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Published in final edited form as: J Consult Clin Psychol. 2012 Mar 12;80(4):694–699. doi: 10.1037/a0027695

Predictors of Treatment Response to Cognitive-Behavioral Therapy for Depression in Parkinson’s Disease

Roseanne D Dobkin 1, Jade Tiu Rubino 2, Lesley A Allen 3, Jill Friedman 4, Michael A Gara 5, Margery H Mark 6, Matthew Menza 7
PMCID: PMC3376684  NIHMSID: NIHMS357484  PMID: 22409644

Abstract

Objective

The purpose of this study was to examine predictors of treatment response to cognitive-behavioral therapy (CBT) for depression in Parkinson’s disease (PD).

Methods

The sample comprised 80 depressed (DSM-IV criteria) adults with PD [60% male] and their caregivers who participated in an NIH-sponsored randomized-controlled trial of CBT vs. clinical monitoring from April 2007 until July 2010. Individually-administered CBT was provided to people with PD for 10 weeks, modified to address the unique needs of the medical population, and supplemented with up to 4 separate caregiver educational sessions. Treatment response was defined a priori as a rating of depression much improved or very much improved on the Clinical Global Impression-Improvement Scale or ≥ 50% reduction in the baseline Hamilton Depression Rating Scale score. It was hypothesized (a priori) that caregiver participation in treatment, motor disability, psychiatric comorbidity, and executive functioning would be significant predictors of response to CBT at end-of-treatment (week 10) and short-term follow-up (week 14).

Results

At week 10, caregiver participation was the only significant predictor of treatment response in the CBT group. At week 14, both caregiver participation and executive functioning predicted response to CBT. Treatment group, baseline depression severity, executive functioning, motor disability, psychiatric comorbidity, marital status, and caregiver burden were also related to change in depression scores, for all participants, in secondary and exploratory models.

Conclusions

Caregiver participation may enhance acute treatment response to psychosocial interventions for depression in PD. Further research is needed to extend and replicate these findings.

Keywords: Parkinson’s disease, depression, cognitive-behavioral therapy, caregiver, predictors of treatment response

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by tremor, rigidity, and bradykinesia. PD affects up to 1 million people in the United States and as many as 6 million individuals worldwide (National Parkinson Foundation, 2010). The majority of people with Parkinson’s disease also experience non-motor complications such as depression, anxiety, sleep disturbance, psychosis, and cognitive changes (Weintraub & Burn, 2011). These neuropsychiatric features of the illness are larger determinants of disability and distress, for both people with PD and their family members, than are the physical aspects of the disease (Carter, Stewart, Lyons, & Archbold, 2008; Forsaa, Larsen, Wentzel-Larsen, Herlofson, & Alves, 2008).

Depression is the most frequently cited non-motor complaint in PD (Cummings, 1992). Affecting up to 50% of people with PD (Reijnders, Ehrt, Weber, Aarsland, & Leentjens, 2008), the incidence of depression in PD is more than double that observed in the general population and significantly higher than the rates reported in other medical conditions (Tandberg, Larsen, Aarsland, & Cummings, 1996). Depression in PD (dPD) may predate the onset of motor symptoms (Leentjens, Van den Akker, Metsemakers, Lousberg, & Verhey, 2003) and is often under-diagnosed (Shulman, Taback, Rabinstein, & Weiner, 2002) and inadequately managed by healthcare providers (Ravina et al., 2007). The sub-optimal treatment of dPD is of great clinical concern as depression is associated with more rapid physical and cognitive deterioration (Starkstein, Mayberg, Leiguarda, Preziosi, & Robinson, 1992), poorer quality of life (Forsaa et al., 2008), and increased caregiver distress in Parkinson’s disease (Carter et al., 2008).

Despite these negative consequences of dPD, there is a paucity of controlled research to guide the treatment of this psychiatric complication. To date, pharmacological approaches for the treatment of dPD have received the most preliminary support (e.g., Menza et al., 2009). In contrast, little is known about the usefulness of psychosocial interventions for treating depression in the context of this comorbid medical condition. To the best of our knowledge, we recently conducted the first randomized-controlled trial (RCT) of cognitive-behavioral therapy (CBT) for depression in PD (Dobkin et al., 2011). In this RCT, we demonstrated that CBT was associated with notable improvements in depression, anxiety, coping, quality of life, and motor disability in people with PD, compared to clinical monitoring, over 14-weeks. Given the paucity of available research to guide the management of dPD, identifying factors that may facilitate depression treatment response in this medical population may have significant clinical implications.

