Depressive Symptoms In Parkinson's Disease Research Articles

Aerobic exercise improves depressive symptoms in the unilateral 6-OHDA-lesioned rat model of Parkinson’s disease

Aerobic exercise has been shown to have established benefits on motor function in Parkinson's disease (PD). However, the impact of exercise on depressive symptoms in PD remains unclear. This study aimed to investigate the effects of regular exercise, specifically using a forced running wheel, on both motor performance and the prevalence of depression in a unilateral 6-OHDA-lesioned rat model of PD. The behavioral outcomes of exercise were assessed through the rotarod test (RT), forelimb adjusting step test (FAST), sucrose consumption test (SCT), and novelty sucrose splash test (NSST). Our data revealed evident depressive symptoms in the PD animals, characterized by reduced sucrose consumption in the SCT and diminished exploratory activity in the NSST compared to the naïve control group. Specifically, after 11 weeks of exercise, the PD exercise group demonstrated the most significant improvements in sucrose consumption in the SCT. Additionally, this group exhibited reduced immobility and increased exploratory behavior compared to the PD control group in the NSST. Furthermore, the PD exercise group displayed the greatest improvement in correcting forelimb stepping bias. Our results suggested that a regimen of running wheel exercise enhances motor abilities and mitigates the occurrence of depressive behaviors caused by 6-OHDA dopamine depletion in the PD rat model.

Disrupted topologic efficiency of brain functional connectome in de novo Parkinson's disease with depression.

Growing evidence supports that depression in Parkinson's disease (PD) depends on disruptions in specific neural networks rather than regional dysfunction. According to the resting-state functional magnetic resonance imaging data, the study attempted to decipher the alterations in the topological properties of brain networks in de novo depression in PD (DPD). The study also explored the neural network basis for depressive symptoms in PD. We recruited 20 DPD, 37 non-depressed PD and 41 healthy controls (HC). The Graph theory and network-based statistical methods helped analyse the topological properties of brain functional networks and anomalous subnetworks across these groups. The relationship between altered properties and depression severity was also investigated. DPD revealed significantly reduced nodal efficiency in the left superior temporal gyrus. Additionally, DPD decreased five hubs, primarily located in the temporal-occipital cortex, and increased seven hubs, mainly distributed in the limbic cortico-basal ganglia circuit. The betweenness centrality of the left Medio Ventral Occipital Cortex was positively associated with depressive scores in DPD. In contrast to HC, DPD had a multi-connected subnetwork with significantly lower connectivity, primarily distributed in the visual, somatomotor, dorsal attention and default networks. Regional topological disruptions in the temporal-occipital region are critical in the DPD neurological mechanism. It might suggest a potential network biomarker among newly diagnosed DPD patients.

Autophagy markers, cognitive deficits and depressive symptoms in Parkinson's disease.

Depressive symptoms are common in Parkinson's disease (PD). The relationships between autophagy and PD or depression have been documented. However, no studies explored the role of autophagy markers associated with depressive symptoms in PD. Our study aimed to investigate the relationships between autophagy markers, cognitive impairments and depressive symptoms in PD patients.A total of 163 PD patients aged 50-80years were recruited. Plasma concentrations of autophagy markers (LC3-I, LC3-II and p62/SQSTM1) and glycolipid parameters were measured. Depressive symptoms, cognitive impairments, and motor function were assessed using the Hamilton Depression Rating Scale-17 (HAMD-17), the Montreal Cognitive Assessment (MoCA), and the Movement Disorders Society Unified Parkinson's Rating Scale Part III (MDS-UPDRS-III), respectively.There were no significant differences between depressed and non-depressed PD patients for LC3-I, LC3-II, LC3-II/LC3-I and p62/SQSTM1. After controlling confounding variables, LC3-II/LC3-I showed an independent relationship with depressive symptoms in PD patients (Beta = 10.082, t = 2.483, p = 0.014). Moreover, in depressive PD patients, p62/SQSTM1 was associated with MoCA score (Beta = -0.002, t = -2.380, p = 0.020); Further, p62/SQSTM1 was related to naming ability; in addition, p62/SQSTM1 was independently associated with delayed recall (Beta = -0.001, t = -2.452, p = 0.017).LC3-II/LC3-I was related to depressive symptoms in PD patients. In depressive PD patients, p62/SQSTM1 was associated with cognitive function, especially naming ability and delayed recall.

