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

Fatigue or piercing feeling of weakness, lack of strength and energy or total exhaustion is a common complaint of patients with neurological disorders. From 40 to over 90 per cent of individuals with multiple sclerosis, Parkinson disease, amyotrophic lateral sclerosis, neuroboreliosis, post polio syndrome or stroke confirm its experience. It is not infrequently numbered among most disabling complaints. A separate entity, with fatigue as a cardinal sign, is a chronic fatigue syndrome, a disorder, though controversial, more and more frequently diagnosed. Fatigue ought to be discriminated from fatigability, paresis, somnolence and, first of all depression which commonly coexists in chronic disorders. The assessment is almost entirely based on self-estimate scales filled in by a patient. Attainable results of neuroimaging, electrophysiological, polisomnographic, vegetative, psychological and biochemical surveys have not allowed yet to define the pathogenesis of fatigue. The treatment basis consists of behavioral therapy, psychotherapy and a proper treatment of the basic disease.
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PMID:[The problem of fatigue in neurological disorders]. 1733 30

Parkinson's disease (PD) is a motor disease including disorders of mobility, fine tremor, rigidity and posture caused by a relentless deterioration of dopaminergic cells in the substantia nigra (SN). Disorders of affect and a range of other symptoms including fatigue, cognitive dysfunction and mental confusion, sleep disorder and addictions are also seen as other CNS sites are also affected. Idiopathic and genetic causes together with inflammatory and degenerative disorders of ageing have been postulated as contributing to PD. Autoimmunity affecting certain vasoactive neuropeptides (VNs) has been postulated as contributing to certain fatigue-related conditions in humans and may be consistent with compromise of receptors associated with VNs and including receptors for vasoactive intestinal polypeptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP). Pro-inflammatory responses are seen in PD patients consistent with apoptotic neurodegeneration. Involvement of the Th1 directed cytokine interferon-gamma has been demonstrated and Th2 directed cytokines such as IL-10 protect against inflammation-mediated degeneration of dopaminergic neurons in the SN. Nitric-oxide dysregulation is also postulated in PD by fostering dopamine depletion via nitric-oxide synthase (iNOS). Both PACAP and VIP have neuroprotective effects in PD models by inhibiting the production of inflammatory mediators. PACAP specifically protects against the neurotoxicity induced by rotenone as well as protecting against oxidative stress-induced apoptosis. These findings suggest that a defect in VN function may act adversely on SN cells and hence contribute to a clinical presentation consistent with PD. The conclusion drawn from these findings is that PD may be an autoimmune disorder of VNs, specifically PACAP and VIP. Possibly unusual or anatomically specific receptors for these VNs may be involved. If proven, this hypothesis would have significant implications for immunological and pharmacological treatment and prevention of PD.
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PMID:Is Parkinson's disease an autoimmune disorder of endogenous vasoactive neuropeptides? 1756 59

Parkinson's disease is a progressive and debilitating movement disorder that is diagnosed by its motor signs. The behavioral manifestations of Parkinson's disease are prevalent and frequently complicate the course of the disease. These may be due to the illness itself or its treatment and are often more disabling than the motor symptoms. This review focuses on the management of the most common behavioral symptoms of Parkinson's disease, including depression, anxiety, psychosis, dementia, delirium, sleep disorders, fatigue, apathy, emotionalism and compulsive behaviors.
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PMID:Management of the behavioral aspects of Parkinson's disease. 1756 53

