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Cognitive-Behavioral Therapy for Depression in Parkinson's Disease: A Randomized, Controlled Trial
Roseanne D. Dobkin, Ph.D.; Matthew Menza, M.D.; Lesley A. Allen, Ph.D.; Michael A. Gara, Ph.D.; Margery H. Mark, M.D.; Jade Tiu, Psy.M.; Karina L. Bienfait, Ph.D.; Jill Friedman, Ph.D.
Am J Psychiatry 2011;168:1066-1074. doi:10.1176/appi.ajp.2011.10111669
View Author and Article Information

Received Nov. 20, 2010; revision received Jan. 31, 2011; accepted Feb. 17, 2011.

Dr. Dobkin has received research support from the National Institutes of Health/National Institute of Neurological Disorders and Stroke. Dr. Menza has received research support from AstraZeneca, Boehringer Ingelheim, Bristol-Myers Squibb, Forest Laboratories, GlaxoSmithKline, Lilly, the National Institutes of Health/National Institute of Neurological Disorders and Stroke, Pfizer, Sanofi-Aventis, Sepracor, Takeda, and Wyeth; he has served as a consultant to GlaxoSmithKline, Kyowa, Lilly Research Laboratories, the National Institutes of Health/National Institute of Neurological Disorders and Stroke, Pfizer, Sepracor, and Takeda; and he has served as a speaker for Sanofi-Aventis. Dr. Allen has received research support from the National Institute of Mental Health and Sepracor. Dr. Gara has received research support from the National Institute of Mental Health. Dr. Mark has received research support from Cephalon, Kyowa, and the National Institutes of Health/National Institute of Neurological Disorders and Stroke; and she has served as a speaker for Allergan, Boehringer Ingelheim, GlaxoSmithKline, and Valeant. Dr. Bienfait was a postdoctoral fellow at the Robert Wood Johnson Medical School (2007–2009) while this study was in progress; upon completion of her fellowship, she accepted a position with Merck, where she is currently employed. Ms. Tiu and Dr. Friedman report no financial relationships with commercial interests.

Supported by the National Institutes of Health/National Institute of Neurological Disorders and Stroke grant 1 K23 NS052155-01A2 (Dr. Dobkin).

Dr. Dobkin had full access to all of the data in this study and takes responsibility for the integrity of the data and the accuracy of the data analysis. The full trial protocol can be assessed by contacting Dr. Dobkin.

The National Institute of Neurological Disorders and Stroke had no role in the design and conduct of this study; in the collection, management, analysis, and interpretation of the data; or in the preparation, review, or approval of the article.

This content is solely the responsibility of the authors and does not represent the views of the National Institute of Neurological Disorders and Stroke, the National Institutes of Health, or the Robert Wood Johnson Medical School.

ClinicalTrials.gov registry number, NCT004644 (www.clinicaltrials.gov).

From the Departments of Psychiatry and Neurology, University of Medicine and Dentistry of New Jersey–Robert Wood Johnson Medical School, Piscataway, N.J.; and Merck and Co., Whitehouse Station, N.J.

Address correspondence to Dr. Dobkin (dobkinro@umdnj.edu).

Received November 20, 2010; Revised January 31, 2011; Accepted February 17, 2011.

Copyright © American Psychiatric Association

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-behavioral therapy (CBT), relative to clinical monitoring (with no new treatment), for depression in this medical population.

Method:  Eighty depressed (based on DSM-IV criteria) patients with Parkinson's disease participated in a randomized, controlled trial of CBT relative to clinical monitoring (1:1 ratio) in an academic medical center from April 2007 to July 2010. All patients continued to maintain stable medication regimens under the care of their personal physicians. The 17-item Hamilton Depression Rating Scale (HAM-D) total score was the primary outcome. CBT was modified to meet the unique needs of the Parkinson's disease population and provided for 10 weeks. Assessments were completed by blind raters at baseline and 5 (midpoint), 10 (end of treatment), and 14 weeks (follow-up evaluation) postrandomization.

Results:  The CBT group reported greater reductions in depression (change in HAM-D score) than the clinical monitoring group. At week 10, the mean HAM-D score change was 7.35 for CBT relative to 0.05 for clinical monitoring. CBT was also superior to clinical monitoring on several secondary outcomes (i.e., Beck Depression Inventory scores, anxiety, quality of life, coping, Parkinson's disease symptom ratings). There were more treatment responders in the CBT group than the clinical monitoring group (56% versus 8%, respectively).

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.

Abstract Teaser
Figures in this Article

Parkinson's disease, the second most common neurodegenerative disorder in the United States, is defined by the motor triad of tremor, rigidity, and bradykinesia. The majority of patients also experience nonmotor complications (1), which are more closely associated with rates of disability and distress than the motor symptoms of the disease (2). Depression, the most prevalent nonmotor concern (3), affects approximately 50% of Parkinson's disease patients (4). Depression in Parkinson's disease is characterized by high rates of psychiatric comorbidity (5) and executive dysfunction (6) and is linked to faster physical and cognitive decline (7), poorer quality of life (8), and increased caregiver burden (9). Despite these negative effects, there is currently no evidence-based standard of care.

Pharmacological interventions have received the most empirical attention to date. Antidepressants (10, 11), dopamine agonists (12), and alternative treatments, such as omega-3 fatty acids (13), have demonstrated beneficial effects in preliminary controlled studies. Psychotherapeutic approaches, such as cognitive-behavioral therapy (CBT), have been the focus of fewer scientific investigations, despite demonstrated efficacy among the aged (14) and in other debilitating medical conditions (15). Only small pilot studies have examined the utility of CBT for depression in Parkinson's disease, with promising results (1621). In other patient groups, CBT has shown effects comparable to those of antidepressants for mild depression, with combination treatment appearing most effective for moderate-to-severe forms of depression (22). Additional research is needed to inform the development of specific treatment recommendations for this medical population.

The purpose of the present study was to conduct the first randomized, controlled trial of CBT for depression in Parkinson's disease. We hypothesized that CBT would result in greater decreases in depressive symptoms, anxiety, negative thoughts, sleep disturbance, and caregiver burden, as well as greater improvements in quality of life, coping, and social support, than clinical monitoring (with no new treatment). Furthermore, we hypothesized that there would be more treatment responders in the CBT group. The effect of CBT on Parkinson's disease symptom ratings was also examined.

This study received full approval by the Robert Wood Johnson Medical School Institutional Review Board. After complete description of the study to participants, written informed consent was obtained (prior to the initiation of any study procedures). Participants received the study treatment at no cost and were compensated $20.00 for each in-person assessment and $10.00 for each telephone assessment. Treatment and evaluation occurred at the Robert Wood Johnson Medical School. Participants enrolled in the study with a caregiver.