Neurobiology of depression in Parkinson's disease: Insights into epidemiology, molecular mechanisms and treatment strategies.

Parkinson's disease (PD) is characterized mainly by motor dysfunctions due to theprogressive loss of dopaminergic neurons. However, PD patients experience a multitude of debilitating non-motor symptoms, including depression, which may have deleteriously detrimental effects on life. Depression is multifactorial and exhibits a bimodal progression in PD, but its underlying molecular mechanisms are poorly understood. Studies demonstrating the pathophysiology of depression in PD and the specific treatment strategies for depression-like symptoms in PD patients are largely lacking, often underrated, under-recognized and, consequently, inadequately/under-treated. Nevertheless, reports suggest that the incidence of depression is approximately 20-30% of PD patients and may precede the onset of motor symptoms. Diagnosing depression in PD becomes difficult due to the clinical overlap in symptomatology between the two diseases, and the nigrostriatal dysfunction alone is insufficient to explain depressive symptoms in PD. Therefore, the current study provides an overview of the molecular mechanisms underlying the development of depression in PD and new insights into developing current antidepressant strategies to treat depression in PD. This review will identify and understand the molecular pathological mechanisms of depression in PD that will fundamentally help tailoring therapeutic interventions for depressive symptoms in PD.

Cover Image, Volume 530, Issue 10

The cover image is based on the Research Article Diffusion tensor imaging correlates of depressive symptoms in Parkinson disease by Lauren Uhr, Evangelia Tsolaki, and Nader Pouratian., https://doi.org/10.1002/cne.25310.

Dynamic interplay of cognitive functioning and depressive symptoms in patients with Parkinson's disease.

We examine the trajectories of and the dynamic interplay between cognitive functioning and depressive symptoms in patients with Parkinson's disease (PD) in comparison to healthy controls (HC) from an intraindividual perspective. The DeNoPa study is a single-center, observational, longitudinal study with biennial follow-ups over 8 years. The present analyses are based on 123 PD (79 male) and 107 HC (64 male) with a mean age of 64.1 years (SD = 8.3). PD and HC completed a battery of neuropsychological tests and scales assessing depressive symptoms. We used a random-intercept cross-lagged panel model (RI-CLPM) to study their trajectories and the dynamic interplay. Cognitive abilities of PD were on average d = -0.67 worse at baseline and d = -1.22 at 8-years follow-up in comparison to HC. Depressive symptoms in PD showed large variability and followed a U-shaped trajectory. From an intraindividual perspective, greater impairments in cognitive abilities were subsequently associated with increased depressive symptoms (b = -0.60, p = .03), whereas the effect in the opposite direction was not significant. We found indication that a decline on a global composite scale of cognition can be seen as a precursor of depressive symptoms in patients with PD. To counter cognitive losses and the subsequent mood deterioration, patient education and early cognitive (and behavioral) enrichment seem promising candidates for treatment. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Diffusion tensor imaging correlates of depressive symptoms in Parkinson disease.

Depression is a heterogeneous clinical syndrome prevalent in patients with Parkinson disease (PD) that remains incompletely understood. Further, the differences in biomarkers of depression in PD and in non-PD patients are unclear. The subcallosal cingulate cortex (SCC) and its connections have been implicated in the pathophysiology of major depressive disorder (MDD). Diffusion tensor imaging (DTI) provides a tool to quantify MDD-related structural abnormalities underlying depressive symptoms in PD. Diffusion-weighted magnetic resonance imaging data were collected from 31 patients with PD. Depression symptom severity was measured using the Beck Depression Inventory (BDI-II), and assessed using three subscales: dysphoric mood, loss of interest/pleasure, and somatic symptoms. Probabilistic tractography methods were used to quantify the SCC connectivity to target regions in cortico-limbic-striatal network (ventral striatum, medial prefrontal cortex [mPFC], dorsal anterior cingulate cortex, and uncinate fasciculus), while fractional anisotropy (FA) was calculated in predefined white matter regions of interest. DTI data were correlated with severity of depression across three domains. SCC-mPFC connectivity in the left hemisphere was positively correlated with severity of dysphoric mood (Benjamini-Hochberg adjusted p=.02). Region of interest-based analyses demonstrated a significant and distinct topographic association between FA and dysphoric mood, loss of interest/pleasure, and somatic symptom severity, although these findings did not maintain significance after applying the false discovery rate correction. Abnormal SCC connectivity underlies depressive symptoms in both PD and MDD, suggesting that interventions used for MDD should be explored in treating depressive symptoms in PD, particularly depression dominated by dysphoric mood.

