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)

Surgical treatments for PD and ET are promising. Medial Pallidotomy, the surgical lesioning of the pallidum, often improves symptoms of long-standing PD. We enrolled twenty-seven late stage PD patients for unilateral medial pallidotomy who were then assessed by the Core Assessment Program for Intracranial Transplantation (CAPIT) protocol. One year after surgery persistent improvement was seen contralateral to the lesion in the following features: drug-induced dyskinesias (92%), akinesia (38%), rigidity (51%), and tremor (42%). Complications included transient dysarthria (7 patients), facial weakness (9 patients), limb weakness (1 patient), swallowing problems (4 patients) and intracerebral haemorrhage (1 patient). Thalamic DBS may improve tremor in PD and ET patients. Therefore, we enrolled fifteen patients (9 PD and 6 ET patients) with disabling tremor, unresponsive to medication. They were assessed by the United Parkinson's Disease Rating Scale (UPDRS) and the Tremor Rating Scale (for PD and ET patients, respectively). Three months after surgery, limb tremor contralateral to stimulation improved by 71% in PD patients and 76% in ET patients. Complications included transient paresthesias (all), confusional state (1 patient) and intracerebral bleed (1 patient). Unilateral medial pallidotomy safely improves some Parkinsonian symptoms contralateral to the lesion. Thalamic DBS may effectively and safely improve contralateral limb tremor in PD and ET.
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PMID:Surgical interventions in the treatment of Parkinson's disease (PD) and essential tremor (ET): medial pallidotomy in PD and chronic deep brain stimulation (DBS) in PD and ET. 929 83

Weakness, easy fatiguing, and lack of endurance are commonly perceived by patients with Parkinson's disease (PD). Although the slowed motor repertoire in PD may underlie these experiences, other abnormalities in skeletal muscle utilization also may be involved. We investigated whether an index of metabolic efficiency during a continuous exercise task, the latency until anaerobic threshold (AT), is altered by L-DOPA (LD). While pedalling a bicycle ergometer against a uniform workload, subjects were monitored for expired O2 and CO2. As compared to an unmedicated state, LD treatment delayed AT by a mean (+/-SE) of 5.67 +/- 0.89 to 6.62 +/- 1.23 min (p < 0.05), paired t test). Subjects did not differ in their perceived exertion upon reaching AT. With relief of parkinsonism by LD, the efficiency of energy utilization is also increased in exercised skeletal muscle.
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PMID:Perceived exertion and muscle efficiency in Parkinson's disease: L-DOPA effects. 931 95

The authors examined the British medical literature published in the 45-year-period following Parkinson's treatise on the shaking palsy to determine the number and type of references to the shaking palsy or paralysis agitans during this particular period. Several sources suggest that Parkinson's 1817 treatise on the shaking palsy received little immediate attention in his native country, England, and that not until 1861, in France, did Charcot began to elucidate the clinical features of this entity, separating it from other neurologic disorders (for example, multiple sclerosis). A review of the British medical literature from the 45-year-period 1817-1861 revealed a number of references to paralysis agitans, including those by Cooke (1820), Good (1824 and 1829), Elliotson (1827, 1829, 1830, 1831, and 1833), Gowry (1831), anonymous (1832), Todd (1833), Watson (1836), Gibson (1839), Hall (1838 and 1841), Thompson (1842), Graves (1843), Birkett (1853), Paget (1855), and Reynolds (1855). Many of these did not report new or personally observed cases, did not separate Parkinson's disease from other disease entities characterized by both "shaking" and "palsy" (for example, tonic-clonic seizures), or misattributed motor signs to dysfunction of the pyramidal system rather than an extrapyramidal system (that is, attributing bradykinesia or rigidity to weakness). Although there were several references to "shaking palsy" in the early- to mid-19th-century British medical literature, there were few original case reports of Parkinson's disease. This may have contributed to the fact that during this period little was added to the original observations made by Parkinson in 1817. In particular, the separation of bradykinesia and weakness did not become apparent until later work by the French.
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PMID:The shaking palsy, the first forty-five years: a journey through the British literature. 939 40

We have previously shown that action tremor persists during maximal wrist extension in patients with Parkinson's disease, and that this contributes to weakness at this joint by preventing the fully fused contraction of the forearm extensor muscles. Antiparkinsonian medication reduces the action tremor in torque and electromyographic (EMG) records, thereby improving strength at the wrist. In the present experiments, peak torque and action tremor were recorded during maximal extension of the elbow in nine patients with Parkinson's disease while they were on and off antiparkinsonian medication, and in eight age- and sex-matched healthy subjects. Peak torque and mean rectified EMG levels were reduced by 34% and 36%, respectively, during maximal elbow extension when patients off medication were compared to those in the treated state. Action tremor was visible in torque records and had a frequency of approximately 10 Hz both in parkinsonian patients and in normal controls. Activity of a similar frequency was often detected in EMG records, especially in patients off therapy. The absolute amplitude of action tremor in torque (A[torque]) and EMG (A[EMG]) records from the elbow was unaffected by therapy and was little different from that recorded in healthy controls. The relative action tremor in torque ([A(torque)/peak torque] x 100) and EMG ([A(EMG)/mean rectified EMG] x 100) was reduced by treatment, but this was the result of the increase in peak torque and mean rectified EMG. Thus, in contrast to the results at the wrist, antiparkinsonian medication has little effect on the 10-Hz action tremor at the elbow. Increased strength is produced by a different mechanism which allows recruitment of triceps motor units outside of this synchronizing influence.
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PMID:Action tremor and weakness in Parkinson's disease: a study of the elbow extensors. 945 27