One-half of the participants received CBT plus clinical monitoring. The other half received clinical monitoring only. This additive design has been recommended for use when exploring the relative efficacy of a new psychotherapy intervention (23).

All participants continued to maintain stable medical regimens under the care of their personal physicians. Depression was addressed in the same manner in which it was handled prior to the study (e.g., antidepressant medication at a stable dose). No new depression treatment (other than CBT in the experimental condition) was provided to study participants. Those assigned to the comparison group (clinical monitoring only) had the option to receive the CBT treatment package after week 14.

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Participants

Patients were recruited from the Richard E. Heikkila Movement Disorders Clinic, local newspapers, and the New Jersey Chapter of the American Parkinson's Disease Association between April 2007 and March 2010. The final follow-up evaluation occurred in July 2010. Patients were eligible for participation in the study if they 1) had a diagnosis of Parkinson's disease per research criteria (24); 2) had a diagnosis of primary major depression, dysthymia, or depression not otherwise specified per DSM-IV criteria; 3) had a Clinical Global Impression–Severity scale score ≥4 (at least moderately ill [25]); 4) were between 35 and 85 years old; 5) were receiving a stable medication regimen for a duration of ≥6 weeks; and 6) had a family member or friend willing to participate.

Expert panel guidelines were followed regarding the diagnosis of depression in Parkinson's disease (26). Patients with comorbid anxiety disorders were eligible to enroll as long as their depressive disorder was primary.

Participants in both study groups (CBT plus clinical monitoring and clinical monitoring only) continued with mental healthcare (other than CBT) that was stabilized (≥6 weeks) prior to baseline. Medication use and mental healthcare utilization were tracked throughout the study. New depression treatment was a criterion for early termination.

Exclusion criteria were 1) dementia (a score below the 5th percentile for age on memory and on at least one other subscale of the Mattis Dementia Rating Scale [27]); 2) off-time (time when medication is not effective and symptoms return) ≥50% of the day; 3) suicidal ideation; 4) unstable medical conditions; 5) bipolar, schizophrenia spectrum, or substance abuse disorders (as determined by DSM-IV criteria); and 6) receiving CBT elsewhere.

Caregiver inclusion criteria were 1) ages 25–85 years, 2) daily contact with the study participant, and 3) no unstable medical or psychiatric conditions (as determined via clinical interview).

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Randomization and Masking

Appropriate candidates were allocated to receive CBT plus clinical monitoring or clinical monitoring only (1:1 ratio) by computer-generated random assignment (run by the statistical consultant [M.A.G.]). Randomization was stratified by antidepressant use at screening (yes/no) and conducted in blocks of six consecutive participants within each stratum.

All follow-up (i.e., postbaseline) assessments were conducted by independent evaluators without knowledge of the treatment condition. Participants were instructed not to reveal their group assignment to raters. Participants and therapists were not blind given the nature of the treatment.

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Procedure

Potential participants called our office to receive information about the study and to complete preliminary screening (see Figure 1 in the data supplement accompanying the online version of this article). Appropriate individuals were scheduled for a face-to-face appointment, where a statement of informed consent (for both patient and caregiver) was reviewed and signed, demographic information was obtained, inclusion/exclusion criteria were assessed (by R.D.D., M.H.M., and M.M.), and baseline evaluations were completed. Those who met eligibility criteria were enrolled and randomly assigned to one of the two aforementioned treatment arms. Participants were reassessed at 5 (midpoint), 10 (end of treatment), and 14 weeks postrandomization (1-month follow-up evaluation). Telephone calls to participants were made at weeks 2 and 7 to assess patient safety.

Raters received extensive training from the first author (R.D.D.) in administration of the Structured Clinical Interview for DSM-IV, the 17-item Hamilton Depression Rating Scale (HAM-D [28]), and the Hamilton Anxiety Rating Scale (HAM-A [29]). Interviews for both Hamilton rating scale measures were standardized (by R.D.D.) at the outset of the trial, and a coding dictionary was developed to facilitate accurate scoring of participant responses.

Change in the HAM-D total score was the primary outcome. HAM-D interrater reliability was >0.95 (intraclass correlation coefficient, based on 234 interviews [with 50 participants] selected by computer-generated random numbers). Secondary outcomes were 1) responder status (defined a priori as depression much improved or very much improved based on Clinical Global Impression–Improvement scale ratings or a reduction of at least 50% from baseline in the HAM-D total score [30]); 2) depression (measured by the Beck Depression Inventory [BDI] [31]); 3) anxiety (based on the HAM-A score); 4) negative thoughts (measured by the Inference Questionnaire [32]); 5) sleep (measured by the Pittsburgh Sleep Quality Index [33]); 6) quality of life (measured by the social functioning, physical role limitations, and physical disability subscales of the Medical Outcomes Study Short-Form Health Survey [34]); 7) coping (measured by the positive reframing and problem-focused subscales of the brief COPE scale [35]); 8) social support (measured by the Social Feedback Questionnaire [36]); 9) caregiver burden (measured by the Caregiver Distress Scale [37]); and 10) Parkinson's disease symptoms (based on the Unified Parkinson's Disease Rating Scale total score [38]).

All scales were completed at baseline, week 5, endpoint (week 10), and the week 14 follow-up evaluation except the Unified Parkinson's Disease Rating Scale, which was given only at baseline and endpoint.

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Intervention

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CBT.

The CBT employed in this trial was tailored to the unique needs of the Parkinson's disease population and is described in detail elsewhere (19, 39). In brief, specific modifications included 1) a stronger emphasis on behavioral and anxiety management techniques than what is traditionally integrated into CBT protocols for depression and 2) inclusion of a supplemental caregiver educational program. These changes were intended to address the psychiatric complexity and executive dysfunction that characterize this patient population.

Participants received 10 weekly individual sessions (60–75 minutes) of manualized CBT. Treatment incorporated exercise, behavioral activation, thought monitoring and restructuring, relaxation training, worry control, and sleep hygiene and was augmented with four separate individual caregiver educational sessions (30–45 minutes) that were intended to provide caregivers with the skills needed to facilitate participants' home-based practice of CBT techniques. For example, caregivers were taught to help participants identify negative thoughts and replace them with more balanced alternatives and were given tools to assist them in completing therapy goals (i.e., exercise, socializing). The primary focus was not to address the caregivers' own personal concerns. (The treatment manual is available upon request from the first author.)