The purpose of the current study was to examine predictors of treatment response to CBT for depression in PD. It was hypothesized (a priori) that caregiver participation in treatment, motor disability, psychiatric comorbidity, and executive functioning would be significant predictors of response to CBT at end-of-treatment (week 10) and short-term follow-up (week 14). These a priori predictors were selected for several reasons. First, the inclusion of family members in psychosocial interventions for chronic medical conditions has been linked with improved patient outcomes across a range of physical illnesses versus usual care (Martire, Lustig, Schulz, Miller, & Helgeson, 2004). Second, estimates suggest that informal caregivers assist people with PD an average of 11 times per day in early PD and up to 30 times per day in later stage disease (Carter et al., 1998). The beneficial impact of caregiver involvement on mental and physical health in PD has been well demonstrated (e.g., Ravenek & Schneider, 2009). Third, in addition to the physical disability observed in this medical group, dPD is characterized by high rates of executive dysfunction (Santangelo et al., 2009) and psychiatric comorbidity (Menza, Robertson-Hoffman, & Bonapace, 1993), factors which have been associated with depression treatment response in older adults (Andresscu et al., 2009; Mohlman & Gorman, 2005; Weinberger, Raue, Meyers, & Bruce, 2009) and in the few pharmacologic studies that have examined these relationships in PD (e.g., Dobkin et al., 2010). The extent to which these a priori factors moderated treatment effects and predicted change in depression scores over time across both study treatments, as well as the degree to which demographic and clinical variables (previously linked with dPD) influenced improvement in this trial, were also examined.

Method

Participants and Procedures

The sample comprised 80 depressed (DSM-IV criteria; SCID-I) people with Parkinson’s disease (PWP) [60% male, 40% female; 5% Asian, 1% African-American, 1% Pacific Islander, 3% Hispanic Caucasian, 90% Non-Hispanic Caucasian] and their caregivers (e.g., a family member or friend) who participated in a randomized-controlled trial of CBT vs. clinical monitoring (with no new treatment) for dPD at an academic medical center in the Northeast. Sixty-five PWP (81%) had primary Major Depressive Disorder; 45 (56.3%) had a secondary anxiety disorder diagnosis. The spouse was the identified caregiver in 62% of cases. Additional participant characteristics, study inclusion criteria, recruitment strategies, flow of participants through the trial, sample size and power calculations, as well as study treatments and procedures are described in detail in the main outcome paper from this trial (Dobkin et al., 2011).

In brief, the study had full IRB approval. Written informed consent was obtained prior to the initiation of any study procedures. As described by Dobkin et al. (2011), participants were allocated to receive CBT plus clinical monitoring (N = 41) or clinical monitoring alone (N = 39) by computer-generated random assignment. The 10-session individually-administered CBT protocol was tailored to the unique needs of the PD population and supplemented with up to four separate caregiver educational sessions. CBT was provided by doctoral level psychologists. All participants received close clinical monitoring of their depressive symptoms by study staff (four, two-hour, in-person assessments and two, 30-minute phone calls) and their personal physicians.

Measures

Depression outcome measures

The Hamilton Depression Rating Scale (HAM-D 17; Hamilton, 1960), Beck Depression Inventory (BDI; Beck, Rush, Shaw, & Emery, 1979), and the Clinical Global Impression-Improvement Scale (CGI-I; Guy, 1976) were used to assess depression severity and change. CGI-I ratings for depression in the current trial were determined not only by symptom change but also by the impact of that change on quality of life and daily functioning, based in response to a scripted interview standardized at the outset of the trial. Treatment response was defined a priori as a score of 1 (very much improved) or 2 (much improved) on the CGI-I or ≥ 50% reduction in the baseline HAM-D 17 score (Frank et al., 1991). This categorical construct of treatment response was the primary depression outcome of interest in the current paper.

Potential predictor measures

All potential predictors of treatment response and symptom change, except caregiver participation in CBT, were evaluated at baseline.

A priori model
Caregiver participation

The number of caregiver sessions attended were tabulated.

Motor disability

The Unified Parkinson’s Disease Rating Scale (UPDRS; Fahn et al., 1987) is a 42-item clinician-administered scale used to evaluate the severity of PD symptoms. The motor subscale assesses key motor symptoms including bradykinesia, resting and action tremor, rigidity, postural instability and gait disorder. Higher scores indicate greater severity.

