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)

Some investigators have proposed that Parkinson's disease (PD) patients often exhibit a worsening of tremor before the emergence of levodopa-induced dyskinesia (LDD). It is not clear, however, whether the presence of tremor depends on the severity of dyskinesia, nor is the precise time course of tremor relative to dyskinesia well understood. This report describes an objective study of the relationship between postural tremor and dyskinesia in eight PD patients who showed signs of choreoathetoid hand movements after a single dose of levodopa. Spectral analysis of sustained hand force provided an objective and sensitive method of detecting worsening of tremor in patients with LDD. Severity of clinical symptoms was highly correlated with severity of dyskinesia. Six of the patients exhibited increased tremor amplitude within 45 min of exposure to levodopa, with two of the six patients experiencing bilateral and four of the six having unilateral worsening of postural tremor. Tremor was more severe on the side with the more severe dyskinesia. These findings provide objective support for the notion that dyskinesia and postural tremor may stem from a common pathophysiologic mechanism.
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PMID:Worsening of postural tremor in patients with levodopa-induced dyskinesia: a quantitative analysis. 850 41

We report a right-handed 78-year-old man with early onset parkinsonism. The patient had an onset of micrographia at 23 years of the age in 1939. Seven years later he started to drag his right foot, and at 38 years of age, he walked with small steps with festination. Tremor was also present in his right hand. His daily life was independent as a otorhinolaryngologist. He visited our clinic on March 24, 1977 when he was mentally sound and showed mild parkinsonism consisting of masked face, stooped posture, small step gait, bradykinesia, and right side dominant rigidity and tremor. He showed good response to trihexyphenidyl and amantadine HCl. Two month later, he developed dyskinesia and some worsening of parkinsonism, and was admitted to our hospital for the first time. He was treated with 400 to 600 mg/day of levodopa/ carbidopa. He showed marked improvement, however, dyskinesia remained in his mouth. He was doing well until 77 years of age (June of 1993) when he developed hallucination and motor fluctuations. He was admitted again to our hospital on June 22, 1993. On admission, he was alert and appeared mentally sound. However, Hasegawa dementia scale was 18/30. Upward gaze was slightly restricted (3/5). Voice was somewhat small but no masking was noted. His posture was stooped and the gait was of small step. Dyskinesia was noted during walk. No rigidity nor tremor was noted. Deep tendon reflexes were lost but no sensory loss or motor weakness was noted. Routine laboratory studies were unremarkable. A cranial CT scan revealed only mild to moderate cortical atrophy. Motor and sensory conduction velocities were within normal limits, however, motor action potentials could not be obtained with stimulation to the right common peroneal nerve. He was treated with 600 mg/day of levodopa with carbidopa, 100 mg of amantadine HCl, 300 mg of Dops, and 25 mg of tiapride. He continued to show motor fluctuations, and was discharged on July 23, 1993. Since then his motor functions had become progressively worse with frequent falls, but he was still able to walk without support. On October 3 of 1994, he went to bed as usual. On the next morning, he was found dead in his bed at 9: 30. The patient was discussed in neurological CPC, and the chief discussant arrived at the conclusion that the patient had young-onset Parkinson's disease with Lewy bodies in the substantia nigra. Opinions were divided between Parkinson's disease and Lewy body negative young onset parkinsonism. Postmortem examination revealed obstruction of the trachea by aspirated foods, and the cause of death appeared to have been suffocation by the foods. Macroscopically, the external appearance of the brain was unremarkable except for slight frontal atrophy. The substantia nigra showed depigmentation in the lateral part, but the pigmentation of the medial part was well preserved. Upon histologic examination, the number of pigmented neurons in the dorsomedial part was well preserved. In the lateral part, pigmented neurons were well preserved in the dorsal area, however, in the ventral area, only non-pigmented neurons were seen; they appeared to be neurons in the pars reticulata. No gliosis was seen in any of the nigral areas. No Lewy bodies were seen in the remaining neurons. So-called immature neurons with rounded shape without neuromelanin could not be detected. The locus coeruleus neurons were well preserved. The putamen and the other basal ganglia structures were also intact. Slight myelin pallor was noted in the subcortical white matter, however, otherwise cerebral cortices were normal. The histology of this patient is unique in that only the ventrolateral part of the substantia nigra showed abnormal finding consisting of lack of pigmented neurons without gliosis. It is not clear whether the nigral change represents degeneration or a congenital "hypoplasia'. To our knowledge, such a unique pathology of the substantia nigra has not been reported in the literature. Our patient ma
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PMID:[A 78-year-old man with young onset parkinsonism and sudden death]. 867 9