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Therapist Training and Treatment Fidelity

The first author (R.D.D.) and two doctoral-level psychologists (K.L.B. and J.F.) conducted CBT. Prior to treating the study participants, the latter two authors received extensive training in CBT for depression in Parkinson's disease, which included treating two nonstudy patients each, with audiotape review of all their sessions by the first author (N=40). Throughout the trial, the first author and an independent expert in CBT in medical populations (L.A.A.) reviewed audiotapes from the therapy sessions (N=150), based on training and supervision needs, and assessed therapist skill and treatment fidelity, on the Cognitive Therapy Scale (40), a widely used and validated CBT competence measure (with a score ≥40 reflecting proficiency; mean score=55.74 [SD=6.52]).

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Clinical Monitoring

All participants received close clinical monitoring of their depressive symptoms by study personnel via follow-up telephone calls (at weeks 2 and 7 [30 minutes at each timepoint]) and evaluations (at weeks 5, 10, and 14 [60–90 minutes at each timepoint]). All participants remained on stable treatment regimens under the care of their personal physicians, who also monitored their medical and psychiatric status. No new depression treatment (other than CBT in the experimental condition) was provided.

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Statistical Analyses

Data were analyzed using SAS, version 9.1 (SAS Institute, Cary, N.C.). An intent-to-treat approach was employed in all analyses, which included all 80 randomly assigned participants. The primary outcome (change in HAM-D total score) was evaluated at baseline and weeks 5, 10, and 14 using mixed-models repeated-measures analysis of variance (SAS PROC MIXED) with restricted maximum likelihood estimation. Treatment group (CBT plus clinical monitoring and clinical monitoring only), assessment point (baseline and weeks 5, 10, and 14), and their interaction were fixed effects. The randomly assigned participant was treated as a random effect. The group-by-time interaction was the fixed effect of interest. Spatial power (a function of the square root of days that a given assessment occurred for a given participant) was used to model the covariance structure for all analyses, since this model yielded the best fit for the data among all covariance structures examined. Gender, block, strata (antidepressant use), and baseline cognition (based on the Dementia Rating Scale total score) were examined as covariates. Because there was no significant effect for any of these variables, they were removed from the final model.

Responder status was examined separately at weeks 10 and 14 and cross-tabulated with treatment group. The Fisher's exact test was used to compare the rate of response between CBT plus clinical monitoring and clinical monitoring only. The aforementioned mixed-models analyses were used to explore all other secondary outcomes. Because multiple tests capitalize on chance, all p values for these secondary outcomes were adjusted for multiple tests by the Holm method using permutation-type resampling (100,000 resamples; two-tailed) in SAS PROC MULTTEST. Effect sizes were calculated for all primary and secondary outcomes. Planned contrasts to examine changes specific to a particular timepoint (i.e., week 10) were only conducted if the overall omnibus statistical test remained significant after adjustment for multiple comparisons. Least squared means are presented.

Sample size was determined a priori based on power analyses. Power calculations were based on the HAM-D total score, an alpha set at 0.05, power set at 0.80, a predicted effect size of Cohen's d (0.70), based on a previous CBT pilot investigation in Parkinson's disease conducted by the first author (19) as well as published literature on CBT for depression (41), and the potential for 20% attrition. These parameters indicated that 40 participants per group were needed to obtain the desired effect.

Eighty individuals with Parkinson's disease, along with their caregivers, were enrolled in the study. Forty-one patients (51%) were randomly assigned to receive CBT plus clinical monitoring and 39 (49%) were assigned to receive clinical monitoring only. Ninety percent of participants (N=72) completed the study (see the data supplement). The mean number of CBT sessions attended was 9.17 ([SD= 2.32]). The mean number of caregiver sessions completed was 2.90 ([SD=1.43]). Forty-three participants (54%) were receiving a stable dose of antidepressant medication at baseline and reported compliance with their prescribed regimen throughout the trial. Baseline clinical and demographic characteristics are presented in Table 1.

 
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TABLE 1.

Baseline Demographic and Clinical Characteristics Among Depressed Parkinson's Disease Patients Randomly Assigned to Receive CBT Plus Clinical Monitoring or Clinical Monitoring Alone

Table Footer Note

a CBT and clinical monitoring were compared at baseline on relevant demographic and clinical variables to determine group equivalence, using t or chi-square tests as appropriate.

Table Footer Note

b For participants receiving antidepressant medications, the average length of treatment with the stable regimen was 2 years; this did not differ between treatment groups.

Table Footer Note

c A nominal baseline difference was observed for the Dementia Rating Scale total score; the baseline score was added as a covariate in the analysis of the primary outcome (change in Hamilton Depression Rating Scale score); this was not a significant covariate and thus was removed from the final analysis. No significant differences emerged for any other variable.

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Overall Treatment-by-Time Effects

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Primary outcome.

As seen in Table 2, the CBT plus clinical monitoring group reported significantly greater reductions in depression (HAM-D total score) compared with the clinical monitoring only group (F=30.74, df=3, 215, p<0.0001).

 
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TABLE 2.

Outcome Variables Among Depressed Parkinson's Disease Patients Randomly Assigned to Receive CBT Plus Clinical Monitoring or Clinical Monitoring Alone

Table Footer Note

a Data indicate least squares means.

Table Footer Note

b All p values for secondary outcomes have been adjusted using the Holm method. Raw p values are not reported.

Table Footer Note

c Data were calculated for the acute treatment period of baseline to endpoint.

Table Footer Note

d Lower scores indicate symptom improvement.

Table Footer Note

e Higher scores indicate symptom improvement.

Table Footer Note

* p≤0.01 (change significant from baseline).

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Secondary outcomes.

Notable effects were also observed on depression (BDI scores), anxiety, social functioning, positive reframing, and Parkinson's disease symptom ratings for those in the experimental group relative to the comparison group (Table 2). No significant group-by-time improvements were noted for sleep, inferences, problem-focused coping, physical disability, physical role limitations, social support, or caregiver burden.

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End of Treatment (Week 10)

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Primary outcome.

The mean HAM-D score was 13.58 (95% confidence interval [CI]=12.12-15.03) for CBT plus clinical monitoring and 19.33 (95% CI=17.89–20.77) for clinical monitoring only (Table 2). Mean change from baseline was 7.35 for CBT plus clinical monitoring compared with 0.05 for clinical monitoring only (F=76.34, df=1, 215, p<0.0001; Cohen's d=1.59) (Figure 1).

 
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FIGURE 1.

Hamilton Depression Rating Scale (HAM-D) Change Scores Among Parkinson's Disease Patients Randomly Assigned to Receive CBT Plus Clinical Monitoring or Clinical Monitoring Alone

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Secondary outcomes.