Factor structure of the BDI-II in Parkinson's disease.

There is substantial heterogeneity in depressive symptomology for individuals with Parkinson's disease (PD). It is unknown whether the Beck Depression Inventory-Second Edition (BDI-II) is capable of identifying such phenotypic variations of depression. We investigated the factor structure of the BDI-II and its associations with demographic characteristics and other nonmotor symptoms in PD. We reviewed the cases of 236 patients with a confirmed PD diagnosis. Evaluations included the BDI-II, Montreal Cognitive Assessment (MoCA), Apathy Scale (AS), and Geriatric Anxiety Inventory (GAI). We used exploratory structural equation modeling (ESEM) with target rotations as this method integrates aspects of exploratory and confirmatory factor analysis. We conducted hierarchical regressions to assess for associations between the BDI-II factors and gender, age, education, disease duration, cognition, anxiety, and apathy. ESEM supported the retention of a Somatic factor and an Affective factor that accounted for 53% of the model variance. Model goodness-of-fit measures were within normal limits. Higher AS scores were positively associated with the Somatic and Affective factors. Higher GAI scores were positively associated only with the Affective factor. There were no other significant relationships with factor scores. This study supports the retention of a two-factor model of the BDI-II in PD. These unique clusters of depressive symptoms in PD can be used to guide clinical decisions about the need for further psychiatric evaluation and the appropriateness of different therapeutic interventions. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Efficacy and safety of 5-hydroxytryptophan on depression and apathy in Parkinson's disease: a preliminary finding.

Several studies have indicated that altered serotonergic neurotransmission may contribute to non-motor features commonly associated with Parkinson's disease (PD) such as apathy and depression. 5-hydroxytryptophan (5-HTP) is the intermediate metabolite of L-tryptophan in the production of serotonin. To date, there has been inconsistent research on the use of 5-HTP in PD. The purpose of this study was to compare the effects of 5-HTP with those of placebo on apathy and depressive symptoms in patients with PD. A single-center, randomized, double-blind placebo-controlled cross-over trial was employed; 25 individuals were subsequently enrolled into the study. Patients received placebo and 50mg of 5-HTP daily over a period of 4weeks. For the assessment of efficacy on depressive and apathy symptoms the Beck Depression Inventory-II (BDI-II), Hamilton Depression Rating Scale (HDRS) and Apathy Scale (AS) were respectively administered at screening, baseline and weeks 4, 8, 12 and 16. Primary efficacy outcomes were the comparison of 5-HTP to placebo in mean change from baseline to weeks 4, 8, 12 and 16 in total score on the AS, BDI-II and HDRS. Repeated-measures analysis revealed a significant improvement of depressive symptoms during the 50-mg 5-HTP treatment compared with placebo as assessed by the HDRS. No effect of 5-HTP was seen on apathy symptoms assessed by the AS. This study provides preliminary evidence of clinical benefit of 5-HTP for treating depressive symptoms in PD. Larger studies with a longer treatment duration are needed to corroborate these early findings.

Cognitive behavioral therapy improves diverse profiles of depressive symptoms in Parkinson's disease.

