to be most effective for PD patients, CBT should be tailored to their unique needs. Additional controlled research is needed to further explore the efficacy of CBT for dPD.