The mean BDI score was 9.74 (95% CI=7.46–12.02) for CBT plus clinical monitoring relative to 17.45 (95% CI=15.19–19.72) for clinical monitoring only. Mean change from baseline was 9.44 for CBT plus clinical monitoring and 1.60 for clinical monitoring only (F=27.25, df=1, 210, p<0.0001; Cohen's d=1.1). Significant improvements were also observed on measures of anxiety (F=25.83, df=1, 214, p<0.0001), social functioning (F=14.27, df=1, 209, p<0.001), and positive reframing (F=10.69, df=1, 204, p=0.001) for CBT plus clinical monitoring relative to clinical monitoring only (Table 2). Although there was no significant group-by-time interaction on negative inferences, exploratory analyses suggested that treatment responders exhibited greater decreases in negative thoughts than nonresponders (F=4.70, df=2, 77, p=0.01).

Moreover, exploratory subscale analysis of the Unified Parkinson's Disease Rating Scale (significant group-by-time effect noted for the total score) indicated statistically significant change for mood (F=39.75, df=1, 68, p<0.0001) and motor functioning (F=5.90, df=1, 68, p=0.02) favoring CBT. Specifically, the mean motor score was 21.10 (95% CI=17.95–24.26) for CBT plus clinical monitoring and 25.38 (95% CI=22.26–28.50) for clinical monitoring only. Mean motor change was 1.11 (improvement) for CBT plus clinical monitoring compared with –2.16 (worsening) for clinical monitoring only.

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One-Month Follow-Up Evaluation (Week 14)

Planned contrasts (baseline to week 14) demonstrated that improvements in depression (HAM-D score: F=55.62, df=1, 215, p<0.0001; BDI score: F=11.14, df=1, 210, p=0.001), anxiety (F=18.88, df=1, 214, p<0.0001), and social functioning (F=7.09, df=1, 209, p=0.008) were maintained at the follow-up evaluation (Table 2). Treatment responders continued to exhibit larger decreases in negative thoughts than nonresponders (F=3.04, df=3, 76, p=0.03). Parkinson's disease symptom ratings were not conducted at week 14.

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Treatment Response

At week 10, 23/41 (56%) participants receiving CBT plus clinical monitoring and 3/39 (8%) receiving clinical monitoring only met criteria for treatment response (Fisher's exact test: p<0.0001). At week 14, 21 (51%) participants in the CBT plus clinical monitoring group and none in the clinical monitoring only group met criteria for response (Fisher's exact test: p<0.0001).

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Number Needed to Treat

The number needed to treat based on responders for CBT plus clinical monitoring compared with clinical monitoring only was 2.1, with an absolute risk reduction of 48%.

The results of this first randomized, controlled trial suggest that CBT may be a feasible and possibly efficacious approach for treating depression in Parkinson's disease. Ninety percent of the sample completed the study, and 88% of participants randomly assigned to CBT plus clinical monitoring attended all 10 treatment sessions. CBT was associated with significant improvements on all clinician-rated and self-reported measures of depression. Gains were observed by the end of treatment (week 10) and maintained during the follow-up evaluation (week 14). Effect sizes were large for both the HAM-D (1.59) and BDI (1.1). Response rates favored CBT plus clinical monitoring relative to clinical monitoring only at weeks 10 (56% versus 8%, respectively) and 14 (51% versus 0%, respectively).

The CBT plus clinical monitoring group also reported greater improvements in quality of life, coping, and anxiety as well as less motor decline. These results underscore several points. First, CBT participants reported less avoidance of and greater enjoyment from social activities as well as the use of positive reframing as a coping strategy in response to daily stress. Second, treatment effects may generalize to the negative thoughts and avoidance behaviors that maintain anxiety. Third, the incorporation of anxiety management strategies, such as worry control and relaxation, into a CBT program for primary depression in Parkinson's disease may be useful. Lastly, consistent with previous findings, suboptimally treated depression may accelerate Parkinson's disease-related physical disability (7, 42).

Although there was no significant group-by-time interaction on inferences, treatment responders exhibited larger decreases in negative thinking compared with nonresponders. Since negative thoughts are a primary target of CBT, it follows that people who did not respond to treatment would not exhibit changes in thinking patterns. Despite moderate effect sizes, the effect of CBT on problem-focused coping and perceptions of role limitations and physical disability was no longer significant after controlling for multiple comparisons. CBT also had no substantial effects on sleep, social support, or caregiver burden.

There are no controlled trials, to our knowledge, of CBT for depression in Parkinson's disease with which to compare these results. However, completion and response rates, as well as effect sizes, are comparable to those observed in randomized trials of CBT in other populations (41). For example, the literature suggests that the average effect size of CBT for depression relative to a comparison condition similar to the one utilized in this study (i.e., no new treatment) is 0.67 (41). Thus, this initial randomized, controlled trial offers preliminary data to suggest that the beneficial effects of CBT observed in other patient groups might not be attenuated by the disease process (i.e., neurodegeneration, neurotransmitter changes, dysfunction in brain regions/pathways).

This study has several limitations related to the interpretation of efficacy. First, the study design did not include an attention-matched control or alternative psychosocial intervention. Although the additive approach and comparison condition employed did control for threats to internal validity (i.e., time, spontaneous remission, regression to the mean, treatment history, effects of repeated testing) and are appropriate for use in early-phase psychotherapy trials (23, 43), the role of nonspecific factors, such as the increased attention and social contact received by the CBT group, cannot be adequately explored. It is also not possible to isolate which aspects of the CBT package (e.g., caregiver sessions, exercise) were most helpful. Related to this, we cannot rule out the placebo effect as a partial explanation for differences between groups. However, several factors make this explanation less likely. Throughout the trial, it was emphasized that the effects of both study treatments (CBT plus clinical monitoring and clinical monitoring only) on depression in Parkinson's disease were not yet known and that there may not be any personal benefit from participation. Additionally, the chronic nature of depression in the sample, progressive nature of Parkinson's disease (i.e., not an acute stressor), durability of CBT gains exhibited over 14 weeks, changes in negative cognition that accompanied treatment response, minimal improvement observed in the clinical monitoring only condition, and comparability of results with CBT trials in other populations suggest that the effect of CBT may be larger than that which can be explained by placebo response alone. Of note, a CBT effect size of 0.75 is obtained when comparing CBT data from this study with pill-placebo data from our recent double-blind placebo-controlled antidepressant trial for depression in Parkinson's disease (10).

