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)

The pathophysiology of dystonia is unclear, but several clues implicate striatal dopamine dysfunction. In contrast, the causal relationship between striatal dopamine deficiency and parkinsonism is well defined. We now suggest that parkinsonism or dystonia may occur following striatal dopamine deficiency. Baboons treated with intracarotid 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) developed transient hemidystonia prior to hemiparkinsonism. The day after MPTP treatment, most animals had spontaneous ipsilateral turning. Within a few days, all developed contralateral hemidystonia, with the arm and leg extended and externally rotated. This transient dystonia preceded hemiparkinsonism with flexed posture, bradykinesia, and postural tremor that persisted for up to 1.5 years. Dystonia corresponded temporally with a decreased striatal dopamine content and a transient decrease in D2-like receptor number. The time course of dystonia and parkinsonism is analogous to lower limb dystonia as the first, frequently transient, symptom of Parkinson's disease in humans. The association of striatal dopamine deficiency with dystonia and parkinsonism implies that other factors influence clinical manifestations.
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PMID:MPTP induces dystonia and parkinsonism. Clues to the pathophysiology of dystonia. 937 34

A 66-year-old woman presented with a 3-year history of predominantly right-sided blepharospasm and a 1-year history of progressive predominantly left-sided hemiparkinsonism manifested by a left upper extremity resting tremor and left-sided bradykinesia. Magnetic resonance imaging of the brain revealed a large right mesencephalic cyst with mass effect. Positron emission tomography revealed bilateral striatal hypometabolism consistent with nigrostriatal dopaminergic dysfunction. The association of predominantly ipsilateral blepharospasm and predominantly contralateral hemiparkinsonism is very rare, and its association with a posterior fossa space-occupying lesion has been reported only once. This is the second report of such an association and the first description of adult-onset symptomatology.
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PMID:Asymmetric predominantly ipsilateral blepharospasm and contralateral parkinsonism in an elderly patient with a right mesencephalic cyst. 945 38

Five female adult Macaca nemestrina monkeys, given a unilateral intracarotid (ic) infusion of 2.3-3.5 mg of MPTP-HCl, were studied for 6-8 years. Two to 3 days after MPTP, the animals developed hemiparkinsonism characterized by rigidity and flexed posture of the arm contralateral to the side of infusion with episodes of tremor, circling ipsilateral to the lesioned side, a slight balance disturbance, and stooped posture. Rating of parkinsonian features 4 months after ic infusion, and yearly thereafter, did not show any statistically significant changes. The animals maintained their usual appetite and body weight increased normally. Each animal responded to l-DOPA methyl ester with decreased parkinsonian signs and symptoms and increased contralateral turning. In contrast, after control vehicle administration, the animals continued to have the same parkinsonian signs and predominant ipsilateral turns. In three of the five monkeys, contralateral turns after vehicle significantly increased after 6-8 years. Unilateral intracarotid MPTP induced asymmetric motor behavior that remained stable after 6-8 years. Animals that showed an increased frequency of contralateral circling after control vehicle showed a decrease in contralateral turns after l-DOPA methyl ester, suggesting neuroplastic changes over the years.
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PMID:MPTP-Induced hemiparkinsonism in nonhuman primates 6-8 years after a single unilateral intracarotid dose. 971 May 20