Depression is among the most common and debilitating nonmotor complaints in Parkinson's disease (PD), yet there is a paucity of controlled research to guide treatment. Little research has focused on the extent to which specific depressive symptom profiles may dictate unique clinical recommendations to ultimately improve treatment outcomes. The current study examined the impact of cognitive behavioral therapy (CBT) on different types of depressive symptoms in PD. It was hypothesized that the cognitive (eg, guilt, rumination, and negative attitudes towards self) and behavioral (eg, avoidance and procrastination) symptoms targeted most intensively by the treatment protocol would show the most robust response. The extent to which stabilized antidepressant use moderated specific symptom change was examined on an exploratory basis. Eighty depressed people with PD participated in a randomized controlled trial of CBT plus clinical management, versus clinical management only. Hamilton Depression Rating Scale (HAMD) and Beck Depression Inventory (BDI) subscale scores, reflecting depressive symptom heterogeneity in PD, were the focus of this investigation. CBT response was associated with significant improvements in mood, sleep, anxiety, and somatic symptoms (HAMD), and negative attitudes toward self, performance impairment, and somatic symptoms (BDI). As hypothesized, the largest effect sizes were observed for cognitive and behavioral (vs somatic) symptoms of depression. Stabilized antidepressant use moderated the effect of CBT on somatic complaints (HAMD and BDI). CBT may improve a diverse array of depressive symptoms in PD. Cognitive and behavioral (vs somatic) symptoms showed the greatest change. Combining CBT with antidepressants may help optimize the management of somatic complaints in depression in PD (dPD).

Echogenic alteration in the raphe nuclei measured by transcranial sonography in patients with Parkinson disease and depression.

Background:Recently, several studies using transcranial sonography (TCS) have demonstrated reduced echogenicity of the mesencephalic midline in unipolar depression and patients with comorbid depression and Parkinson disease (PD). However, there is no consensus on the conclusion that raphe nuclei (RN) hypoechogenicity is associated with depression in PD. The methods used in previous studies lack quantitative and objective indicators to some extent; therefore, the present study used the level of platelet 5-hydroxytryptamine (5-HT) as an objective indicator of depression. Additionally, the reason for the reduced echogenicity of the brainstem raphe is still unclear.Objectives:The purpose of the present study was to assess the correlation between alterations in RN echogenicity and depressive symptoms in patients with PD using transcranial sonography (TCS). This information could provide a meaningful clinical reference for the antidiastole between depressive symptoms in PD and unipolar depression in patients with PD in whom depressive symptoms occur before motor symptoms.Methods:TCS was performed in patients with PD, patients with PD and depression, patients with depression and no PD, and healthy controls. Using the red nucleus as a reference, the RN was rated from grades 0 to 1 (grade 0: invisible, slightly echogenic, or interrupted RN; grade 1: hyperechogenicity in the RN observed as a continuous line).Results:The rate of abnormal RN (grade 0) was found to be 16.67% in patients with PD (5/30) and 14.29% in healthy controls (4/28). The presence of abnormal RN was significantly higher (χ2 = 15.983, P < .05) in patients with depression and PD (40%, 12/30) and in patients with depression only (58.33%, 14/24) than in those without depression and healthy controls. No correlation was found between RN changes and depression severity (P > .05). There were no statistical differences in the concentration of platelet serotonin among the 4 groups (P > .05).Conclusions:TCS of the mesencephalic midline may be useful for detecting depression, which is an early symptom of PD. However, further neuropathological studies are needed to understand the principles underlying the use of platelet serotonin as a peripheral biomarker, as well as the connection between PD and depression.

Effects of personalized transcranial alternating current stimulation associated with physical therapy on motor and cognitive functions in people with Parkinson's disease