Second, despite an average reduction of 7.35 points, the mean HAM-D score of 13.58 for the CBT group at week 10 still reflects moderate depressive symptoms. This finding may be in part a result of the high rate of somatic complaints experienced by Parkinson's disease patients, independent of depression, as well as the inclusive scoring approach employed (44). For example, all reported symptoms were counted toward HAM-D ratings, despite potential overlap with the physical symptoms of Parkinson's disease (i.e., psychomotor slowing, fatigue). Importantly, the BDI emphasizes cognitive symptoms of depression (i.e., guilt, hopelessness), and the mean week-10 BDI score of 9.7 for the CBT group indicates minimal symptoms of depression. Third, given the psychiatric comorbidity in the sample and the inclusion of two anxiety management modules in the CBT package, it is possible that reduced anxiety could have influenced depression treatment response. Because the depression effect remained robust (p<0.0001) when controlling for change in the HAM-A score (exploratory analyses), it is unlikely that improved anxiety was a main mechanism of action. Fourth, motor functioning results warrant prudent interpretation. Although the group-by-time interaction on motor scores at week 10 was statistically significant, the effect size was small (0.13) and may be an artifact of the sample.

It is also necessary to acknowledge that our results may not generalize to those in more advanced stages of disease or with severe depression, dementia, suboptimal social supports, inability to travel to weekly therapy, and limited access to specialized mental health resources. In addition, we could not explore the longer-term durability of treatment gains because the follow-up period was limited to 1 month for ethical reasons (protocol restrictions regarding changing depression treatment). Lastly, treatment side effects were not assessed prospectively. Collectively, these limitations suggest that the results should be viewed as a preliminary first step in the establishment of an evidence base for CBT in the treatment of the psychiatric complications of Parkinson's disease.

The precise cause of depression in Parkinson's disease is unclear, with both biological and psychosocial factors implicated in its onset and maintenance (45). As a whole, the results of this trial suggest that CBT for depression in patients with Parkinson's disease may be beneficial, independent of etiology. Further research is needed to replicate and extend these findings.

Patient Perspective

A 64-year-old man with an 11-year history of Parkinson's disease was experiencing significant depression. Despite only mild motor symptoms, he rarely left the house because he believed that he would be viewed as frail. He stated, “People will view me as weak if I tremor in public.” In order to test the accuracy of this belief, the patient and therapist walked around the medical school where the therapist worked, and 25 people were approached at random and asked what they think when they see someone in public who is struggling with a physical handicap. Twenty-four expressed that they would view the person as “strong or admirable” for living a full life despite physical limitations while only one indicated that she might view the person with pity. This experiment was a turning point for the patient, who learned that it is important to evaluate evidence for his negative thoughts before assuming they are true. Based on this new information, he changed his thought to: “While some people might view me as weak if I tremor in public, the majority will see me as strong.” The patient's activity level increased, and his mood improved following this change in his thinking.

The authors thank Dr. Laura Marsh for her comments on the revised version of this article.

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[PubMed]
[CrossRef]
 
Menza  M;  Dobkin  RD;  Marin  H;  Mark  MH;  Gara  M;  Buyske  S;  Bienfait  K;  Dicke  A:  A controlled trial of antidepressants in patients with Parkinson's disease and depression.  Neurology 2009; 72:886–892
[PubMed]
[CrossRef]
 
Devos  D;  Dujardin  K;  Poirot  I;  Moreau  C;  Cottencin  O;  Thomas  P;  Destee  A;  Bordet  R;  Defebvre  L:  Comparison of desipramine and citalopram treatments for depression in Parkinson's disease: A double-blind, randomized placebo controlled study.  Mov Disord 2008; 23:850–857
[PubMed]
[CrossRef]
 
Barone  P;  Poewe  W;  Albrecht  S;  Debieuvre  C;  Massey  D;  Rascol  O;  Tolosa  E;  Weintraub  D:  Pramipexole for the treatment of depressive symptoms in patients with Parkinson's disease: a randomised, double-blind, placebo-controlled trial.  Lancet Neurol 2010; 9:573–580
[PubMed]
[CrossRef]
 
da Silva  TM;  Munhoz  RP;  Alvarez  C;  Naliwaiko  K;  Kiss  A;  Andreatini  R;  Ferraz  AC:  Depression in Parkinson's disease: a double-blind, randomized, placebo-controlled study of omega 3 fatty acid supplementation.  J Affect Disord 2008; 111:351–359
[PubMed]
[CrossRef]
 
Serfaty  MA;  Haworth  D;  Blanchard  M;  Buszewicz  M;  Murad  S;  King  M:  Clinical effectiveness of individual cognitive behavioral therapy for depressed older people in primary care.  Arch Gen Psychiatry 2009; 66:1332–1340
[PubMed]
[CrossRef]
 
Mohr  DC;  Likosky  W;  Bertagnolli  A;  Goodkin  DE;  van der Wende  J;  Dwyer  P;  Dick  LP:  Telephone-administered cognitive-behavioral therapy for the treatment of depressive symptoms in multiple sclerosis.  J Consult Clin Psychol 2000; 68:356–361
[PubMed]
[CrossRef]
 
Veazey  C;  Cook  KF;  Stanley  M;  Lai  EC;  Kunik  ME:  Telephone-administered cognitive behavioral therapy: a case study of anxiety and depression in Parkinson's disease.  J Clin Psychol Med Settings 2009; 16:243–253
[PubMed]
[CrossRef]
 
Feeney  F;  Egan  S;  Gasson  N:  Treatment of depression and anxiety in Parkinson's disease: a pilot study using group cognitive behavioural therapy.  Clin Psychol 2005; 9:31–38
[CrossRef]
 
Cole  K;  Vaughan  FL:  Brief cognitive-behavioral therapy for depression associated with Parkinson's disease: a single case series.  Behav Cogn Psychother 2005; 33:89–102
[CrossRef]
 
Dobkin  RD;  Allen  LA;  Menza  M:  Cognitive behavior therapy for depression in Parkinson's disease: a pilot study.  Mov Disord 2007; 22:946–952
[PubMed]
[CrossRef]
 
Dreising  H;  Beckmann  J;  Wermuth  L;  Skovlund  S;  Bech  P:  Psychologic effects of structured cognitive psychotherapy in young patients with Parkinson's disease: a pilot study.  Nordic J Psychiatry 1999; 53:217–221
[CrossRef]
 
Farabaugh  A;  Locascio  JJ;  Yap  L;  Growdon  J;  Fava  M;  Crawford  C;  Matthews  J;  McCutchen  J;  Bunchin  J;  Pava  J;  Alpert  JE:  Cognitive-behavioral therapy for patients with Parkinson's disease and comorbid major depressive disorder.  Psychosomatics 2010; 51:124–129
[PubMed]
 