A 58-year-old Chamorro female patient, who died in 1993, was examined clinicopathologically. At the age of 51, she suffered from hemiparkinsonism, then bradykinesia, rigidity without tremor, and dementia. Extrapyramidal symptoms developed, and at the age of 57, vertical gaze palsy was noted. The clinical diagnosis was parkinsonism-dementia complex (PDC) with vertical gaze palsy. The brain showed atrophy in the frontal and temporal lobes, and the atrophy was accentuated in the dentate gyrus, Ammon's horn and parahippocampal gyrus. The basal ganglia, thalamus and midbrain were moderately atrophic. The substantia nigra and locus ceruleus were completely depigmented. Numerous neurofibrillary tangles (NFTs) were seen in the subiculum and amygdaloid nucleus. Many NFTs were evident in the parahippocampal gyrus, lateral occipitotemporal gyrus, insula, Sommer sector, basal nucleus of Meynert, lateral nucleus of the thalamus, subthalamic nucleus and brain stem, and several were observed in the globus pallidus and hypothalamus. The Sommer sector, substantia nigra, locus ceruleus and basal nucleus of Meynert showed severe loss of neurons, and a moderate loss of neurons was exhibited by the globus pallidus. These findings were apparently consistent with those associated with PDC. However, in this patient, severe neuronal loss was seen in the subthalamic nucleus and lateral nucleus of the thalamus, and grumose degeneration, which has not previously been reported in PDC, was seen in the dentate nucleus. In addition, many tufted astrocytes, which have been reported to occur in progressive supranuclear palsy (PSP) and postencephalitic parkinsonism, but scarcely observed in PDC, were present. Furthermore, astrocytic plaques, which have been considered as a specific finding of corticobasal degeneration (CBD), were observed in the cerebral cortex. On the other hand, granular hazy astrocytic inclusions, previously reported to occur in PDC, were not seen. Chromatolytic neurons were not observed. The question thus arises as to whether it is appropriate to consider this patient as having suffered from a combination of PDC, PSP and CBD. From the view points of absence of granular hazy astrocytic inclusions and chromatolytic neurons, and of tufted astrocytes in the neostriatum, it is conceivable that this patient is a case of a new disease entity.
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PMID:Parkinsonism, dementia and vertical gaze palsy in a Guamanian with atypical neuroglial degeneration. 1065 Oct 31

Several neurological conditions have been reported to be associated with peripheral or central deficits of olfactory system. In recent years particular emphasis has been placed on the early and severe olfactory impairment in Parkinson's disease (PD), in which limited neuropathological studies have revealed a marked dopaminergic deficit in the olfactory tubercles. Moreover, indirect evidence suggests that dysfunction of the dopaminergic pathways from mesencephalon to the piriform cortex may play a role in olfactory impairment in PD. A large number of clinical studies have reported that olfactory loss in idiopathic PD is bilateral, present in hemiparkinsonism, unrelated to the stage or clinical subtype of the disease, and independent of antiparkinsonian medication. In addition, major olfactory alterations have been reported in familial PD and dementia with Lewy bodies but not in progressive supranuclear palsy and essential tremor. These findings might stimulate further research targeted to determine the biological substrate of dissimilar olfactory performances in these movement disorders. The present review summarizes standardized procedures for the assessment of olfactory acuity (detection threshold), identification (multiple choice odor naming), discrimination (differentiation between similar/dissimilar odorants), and memory (recognition of a substance previously smelled). Specific suggestions concerning the psychometric and neuropsychological evaluation of PD patients are provided.
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PMID:Olfaction in Parkinson's disease: methods of assessment and clinical relevance. 1075 Nov 9

A 66-year-old woman presented with a 3-year history of progressive right-sided hemiparkinsonism manifested by a right-hand resting tremor and right-sided bradykinesia. Magnetic resonance imaging (MRI) of the brain revealed a non-enhanced polycystic mass in the left midbrain. (11)C-methylspiperone ((11)C-NMSP) and (18)F-fluorodopa ((18)F-DOPA) positron emission tomography (PET) revealed a striatal hypometabolism that was restricted to the left side. These findings are consistent with a dysfunction in the left nigrostriatal dopaminergic pathway that is presumably induced by the cystic mass in the left midbrain. This case is significant due to the paucity of reports regarding the occurrence of a relatively pure parkinsonism that is associated with a mesencephalic space-occupying lesion.
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PMID:Hemiparkinsonism associated with a mesencephalic tumor. 1199 73