Hypersynchronization of oscillatory brain activity, prevalent in the beta band, is a neurophysiological signature of Parkinson's disease (PD). Transcranial alternating current stimulation (tACS) can entrain cortical activity at the stimulation frequency. The aim of this study was to provide a personalized neurostimulation treatment associated with physical therapy to improve motor and cognitive functions in PD. Seventeen persons with PD were recruited. Fourteen concluded the protocol (2 changes of diagnosis, 1 refusal to continue). A resting state EEG was acquired and analyzed with Fast Fourier Transform to obtain power spectral density maps. Comparison of a control group versus each patient was performed using a z-test. Statistical maps provided site and frequency of stimulation (stimulation frequency was set at 30 Hz in theta prevailing group and at 4 Hz in beta prevailing group). Stimulation site was identified as the scalp area in which the prevailing band was more represented. The experiment consisted of two-weeks sessions of randomized real tACS or transcranial random noise stimulation (sham) followed by a 1-hour physiotherapy session. EEG and clinical assessments with Unified Parkinson Disease Rating Scale (UPDRS-III) and a neuropsychological battery were performed before stimulation (T 0 ), after stimulation (T 1 ) and 4 weeks follow-up (T 2 ). Ten subjects showed a prevailing beta band and 4 a prevailing theta. A reduction of beta rhythm emerged at T 1 over the bilateral sensorimotor and right frontal area and at T 2 over the left frontal area in the real group. No significant modulation of EEG activity emerged in theta prevailing group. UPDRS-III scores improved at T 1 and T 2 in the real group. A score reduction emerged at T 1 in both groups for Beck Depression Inventory and at T 2 in the real group for Geriatric Depression Scale. Personalized tACS appears a valid add-on treatment for motor dysfunction and depressive symptoms in PD.

The Gender-Biased Effects of Intranasal MPTP Administration on Anhedonic- and Depressive-Like Behaviors in C57BL/6 Mice: the Role of Neurotrophic Factors.

Depression is a highly prevalent and debilitating non-motor symptom observed during the early stages of Parkinson's disease (PD). Although PD prevalence is higher in men, the depressive symptoms in PD are more common in women. Therefore, the aim of this study was to investigate the development of anhedonic- and depressive-like behaviors in male and female mice and thepotential mechanisms related to depressive symptoms in an experimental model of PD. Young adult male and female C57BL/6 mice (3months old) received a single intranasal (i.n.) administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and were submitted to a battery of behavioral tasks (sucrose consumption, splash test, tail suspension, forced swimming and open field tests) to assess their emotional and motor profiles. Considering the role of sexual hormones in emotional behaviors, the same protocol of i.n. MPTP administration and the splash, tail suspension, and open field tests were conducted in ovariectomized (OVX) and aged C57BL/6 female (20months old) mice. We also investigated the immunocontent of neurotrophins (BDNF, GDNF, and VEGF) in the hippocampus and prefrontal cortex by western blot. I.n. MPTP administration induced more pronounced anhedonic- and selective depressive-like behaviors in female adult mice, also observed in OVX and aged female mice, with the absence of motor impairments. Furthermore, MPTP induced a more pronounced depletion of neurotrophins in the prefrontal cortex and hippocampus in female than male mice. This study provides new evidence of increased susceptibility of female mice to anhedonic- and depressive-like behaviors following i.n. MPTP administration. The observed gender-related effects of MPTP on emotional parameters seem to be linked to increased depletion of neurotrophins (particularly BDNF and GDNF) in the hippocampus and prefrontal cortex of female mice.

Efficacy and tolerability of antidepressants in Parkinson's disease: A systematic review and network meta-analysis.

To systematically review and analyze the efficacy and tolerability of different antidepressant pharmacologic treatments for depressive symptoms in Parkinson's disease (PD) METHODS: We searched PubMed, EMBASE, Cochrane database (CENTRAL), clinicaltrials.gov, and bibliographies for randomized controlled trials investigating the efficacy of antidepressant medications versus a non-treatment, placebo, or active treatment groups for depressive symptoms in PD. Twenty of 3191 retrieved studies (1893 patients) were included, but not all could be meta-analyzed. We used a random-effects model meta-analysis to compare depression scores between an active drug and placebo or control group then used a network meta-analysis to compare the effectiveness of different antidepressant classes. The primary outcome was the efficacy of different classes of antidepressant medications in PD patients with depressive symptoms, measured by standardized mean difference (SMD) in depression score from baseline compared with control. Pairwise meta-analysis suggested that type B-selective monoamine oxidase inhibitors (SMD=-1.28, CI=-1.68, -0.88), selective serotonin reuptake inhibitors (SMD=-0.49, CI=-0.93, -0.05), and tricyclics (SMD=-0.83, CI=-1.53, -0.13) are effective antidepressants in PD. Network meta-analysis showed that monoamine oxidase inhibitors had the largest effect on depression in PD (SMD (vs selective serotonin reuptake inhibitors)=-0.78, CI=-1.55, -0.01), but these might not be considered traditional antidepressants given their type B selectivity. Although limited by few data, this review suggests that multiple antidepressant classes are potentially efficacious in the treatment of depression in PD, but that further comparative efficacy and tolerability research is needed.