Hollon  SD;  Jarrett  RB;  Nierenberg  AA;  Thase  ME;  Trivedi  M;  Rush  AH:  Psychotherapy and medication in the treatment of adult and geriatric depression: which monotherapy or combined treatment? J Clin Psychiatry 2005; 66:455–468
[PubMed]
[CrossRef]
 
Borkovec  T;  Sibrava  NJ:  Psychotherapy research, suggested alternatives, and some strategies for the pursuit of the placebo phenomenon.  J Clin Psychol 2005; 61:805–818
[PubMed]
[CrossRef]
 
Gelb  DJ;  Oliver  E;  Gilman  S:  Diagnostic criteria for Parkinson disease.  Arch Neurol 1999; 56:33–39
[PubMed]
[CrossRef]
 
Guy  W:  ECDEU Assessment Manual for Psychopharmacology .  Washington, DC,  US Department of Health, Education, and Welfare, 1976
 
Marsh  L;  McDonald  WM;  Cummings  J;  Ravina  BNINDS/NIMH Work Group on Depression and Parkinson's Disease:  Provisional Diagnostic Criteria for Depression in Parkinson's Disease: report of an NINDS/NIMH Work Group.  Mov Disord 2006; 21:148–158
[PubMed]
[CrossRef]
 
Mattis  S:  Dementia Rating Scale .  Odessa, Fla,  Psychological Assessment Resources, 1988
 
Hamilton  M:  A rating scale for depression.  J Neurol Neurosurg Psychiatry 1960; 23:56–62
[PubMed]
[CrossRef]
 
Hamilton  M:  The assessment of anxiety status by rating.  Br J Med Psychol 1959; 32:50–55
[PubMed]
[CrossRef]
 
Frank  E;  Prien  RF;  Jarrett  RB;  Keller  MB;  Kupfer  DJ;  Lavori  PW;  Rush  AJ;  Weisman  MM:  Conceptualization and rationale for consensus definitions of terms in major depressive disorder.  Arch Gen Psychiatry 1991; 48:851–855
[PubMed]
[CrossRef]
 
Beck  AT;  Rush  AJ;  Shaw  BF;  Emery  G:  Cognitive Therapy of Depression .  New York,  Guilford Press, 1979
 
Alloy  LB;  Abramson  LY:  The Temple-Wisconsin Cognitive Vulnerability to Depression (CVD) project: conceptual background, design, and methods.  J Cogn Psychother 1999; 13:227–262
 
Buysse  DJ;  Reynolds  CF  III;  Monk  TH;  Berman  SR;  Kupfer  DJ:  The Pittsburgh Sleep Quality Index: a new instrument for psychiatric research and practice.  J Psychiatr Res 1989; 28:193–213
[CrossRef]
 
Ware  JE;  Sherbourne  CD:  The MOS 36-Item Short-Form Health Survey (SF-36).  Med Care 1992; 30:473–483
[PubMed]
[CrossRef]
 
Carver  CS:  You want to measure coping but your protocol is too long: consider the brief COPE.  Int J Behav Med 1997; 4:92–100
[PubMed]
[CrossRef]
 
Dobkin  RD;  Panzarella  C;  Alloy  LB;  Cascardi  M;  Truesdell  K;  Gara  M:  Assessing an interpersonal- cognitive risk factor for depression: preliminary validation of the Social Feedback Questionnaire.  J Soc Pers Relat 2007; 24:765–780
[CrossRef]
 
Cousins  R;  Davies  ADM;  Turnball  CJ;  Playfer  JR:  Assessing caregiver distress: a conceptual analysis and brief scale.  Br J Clin Psychol 2002; 41:387–403
[PubMed]
[CrossRef]
 
Fahn  S;  Elton  RLUPDRS Development Committee:  Unified Parkinson's Disease Rating Scale, in Recent Developments in Parkinson's Disease . Edited by Fahn  S;  Marsden  CD;  Calne  DB;  Goldstein  M.  Florham Park, NJ,  Macmillan Health Care Information, 1987, pp 153–163
 
Dobkin  RD;  Menza  M;  Bienfait  KL:  CBT for the treatment of depression in Parkinson's disease: a promising non-pharmacological approach.  Expert Rev Neurother 2008; 8:27–35
[PubMed]
[CrossRef]
 
Young  J;  Beck  AT:  Cognitive Therapy Scale Rating Manual .  Philadelphia,  University of Pennsylvania Psychotherapy Research Unit, 1980
 
Driessen  E;  Hollon  SD:  Cognitive behavioral therapy for mood disorders: efficacy, moderators, and mediators.  Psychiatr Clin N Am 2010; 33:537–555
[CrossRef]
 
Marsh  L;  Williams  JR:  Effect of depression remission status on physical disability in Parkinson's disease: longitudinal cohort study (abstract).  Mov Disord 2007; 22:XIV–XV
 
Mohr  DC;  Spring  B;  Freedland  KE;  Beckner  V;  Arean  P;  Hollon  SD;  Ockene  J;  Kaplan  R:  The selection and design of control conditions for randomized controlled trials of psychological interventions.  Psychother Psychosom 2009; 78:275–284
[PubMed]
[CrossRef]
 
Schrag  A;  Barone  P;  Brown  RG;  Leentjens  AFG;  McDonald  WM;  Starkstein  S;  Weintraub  D;  Poewe  W;  Rascol  O;  Sampaio  C;  Stebbins  GT;  Goetz  CG:  Depression rating scales in Parkinson's disease: critique and recommendations.  Mov Disord 2007; 22:1077–1092
[PubMed]
[CrossRef]
 
Weintraub  D;  Stern  MB:  Psychiatric complications in Parkinson's disease.  Am J Geriatr Psychiatry 2005; 13:844–851
[PubMed]
 
References Container

FIGURE 1. 

Hamilton Depression Rating Scale (HAM-D) Change Scores Among Parkinson's Disease Patients Randomly Assigned to Receive CBT Plus Clinical Monitoring or Clinical Monitoring Alone

Anchor for Jump
TABLE 1.

Baseline Demographic and Clinical Characteristics Among Depressed Parkinson's Disease Patients Randomly Assigned to Receive CBT Plus Clinical Monitoring or Clinical Monitoring Alone

Table Footer Note

a CBT and clinical monitoring were compared at baseline on relevant demographic and clinical variables to determine group equivalence, using t or chi-square tests as appropriate.

Table Footer Note

b For participants receiving antidepressant medications, the average length of treatment with the stable regimen was 2 years; this did not differ between treatment groups.

Table Footer Note

c A nominal baseline difference was observed for the Dementia Rating Scale total score; the baseline score was added as a covariate in the analysis of the primary outcome (change in Hamilton Depression Rating Scale score); this was not a significant covariate and thus was removed from the final analysis. No significant differences emerged for any other variable.

