Vigilance Performance in Parkinson's Disease and Depression

Patients with Parkinson's disease (PD), patients with Major Depression (MD) and normal control (NC) subjects were administered a continuous performance test (CPT) under neutral and incentive conditions. Patients made more errors than NC subjects with the MD group making a disproportionately large number of omission errors and the PD group tending to make commission errors. Incentive reduced errors across groups. Reaction times were slowest in the MD group. The pattern of findings in patients with MD is consistent with a failure of effort-demanding cognitive processes. In contrast, nondemented patients with PD appeared to have deficiencies in executive control. A previously reported paradoxical effect of incentive on recognition memory performance in depressed patients did not generalize to a vigilance task.     

Psychosis in Parkinson's disease

Psychosis in Parkinson's disease (PD) is a fairly common and vexing problem. Although it can occur at any stage of the illness, it is a particularly important issue for patients who are in the later stages of PD and have been chronically treated with anti-PD medications. The exact pathophysiology of PD-related psychosis remains a mystery. Neurochemical imbalances, sleep disturbances, and visual processing abnormalities in PD have been implicated in its pathogenesis. Treatment of psychotic symptoms should occur only after potential medical and environmental causes of delirium have been eliminated or addressed. Initial pharmacologic changes should include limiting the patient's anti-PD medications to those that are necessary to preserve motor function. Should that fail, an atypical antipsychotic agent is presently the treatment of choice. An emerging treatment option is the use of acetylcholinesterase inhibitors. This article reviews what is known about the epidemiology, risk factors, pathophysiology, and treatment of PD-related psychosis.     

Optimal Treatment of Depression and Anxiety in Parkinson's Disease

Depression and anxiety are highly prevalent and have major adverse effects on function and quality of life in Parkinson's disease (PD). Optimal management requires that motor symptoms and psychiatric symptoms be simultaneously addressed. While there is fairly robust evidence for the treatment of motor symptoms, there are no completed randomized controlled trials to guide pharmacological treatment of anxiety in PD and no nonpharmacologic interventions have proven efficacious. Several high-quality trials for depression in PD suggest a number of antidepressants and cognitive behavioral therapy may help, but there is no data on rates of recurrence, comparative efficacy, or augmentation strategies. In order to address the gaps in knowledge, the authors provide a summary of the current evidence for treating depression and anxiety in PD and offer an algorithm that extends beyond the current literature based on clinical experience working in a multidisciplinary specialty center.     

Depression Antedating the Onset of Parkinson's Disease

Abstract: Neurological and depressive symptoms in a subtype of Parkinson's disease (PD), in which a depressive state precedes the clinical manifestation of neurological symptoms, were examined on the basis of clinical observations for 3 years or more. PD, in which depression preceded, was different from PD with preceding neurological symptoms, in the severity of not only neurological but also depressive symptoms. These results suggest that PD in which depression precedes neurological symptoms is a specific subtype of PD. It was speculated that the differences in clinical symptoms might be due to a biological background, in particular the dopaminergic system.     

Dysarthria During ECT Given for Parkinson's Disease and Depression

A patient with recurrent major depression, parkinsonism, and pseudobulbar symptoms underwent a course of electroconvulsive therapy. Although his depression and parkinsonian symptoms markedly improved, his dysarthria worsened, resulting in cessation of further treatments. Possible mechanisms are explored.     

Depression and Parkinson's Disease: study of a series of 135 Parkinson's patients

OBJECTIVE: The prevalence of depression in Parkinson's disease (PD) raises the issues of the difficulties of diagnosing the condition and of the relationships between depression and the natural history of the disease. METHODS: A cohort of 135 consecutive patients with idiopathic PD underwent psychiatric (DSM-III-R, Goldberg depression scale), neurological (distinguishing "axial" signs from other signs of parkinsonism), and neuropsychological (particularly frontal tests) evaluations. RESULTS: Depression is present in more than half of the patients and it seems to be more frequent in patients with the akinetic and fluctuating forms of the disease. The subjects who are depressed do not have a greater degree of cognitive impairment, but their scores on frontal tests are higher. Moreover, the axial signs of the disease (postural instability, axial rigidity) are more severe in depressed parkinsonians suggesting a link between depression and the non-dopaminergic lesions of the disease. Even though slowness, appetite and sleep disturbances, and fatigue may be encountered in non-depressed parkinsonian patients, separation of the parkinsonian population into subgroups shows that certain symptoms are never seen in parkinsonians who are not depressed: it is thus evident that "the impression that life is not worth living", "the hopelessness", "the impression of being worthless and incompetent", "the low level of energy", "the morning sadness" are characteristic of parkinsonian depression. Parkinsonian depression has two major clinical forms. The first one is associated with a greater number of somatic manifestations: sleep disturbances, morning fatigue. corresponding to more severe depression with hopelessness and loss of self confidence. The second exhibits few somatic manifestations with apathy and slowness as frequent complaints. CONCLUSIONS: This study defines the symptoms of parkinsonian depression which should be better recognised in order to be treated. The link between depression and axial signs of the disease may explain why L-dopa and dopaminergic agonists improve the motor signs of depression without influencing depressive manifestations in most cases.     

