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)

Parkinson's disease is a neurodegenerative disorder characterized mainly by damage to the dopaminergic nigrostriatal system. Recently, the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been shown to induce damage in the nigrostriatal system, accompanied by Parkinson-like symptoms in humans. We present here evidence that MPTP treatment in aged 21-month-old mice produced a marked reduction in the presence and intensity of fluorescence in noradrenergic neurons of the locus coeruleus and in dopaminergic neurons of the ventral tegmental area in addition to extensive damage to the substantia nigra. Aged mice treated with MPTP also showed physical signs of movement disability characterized by marked akinesia, rigidity of the hind limbs, and an initial resting tremor of the entire body. Such symptoms were less evident in young mice treated with MPTP. These remarkable initial behavioral effects of MPTP treatment in aged mice and evidence of reduced catecholamine fluorescence in the locus coeruleus and ventral tegmental area suggest that aged mice are more sensitive to, and more severely affected by MPTP treatment than young mice. We suggest that these MPTP-treated aged mice provide a useful animal model for studying both anatomical and functional characteristics of Parkinson's disease.
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PMID:Aged mice are more sensitive to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine treatment than young adults. 349 Jun 39

Thalamic targets in the treatment of involuntary movements include the lateral and usually the intermediary ventral nuclei. Destruction of their afferents in Forel's fields provides the same therapeutic result but the size of the lesion must then be very small due to the proximity of essential structures, particularly corpus Luysi. Efficacy of treatment depends partly on the aetiology of the involuntary movement (and thus from the indication for surgery) and also on the technical possibilities of electrophysiologic mapping. The true dystonic element of the involuntary movement is usually little improved whereas tremors of all types are improved or suppressed. Essential tremor, familial or not, of large amplitude and very disabling, is an ideal indication for stereotaxic surgery when it presents as intention tremor. In Parkinson's disease, the treatment is effective against tremor and rigidity but akinesia is unaltered and the progressive course of the disease uninterrupted. Indications for surgery have become rare since the availability of L-dopa, perhaps too rare for the slowly progressive forms with predominant tremor poorly relieved by dopa-therapy, surgery has a curative and probably preventive effect on the involuntary movements of limbs induced by this treatment. Suppression of post-traumatic tremor and that due to multiple sclerosis is dependent on various factors: electrophysiologic precise mapping of the target since "electrical silences or holes" exist that disturb or prevent collection of evoked potentials or spike activity; multiple neurologic lesions that may be worsened by an additional thalamic lesion; finally residual cerebellar disturbance unmasked by the suppression of tremor, a poor "functional" result despite a good operative result.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of abnormal movements by thalamic lesions]. 353 89

The motor score with and without levodopa was estimated in 193 parkinsonian patients with variable length of evolution. The effect of levodopa on akinesia, rigidity, and tremor remained quite stable during the course of the disease. In contrast, the aggravation of gait disorder, postural instability, and dysarthria was more severe, with decreased percentage of improvement on levodopa in patients with longer evolution. It is suggested that aggravation of Parkinson's disease mainly results from increasing severity of cerebral nondopaminergic lesions.
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PMID:Does long-term aggravation of Parkinson's disease result from nondopaminergic lesions? 362 54

The long-term effects of mesulergine, a new drug with dopamine agonistic properties, were studied in 28 patients with Parkinson's disease. In 18 patients with late side effects of levodopa, the addition of mesulergine (10.9 mg/day) induced significant decreases in the global (-48%), rigidity (-62%), and akinesia (-37%) scores. The drug was found to be very effective on tremor (-71%). Mesulergine was useful in cases of inefficacy of levodopa alone or persistent intolerable side effects. The decrease in levodopa dose and the addition of mesulergine permitted a significant reduction in dyskinesia. Used as sole therapeutic agent (10.9 mg/day), mesulergine was found to be active on tremor and rigidity scores but not on akinesia or global scores. Mesulergine induced few side effects. These results show the antiparkinsonian properties of mesulergine that seem to be of significant therapeutic value in patients with tremor or in combination with levodopa.
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PMID:Mesulergine (CU 32-085) in the treatment of Parkinson's disease. 370

L-Dopa was administered to 122 patients with Parkinson's disease over a time period up to 14 years. The results were summarized below. The akinesia and postural instability scores were significantly improved up to the 9th year. The rigidity and static tremor scores and the Parkinson score were significantly improved up to the 11th year. The Yahr stage was significantly improved up to the 8th year. The time course of Parkinson score was investigated in three groups, Yahr stage I/II group, Yahr stage III group, and Yahr stage IV/V group, taking into account the time interval between the onset of the disease and initiation of L-dopa therapy. No significant difference was found among the three groups. The above results suggested that the long-term prognosis of patients on L-dopa therapy in Japan was better than in Western countries. It was also though that L-dopa therapy should be instituted at the earliest possible stage of the disease.
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PMID:An analysis of long-term L-dopa therapy in 122 cases of Parkinson's disease over 14 years--when should L-dopa therapy be initiated? 374 58