We present the clinical features of 17 patients from 12 Japanese families with familial juvenile parkinsonism suggesting autosomal-recessive inheritance (AR-JP). Because the marriages of the parents in all but one family were consanguineous and all patients were only first generation, an autosomal-recessive trait was strongly suspected. Analysis of the clinical features showed female predominance, mean age at onset 27.8 years, and slow progression. The symptoms of the parkinsonian triad (tremor, rigidity, and bradykinesia) were mild, but gait freezing, hyperreflexia, foot dystonia, and retropulsion were relatively prominent. A characteristic finding was amelioration of parkinsonian symptoms after sleep in all patients. Response to levodopa was satisfactory, but dopa-induced choreic limb dyskinesia and wearing-off phenomenon occurred frequently. Juvenile parkinsonism is a syndrome that encompasses several clinical entities. The similarity of clinical findings in these patients, and the differences from other types of parkinsonism, indicates that AR-JP is distinct clinical entity.
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PMID:Clinical analysis of 17 patients in 12 Japanese families with autosomal-recessive type juvenile parkinsonism. 871 71

Regional cerebral glucose metabolism (rCMRGlu-18FDG) was measured in 6 cases with rigid type Parkinson's disease (PD) (2 cases with dopa-induced dyskinesia = DID), 6 cases with chorea (Ch), 5 cases with essential tremor (EssT) and 2 cases with normal subjects (N). The effects of L-Dopa on rCMRGlu was studied in 3 cases with PD. With the aid of depth microrecording study, stereotactic pallidotomy was performed in all cases with PD. Thalamotomy was performed in 3 cases with Ch. In the EssT and N group, the metabolic pattern was high in the frontal cortex (FCx) but low in the lenticular nucleus (LN). In contrast, all cases with a rigid type PD showed lower rCMRGlu in FCx (premotor, prefrontal area). However, 4 out of 6 cases were higher in LN than the control group. Administration of L-Dopa shifted rCMRGlu toward the normal pattern in this group. Five out of 6 cases with Ch represented higher rCMRGlu in FCx (3 focal, 2 diffuse) but lower in LN. Moreover, when DID occurred, it showed almost the same pattern as in Ch. Electrophysiological studies showed high background neuronal activity (BNA) in the medial segment of the globus pallidus (GP) but low BNA in the lateral segment of the GP in the rigid type of PD. In cases with Ch, irregular burst discharges were often encountered in ventro-oral thalamus. From these results, the on-going changes of basal ganglia-thalamocortical motor circuit in cases with a rigid type PD, DID and Ch are discussed. The underlying mechanisms of Parkinsonian rigidity was considered to contrast with those of DID and Ch within the same motor circuit.
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PMID:Parkinsonian rigidity, dopa-induced dyskinesia and chorea--dynamic studies on the basal ganglia-thalamocortical motor circuit using PET scan and depth microrecording. 874 74