Isokinetic strength of knee extension and flexion was measured at two speeds of movement in 23 patients with Parkinson's disease, to clarify whether muscle weakness is inherent to the disease. To counteract normal variation among subjects, we selected patients with symptoms completely or largely confined to one side and compared sides for each patient. The affected side was weaker than the other in both slow and fast movements early in the disease. In more advanced disease, the difference between sides diminished at the slow speed but remained significant at the faster speed. These observations suggest that weakness is inherent to Parkinson's disease and influenced by movement speed.
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PMID:Muscle weakness in Parkinson's disease: isokinetic study of the lower limbs. 963 72

Exercise provides important benefits for older adults in the areas of cardiovascular function, strength and muscle mass, postural stability, and psychological function. These benefits can be achieved by those who are healthy, as well as by the frail and very old. Physicians can use a simple screening test to identify patients at risk for loss of mobility and function due to muscle weakness. Exercise helps prevent hip fractures from falls by increasing bone density, coordination, balance, and muscle strength. It is also an important treatment for patients with arthritis, Parkinson's disease, stroke, and other chronic diseases of aging. Patients who exercise show improvements in depressive symptoms and sleep disorders.
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PMID:Physical fitness: benefits of exercise for the older patient. 2. 979 Nov 96

We measured isokinetic muscle strength of knee extension and flexion in 18 patients with Parkinson's disease who showed marked laterality in symptom severity and compared strength between the sides in the same patient. In all patient groups, the maximum peak torque of the more affected side was significantly less than for the less affected side at 15 revolutions per minute (r.p.m.) and 30 r.p.m. with the difference between the sides being larger at 30 r.p.m. than at 15 r.p.m., while at 5 r.p.m. there were no significant differences between sides. In the Yahr stage I group, the maximum peak torque in both extension and flexion at each velocity showed no significant difference between the sides. In contrast, in the stage II and III groups the maximum peak torque at 5 r.p.m. showed no significant difference between the sides, while at 15 r.p.m. and 30 r.p.m. these values showed a tendency and a significant difference between the sides, respectively, with the more affected side being weaker. These results suggest that muscle weakness in patients with Parkinson's disease increases with performance velocity, especially as the disease progresses.
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PMID:Movement velocity dependent muscle strength in Parkinson's disease. 1010 Sep 58

An autopsy case of myotonic dystrophy (MD) is reported. The patient was a 58-year-old male. He presented with muscular weakness and muscular atrophy at the age of 33 and was diagnosed as having MD from myotonic symptoms (i.e. percussion and grip myotonia) at 49 years old. Mental disorders including a delusional hallucinatory state, mental slowness, indifference, and lack of spontaneity as well as visual cognitive impairments were noted at the age of 55. He showed Parkinsonism and died of septic shock. T2-weighted magnetic resonance imaging demonstrated diffuse cortical atrophy with a marked frontal atrophy and high-intensity signals in the white matter. Single photon emission computed tomography demonstrated hypoperfusion in the frontal cortex. Neuropathologic observation revealed neuronal loss in the superficial layer of the frontal and parietal cortices and extensive neuronal loss in the occipital cortex, intracytoplasmic inclusion body in the nerve cell of the medial thalamic nuclei, neuronal loss and presence of Lewy bodies in the substantia nigra and locus ceruleus corresponding to the pathologic features of Parkinson's disease, as well as abnormalities of myelin in the white matter. The present case suggests that in MD brain, various neuropathologic changes may occur and they contribute to the mental disorders.
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PMID:An autopsy case of myotonic dystrophy with mental disorders and various neuropathologic features. 1020 Dec 84

We counted spontaneous eye blink rate in 11 myotonic dystrophy (MD) patients. Seven healthy subjects as well as 10 Parkinson disease (PD) and 7 facio-scapulo-humeral dystrophy (FSH) patients were used as controls. Blink frequency was significantly decreased in MD and PD patients (7.6 +/- 4.9/min in average and 11.0 +/- 7.5/min, respectively), compared with healthy subjects and FSH patients (17.5 +/- 4.3/min and 17.3 +/- 9.9/min, respectively). Normal blink frequency in FSH suggests that the facial muscle weakness is not responsible for decreased blink frequency in MD. This observation is compatible with prolonged R1 latency in blink reflex in MD, suggesting a dysfunction of central mechanism of blink control system as in the case of PD, although there remains a possibility that the myotonia in levator palpebrae muscles disturbs blinking.
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PMID:[Decreased blink frequency in myotonic dystrophy]. 1020 80

It was observed by Couper in 1837 that manganese dust produces a neurological syndrome characterized by muscle weakness, tremor, bent posture, whispered speech and excess salivation. The similarity of these symptoms to those of Parkinson's disease were not recognized for many years. In addition to its Parkinson-like effects, manganese produces behavioral symptoms in humans including nervousness, hallucinations, memory loss, cognitive problems, bizarre behaviors and flight of ideas. Despite these signs and symptoms, there have been few systematic attempts to study the effects of manganese on behavior using animal models. The need to better understand the effects of manganese on behavior is becoming more important due to the potential of increased environmental exposure to manganese due to its use, or proposed use as a gasoline additive in a number of countries. However, there is debate as to which manganese compounds should receive priority for testing, what route of administration should be used in this testing, what dosing regimens should be used, what species are appropriate for behavioral testing, and what behavioral tests should be selected. Research to answer these questions is needed so that the behavioral effects of manganese can be described comprehensively and the mechanisms underlying these effects can be understood.
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PMID:A brief history of the neurobehavioral toxicity of manganese: some unanswered questions. 1038 8


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