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)

Two women had a syndrome of progressive parkinsonism with ipsilateral rigidity, mild resting tremor, paresis, hyperreflexia, and an extensor plantar response. Symptoms had started 24 and 3 months after a surgical procedure in the affected limb. Neuroimaging studies were unhelpful. Both the parkinsonian features and the pyramidal tract signs responded well to dopaminergic drug treatment. We propose that the syndrome be called "idiopathic hemiparetic parkinsonism".
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PMID:Idiopathic hemiparetic parkinsonism, a syndrome distinct from idiopathic parkinsonism. 135 57

Parkinsonism is a well-known side effect of some calcium channel blockers (CCB). Its long-term evolution, however, is unknown. To clarify this issue, we performed a prospective follow-up study involving 32 patients diagnosed with CCB-induced parkinsonism. After the baseline examination, the CCB were discontinued and serial evaluations were carried out according to the same protocol. Despite a global improvement, cognitive and mood disturbances subsided slowly, and tremor persisted in most patients. After 18 months of CCB withdrawal, 44% of patients had depression, 88% had tremor, and 33% still had criteria for diagnosis of parkinsonism. During the survey, only three patients were found to be fully recovered. The improvement of some clinical symptoms was related to age: Patients younger than 73 years recovered better than older patients did. Our data indicate that CCB-induced parkinsonism is not the benign condition previously thought, and suggest an age-related prognosis of this entity.
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PMID:Parkinsonism associated with calcium channel blockers: a prospective follow-up study. 134 6

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

The effect of arotinolol, a peripherally acting beta-adrenergic-blocking agent, on postural or kinetic tremor was studied in monkeys with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism. Male cynomolgus monkeys (Macaca fascicularis) were treated with three injections of MPTP hydrochloride (0.3 mg/kg, i.v.) at an interval of 3-4 days, followed by several injections of the same dose every 7 days. Four monkeys with persistent parkinsonian symptoms manifested for greater than 1 year were used. The animals developed mild to moderate degrees of postural or kinetic tremor, and their motor activity was reduced. Arotinolol (20-30 mg/kg, s.c.) significantly suppressed postural tremor in a dose-dependent manner. Propranolol (20-30 mg/kg) was also effective in suppressing the tremor. However, the application of propranolol induced emesis, whereas arotinolol had no adverse effects. These results suggest that arotinolol is a useful adjunct to dopaminergic therapy for tremor in Parkinson's disease.
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PMID:Therapeutic effects of arotinolol, a beta-adrenergic blocker, on tremor in MPTP-induced parkinsonian monkeys. 138 70

Dopa-responsive dystonia (DRD) is one form of childhood-onset idiopathic torsion dystonia. Adult-onset parkinsonism has appeared in several previously unaffected members in families with DRD suggesting that this may be an additional phenotypical expression of the disease. We report a family with DRD in which 2 women and 1 man, unaffected by dystonia, developed tremor-onset parkinsonism after age 50 years. The women continue on a low dosage of levodopa after 9 and 13 years of treatment, with a stable, nearly complete, symptomatic response. This contrasts to the typical long-term treatment complications observed in patients with Parkinson's disease. We assessed nigrostriatal dopaminergic function in the proband, with typical DRD, and the 2 women with parkinsonism using 6-[18F]fluoro-L-dopa positron emission tomography. All 3 had normal striatal 6-[18F]fluoro-L-dopa uptake. These observations provide compelling evidence that "benign" adult-onset parkinsonism may be an expression of the disease in some members of families with DRD and does not support consideration of the DRD gene as a risk factor for development of Parkinson's disease. There may be considerable clinical heterogeneity in DRD depending on the age at onset.
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PMID:Long-term treatment response and fluorodopa positron emission tomographic scanning of parkinsonism in a family with dopa-responsive dystonia. 144 40