The natural history of depressive symptoms in patients with incident Parkinson's disease: a prospective cohort study.

Depression is common in patients with Parkinson disease and causes suffering and increased caregiver burden. A better understanding of depressive symptoms in Parkinson disease, their progression, and risk factors may, therefore, benefit management of these patients. The present study included 187 drug-naïve patients with incident PD and 166 controls from the population-based Norwegian ParkWest project. Depressive symptoms were examined with the Montgomery and Aasberg Depression Rating Scale (MADRS) at time of diagnosis and inclusion in the study and after 1, 3, 5, and 7 years of follow-up. Associations between MADRS scores and risk factors were assessed using generalized estimating equations (GEE). The mean MADRS score from all 823 examinations during the study period was 4.2 in patients and 1.3 in 732 examinations among controls. Among controls, the occurrence of depressive symptoms was also lower and rather stable during follow-up, while in patients, we observed a decrease from time of diagnosis and until the 1-year visit, followed by a steady increase in these symptoms over time. Factors associated with higher MADRS score in the multivariable model were female sex, being dependent, higher pain score, higher Unified PD Rating Scale (UPDRS) motor score, and lower Mini-Mental State Examination (MMSE) score. The results from this study underscore the importance and frequency of depressive symptoms in patients with early PD. Furthermore, risk factors that may be considered PD-nonspecific are associated with depressive symptoms as are factors that reflect the progression of PD.

Discordance Between Physician Assessment and Patient-Reported Depressive Symptoms in Parkinson Disease.

To assess concordance between physician assessment and patient-reported symptoms when screening for depression in Parkinson disease (dPD). Depression in Parkinson disease is highly prevalent (∼40%) and has a significant impact on quality of life and disability, yet physician recognition and treatment remain inadequate. One thousand seventy-six patients with PD completed the Brief Symptom Inventory-18 (BSI-18), a screening questionnaire for psychiatric symptoms, which was compared to item #3 (depression) on the Unified Parkinson's Disease Rating Scale (UPDRS). The mean BSI-18 depression score was 51.4 (9.7). Of the 170 (16%) patients screening positive for dPD on the BSI-18, 104 (61%) were not recognized as depressed by neurologists on the UPDRS. Factors associated with lower neurologist recognition included male gender, better mental health quality of life, and lack of antidepressant use. More than 60% of patients screening positive for depression on self-report were not recognized by neurologists on the UPDRS. A patient-reported screening tool for depression may improve recognition and management of dPD.

Depressive symptoms in Parkinson's disease are related to decreased hippocampus and amygdala volume.

Depression and anxiety are common in Parkinson's disease (PD), and are among the non-motor symptoms that interfere with quality of life dramatically. Motor, cognitive, and affective features overlap in PD, hampering diagnosis. To shed more light on the contribution of structural brain changes to the presence of PD-related depressive symptoms, we conducted a Voxel-Based Morphometry (VBM) study. We hypothesized that depressive symptoms in PD are related to regional gray matter (GM) volume loss within the limbic circuit. We analyzed the T1-weigthed magnetic resonance imaging (MRI) images of 67 PD patients with a mean disease duration of 2.95 (±3.39) years. Scores on the Beck Depression Inventory (BDI) and GM probability maps were analyzed by regression analysis to study the association between GM volume and severity of depressive symptoms. Results are reported at both the uncorrected and the family-wise error (FWE) corrected level for multiple comparisons. The BDI scores correlated negatively with bilateral hippocampus and right amygdala volume and positively with the volume of the anterior cingulate cortex. These findings confirm the hypothesized involvement of the limbic circuit in PD-related depressive symptoms. We speculate that non-dopaminergic changes are essential in the pathophysiology of depressive symptoms in PD, because our findings suggest the involvement of extra-striatal brain regions.