There is lack of clarity in the literature over whether patients with Parkinson's disease (PD) show the same post-exercise depression of corticospinal excitability as is usually observed in healthy control. This study set out to resolve the problem. Ten patients with idiopathic PD and 10 age-matched controls were included in this study. Each subject performed a submaximal sustained voluntary contraction of the right first dorsal interosseous muscle (FDI) for 10 min or until force could no longer be sustained. Resting motor threshold, motor-evoked potential (MEP), input-output curve, cortical silent period duration, interference pattern (IP) and M/F ratio were recorded at baseline, immediately after fatigue and after 20 min rest. Immediately after exercise, decreased MEP amplitude and increased cortical SP duration were observed in the control group whilst no such changes were observed in PD patients. The input-output curve was also significantly suppressed only in controls, but not in patients. The amplitude of IP was significantly reduced immediately after exercise in both PD patients and controls. Almost all these changes returned nearly to baseline values after 20 min rest. The amount of exercise was approximately equal in both groups because the effect on M-waves and EMG amplitude was similar. However, the expected decline in corticospinal excitability was absent in PD patients. The absence of this effect in PD patients may reflect reorganization of motor commands in response to basal ganglia deficit.
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PMID:Lack of post-exercise depression of corticospinal excitability in patients with Parkinson's disease. 1759 37

Muscle cramps are involuntary, painful, spasmodic contractions of the skeletal muscle. Although cramps are a common clinical complaint, their etiology and management have not been well established. Exercise-associated muscle cramps occur during or immediately following exercise, and they are associated with muscular fatigue and shortened muscle contraction. The main challenges for treating physicians are to identify whether the complaint represents a true muscle cramp as well as to rule out the presence of an underlying serious clinical condition. Muscle cramps may be a symptom of any of several conditions, including radiculopathies, Parkinson's disease, hypothyroidism, diabetes mellitus, vascular problems, electrolyte disorders, and metabolic myopathies. Cramps also may occur as a side effect of certain drugs (eg, lipid-lowering agents, antihypertensives, beta-agonists, insulin, oral contraceptives, alcohol). Most athletes who experience exercise-associated muscle cramps are healthy individuals without systemic illness. Therapy should focus on preventing premature fatigue by means of appropriate nutrition and adequate training.
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PMID:The athlete with muscular cramps: clinical approach. 1760 31

Neuropsychiatric problems are common in Parkinson's disease (PD) but there is little information regarding how they impact on quality of life. PD patients without dementia (49) were assessed for low mood/depression, fatigue, apathy, sleep problems and hallucinations. Measures of quality of life and motor function were also obtained. Over 77% of the patients reported symptoms consistent with one or more neuropsychiatric problems. Low mood/depression, anxiety and the presence of hallucinations predicted poorer quality of life after controlling for motor symptoms. Additional to the motor symptoms, we found that specific neuropsychiatric problems may impact on quality of life for PD patients.
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PMID:A profile of neuropsychiatric problems and their relationship to quality of life for Parkinson's disease patients without dementia. 1762 63

Non-motor symptoms (NMS) in Parkinson's disease (PD) are common, significantly reduce quality of life and at present there is no validated clinical tool to assess the progress or potential response to treatment of NMS. A new 30-item scale for the assessment of NMS in PD (NMSS) was developed. NMSS contains nine dimensions: cardiovascular, sleep/fatigue, mood/cognition, perceptual problems, attention/memory, gastrointestinal, urinary, sexual function, and miscellany. The metric attributes of this instrument were analyzed. Data from 242 patients mean age 67.2 +/- 11 years, duration of disease 6.4 +/- 6 years, and 57.3% male across all stages of PD were collected from the centers in Europe, USA, and Japan. The mean NMSS score was 56.5 +/- 40.7, (range: 0-243) and only one declared no NMS. The scale provided 99.2% complete data for the analysis with the total score being free of floor and ceiling effect. Satisfactory scaling assumptions (multitrait scaling success rate >95% for all domains except miscellany) and internal consistency were reported for most of the domains (mean alpha, 0.61). Factor analysis supported the a prori nine domain structure (63% of the variance) while a small test-retest study showed satisfactory reproducibility (ICC > 0.80) for all domains except cardiovascular (ICC = 0.45). In terms of validity, the scale showed modest association with indicators of motor symptom severity and disease progression but a high correlation with other measures of NMS (NMSQuest) and health-related quality of life measure (PDQ-8) (both, rS = 0.70). In conclusion, NMSS can be used to assess the frequency and severity of NMS in PD patients across all stages in conjunction with the recently validated non-motor questionnaire.
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PMID:The metric properties of a novel non-motor symptoms scale for Parkinson's disease: Results from an international pilot study. 2623 Jul 48