Risk of Mortality Associated With Atypical Antipsychotic use: A National Cohort Study of Older Adults With Depression and Parkinson's Disease

ObjectivesThis study examined the risk of all-cause-mortality in patients with Parkinson's Disease (PD) and comorbid depression using inappropriate atypical antipsychotics (AAPs), based on the 2015 American Geriatrics Society Beers criteria.MethodsA retrospective analysis of 2007–2010 Minimum Data Set linked Medicare data was conducted using a propensity-matched approach. The cohort included PD patients aged 65 years or older without schizophrenia or bipolar disorder who started AAPs. All patients had a diagnosis of comorbid depression. Risk of 6-month all-cause-mortality was compared across appropriate AAPs (aripiprazole, clozapine, or quetiapine) and inappropriate AAPs (olanzapine, asenapine, brexpiprazole, iloperidone, lurasidone, paliperidone, risperidone, or ziprasidone) using robust Cox regression models involving the matched cohort.ResultsAll-cause mortality rate was 15.65% in appropriate AAP group (n = 6,038) and 16.91% in inappropriate AAP group (n = 6,038) over 6-month follow-up in the matched cohort. The robust Cox proportional hazards models revealed increased risk of all-cause mortality (hazard ratio [HR] 1.13 [95% confidence interval {CI}: 1.01–1.28)] for patients who used inappropriate compared to appropriate AAPs. Risk of death was also higher for risperidone compared to quetiapine (HR: 1.20 [95% CI: 1.03–1.40]) in sensitivity analysis. However, there was a significant relationship between pneumonia and death in all analyses. The impact of inappropriate AAP use on mortality was not significant when pneumonia was modeled as a mediator.ConclusionsInappropriate AAP use is associated with a higher risk of all-cause-mortality in older patients with PD which is mainly mediated by pneumonia. Therefore, inappropriate AAP use should be avoided to improve quality of care in PD.     

Semantic and Cross-Case Identity Priming in Patients With Parkinson's Disease

Semantic and cross-case identity priming were investigated in nondemented patients with Parkinson's disease (PD) and controls using the Lexical Decision Task. Three conditions were administered that consisted of the presentation of prime and target word pairs. In the semantic priming condition the word pairs were semantically related (e.g., table-CHAIR), in the cross-case identity priming condition the word pairs consisted of the same word (e.g., noise-NOISE), and in the unrelated condition the word pairs were not related semantically (e.g., guns-DEEP). A fourth condition was also administered that consisted of the presentation of a prime word and a pronounceable nonword target (e.g., starved-FORVE). Participants were asked to indicate whether the target was a real word or a nonword. The prime and target were separated by either a short or long (250 ms or 1000 ms) stimulus onset asynchrony (SOA). Results indicated that PD patients displayed normal semantic priming (i.e., faster responding to the target in the semantic condition as compared to the unrelated condition) at both the short and long SOA. Similarly, PD patients displayed normal cross-case identity priming (i.e., faster responding to the target in the identity condition relative to the unrelated condition) at the long SOA. At the short SOA, however, PD patients displayed hyper identity priming relative to controls (134 ms vs. 50 ms). These results suggest that semantic processes are normal in nondemented PD patients but that the processes involved in accessing lexical information may be overly activated in these patients.     

Psychosis in Parkinson's disease: case studies

Psychosis is common in patients who have PD and leads to significant disability. Patients often can be managed with non-pharmacologic interventions or with decreasing doses of anti-parkinsonism medications. If these interventions are insufficient, then atypical antipsychotics should be considered. Clozapine is used in more refractory cases and requires stringent monitoring for agranulocytosis.     

Changes in Glucose Metabolism in Cerebral Cortex and Cerebellum Correlate With Tremor and Rigidity Control by Subthalamic Nucleus Stimulation in Parkinson's Disease: A Positron Emission Tomography Study

Objective. Employing [¹⁸F]fluorodeoxyglucose (FDG) positron emission tomography (PET) to assess the correlation between the effect of deep brain stimulation (DBS) on the subthalamic nucleus (STN) and the regional cerebral metabolic rate of glucose (rCMRGlc) in advanced Parkinson's disease patients (N = 8). Materials and Methods. On the basis of patients’ diary records, we performed FDG‐PET during the off‐period of motor activity with on‐ or off‐stimulation by STN‐DBS on separate days and analyzed the correlation between changes in motor symptoms and alterations in the rCMRGlc. Result. When FDG‐PET was performed, the motor score on the unified Parkinson's disease rating scale (UPDRS) was 64% lower with on‐stimulation than with off‐stimulation (p < 0.001, Wilcoxon single‐rank test). STN‐DBS increased the rCMRGlc in the posterior part of the right middle frontal gyrus, which corresponded to the premotor area, and the right anterior lobe of the cerebellum (p < 0.005, paired t‐test). No region exhibited a decrease in rCMRGlc. Among the items of the UPDRS motor score, the changes in resting tremor and rigidity of the left extremities showed a significant correlation with the changes in rCMRGlc observed in the right premotor area (p < 0.02 and p < 0.05, respectively, Spearman's rank correlation). Conclusions. STN‐DBS either activates the premotor area or normalizes the deactivation of the premotor area. These FDG‐PET findings obtained are consistent with the idea that STN‐DBS modifies the activities of neural circuits involved in motor control.     

Depression in Parkinson's disease

Journal of Neurology - Depression is one of the most common non-motor symptoms in Parkinson's disease (PD) affecting 30–40% of patients and it has a major impact on quality of life....