Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report on a 44-year-old woman with a right frontal meningioma, who presented with resting tremor, rigidity and bradykinesia in the left limbs. There were no other neurologic manifestations. A computed tomography scan demonstrated a huge high-density mass in the right frontal lobe and marked surrounding edema causing compression of the basal ganglia. Cerebral angiography showed a typical sunburst tumor stain and three feeding vessels from the bilateral middle meningeal arteries and the right callosomarginal artery. The pathologic diagnosis was transitional type meningioma. Before surgery, treatment with levodopa and bromocriptine was significantly effective in controlling hemiparkinsonism, which completely disappeared after surgical removal of the tumor. This outcome supports the notion that local compression due to edema may cause a functional disorder in the basal ganglia producing reversible contralateral parkinsonism.
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PMID:Hemiparkinsonism in a patient with frontal meningioma. 136 48

Cynomolgus monkeys received intracarotid injections of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to produce a chronic unilateral model of parkinsonism. Extensive dopamine (DA) depletion was observed in the caudate nucleus and putamen on the side ipsilateral to the injection and this was associated with contralateral tremor, rigidity, and bradykinesia. A dose of 1.25 mg of MPTP caused ipsilateral DA loss of 99.4% in the caudate nucleus, 99.8% in the putamen, and 74.2% in the nucleus accumbens. A dose of 2.5 mg caused ipsilateral DA depletion of 99.3% in the caudate nucleus, 99.5% in putamen, and 90.1% in the nucleus accumbens. The unilateral aspect of the lesion was dose sensitive, with the 2.5-mg dose causing bilateral asymmetric DA depletion. Tissue concentrations of serotonin were not affected by the toxin. These findings confirm that intracarotid injection of MPTP may produce a useful primate model of hemiparkinsonism that can be associated with selective unilateral DA depletion when the appropriate dose of toxin is used.
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PMID:Intracarotid 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine administration: biochemical and behavioral observations in a primate model of hemiparkinsonism. 169 Feb 67

After local surgical exposure, we administrated 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) directly into the right common carotid artery of 5 rhesus monkeys. All the monkeys manifested akinesia, rigidity and postural tremor of the contralateral limbs, and spontaneous circling toward the MPTP treated side. These disturbances began to appear 3-4 days after injection, peaking at one month, and continued until the day of sacrifice. After treatment with madopar and apomorphine, marked improvements of the motor impairments appeared and a striking reversal of the direction of rotation away from the MPTP-treated side occurred in a dose-dependent manner. The ipsilateral neurotoxicity was confirmed biochemically by 99% reduction in the caudate-putamen dopamine levels and histologically by selective cell loss in the substantia nigra of the MPTP-treated side. It is concluded that this primate model of hemiparkinsonism is easy to reproduce and life is maintained with good health otherwise. So it may be more feasible for behavioral and pharmacological studies of Parkinson's disease.
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PMID:Hemiparkinsonism in monkeys following unilateral common carotid artery infusion of MPTP. A study of behavior, biochemistry and histology. 193 58

We evaluated 11 patients with hemiparkinson-hemiatrophy syndrome, 6 with body and contralateral cerebral hemispheric hemiatrophy, 4 with only body hemiatrophy, and 1 with just brain hemiatrophy. The mean age of symptom onset was 38.1 years (range, 18 to 54) with 5.2 +/- 3.1 (mean +/- SD) years of illness until the last follow-up visit. The presenting symptom was unilateral tremor in 6 patients, hand dystonia in 2, bradykinesia in 2, and abnormal gait in 1 patient. Three patients had a good response to levodopa, 4 had moderate response, and 2 patients had a poor response. During a mean follow-up period of 1.7 years (range, 4 months to 5 years), the Hoehn and Yahr score changed in only 3 patients: 2 gained 1.5 points and 1 gained 3 points over 2.5 years. We discuss the association between hemiparkinsonism-body hemiatrophy and contralateral hemispheric hemiatrophy, and raise the possibility of early childhood brain insult with delayed-onset parkinsonism.
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PMID:Hemiparkinsonism-hemiatrophy syndrome: clinical and neuroradiologic features. 223 29

Long-term observation over 3-8 postoperative years of cases of Parkinson disease operated by stereotactic thalamotomy using a microelectrode recording technique is reported. The procedure is specifically useful in the following four groups: (1) tremor-dominant cases, (2) hemiparkinsonism, (3) cases with marked asymmetry in motor symptoms and (4) juvenile parkinsonism presenting levodopa-induced dyskinesia.
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PMID:Long-term follow-up study of nucleus ventralis intermedius and ventrolateralis thalamotomy using a microelectrode technique in parkinsonism. 332 71

Isotonic muscle strength measured by a quantitative technique was decreased in early Parkinson's disease compared to age-matched controls. Weakness was present both on the affected and unaffected side in hemiparkinsonism. Similar degrees of weakness occurred in limbs with tremor or rigidity. Muscle weakness appears to be a primary symptom of Parkinson's disease which may relate to disturbed motor programming due to basal ganglia dysfunction.
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PMID:Muscle strength testing in Parkinson's disease. 394 87