Forty-four Parkinson patients (19 patients of the rigid-akinetic type, 13, of the rigid-akinetic-tremor type, and 12, of the tremor type) were included in a study in order to analyse correlations of the expression of the motor symptoms tremor, rigidity, akinesia, with other clinical parameters, computertomographic aspect of brain atrophy and psychometrically assessed cognitive parameters. Rigidity and akinesia are significantly positively correlated with the severity of motor dysability, stage of the disease, and brain atrophy, as is akinesia with a history of pharmacotoxic psychosis. Tremor is significantly negatively correlated with motor dysability, stage of the disease, and history of pharmacotoxic psychosis. Akinesia is correlated with visuomotor dysfunction (tested with Bender Gestalt Test) and rigidity with the depression score (Zung scale). The tremor type is favorable, the rigid-akinetic type unfavorable with respect to motor disability and psychosis.
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PMID:Prognostic implications of the motor symptoms of Parkinson's disease with respect to clinical, computertomographic and psychometric parameters. 378 47

The clinical pattern of symptoms consists of motor disorders (akinesia, tremor, rigor), emotional disorders (depression, abnormal behaviour), autonomic disorders (sweating, salivation, seborrhoea, constipation) and intellectual disorders (bradyphrenia, Alzheimer's dementia)
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PMID:[Clinical picture of Parkinson disease]. 378 88

Recent experimental studies and one clinical case have suggested that grafting tissue from the adrenal medulla into the brain may ameliorate the signs of Parkinson's disease. We describe the treatment of two young patients (35 and 39 years old) with intractable and incapacitating Parkinson's disease, in whom fragments of the adrenal medulla were autotransplanted to the right caudate nucleus. Clinical improvement was noted in both patients at 15 and 6 days (respectively) after implantation and has continued in both. Rigidity and akinesia had virtually disappeared in the first patient at 10 months after surgery, and his tremor was greatly reduced. A similar degree of improvement was present in the second patient at three months. We conclude that autografting of the adrenal medulla to the right caudate nucleus was associated with a marked improvement in the signs of Parkinson's disease in two patients, but our results are preliminary and further work is necessary to see whether this procedure will be applicable over the long term in other types of patients with Parkinson's disease.
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PMID:Open microsurgical autograft of adrenal medulla to the right caudate nucleus in two patients with intractable Parkinson's disease. 382 26

Eleven cases of "pure akinesia without rigidity and tremor and with no effect by L-dopa therapy" were first reported by Imai in 1980. Three cases were added by Hayashi and Hayashi (1983). However there have been so far no autopsy cases, remaining the nosological position of this syndrome uncertain. The authors have had an opportunity of observing the third case in the report by Hayashi and Hayashi for 8 years and autopsy was done as well. Case report The patient was a female farmer. On account of postural-reflex troubles, the pulsion phenomenon and feet freezing, which had progressed since the age of 54, she easily tumbled over. Eight years after the beginning of those symptoms, vertical oculomotor palsy, pseudobulbar palsy and dementia were added; she was diagnosed as a progressive supranuclear palsy. Before this diagnosis, her illness was being regarded as "pure akinesia without rigidity and tremor and with no effect by L-dopa therapy". Neck dystonia was not observed even in the terminal stage. She died at the age of 65. The total clinical course was about 11 years. Pathological observation The brain weighed 1,170 g before fixation. Marked atrophy of the subthalamic nucleus, globus pallidus and pontine tegmentum was observed. The substantia nigra was shown to be severely depigmented. Microscopically, loss of neurons and gliosis were seen in the subthalamic nucleus, globus pallidus, substantia nigra, hypothalamus, superior colliculus, central grey matter, brain stem reticular formation, cerebellar dentate nucleus, etc. The characteristic finding was the appearance of neurofibrillary tangles in these regions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An autopsy case of progressive supranuclear palsy showing "pure akinesia without rigidity and tremor and with no effect by L-dopa therapy (Imai)"]. 382 55

Clinical Neurophysiology brings about 2 major contributions in the study of Parkinson's disease: on the one hand, it makes it possible to measure the motor troubles; on the other, it enables their pathophysiological analysis. The 3 classical signs must be studied separately. Tremor can easily be recorded by electromyography. Moreover, its parkinsonian nature can be specified by studying the resetting of EMG bursts following electrical stimulation of the motor nerve. A pace maker has been demonstrated in the thalamus from where rhythmic messages are first sent to motor cortex and thereafter reverberated to spinal motoneurons. Rigidity can be assessed by sophisticated but not generalized methods. It is easier to evaluate it by long-loop responses evoked by proprioceptive or exteroceptive stimulations. These responses reflect activity in pathways relaying in supraspinal structures. Contrary to spasticity, rigidity is not basically due to dysfunctions in segmentary spinal circuits. It is more likely that it depends on hyperactive and hyperexcitable long loop pathways. This hypothesis is in agreement with well established facts showing that parkinsonian hypertonia vanishes after dorsal root section. Akinesia is complex semeiologically. It is made of various components some of which can be measured. Reaction times and movement times provide interesting data which however are not strictly correlated with the motor handicap. Motor programmes are assembled in normal delays but they are not "called upon" correctly, reflecting a disturbance in the motor planning. A lack of "energetization" of the motor cortex and the pyramidal tract is likely. A functional disconnection between the motor program/plan side and the execution side can be hypothesized to explain the 3 major signs; on the one hand, neural messages are not correctly transferred to the pyramidal system, on the other, spinoencephalospinal loops on the execution side become more active as they escape from the control normally exerted by the plan/program side where basal ganglia play a prominent role.
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PMID:[Clinical neurophysiology in the evaluation and physiopathology of Parkinson's disease]. 383 95


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