Psychiatric comorbidity

The number SCID Axis I diagnoses were tabulated.

Executive functioning

The Trail-making Test (TMT) is a timed neuropsychological test comprised of two parts (Bowie & Harvey, 2006). In Part A, the patient is asked to connect a series of consecutively numbered circles (1–25) in ascending order. In Part B, the patient must connect a series of numbered (1–13) and lettered (A-L) circles in ascending order while alternating between numbers and letters (i.e., 1-A-2-B-3-C, etc.). Parts A and B are timed separately. The time difference between parts B and A is a reflection of executive functioning.

Exploratory models
Demographic variables

Age, gender, marital status, highest level of education, race and ethnicity (per NIH guidelines), and work status were assessed.

Clinical variables

Information on the following clinical variables relevant to the treatment of dPD was also obtained: primary mood disorder diagnosis, length of the current depressive episode, number of past depressive episodes, current use of an antidepressant medication, number of past antidepressant medication trials, history of psychotherapy, comorbid medical conditions, age of PD onset, new onset of PD (in the past year), anxiety (Hamilton Rating Scale for Anxiety; Hamilton, 1959), caregiver burden (Caregiver Distress Scale; Cousins, Davies, Turnball, & Playfer, 2002), global cognition (Dementia Rating Scale Total Score; Mattis, 1988), and negative thoughts (Inference Questionnaire; Alloy & Abramson, 1999).

Results

Data was analyzed with SPSS Version 18. The a priori predictor model was separately examined at end-of-treatment (week 10) and short-term follow-up (week 14) on the following depression outcomes: 1) treatment response (yes/no) [primary outcome], 2) HAM-D ratings [secondary outcome], and 3) BDI scores [secondary outcome]1. The primary outcome of treatment response was examined in the CBT group only with stepwise logistic regression. Secondary and exploratory2 outcomes were tested with stepwise linear regression in the entire sample, controlling for treatment group and baseline score on each respective secondary outcome measure (HAM-D or BDI). We also tested the interaction (i.e., moderating effects) between treatment group and each a priori predictor (controlling for the main effects of each variable and baseline depression severity) on HAM-D and BDI scores. All available participant data, coupled with a multiple imputation approach to missing data, was used to compute all reported statistics.

Recruitment and follow-up occurred between April 2007 and July 2010. Ninety percent of participants completed the study (88% in CBT; 92% in clinical monitoring) and treatment fidelity was high (Dobkin et al., 2011). Detailed results regarding predictors of treatment response to CBT and depression change over time (HAM-D and BDI) across both treatment conditions can be found in Table 1, Table 2, Table 3,and Table 4. In brief, stepwise logistic regression revealed that caregiver involvement accounted for significant variance [21% at week 10 (p = .012) and 25% at week 14 (p = .008)] in CBT response status. Moreover, results of stepwise linear regression suggested that treatment group, baseline depression severity, executive functioning, motor disability, psychiatric comorbidity, marital status, and caregiver burden also influenced change in depression scores over time across both study conditions, while executive functions (in addition to caregiver participation) were related to the short-term maintenance of treatment gains in the CBT group (as demonstrated by stepwise logistic regression). Of note, relationship to patient (i.e., spouse, friend) was also a significant predictor of week 14 HAM-D score when used in place of marital status in the exploratory model. Having a spouse involved in treatment was more beneficial than another family member or friend. No significant moderators of treatment effects were revealed.

Table 1.

Predictors of Treatment Response to CBT

Variables M (SD) Wald χ2 df Exp(B) [95% CI] P Nagelkerke
R2 Change
Week 10 Baseline UPDRS Motor Subscale 22.39 (9.99) 0.76 1 0.97 [0.90, 1.04] .383 8%
Axis I Diagnoses (number) 1.88 (0.81) 0.49 1 0.72 [0.28, 1.81] .482 1%
Trail-making test B-A Time (seconds) 82.15 (71.20) 3.37 1 0.99 [0.97, 1.00] .067 4%
Caregiver Sessions Attended (number) 2.90 (1.42) 6.25 1 2.20 [1.18, 4.08] .012 21%
Week 14 Baseline UPDRS Motor Subscale 22.39 (9.99) 0.23 1 0.98 [0.91, 1.05] .633 6%
Axis I Diagnoses (number) 1.88 (0.81) 0.21 1 1.24 [0.50, 3.09] .648 1%
Trail-making test B-A Time (seconds) 82.15 (71.20) 4.74 1 0.98 [0.97, 1.00] .029 7%
Caregiver Sessions Attended (number) 2.90 (1.42) 7.02 1 2.41 [1.26, 4.60] .008 25%
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Note. CI= confidence interval; UPDRS= Unified Parkinson’s disease Rating Scale

Table 2.