Anchor for Jump
TABLE 2.

Outcome Variables Among Depressed Parkinson's Disease Patients Randomly Assigned to Receive CBT Plus Clinical Monitoring or Clinical Monitoring Alone

Table Footer Note

a Data indicate least squares means.

Table Footer Note

b All p values for secondary outcomes have been adjusted using the Holm method. Raw p values are not reported.

Table Footer Note

c Data were calculated for the acute treatment period of baseline to endpoint.

Table Footer Note

d Lower scores indicate symptom improvement.

Table Footer Note

e Higher scores indicate symptom improvement.

Table Footer Note

* p≤0.01 (change significant from baseline).

+

References

Kulisevsky  J;  Pagonabarraga  J;  Pascual-Sedano  B;  Garcia-Sanchez  C;  Gironell  A:  Prevalence and correlates of neuropsychiatric symptoms in Parkinson's disease without dementia.  Mov Disord 2008; 23:1889–1896
[PubMed]
[CrossRef]
 
Forsaa  EB;  Larsen  JP;  Wentzel-Larsen  T;  Herlofson  K;  Alves  G:  Predictors and course of health-related quality of life in Parkinson's disease.  Mov Disord 2008; 23:1420–1427
[PubMed]
[CrossRef]
 
Cummings  JL:  Depression and Parkinson's disease.  Am J Psychiatry 1992; 149:443–454
[PubMed]
 
Reijnders  MA;  Ehrt  U;  Weber  WEJ;  Aarsland  D;  Leentjens  AF:  A systematic review of prevalence studies of depression in Parkinson's disease.  Mov Disord 2008; 23:183–189
[PubMed]
[CrossRef]
 
Menza  MA;  Robertson-Hoffmann  DE;  Bonapace  AS:  Parkinson's disease and anxiety: comorbidity with depression.  Biol Psychiatry 1993; 34:465–470
[PubMed]
[CrossRef]
 
Santangelo  G;  Vitale  C;  Trojano  L;  Longo  K;  Cozzolino  A;  Grossi  D;  Barone  P:  Relationship between depression and cognitive dysfunctions in Parkinson's disease without dementia.  J Neurol 2009; 256:632–638
[PubMed]
[CrossRef]
 
Starkstein  SE;  Mayberg  HS;  Leiguarda  R;  Preziosi  TJ;  Robinson  RG:  A prospective longitudinal study of depression, cognitive decline, and physical impairments in patients with Parkinson's disease.  J Neurol Neurosurg Psychiatry 1992; 55:377–382
[PubMed]
[CrossRef]
 
Global Parkinson's Disease Survey Steering Committee:  Factors impacting on quality of life in Parkinson's disease: results from an international survey.  Mov Disord 2002; 17:60–67
[PubMed]
[CrossRef]
 
Martinez-Martin  P;  Forjaz  MJ;  Frades-Payo  B;  Rusiñol  AB;  Fernández-García  JM;  Benito-León  J;  Arillo  VC;  Barberá  MA;  Sordo  MP;  Catalán  MJ:  Caregiver burden in Parkinson's disease.  Mov Disord 2007; 22:924–931
[PubMed]
[CrossRef]
 
Menza  M;  Dobkin  RD;  Marin  H;  Mark  MH;  Gara  M;  Buyske  S;  Bienfait  K;  Dicke  A:  A controlled trial of antidepressants in patients with Parkinson's disease and depression.  Neurology 2009; 72:886–892
[PubMed]
[CrossRef]
 
Devos  D;  Dujardin  K;  Poirot  I;  Moreau  C;  Cottencin  O;  Thomas  P;  Destee  A;  Bordet  R;  Defebvre  L:  Comparison of desipramine and citalopram treatments for depression in Parkinson's disease: A double-blind, randomized placebo controlled study.  Mov Disord 2008; 23:850–857
[PubMed]
[CrossRef]
 
Barone  P;  Poewe  W;  Albrecht  S;  Debieuvre  C;  Massey  D;  Rascol  O;  Tolosa  E;  Weintraub  D:  Pramipexole for the treatment of depressive symptoms in patients with Parkinson's disease: a randomised, double-blind, placebo-controlled trial.  Lancet Neurol 2010; 9:573–580
[PubMed]
[CrossRef]
 
da Silva  TM;  Munhoz  RP;  Alvarez  C;  Naliwaiko  K;  Kiss  A;  Andreatini  R;  Ferraz  AC:  Depression in Parkinson's disease: a double-blind, randomized, placebo-controlled study of omega 3 fatty acid supplementation.  J Affect Disord 2008; 111:351–359
[PubMed]
[CrossRef]
 
Serfaty  MA;  Haworth  D;  Blanchard  M;  Buszewicz  M;  Murad  S;  King  M:  Clinical effectiveness of individual cognitive behavioral therapy for depressed older people in primary care.  Arch Gen Psychiatry 2009; 66:1332–1340
[PubMed]
[CrossRef]
 
Mohr  DC;  Likosky  W;  Bertagnolli  A;  Goodkin  DE;  van der Wende  J;  Dwyer  P;  Dick  LP:  Telephone-administered cognitive-behavioral therapy for the treatment of depressive symptoms in multiple sclerosis.  J Consult Clin Psychol 2000; 68:356–361
[PubMed]
[CrossRef]
 
Veazey  C;  Cook  KF;  Stanley  M;  Lai  EC;  Kunik  ME:  Telephone-administered cognitive behavioral therapy: a case study of anxiety and depression in Parkinson's disease.  J Clin Psychol Med Settings 2009; 16:243–253
[PubMed]
[CrossRef]
 
Feeney  F;  Egan  S;  Gasson  N:  Treatment of depression and anxiety in Parkinson's disease: a pilot study using group cognitive behavioural therapy.  Clin Psychol 2005; 9:31–38
[CrossRef]
 
Cole  K;  Vaughan  FL:  Brief cognitive-behavioral therapy for depression associated with Parkinson's disease: a single case series.  Behav Cogn Psychother 2005; 33:89–102
[CrossRef]
 
Dobkin  RD;  Allen  LA;  Menza  M:  Cognitive behavior therapy for depression in Parkinson's disease: a pilot study.  Mov Disord 2007; 22:946–952
[PubMed]
[CrossRef]
 
Dreising  H;  Beckmann  J;  Wermuth  L;  Skovlund  S;  Bech  P:  Psychologic effects of structured cognitive psychotherapy in young patients with Parkinson's disease: a pilot study.  Nordic J Psychiatry 1999; 53:217–221
[CrossRef]
 