Factors at presentation which influenced the course of the disease and response to treatment were assessed in 125 de novo patients with Parkinson's disease. Ninety-eight patients were available for re-assessment at 5 years. Older patients presented earlier after the onset of symptoms, deteriorated more rapidly, and were significantly more likely to develop dementia and impairment of balance. Increasing age and symmetrical disease predicted the new appearance of imbalance. Age of onset did not predict dyskinesia or end of dose failure. A low tremor score at baseline and female gender were predictive of the early appearance of dyskinesia. Patients who experienced end of dose failure were taking a significantly higher dose of levodopa. Once dose and duration of treatment were corrected for, no baseline features were predictive of end of dose failure. The dose of levodopa at 5 years was positively correlated to baseline disease severity as measured by the Columbia score. We conclude that the age of onset of symptoms of Parkinson's disease is a major determinant of the course of the disease and response to treatment.
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PMID:Age at onset: the major determinant of outcome in Parkinson's disease. 875 Jan 10

The purpose of this study was to determine the prevalence and functional and diagnostic correlates of reported shaking in the community-dwelling elderly. We conducted a standardized neurological evaluation of 1,056 nondemented Medicare recipients in Washington Heights-Inwood, Northern Manhattan (New York). Of 1,056 patients, 108 reported shaking (10.2%). The prevalence of reported shaking did not increase with age. It did differ between ethnic groups, but when adjusted for depression and score on the Schwab and England Activities of Daily Living (ADL) scale, this difference was insignificant. The age-adjusted prevalence was similar for women and men. Neurological examination of the 108 who reported shaking showed that 8.3% had tremor at rest, 17.6% had tremor with action, 5.6% had dyskinesia or chorea, and an additional 28.7% had various problems in coordination or movement. The remaining 39.8% had neither tremor nor problems in coordination or movement. Only 2.9% of individuals with reported shaking had Parkinson's disease (PD), 8.7% had essential tremor, and 2.1% had oral-buccal-lingual dyskinesia. Of the remaining 86.3%, 29 (31%) had no identifiable medical condition. Those who reported shaking were less independent with ADLs, regardless of presence of tremor on examination. Shaking is commonly reported by the community-dwelling elderly. It does not necessarily identify individuals with essential tremor and PD, and is related to decreased independence in ADLs.
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PMID:Prevalence of a history of shaking in persons 65 years of age and older: diagnostic and functional correlates. 877 Oct 69

In schizophrenic patients in maintenance treatment, clozapine, compared to classic neuroleptics, induces relatively few extrapyramidal syndromes (EPS), especially less akathisia and tremor and usually no dystonia or rigidity. In patients with dyskinetic movements (acute or tardive) induced by other neuroleptics, clozapine may reduce or even remove dyskinesia or permit it to disappear. It cannot, however, be excluded that clozapine can induce dyskinesia in extremely rare cases, but it seems more likely that this is due to previous treatment with classic neuroleptics. The earlier clozapine is started, the less chance of development of dyskinesia. The low level of EPS with clozapine may be linked to the special receptor-binding profile of this drug: during treatment with therapeutic doses of clozapine, the level of D2 receptor blockade is too low (40% to 50% occupancy by positron emission tomography) to induce EPS, and the D1 receptor blockade (also 40% to 50% occupancy) has a lower EPS potential than D2 blockade. This binding profile may at the same time contribute to the special antipsychotic properties of clozapine. Other receptor affinities may contribute to the beneficial effect of clozapine in EPS and schizophrenia.
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PMID:Extrapyramidal symptoms during long-term treatment with antipsychotics: special focus on clozapine and D1 and D2 dopamine antagonists. 886 42