Hamilton Depression Rating Scale (HAM-D) A Priori Models

Variables M (SD) B [95% CI] β P R2 Change
Week 10 Treatment Condition 6.20 [4.57, 7.83] .59 .000 37%
Baseline HAM-D Total 20.18 (4.27) 0.55 [0.35, 0.76] .44 .000 18%
Baseline UPDRS Motor Subscale Score 22.80 (9.51) 0.10 [0.02, 0.19] .16 .046 2%
Axis I Diagnoses (number) 1.80 (0.92) 0.90 [−0.04, 1.85] .15 .061 2%
Trail-making Test B-A Time (seconds) 91.61 (70.62) 0.01 [0.00, 0.02] .16 .054 2%
Week 14 Treatment Condition 5.66 [3.90, 7.43] .50 .000 26%
Baseline HAM-D Total 20.18 (4.27) 0.88 [0.65, 1.11] .66 .000 34%
Baseline UPDRS Motor Subscale Score 22.80 (9.51) 0.03 [−0.08, 0.13] .04 .623 0%
Axis I Diagnoses (number) 1.80 (0.92) 0.28 [−0.81, 1.37] .04 .614 0%
Trail-making Test B-A Time (seconds) 91.61 (70.62) 0.00 [−0.01, 0.02] .04 .662 0%
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Note. CI= confidence interval; UPDRS= Unified Parkinson’s disease Rating Scale; HAM-D= Hamilton Depression Rating Scale

Table 3.

Hamilton Depression Rating Scale (HAM-D) Exploratory Models

Variables M (SD) B [95% CI] β P R2 Change
Week 10 Treatment Condition 6.13 [4.56, 7.70] .58 .000 37%
Baseline HAM-D Total 20.18 (4.27) 0.51 [0.31, 0.71] .40 .000 18%
Baseline UPDRS Motor Subscale Score 22.80 (9.51) 0.08 [−0.01, 0.17] .14 .091 2%
Axis I Diagnoses (number) 1.80 (0.92) 1.06 [0.13, 1.98] .18 .025 2%
Trail-making Test B-A Time (seconds) 91.61 (70.61) 0.01 [0.00, 0.02] .16 .031 2%
Caregiver Burden 5.66 (3.75) 0.28 [0.07, 0.49] .20 .008 4%
Week 14 Treatment Condition 5.23 [3.48, 6.98] .46 .000 26%
Baseline HAM-D Total 20.18 (4.27) 0.85 [0.63, 1.08] .63 .000 34%
Baseline UPDRS Motor Subscale Score 22.80 (9.51) 0.03 [−0.06, 0.13] .07 .497 0%
Axis I Diagnoses (number) 1.80 (0.92) 0.32 [−0.74, 1.38] .05 .556 0%
Trail-making Test B-A Time (seconds) 91.61 (70.61) 0.00 [−0.01, 0.02] .04 .606 0%
Marital Status 0.84 [0.17, 1.51] .18 .014 3%
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Note. CI= confidence interval; UPDRS= Unified Parkinson’s disease Rating Scale; HAM-D= Hamilton Depression Rating Scale

Table 4.