Depressive symptoms in Parkinson's disease are related to reduced [123I]FP-CIT binding in the caudate nucleus

BackgroundDepression is a common neuropsychiatric symptom in Parkinson's disease (PD). In previous research, PD-related depression was associated with striatal dopaminergic deficits, presumably due to degeneration of brainstem dopaminergic projections. Segregated...

Depressive Symptoms in Parkinson Disease as Measured by Beck's Depression Scale and Its Relationship to Visual Analogue Mood Scale, Motor Symptoms and the Quality of Life Measures (P06.057)

Objective: To ascertain the relationship between depression score and visual analogue mood scale, quality of life and motor severity in Parkinson9s disease. Background Depression is the most common non-motor manifestation of Parkinson disease (PD), affecting up to 40 to 50 % of PD patients, far in excess of its prevalence of 6.7% in the general American population. Design/Methods: All patients seen at the University of Florida Movement Disorders Center, with a confirmed PD diagnosis and a recorded Beck Depression Inventory (BDI) on their first visit were included in this study. Using a cutoff of 14, we determined the prevalence of depressive symptoms in our whole population, in men versus women and in drug naive versus those treated with levodopa. Results: The depressed cohort had a mean BDI score of 19.41 whereas the mean for the non-depressed was 7.06. The HY with the last two having negative coefficients. The best predictor, not surprisingly was the SadTscore. Overall there is not a strong correlation between VAMS and BDI. Conclusions: There is a correlation between the severity of motor symptoms and the presence of depression pointing to the possibility of both organic and reactive components in PD depression. There was only poor correlation between the VAMS score and BDI, but the quality of life PDQ-39 paralleled the BDI score raising questions whether this is cause or effect. Disclosure: Dr. Salardini has nothing to disclose. Dr. Rodriguez has received personal compensation for activities with Allergan, Merz Pharmaceuticals, Lundbeck and Teva Pharmaceuticals as a consultant. Dr. Malaty has received research support from The National Parkinson Foundation. Dr. Okun has received personal compensation for activities with National Parkinson Foundation, Ask the Expert, and Neuropace Devices. Dr. Okun has received research support from the Michael J. Fox Foundation, the National Parkinson Foundation, the Parkinson Alliance and the National Institutes of Health. Dr. Fernandez has received personal compensation for activities with USF CME, Cleveland Clinic CME, Medical Communications Media, Health Professions Conferencing, Ipsen, Merz Pharmaceuticals, and US World Meds Dr. Fernandez has received personal compensation in an editorial capacity for the Movement Disorders Society Website. Dr. Fernandez has received royalty payments from Demos Publishing, Manson Publishing, and Springer Publishing. Dr. Fernandez has received research support from Abbott, Acadia, Biotie Therapeutics, EMD-Serono, Huntington Study Group, Ipsen, Merz Pharmaceuticals, Michael J. Fox Foundation, Movement Disorders Society, National Parkinson Foundation, NIH/NINDS, Novartis, Parkinson Study Group, Teva, but has no owner interest in any pharmaceutical company.

Are verbal fluency and nonliteral language comprehension deficits related to depressive symptoms in Parkinson's disease?

Depression in Parkinson's disease (PD) is frequently associated with executive deficits, which can influence nonliteral comprehension and lexical access. This study explores whether depressive symptoms in PD modulate verbal fluency and nonliteral language comprehension. Twelve individuals with PD without depressive symptoms, 13 with PD and depressive symptoms (PDDSs), and 13 healthy controls completed a semantic and phonemic verbal fluency task and an indirect speech acts comprehension task. All groups had the same performance in the phonemic fluency task while the PDDS group was impaired in the semantic task. For the indirect speech act comprehension task, no difference was observed between the groups. However, the PDDS group had difficulty answering direct speech act questions. As some language impairments in PD become apparent when depressive symptoms are associated with the disease, it would appear to be important to take the presence of depressive symptoms into account when evaluating language abilities in PD.