An Irish kindred is described in which 5 of 10 siblings in the fourth or fifth decade of life developed an akinetic-rigid syndrome clinically indistinguishable from idiopathic Lewy body Parkinson's disease. Four of these patients were scanned by positron emission tomography (PET) with [18F]dopa after clinical diagnosis and in all, a profound impairment of tracer uptake into the striatum was recorded. The fifth patient was initially scanned at a time when he was asymptomatic and normal by clinical examination. His scan showed impaired tracer uptake, indicating a subclinical defect in the presynaptic nigrostriatal system. Within months of his scan, he too developed subtle symptoms and signs of parkinsonism although there was little further clinical progression or change in his PET scan over the following year. A clinically normal sibling was also scanned and found to have subclinical impairment of [18F]dopa uptake in the putamen. The 19-year-old daughter of an affected sibling had a mild postural tremor but no other symptoms or signs. The [18F]dopa uptake in her putamen fell at the borderline between normal and parkinsonian values. This study confirms that PET can identify preclinical parkinsonism in at-risk subjects. The finding of abnormalities in several clinically unaffected family members suggests that family studies based on clinical assessment alone may miss a significant number of subclinically affected individuals, leading to an underestimate of any genetic component to Parkinson's disease.
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PMID:The identification of presymptomatic parkinsonism: clinical and [18F]dopa positron emission tomography studies in an Irish kindred. 144 41

Vascular pseudoparkinsonism may be confused with idiopathic Parkinson's disease. Patients may be unnecessarily treated with anti-parkinsonian drugs while their underlying vascular disease is ignored. We investigated 250 parkinsonian patients seen in our Movement Disorders Clinic for a possible vascular etiology. After excluding those with a known secondary cause such as drug-induced parkinsonism, progressive supranuclear palsy, multiple system atrophy and hyperparathyroidism, brain computed tomography and/or magnetic resonance imaging were performed on those who showed poor or no response to levodopa. In those with an ischemic lesion demonstrated on neuroimaging, anti-parkinsonian drugs were stopped and the patients were reassessed. Eleven patients (4.4%) had ischemic brain lesions accounting for their parkinsonism. All were initially diagnosed as Parkinson's disease because of the prominence of bradykinesia and rigidity. Gait disturbance was also common, but resting tremor was distinctly absent. Three anatomical patterns with different prognosis were identified. Three patients with basal ganglia lacunar infarct recovered spontaneously, three with frontal lobe infarcts remained static and five with periventricular and deep subcortical white matter lesions had progressive deterioration. Autopsy in one patient confirmed bilateral frontal lobe watershed infarcts and the absence of brain stem Lewy bodies. Parkinsonian patients with poor or no response to levodopa therapy should be investigated for a vascular etiology.
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PMID:Vascular pseudoparkinsonism. 148 45

A review is presented of the more important discoveries and advances in the 175-year history of the studies and therapeutic trials on parkinsonism. The personality and achievements of James Parkinson are described, with a brief discussion on his most important paper "An Essay on Shaking Palsy". The important works of clinicians, neuropathologists and pharmacologists in the 19th and 20th centuries, especially in the "era of L-DOPA", are reviewed. The development of neurosurgical methods of parkinsonism treatment, including intracerebral grafting of dopamine-producing cells, is outlined.
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PMID:[History of discoveries and advances in the studies of parkinsonism]. 148 80

The risk of developing drug-induced parkinsonism (DIP) has been related to a number of factors but it remains up to now poorly defined. The aim of this survey has been to evaluate retrospectively the possible role of inherited components in 25 patients with parkinsonism induced by chronic exposure to the calcium-entry blockers cinnarizine and flunarizine. The finding of higher occurrence of a positive family history for Parkinson's disease (PD) and/or essential tremor (ET) and of higher frequency of secondary cases with PD and/or ET among close relatives of the patients as compared to age-matched controls, suggests the involvement of genetic susceptibility in developing this drug-induced disorder. DIP could be regarded as a multifactorial disease process resulting from potential neurotoxicity of drugs on a background of inherited predisposition.
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PMID:Calcium-entry blockers-induced parkinsonism: possible role of inherited susceptibility. 150 27

Hyperkinetic movement disorders may develop as a complication of stereotactic thalamotomy or pallidotomy. However, such movement disorders are uncommon after nonsterotactic intracranial operations. The authors report three cases of involuntary movement disorders unexpectedly developing after intracranial operations. The patients had undergone clipping of an internal carotid aneurysm, removal of an intracerebral hematoma, and resection of a tentorial meningioma. Two patients developed choreic movements and a dystonic posture of the unilateral upper extremity. One patient showed a tremor that had features of both parkinsonism and essential tremor. The symptoms of these patients were medically uncontrollable, and they were successfully treated with stereotactic ventrolateral thalamotomy.
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PMID:Unexpected movement disorders in neurosurgical practice: report of three cases. 150 46


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