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)

Between 1985 and 1990, the authors performed stereotactic posteroventral pallidotomies on 38 patients with Parkinson's disease whose main complaint was hypokinesia. Upon re-examination 2 to 71 months after surgery (mean 28 months), complete or almost complete relief of rigidity and hypokinesia was observed in 92% of the patients. Of the 32 patients who before surgery also suffered from tremor, 26 (81%) had complete or almost complete relief of tremor. The L-dopa-induced dyskinesias and muscle pain had greatly improved or disappeared in most patients, and gait and speech volume also showed remarkable improvement. Complications were observed in seven patients: six had a permanent partial homonymous hemianopsia (one also had transient dysphasia and facial weakness) and one developed transitory hemiparesis 1 week after pallidotomy. The results presented here confirm the 1960 findings of Svennilson, et al., that parkinsonian tremor, rigidity, and hypokinesia can be effectively abolished by posteroventral pallidotomy, an approach developed in 1956 and 1957 by Lars Leksell. The positive effect of posteroventral pallidotomy is believed to be based on the interruption of some striopallidal or subthalamopallidal pathways, which results in disinhibition of medial pallidal activity necessary for movement control.
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PMID:Leksell's posteroventral pallidotomy in the treatment of Parkinson's disease. 150 2

We studied the effects of botulinum toxin A in 12 patients with spasticity and in eight patients with rigidity. The study design was a double-blind, placebo-controlled crossover trial with botulinum toxin A versus saline. Using the Ashworth Scale for spasticity and the Unified Parkinson's Disease Rating Scale for rigidity, we gave the patients a tone grade before and 2 weeks after treatment. Improvement in tone by two grades or more was considered clinically significant. In the spasticity group, botulinum toxin A reduced the tone of all patients significantly, improved functionality and nursing care in eight of 12 patients, and alleviated painful spasms in five of five patients. In the rigidity group, muscle tone was decreased in seven of eight patients, functionality improved in four of seven, and joint and muscle pain decreased in four of five. We conclude that botulinum toxin A is effective against the disabling effects of spasticity and rigidity. The treatment was well tolerated.
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PMID:Botulinum toxin A for spasticity, muscle spasms, and rigidity. 772 60

Muscular pain is the most frequent kind of nondystonic pain associated with Parkinson's disease (PD). It might be related not only to peripheral factors but also to an abnormal nociceptive input processing in the central nervous system. To test this hypothesis, we recorded CO(2) laser-evoked potentials (LEPs) in response to shoulder stimulation (skin over deltoid muscle) in 11 hemiparkinsonian PD patients complaining of muscular pain in the shoulder (ipsilateral to motor symptoms) and compared the results with those obtained in 12 pain-free PD patients with hemiparkinson and in 11 normal subjects. N2/P2 LEP, which is thought to originate from the cingulate cortex and insula, was significantly lower in amplitude in both groups of PD patients than in controls, regardless of the clinically affected body side. In both groups of PD patients, no significant correlation was observed between the severity of motor symptoms and N2/P2 amplitude abnormalities. In PD patients with muscular pain, the N2/P2 amplitude obtained following stimulation of the painful shoulder was significantly reduced compared with that obtained in response to nonpainful shoulder stimulation and compared with the values obtained in pain-free PD patients. No significant correlation was observed between the intensity of muscular pain and N2/P2 amplitude abnormalities in this group of PD patients. These results suggest abnormal nociceptive input processing in PD, which appears to be independent of clinical expression of parkinsonian motor signs. These alterations are more evident in the presence of muscular pain.
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PMID:Muscular pain in Parkinson's disease and nociceptive processing assessed with CO2 laser-evoked potentials. 2006 86

A 66-year-old woman with advanced Parkinson disease (PD) was referred to our center for an adjustment of her antiparkinsonian medication. To reduce daily off-time, we introduced rasagiline 1 mg/d. Three days after starting this new treatment, she presented with intense arthralgia that symmetrically affected the shoulders, hands, and hips without myalgia. Ten days later, while walking, she experienced acute pain on the inner side of her right thigh, with the absence of any trauma. Findings of ultrasonography confirming the diagnosis of partial avulsion of the right harmstrings. Rasagiline was stopped immediately, and the arthralgia disappeared within 48 hours and did not recur. To our knowledge, this is the first reported case of a spontaneous tendon rupture possibly caused by rasagiline. Our observation emphasizes that, although often well tolerated, rasagiline may cause muscle and joint complications that could increase disability in patients with PD.
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PMID:Tendon rupture as an adverse effect of rasagiline. 2461 73

Neuroinflammation is a condition characterized by the elaboration of proinflammatory mediators within the central nervous system. Neuroinflammation has emerged as a dominant theme in contemporary neuroscience due to its association with neurodegenerative disease states such as Alzheimer's disease, Parkinson's disease and Huntington's disease. While neuroinflammation often is associated with damage to the CNS, it also can occur in the absence of neurodegeneration, e.g., in association with systemic infection. The "acute phase" inflammatory response to tissue injury or infections instigates neuroinflammation-driven "sickness behavior," i.e. a constellation of symptoms characterized by loss of appetite, fever, muscle pain, fatigue and cognitive problems. Typically, sickness behavior accompanies an inflammatory response that resolves quickly and serves to restore the body to homeostasis. However, recurring and sometimes chronic sickness behavior disorders can occur in the absence of an underlying cause or attendant neuropathology. Here, we review myalgic enchepalomyelitis/chronic fatigue syndrome (ME/CFS), Gulf War Illness (GWI), and chemobrain as examples of such disorders and propose that they can be exacerbated and perhaps initiated by a variety of environmental stressors. Diverse environmental stressors may disrupt the hypothalamic pituitary adrenal (HPA) axis and contribute to the degree and duration of a variety of neuroinflammation-driven diseases.
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PMID:Neuroinflammation disorders exacerbated by environmental stressors. 3161 Aug 52