Fatigue is a common nonmotor symptom in idiopathic Parkinson disease (IPD) that can prominently affect everyday function. This study was a randomized, double-blind, placebo-controlled trial evaluating methylphenidate for the treatment of fatigue in patients with IPD maintained on their regular medications. Thirty-six patients were randomized to receive either methylphenidate (10 mg three times per day; n = 17) or placebo (n = 19) for 6 weeks. Primary outcomes were the change from baseline on two separate self-report fatigue questionnaires: the Fatigue Severity Scale (FSS) and the Multidimensional Fatigue Inventory (MFI). Secondary outcomes included the Unified Parkinson Disease Rating Scale (UPDRS) motor score and the five individual domains of the MFI. Fourteen patients in the methylphenidate group and 16 patients in the control group remained on the intervention for the entire study period. In the treatment arm, mean FSS score was reduced by 6.5 points (from a baseline of 43.8) and mean MFI score was reduced by 8.4 points (from a baseline of 51.0). Both these reductions were significant (P < 0.04). Smaller reductions in the placebo group were nonsignificant. Mean UPDRS motor score did not change significantly in either group. Analysis of MFI subscores showed a significant reduction in General Fatigue in the methylphenidate group (P < 0.001). Overall, adverse effects of medication were more frequent in the placebo group. In conclusion, methylphenidate was effective in lowering fatigue scores in patients with IPD following a 6-week treatment period.
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PMID:Methylphenidate improves fatigue scores in Parkinson disease: a randomized controlled trial. 1767 15

Sporadic and chronic fatigue are common, but an underlying etiology is identified in only up to 10% of cases. Under-reporting makes fatigue's prevalence unknown. Some estimate up to 50% of elders suffer from mild fatigue. Causes vary, but prevailing theory links most fatigue as a secondary consequence to illness and medication. Fatigue is prominently linked to sleep disorders, depression, heart disease, Parkinson's disease, anemia, and cancer. Fatigue and its consequences should be assessed routinely. Empiric treatment is the norm, focusing on managing fatigue, and, when possible, selecting agents with fewer side effects. Exercise, diet, and promoting good sleep hygiene have beneficial effects in symptom management.
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PMID:Fatigue: implications for the elderly. 1771 1

Sildenafil, a phosphodiesterase-5 inhibitor is widely used for the treatment of erectile dysfunction. Recently, the FDA approved the use of sildenafil in the therapeutic treatment of pulmonary arterial hypertension. Sildenafil crosses the blood-brain barrier and has been shown to enhance memory. Tremor, rigidity and akinesia are the most common symptoms seen in Parkinson's disease. Fatigue and sexual dysfunction are the other prominent features seen in Parkinson's disease. Interestingly, sildenafil is used therapeutically to treat sexual dysfunction in Parkinson's disease patients. Currently research on Parkinson's disease focuses on developing novel drug therapies for retarding the nigral dopaminergic neurodegeneration. Hence, we investigated the anti-fatigue and neuroprotective effects of sildenafil. In this study, the effect of sildenafil on fatigue was evaluated using forced swim test in mice. Sildenafil had no effect on fatigue as seen by the swim time. With regard to neuroprotective effects, we investigated the effects of sildenafil using two animal models of Parkinson's disease. In this study, 6-hydroxydopamine-lesioned (unilateral) rats and MPTP-treated mice were used as the animal models of Parkinson's disease. 6-Hydroxydopamine-lesioned rats were used to determine the effect of sildenafil on rotational behavior. Ipsilateral or contralateral rotational behavior can indicate the amphetamine-like activity or apomorphine-like activity of sildenafil. Sildenafil did not induce contralateral or ipsilateral rotations in 6-hydroxydopamine-lesioned rats. Sildenafil did not protect against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dopamine depletion in the striatum.
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PMID:Evaluation of neuroprotective and anti-fatigue effects of sildenafil. 1782 48


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