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)

A patient with Alzheimer's disease and mild features of parkinsonism was treated with tacrine. Tremor and gait dysfunction worsened but responded to the addition of levodopa without adversely affecting cognitive function. The implications for experimental treatment strategies of patients with combined Alzheimer's and Parkinson's disease are discussed.
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PMID:Exacerbation of parkinsonism by tacrine. 151 77

Peak dose dyskinesia is a major problem in the treatment of parkinsonian patients with levodopa and yet this remains the best pharmacological agent for treating the condition. The hypothesis which this research set out to test was that thalamotomy in the area of the thalamus which receives the input from the medial segment of the globus pallidus would decrease or prevent the dyskinesia. A well established primate model of parkinsonism was used. Eight monkeys (Macaca fascicularis) were rendered parkinsonian with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Regular dosing with levodopa or apomorphine reliably resulted in peak dose dyskinesia. Thalamotomy was carried out using a radiofrequency electrode. To ensure that the appropriate area of the thalamus was targeted, that is the area receiving the pallidal input, an anatomical tracing study was carried out. The anterograde anatomical tracer horseradish peroxidase, covalently bound to wheatgerm agglutinin, was injected into the medial segment of the globus pallidus bilaterally in three monkeys. The target site for thalamotomy was accurately worked out from the tracings obtained. Chorea was usually abolished and always reduced by a thalamotomy in the pallidal terminal territory. This result was obtained after 10 thalamotomies: 4 animals receiving bilateral lesions, with an interval between operations, and 2 animals undergoing unilateral surgery. Lesions in three control sites were carried out and had no permanent effect on chorea. The effect of lesions in other areas was also assessed. Dystonia was not relieved by any thalamic lesion. Thalamotomy is a long established procedure used to help parkinsonian tremor. Appropriately placed thalamotomy should be considered for the relief of disabling peak dose dyskinesia, which is predominantly choreic, in parkinsonian patients on otherwise successful levodopa therapy.
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PMID:The use of thalamotomy in the treatment of levodopa-induced dyskinesia. 158 Jan 97

The causes of symptomatic parkinsonism are enumerated and discussed including drug-induced, vascular, toxic, postencephalitic and posttraumatic parkinsonism. The environmental hypothesis and the concept of oxidative stress in the pathogenesis of Parkinson's disease are illustrated. The clinical diagnosis, the differential diagnosis and the possible diagnostic errors originating from the cardinal symptoms akinesia, rigor und tremor in the early stages of the disease are delineated. At last the contributions of EEG, CCT, evoked potentials, MRI, PET und the apomorphine test to the diagnosis especially early diagnosis are evaluated.
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PMID:[Current aspects in diagnosis of Parkinson disease]. 158 88

We report an autopsy case of a 73 year-old female with idiopathic parkinsonism, characterized pathologically by the wide spread appearance of Lewy bodies (LBs) not only in the pigmented neurons in the midbrain and brainstem but also in the cerebral cortex. Initial symptoms at the age of 62 were finger tremor and gait disturbance, which were followed mainly by mental deterioration, such as regression, dependency, auditory hallucination, depression, emotional incontinence, and a personality change. In the terminal stage, nuchal stiffness in extension, one of the hallmarks of progressive supranuclear palsy, and slow and generalized tremor in all 4 extremities were noted. She died of aspiration pneumonia. The brain was somewhat small and weighed 1100 g after the fixation by formalin. Macroscopical findings included mild cerebral atrophy with mild pial thickening both in the frontal and temporal lobes and slight expansion of the ventricular system. Histopathologically, severe loss of neuronal cells in both the pallidum and Luy's body and moderate loss of large cells in the putamen were noted in addition to the typical findings of Parkinson's disease in the substantia nigra and locus caeruleus including neuronal cell loss, depigmentation, and gliosis. These findings in the basal ganglia were more conspicuous than the two controls of classical Parkinson's disease. The distribution, stainability in the routine methods of staining, and shape of Lewy bodies in the cerebral cortex conformed to those of previous reports. The similar case reports in the literatures do not seem to have paid much attention to the findings of the basal ganglia observed in our case.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An autopsy case of idiopathic parkinsonism with numerous Lewy bodies in the cerebral cortex--diffuse Lewy body disease]. 165 48