Farabaugh  A;  Locascio  JJ;  Yap  L;  Growdon  J;  Fava  M;  Crawford  C;  Matthews  J;  McCutchen  J;  Bunchin  J;  Pava  J;  Alpert  JE:  Cognitive-behavioral therapy for patients with Parkinson's disease and comorbid major depressive disorder.  Psychosomatics 2010; 51:124–129
[PubMed]
 
Hollon  SD;  Jarrett  RB;  Nierenberg  AA;  Thase  ME;  Trivedi  M;  Rush  AH:  Psychotherapy and medication in the treatment of adult and geriatric depression: which monotherapy or combined treatment? J Clin Psychiatry 2005; 66:455–468
[PubMed]
[CrossRef]
 
Borkovec  T;  Sibrava  NJ:  Psychotherapy research, suggested alternatives, and some strategies for the pursuit of the placebo phenomenon.  J Clin Psychol 2005; 61:805–818
[PubMed]
[CrossRef]
 
Gelb  DJ;  Oliver  E;  Gilman  S:  Diagnostic criteria for Parkinson disease.  Arch Neurol 1999; 56:33–39
[PubMed]
[CrossRef]
 
Guy  W:  ECDEU Assessment Manual for Psychopharmacology .  Washington, DC,  US Department of Health, Education, and Welfare, 1976
 
Marsh  L;  McDonald  WM;  Cummings  J;  Ravina  BNINDS/NIMH Work Group on Depression and Parkinson's Disease:  Provisional Diagnostic Criteria for Depression in Parkinson's Disease: report of an NINDS/NIMH Work Group.  Mov Disord 2006; 21:148–158
[PubMed]
[CrossRef]
 
Mattis  S:  Dementia Rating Scale .  Odessa, Fla,  Psychological Assessment Resources, 1988
 
Hamilton  M:  A rating scale for depression.  J Neurol Neurosurg Psychiatry 1960; 23:56–62
[PubMed]
[CrossRef]
 
Hamilton  M:  The assessment of anxiety status by rating.  Br J Med Psychol 1959; 32:50–55
[PubMed]
[CrossRef]
 
Frank  E;  Prien  RF;  Jarrett  RB;  Keller  MB;  Kupfer  DJ;  Lavori  PW;  Rush  AJ;  Weisman  MM:  Conceptualization and rationale for consensus definitions of terms in major depressive disorder.  Arch Gen Psychiatry 1991; 48:851–855
[PubMed]
[CrossRef]
 
Beck  AT;  Rush  AJ;  Shaw  BF;  Emery  G:  Cognitive Therapy of Depression .  New York,  Guilford Press, 1979
 
Alloy  LB;  Abramson  LY:  The Temple-Wisconsin Cognitive Vulnerability to Depression (CVD) project: conceptual background, design, and methods.  J Cogn Psychother 1999; 13:227–262
 
Buysse  DJ;  Reynolds  CF  III;  Monk  TH;  Berman  SR;  Kupfer  DJ:  The Pittsburgh Sleep Quality Index: a new instrument for psychiatric research and practice.  J Psychiatr Res 1989; 28:193–213
[CrossRef]
 
Ware  JE;  Sherbourne  CD:  The MOS 36-Item Short-Form Health Survey (SF-36).  Med Care 1992; 30:473–483
[PubMed]
[CrossRef]
 
Carver  CS:  You want to measure coping but your protocol is too long: consider the brief COPE.  Int J Behav Med 1997; 4:92–100
[PubMed]
[CrossRef]
 
Dobkin  RD;  Panzarella  C;  Alloy  LB;  Cascardi  M;  Truesdell  K;  Gara  M:  Assessing an interpersonal- cognitive risk factor for depression: preliminary validation of the Social Feedback Questionnaire.  J Soc Pers Relat 2007; 24:765–780
[CrossRef]
 
Cousins  R;  Davies  ADM;  Turnball  CJ;  Playfer  JR:  Assessing caregiver distress: a conceptual analysis and brief scale.  Br J Clin Psychol 2002; 41:387–403
[PubMed]
[CrossRef]
 
Fahn  S;  Elton  RLUPDRS Development Committee:  Unified Parkinson's Disease Rating Scale, in Recent Developments in Parkinson's Disease . Edited by Fahn  S;  Marsden  CD;  Calne  DB;  Goldstein  M.  Florham Park, NJ,  Macmillan Health Care Information, 1987, pp 153–163
 
Dobkin  RD;  Menza  M;  Bienfait  KL:  CBT for the treatment of depression in Parkinson's disease: a promising non-pharmacological approach.  Expert Rev Neurother 2008; 8:27–35
[PubMed]
[CrossRef]
 
Young  J;  Beck  AT:  Cognitive Therapy Scale Rating Manual .  Philadelphia,  University of Pennsylvania Psychotherapy Research Unit, 1980
 
Driessen  E;  Hollon  SD:  Cognitive behavioral therapy for mood disorders: efficacy, moderators, and mediators.  Psychiatr Clin N Am 2010; 33:537–555
[CrossRef]
 
Marsh  L;  Williams  JR:  Effect of depression remission status on physical disability in Parkinson's disease: longitudinal cohort study (abstract).  Mov Disord 2007; 22:XIV–XV
 
Mohr  DC;  Spring  B;  Freedland  KE;  Beckner  V;  Arean  P;  Hollon  SD;  Ockene  J;  Kaplan  R:  The selection and design of control conditions for randomized controlled trials of psychological interventions.  Psychother Psychosom 2009; 78:275–284
[PubMed]
[CrossRef]
 
Schrag  A;  Barone  P;  Brown  RG;  Leentjens  AFG;  McDonald  WM;  Starkstein  S;  Weintraub  D;  Poewe  W;  Rascol  O;  Sampaio  C;  Stebbins  GT;  Goetz  CG:  Depression rating scales in Parkinson's disease: critique and recommendations.  Mov Disord 2007; 22:1077–1092
[PubMed]
[CrossRef]
 
Weintraub  D;  Stern  MB:  Psychiatric complications in Parkinson's disease.  Am J Geriatr Psychiatry 2005; 13:844–851
[PubMed]
 
References Container
+
+

Self-Assessment Quiz - Expired

Did you know? You can add a subscription now to earn CME Credits!

1.
The CBT employed in this trial was tailored to the unique needs of the Parkinson's disease population in which of the following ways?
2.
Why were caregivers of patients with Parkinson's disease included in the CBT protocol?
3.
CBT was associated with which of the following benefits for people with Parkinson's disease, relative to clinical monitoring with no new treatment?
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