To evaluate the effect of stereotactic thalamotomy on the function of the corticospinal tract, we studied motor evoked potentials (MEPs) recorded by surface electromyography (EMG) in the left extensor carpi radialis (ECR) and flexor carpi radialis (FCR) with magnetic stimulation of the contralateral motor cortex in a 43-year-old patient with a severe postural and resting tremor of the left hand. The patient was diagnosed eight years previously with left hemiparkinsonism. The tremor was unresponsive to various medications. After thalamotomy the tremor had disappeared, confirmed by EMG studies. MEP latencies at rest were normal and did not change after thalamotomy. Volitional contraction of either ECR or FCR shortened the latency of the corresponding MEP before and after thalamotomy. However, before thalamotomy responses at rest were less well synchronized and followed by EMG silence with subsequent long duration tonic after discharges. Furthermore, during voluntary contraction the responses only slightly enhanced. After surgery MEPs at rest in both muscles were more synchronized and after-discharges had disappeared. Moreover, with volitional contraction of either ECR of FCR, the MEPs enhanced more dramatically. The silent periods (SPs) following the MEP during sustained voluntary contraction were longer after thalamotomy. The consistent MEP latencies suggest that the conduction of the pyramidal tract is unaffected by thalamotomy. The better synchronized responses, the alleviation of after-discharges and the longer SPs in this patient with hemiparkinsonism following thalamotomy suggest an improved sensorimotor integration, which may be the result of a reduced thalamic input onto suprasegmental levels.
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PMID:Alterations of motor evoked potentials by thalamotomy. 822 31

We recorded spontaneous magnetoencephalographic (MEG) activity and somatosensory-evoked fields (SEFs) with a 24-channel planar SQUIDgradiometer in five patients with hemiparkinsonism. The SEFs of the patients were within normal limits. During tremorless periods, the spontaneous activity over the somatomotor cortex had a frequency peak at approximately 10 Hz in all five patients and another at approximately 20 Hz in three. Tremor dampened the 10-Hz activity in all patients; in three the effect was bilateral. Tremor did not increase MEG activity at the tremor frequency. The suppression of the mu rhythm by the parkinsonian tremor resembled that occurring during voluntary movements in healthy subjects.
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PMID:Suppression of magnetic mu rhythm during parkinsonian tremor. 840 46

A group of 10 healthy control subjects and 10 patients with hemiparkinsonism (HD) were studied by positron emission tomography (PET) using 6-[18F]fluorodopa (FDOPA). FDOPA metabolism in the caudate nucleus and the putamen was separately estimated by measuring target-to-background ratios (TBRs) using composite images added between 30 and 60 min after FDOPA injection and by TBR-versus-time slopes during PET study. TBRs in the caudate nucleus and the putamen were 1.81 +/- 0.23 (mean +/- SD) and 1.92 +/- 0.28 in the 10 controls, respectively. In HD patients, on the dominantly affected hemisphere related to main clinical symptoms, TBRs were significantly decreased in the caudate nucleus (P < 0.01) and the putamen (P < 0.05) compared with those in the corresponding areas on the contralateral hemisphere, though those TBRs on both hemispheres were significantly decreased compared with the TBRs of normal subjects (P < 0.01). TBRs and TBR slopes in both the caudate nucleus and the putamen were correlated with disease severity according to Hoehn and Yahr. On the dominantly affected hemisphere, TBR and TBR slopes in the putamen were well correlated with individual clinical measures for bradykinesia and rigidity, and those in the caudate nucleus were also correlated with the severity of tremor. Our data suggest that in HD patients, PET study using FDOPA may provide unique and efficient information on the dysfunction of the dominantly affected caudate nucleus and the putamen which are correlated with diseased severity and individual clinical symptoms.
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PMID:6-[18F]fluorodopa metabolism in patients with hemiparkinsonism studied by positron emission tomography. 848 75

A 47 year old female dentist suffered from hemiparkinsonism which had started eighteen months earlier and was manifested mainly by resting tremor and cogwheel rigidity. A baseline quantitative urinary mercury excretion was 46 micrograms/day. The patient was treated with chelating agent d-penicillamine for a week. Chelation therapy resulted in clinical improvement of parkinsonism and in dynamic changes in daily urinary mercury excretion with a prompt increase to 79 micrograms/day, a subsequent decline followed by increase in the mercury urinary excretion. After a week chelation therapy was stopped. During a follow-up period of five years, the neurological status remained unchanged after the initial penicillamine-induced improvement. This case may be evidence, therefore, of a rare clinical variant of elemental mercury intoxication associated with parkinsonism, in the absence of most classical neuropsychiatric signs of chronic mercurialism.
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PMID:The enigma of parkinsonism in chronic borderline mercury intoxication, resolved by challenge with penicillamine. 878 40


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