The authors studied motor associated brain potentials (MABP) in patients with disturbed motor function (hypertonia, tremor) due to affection of the basal ganglia (parkinsonism) and studied the changes of these potentials after stereotaxic operations conducted for the correction of the motor pathology. It was found that in a favourable effect of operative treatment manifested by decrease of the tonus and inhibition of tremor in patients with parkinsonism, there was a tendency towards normalization of MABP. Restoration of some of the components of the motor response and in certain cases of the MABP on the whole occurred on the 14-16th postoperative day. No clearly defined changes of motor associated potentials characteristic of different forms of parkinsonism were discovered.
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PMID:[Movement-related brain potentials during the treatment of parkinsonism]. 166 36

Abnormally increased subthalamic nucleus output to the internal pallidal segment and the reticular part of the substantia nigra plays a critical pathophysiological role in the development of parkinsonism. Because synaptic transmission of subthalamic output is glutamatergic and mediated, in part, by the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) subtype of glutamate receptor, AMPA receptor antagonists may possess antiparkinsonian properties. We report that in monoamine-depleted rats, 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)quinoxaline (NBQX) (Novo-Nordisk, Copenhagen, Denmark)--a selective antagonist of the AMPA subtype of glutamate receptor--suppressed muscular rigidity but had no effect on akinesia. NBQX microinjected into the subthalamic nucleus, internal pallidal segment, and reticular part of the substantia nigra, but not into the laterodorsal neostriatum of the rats, stimulated locomotor activity and reduced muscular rigidity. In aged Rhesus monkeys with bilateral 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced parkinsonism, intramuscular NBQX produced clinically apparent improvement in akinesia, tremor, posture, and gross motor skills. NBQX also potentiated the antiparkinsonian effects of L-3,4-dihydroxyphenylalanine in both rats and monkeys. Blockade of excitatory synaptic transmission by AMPA receptor antagonists may provide a new therapeutic strategy for Parkinson's disease (PD).
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PMID:The AMPA receptor antagonist NBQX has antiparkinsonian effects in monoamine-depleted rats and MPTP-treated monkeys. 166 77

We evaluated 21 right-handed psychiatric patients with tardive dyskinesia (TD) for the presence and laterality of neuroleptic-induced tremor and rigidity. The goals of the study were to assess the frequency and coexistence of TD and neuroleptic-induced parkinsonism (NIP) using instrumental and clinical measurements and to evaluate the hypothesis that when TD and NIP coexisted in the same patient, they were more likely to appear in opposite limbs. Results indicated that a high percentage of TD patients had coexisting rigidity and tremor on the basis of both clinical ratings and instrumental procedures; however, only instrumental procedures were useful in identifying tremor and rigidity asymmetries. We found that TD and tremor or rigidity did not lateralize to opposite limbs, thus weakening the hypothesis that TD and NIP stemmed from reciprocal pathophysiological mechanisms.
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PMID:Clinical and instrumental assessment of neuroleptic-induced parkinsonism in patients with tardive dyskinesia. 167 45

Drug-induced parkinsonism is usually reversible, except in a small percentage of elderly patients. We describe two relatively young patients, who developed drug-induced parkinsonism during chronic treatment with neuroleptics for a psychotic disorder. Parkinsonism persisted, and markedly and progressively deteriorated after discontinuation of neuroleptic drugs. One patient had tremor as the most prominent sign and the other had mainly an akinetic-rigid syndrome. Neither had ever developed tardive dyskinesia. Both responded to levodopa therapy. Persistent drug-induced parkinsonism in our, and other reported on, elderly patients may be due to unmasking of preexisting subclinical idiopathic Parkinson's disease by neuroleptics. Theoretically, these drugs may precipitate degeneration of vulnerable, nigrostriatal neurons by generating cytotoxic free radicals or by attrition, due to accelerated neuronal firing rates.
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PMID:Persistent and progressive parkinsonism after discontinuation of chronic neuroleptic therapy: an additional tardive syndrome? 167 33

Six patients autopsied by the neuropathology service at UMDNJ-Robert Wood Johnson Medical School between 1985 and 1988 had pathologically typical Lewy-body Parkinson's disease (PD). Review of their clinical records revealed that none had clinically typical PD. Atypical clinical features included juvenile onset, retrocollis, strong family history, and absence of tremor, flexed posture, or levodopa response. One patient had dementia without parkinsonism. We conclude that the clinical spectrum of Lewy-body PD is wider than is generally assumed and that the diagnosis of pathologically typical Parkinson's disease cannot be excluded on clinical grounds alone.
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PMID:Clinically atypical expression of pathologically typical Lewy-body parkinsonism. 168 15

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


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