We analyzed parkinsonian features in multiple system atrophy (MSA) compared with age- and disease duration-matched Parkinson's disease (PD) patients, and assessed the applicability of the Unified Parkinson's Disease Rating Scale (UPDRS) -III motor scale as a means of rating their severity. Cross-sectional analysis of parkinsonism was done using UPDRS-III, International Cerebellar Atatia Rating Scale, and disability scales (Hoehn and Yahr [H&A], Schwab and England, Katz and Lawton) in 50 unselected MSA patients and in 50 matched PD patients. At symptom onset, falls occurred 10 times more frequently in MSA, whereas limb tremor was 10 times more common in PD. At first visit (10.2 months), hemiparkinsonism and pill-rolling rest tremor were less common in MSA. Hypomimia, atypical rest, postural or action tremor, as well as postural instability were more frequent in MSA. At study examination (62.4 months), parkinsonian signs in MSA patients were more frequently symmetrical and associated with axial rigidity, antecollis and postural instability. A levodopa response of >50% was seen in <10% of MSA patients. Modified H&Y stages (3.2 +/- 1.3 vs. 2.2 +/- 0.78) and UPDRS-III scores (48.14 +/- 19.5 vs. 31.74 +/- 12.9) were significantly (P = 0.0001) higher in MSA. The internal consistency of the UPDRS-III was fair in MSA patients (Cronbach's alpha >0.90), and correlated well with marked dependency on the Schwab and England and Katz and Lawton scales. Factor structure analysis of UPDRS-III in MSA showed five clinically distinct subscores accounting for 74% of the variance, differing from PD by the dependency of the face-speech and limb bradykinesia items and independence of the postural-action tremor from the rest tremor items. There was a significant correlation (R(2) = 0.70, P = 0.001) between ICARS ataxia and UPDRS-III scores in MSA patients. Results confirm a distinct profile of parkinsonism in MSA and greater severity and disability compared with PD. It also indicates that the UPDRS-III provides a useful severity measure of parkinsonism in MSA, albeit contaminated by additional cerebellar dysfunction.
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PMID:Parkinsonism in multiple system atrophy: natural history, severity (UPDRS-III), and disability assessment compared with Parkinson's disease. 1221 Aug 59

A 54-year-old woman was admitted to our hospital because of left-sided rigidity. Neurological examination revealed cogwheel-type rigidity in the left upper and lower limbs without tremor. A brain MRI showed no abnormal findings. She was diagnosed as having left-sided hemiparkinsonism. A 99mTc-ECD SPECT detected a decrease in regional cerebral blood flow (rCBF) in the right corpus striatum. Administration of levodopa/DCI (100 mg/day) improved not only her left-sided rigidity but also the rCBF in the right corpus striatum. The ratio of rCBF in the right corpus striatum to that in the left corpus striatum increased from 96.03% to 99.26% on the three-dimensional stereotactic ROI template. These findings suggest that L-dopa may directly activate the metabolism in the bilateral corpus striatum, and that rCBF in the corpus striatum may be increased indirectly according to the increase of movement in the legs. And also it is suggested that denervation supersensitivity to dopamine may exist in the corpus striatum on the contralateral side of the signs and symptoms in this patient with hemiparkinsonism.
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PMID:[Increase in regional cerebral blood flow of striatum induced by low dose levodopa in a patient with hemiparkinsonism]. 1538 6

We present a patient with tremor-dominant hemiparkinsonism after a focal lesion to the substantia nigra. An excellent response to levodopa was complicated by rapid development of motor fluctuations and disabling dyskinesias. Stereotactic thalamotomy resulted in a persistent extinction of parkinsonism and of dyskinesias along with stopping dopaminergic treatment.
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PMID:Hemiparkinsonism and levodopa-induced dyskinesias after focal nigral lesion. 1707 68

Controversy exists as to whether muscle weakness is present in Parkinson's disease (PD). Computerized literature searches identified clinical trials and reviews about muscular strength assessment in patients with Parkinson's disease, using the following databases: PubMed, Ovid MEDLINE, Ovid EMBASE, the Cochrane Database of Systematic Reviews, Cumulative Index to Nursing and Allied Health Literature, and Physiotherapy Evidence Database. Seventeen articles fulfilled all criteria for selection. These studies suggested that isokinetic muscle strength was decreased in patients with Parkinson's disease and that muscle weakness was not specifically related to tremor or rigidity. Bilateral asymmetrical muscle weakness was present in Parkinson's disease when presenting with clinical unilateral hemiparkinsonism. Recent studies using sensitive mechanical devices have provided evidence that muscle strength is reduced in patients with Parkinson's disease compared with age-matched controls. The specific cause of this weakness is not known. Questions under debate were whether this weakness was of central or peripheral origin and whether it was intrinsic to the disease or a secondary phenomenon.
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PMID:Is there muscular weakness in Parkinson's disease? 1948 24


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