Beck Depression Inventory (BDI) A Priori Models

Variables M (SD) B [95% CI] β P R2 Change
Week 10 Treatment Condition 6.76 [3.70, 9.82] .43 .000 20%
Baseline BDI Total 19.30 (7.97) 0.34 [0.15, 0.54] .36 .001 12%
Baseline UPDRS Motor Subscale Score 22.80 (9.51) 0.16 [−0.02, 0.33] .18 .078 4%
Axis I Diagnoses (number) 1.80 (0.92) 0.94 [−0.87, 2.75] .11 .309 1%
Trail-making Test B-A Time (seconds) 91.61 (70.61) 0.01 [−0.01, 0.03] .10 .345 0%
Week 14 Treatment Condition 3.72 [1.06, 6.39] .26 .006 10%
Baseline BDI Total 19.30 (7.97) 0.46 [0.29, 0.63] .51 .000 21%
Baseline UPDRS Motor Subscale Score 22.80 (9.51) 0.13 [−0.02, 0.29] .16 .085 5%
Axis I Diagnoses (number) 1.80 (0.92) 0.05[−1.59, 1.68] −.01 .957 0%
Trail-making Test B-A Time (seconds) 91.61 (70.61) 0.03 [0.01, 0.04] .26 .011 5%
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Note. CI= confidence interval; UPDRS= Unified Parkinson’s disease Rating Scale; BDI= Beck Depression Inventory

Discussion

This was the first study to examine predictors of treatment response to CBT for dPD. Results suggest that caregiver participation in treatment may positively influence acute depression response to CBT in PD. While several additional factors (as described above) also predicted depression change over time for all participants, the effect sizes for these measures were small, relative to treatment group and baseline depression severity.

The findings from this study provide preliminary support for supplementing individually-administered CBT with a standardized caregiver educational intervention in the treatment of dPD. Further research is needed to determine if the impact of caregiver involvement is specific to CBT or if these results will generalize to any active treatment for depression in PD. However, the skills-based nature of treatment, the focus on tangible thoughts and behaviors, and the importance of homework and practice (i.e.., behavioral experiments, cognitive restructuring) between sessions (and after therapy has ended) may make CBT especially well-suited for the inclusion of PD caregivers in treatment.

The study has several limitations. First, the sample size is modest by clinical trial standards and it is possible that additional variables of clinical relevance and moderators of treatment response would have been identified in a larger sample. Second, the specific mechanisms (i.e., practicing CBT skills, increased treatment adherence, non-specific factors) by which caregivers positively impacted patient outcomes cannot be elucidated from the current data. Third, because the follow-up period was limited to one-month, it is not possible to explore predictors of long-term outcomes or to identify patterns of relapse or recurrence in this medical population. Lastly, our results may not generalize to all individuals with dPD as the majority of participants were Caucasian and highly educated with no evidence of dementia.

In sum, despite the negative effects of depression in PD, there is a dearth of information available to guide clinical care. The results of the current study offer preliminary guidance regarding treatment strategies, such as caregiver participation, that may help to optimize the acute management of dPD. Further research is needed to extend and replicate these findings given the modest sample size and small effects observed across several outcome measures.

Acknowledgments

This study was funded by 1 K23 NS052155-01A2 awarded to Roseanne D. Dobkin by the National Institute of Neurological Disorders and Stroke (NIH/NINDS). This trial is registered at clinicaltrials.gov: Identifier NCT00464464.

Footnotes

1

As caregiver participation is confounded with treatment arm (i.e., caregivers in the clinical monitoring group did not have the option to attend sessions), this variable was removed from the a priori model for analyses of secondary outcomes.

2

Exploratory correlations between demographic and clinical factors that have been previously linked to dPD and each respective depression outcome measure (at weeks 10 and 14) were conducted. Variables that correlated with outcome at p ≤ .025 were tested in exploratory regression models. Those that contributed unique variance above and beyond the a priori model (p levels ≤ .05 adjusted via the Holm Method) were retained in the final exploratory models.

Publisher's Disclaimer: The following manuscript is the final accepted manuscript. It has not been subjected to the final copyediting, fact-checking, and proofreading required for formal publication. It is not the definitive, publisher-authenticated version. The American Psychological Association and its Council of Editors disclaim any responsibility or liabilities for errors or omissions of this manuscript version, any version derived from this manuscript by NIH, or other third parties. The published version is available at www.apa.org/pubs/journals/ccp

Contributor Information

Roseanne D. Dobkin, Department of Psychiatry, Robert Wood Johnson Medical School

Jade Tiu Rubino, Department of Psychiatry, Robert Wood Johnson Medical School.

Lesley A. Allen, Department of Psychiatry, Robert Wood Johnson Medical School

Jill Friedman, Department of Psychiatry, Robert Wood Johnson Medical School.

Michael A. Gara, Department of Psychiatry, Robert Wood Johnson Medical School

Margery H. Mark, Departments of Psychiatry and Neurology, Robert Wood Johnson Medical School

Matthew Menza, Departments of Psychiatry and Neurology, Robert Wood Johnson Medical School.

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