Although there is a consensus that orofacial and limbtruncal subtypes of tardive dyskinesia (TD) exist and may represent distinct pathophysiologic entities, few studies have examined the incidence of and risk factors associated with the development of these TD subtypes. Two hundred and sixty-six middle-aged and elderly outpatients with a median duration of 21 days of total lifetime neuroleptic exposure at study entry were evaluated at 1- to 3-month intervals. Using "mild" dyskinesia in any part of the body for diagnosis of TD, the cumulative incidence of orofacial TD was 38.5 and 65.7% after 1 and 2 years, respectively, whereas that of limbtruncal TD was 18.6 and 32.6% after 1 and 2 years. Preclinical dyskinesia was predictive of both orofacial and limbtruncal TD. History of alcohol abuse or dependence was a significant predictor of orofacial TD only whereas tremor was a significant predictor of limbtruncal TD only. Findings support suggestions that orofacial and limbtruncal TD may represent specific subsyndromes with different risk factors.
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PMID:Risk factors for orofacial and limbtruncal tardive dyskinesia in older patients: a prospective longitudinal study. 886 68

Twenty-eight centers completed a survey about their current practice of pallidotomy. This sample represents a non-exhaustive survey of the current practice of pallidotomy in North America and is not a study of outcomes. 1015 patients underwent 1219 pallidotomies: 811 (80%) unilateral, 72 (7%) staged bilateral, and 132 (13%) simultaneous bilateral. Pallidotomy has long been an accepted procedure and the indications for this surgery, in the opinion of the responding centers, were rated on a scale of 1 (poor) to 4 (excellent) and demonstrated dyskinesia as the best indication (median = 4); on-off fluctuations, dystonia, rigidity, and bradykinesia as good indications (median = 3); and freezing, tremor and gait disturbance as fair indications (median = 2). Most centers used MRI alone (50%) or in combination with CT scan (n = 6) or ventriculopathy (n = 5) to localize the target. The median values of pallidal coordinates were: 2 mm anterior to the midcommissural point 21 mm lateral to the midsagittal plane and 5 mm below the intercommissural line. Microrecording was performed by half of the centers (n = 14) and half of the remaining centers were considering starting it (n = 7). Main criteria used to define the target included the firing pattern of spontaneous neuronal discharges (n = 13) and the response to joint movement (n = 10). Most centers performed motor (n = 26) and visual (n = 23) macrostimulation. Twenty four centers performed test lesions using median values of 55 degrees C temperatures for 30 s. Final lesions consisted of 3 permanent lesions placed 2 mm apart, each lesion created with median values of 75 degrees C temperatures for 1 minute. Median hospital stay was 2 days.
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PMID:Pallidotomy: a survey of current practice in North America. 888 Jul 89

We report a 43-year-old woman who died after 18 years history of parkinsonism. She was well until 25 years of the age (1976) when she noted a difficulty in stepping her feet. In the next year, she started to drag her feet. She was treated with levodopa with good response, however, she developed dyskinesia when she was 33 years of the age. She was evaluated in another hospital in 1984. She showed normal intelligence, normal ocular movement, masked face, small voice, small step gait, stooped posture, freezing of the gait, retropulsion, and cogwheel rigidity in limbs. No tremor or ataxia was noted. She received left ventrolateral thalamotomy at that time. Rigidity on the right side markedly reduced, however, she continued to show bradykinesia and motor fluctuations. On August 1 of 1994, she developed fever of 40 degrees C and dyspnea. On the next day, she expired from acute respiratory distress. She was able to walk unsupported until just before her last admission. The patient was discussed in a neurological CPC. The chief discussant arrived at the conclusion that this patient had Lewy body-positive young onset Parkinson's disease. Opinions were divided into two groups, i.e., young onset Lewy-body positive Parkinson's disease and Lewy-body negative young onset parkinsonism. Post-mortem examination revealed moderate loss of pigmented neurons in the substantia nigra more in the ventro-lateral part. Lewy bodies were found in the remaining neurons. Lewy bodies were more frequently seen in the locus coeruleus, although neuronal loss was less prominent in the locus coeruleus. The dorsal vagal motor nucleus showed moderate loss of neurons. Otherwise, the central nervous system was unremarkable. To our knowledge, this patient had the second youngest age of the onset so far reported in the literature for Lewy-body positive typical Parkinson's disease.
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PMID:[A 43-year-old woman with 18 years history of parkinsonism]. 892 38


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