Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Depressive disorders occur in Parkinson's disease in about 40%. They often manifest--not seldom preceding diagnosis of Parkinson's syndrome--like monopolar depression. Their cause has not yet been explained in a satisfactory way. Neurotransmitter disturbances are discussed as well as psychogenic factors. There seems to be a subtype of Parkinson's disease with more frequent depression, which is characterized by increased rigidity and bradykinesia, lower age at onset and family history of Parkinson's disease. Especially antidepressants, but also sleep deprivation and electroconvulsive therapy are efficient. The review is illustrated by a case report.
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PMID:[Depression in Parkinson disease. A literature review]. 818 90

Patients suffering from Parkinson's disease (PD) often report about sleep disorders and excessive daytime sleepiness. To some extent, motor disabilities or neural degeneration of sleep modulating structures may be responsible for these effects. Depressive disorders also contribute to the occurrence of insomnia and daytime sleepiness. Nevertheless, dopaminergic, anticholinergic, and other drugs used in PD have a great impact on sleep/wakefulness mechanisms. They may indirectly improve or worsen sleep by changing motor symptoms such as akinesia, hyperkinesia, or tremor. Although their is only little information on the complex regulation of vigilance, it is well known that monoaminergic and cholinergic drugs could influence it directly. Data from animal experiments and clinical experiences led to the hypothesis of a biphasic influence on sleep by dopaminergic substances: small doses of L-Dopa e. g. appear to improve sleep whilst higher doses led to insomnia. Different dopaminergic receptor types or changes in receptor sensitivity may explain these phenomena. Dopaminergic and anticholinergic drugs suppress REM sleep. Recently, initial data on 'sleep attacks' after pramipexole or ropinirole treatment were published. Our preliminary results using 24 h polygraphic recordings showed excessive daytime sleepiness in patients taking ropinirole and L-Dopa which disappeared when changed to ropinirole monotherapy. Sleepiness did never appear as an irresistible attack. Current hypotheses on this topic are reviewed.
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PMID:Effects of parkinsonian medication on sleep. 1119 13

Depressive disorders (DDs) are frequent psychiatric comorbidities of neurological disorders like multiple sclerosis, stroke, dementia, migraine, Parkinson's disease, and epilepsy. The clinical manifestations of DDs in these neurological disorders are identical to those of idiopathic mood disorders. In epilepsy, however, DDs can frequently also present with clinical characteristics that differ from those of idiopathic depression and fail to meet the criteria included in the Diagnostic and Statistical Manual of Psychiatric Disorders-Fourth Edition. Despite their multifaceted clinical expressions and their relatively high prevalence in epilepsy, DDs very often go unrecognized and untreated. The aim of this article is to review some of the more relevant aspects of DDs in epilepsy, to highlight their various clinical expressions, and their impact on the quality of life of patients with epilepsy, and to review the basic principles of treatment.
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PMID:Depression in epilepsy: a frequently neglected multifaceted disorder. 1465 23

Depressive disorders as well as depressive symptoms are common in Parkinson's disease (PD) and an important factor affecting quality of life. Treatment of depressive symptoms not only improves mood but is also associated with improvement of motor symptoms, disability and cognitive symptoms. Currently, dopamine agonists are being suggested as an alternative to antidepressants for the treatment of depression in PD. The aim of this article is to systematically review the efficacy of dopamine agonists in the treatment of depression in PD. Since 1983, 19 studies have reported on the effects of dopamine agonists on depressive disorder, depressive symptoms or mood in PD. To date, no double-blind, placebo-controlled, randomized controlled trial of the treatment of major depressive disorder in PD with a dopamine agonist has been conducted. Studies of the effects of treatment with dopamine agonists on depressive symptoms in PD, or on mood in non-depressed PD patients, have yielded inconclusive results. Most studies are not designed to test effects on mood and are limited by methodological flaws. It can be concluded that, although the preliminary evidence of the effects on mood and depression in PD is interesting and in need of further study, there is as yet insufficient evidence to recommend dopamine agonists in the treatment of either depressive disorder or depressive symptoms in patients with PD. Treatment of depressive disorder and clinically relevant depressive symptoms should be based on pharmacological or non-pharmacological interventions with known efficacy in this population, such as citalopram, nortriptyline, desipramine or cognitive behavioural therapy. This strategy has the additional advantage of enabling the clinician to treat depressive symptoms independently of motor symptoms, thus avoiding potential complications of dopaminergic therapy.
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PMID:The role of dopamine agonists in the treatment of depression in patients with Parkinson's disease: a systematic review. 2131 66

Dynamic feedback based closed-loop medical devices offer a number of advantages for treatment of heterogeneous neurological conditions. Closed-loop devices integrate a level of neurobiological feedback, which allows for real-time adjustments to be made with the overarching aim of improving treatment efficacy and minimizing risks for adverse events. One target which has not been extensively explored as a potential feedback component in closed-loop therapies is mitochondrial function. Several neurodegenerative and psychiatric disorders including Parkinson's disease, Major Depressive disorder and Bipolar disorder have been linked to perturbations in the mitochondrial respiratory chain. This paper investigates the potential to monitor this mitochondrial function as a method of feedback for closed-loop neuromodulation treatments. A generic model of the closed-loop treatment is developed to describe the high-level functions of any system designed to control neural function based on mitochondrial response to stimulation, simplifying comparison and future meta-analysis. This model has four key functional components including: a sensor, signal manipulator, controller and effector. Each of these components are described and several potential technologies for each are investigated. While some of these candidate technologies are quite mature, there are still technological gaps remaining. The field of closed-loop medical devices is rapidly evolving, and whilst there is a lot of interest in this area, widespread adoption has not yet been achieved due to several remaining technological hurdles. However, the significant therapeutic benefits offered by this technology mean that this will be an active area for research for years to come.
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PMID:An investigation into closed-loop treatment of neurological disorders based on sensing mitochondrial dysfunction. 2943 44