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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since the description by Galen in the 2nd Century, A.D., clinical neurology has acknowledged the existence of two types of tremor: that which occurs at rest and that occuring during the execution of movement. With the help of refined methods of analysis, E.M.G. and cinephotography, the authors have carried out a detailed clinical assessment in more than 400 patients. The basic criterion used to define a tremor was the classical definition of Dejerine: "An involuntary, rhythmical and symmetrical movement about an axis of equilibrium." As a result of this study, the conclusion has been reached that there are two types of tremor: postural tremor and tremor of attitude. Both are present while the limb remains immobile, whether by wilful design or when at rest in a position of posture and subject only to the action of gravity. During voluntary movement, tremor is not present. Irregular, asymmetrical and non-rhythmic oscillations may appear however - as in so-called intention tremor, of cerebellar origin - but this abnormal movement can hardly be called a real tremor. It is merely a manifestation of ataxia. As a consequence of this study, it is suggested that further understanding of the basic mechanism of tremor can be reached by the investigation of the central neural structures which are involved in the physiology of posture and attitude.
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PMID:Semiology of Tremors. 109 80

Lesions were placed in a number of brain stem and cerebellar structures to determine their importance to the control of posture and movement in rats. Lesions of the lateral vestibular nucleus, superior vestibular nucleus, or inferior olive produced severe disturbances of posture and movement. Rats with such lesions had pronounced tremor, abnormal head posture and asymmetrical trunk posture, and failed in a balance beam test. Lesions of the medial medullary reticular formation and medial vestibular nucleus had less overall effect on posture and movement, while animals with lesions of the deep cerebellar nuclei were relatively unimpaired. All lesion groups showed some recovery of function during the course of postoperative testing.
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PMID:Brain stem and cerebellar lesions in female rats. I. Tests of posture and movement. 126 11

A mutant strain of Han-Wistar rat carries an autosomal recessive gene producing spastic paresis which is characterized by ataxia, tremor and hind limb rigidity. Brains of affected rats and unaffected littermate controls were transected at the mesencephalon into rostral and caudal portions (the caudal portion contained the cerebellum and brainstem). Poly(A)+ mRNA was isolated from pooled rostral or caudal portions and injected into Xenopus oocytes. The oocytes were voltage-clamped and exposed to 1 mM L-glutamate, 500 microM kainate, 500 microM quisqualate, 200 microM N-methyl-D-aspartate (NMDA) or 1 mM gamma-aminobutyric acid (GABA). Oocytes injected with mRNA isolated from the caudal portions of the affected rat brains exhibited statistically significant increases in glutamate and kainate peak current responses compared to oocytes injected with mRNA from other brain samples. No differences were noted in the responses of the groups when exposed to quisqualate, NMDA or GABA. Cerebellar and brain stem mRNA were also isolated separately in different groups of mutants and unaffected littermates. Only oocytes injected with cerebellar mRNA from mutants displayed statistically significant increases in responses to glutamate and kainate. In parallel morphological studies changes in the cerebellum of mutants were also observed. These consisted of a loss of Purkinje cells and an asymmetrical disarrangement of the granule cell layer of cerebellar cortex. Taken together, the physiological and morphological results suggest that alterations in glutamate/kainate receptors in the cerebellum are phenotypic manifestations of the Han-Wistar mutation. The results are consistent with the hypothesis that this mutant rat might serve as a model of glutamate/kainate excitotoxicity in the brain.
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PMID:Altered excitatory amino acid function and morphology of the cerebellum of the spastic Han-Wistar rat. 168 5

Spectral analysis of a tremor record can sometimes produce a spectrum with multiple components of significant amplitude. The problem is to determine whether the presence of several peaks represents the coexistence of separate tremor mechanisms or be a consequence of fluctuations in the frequency or amplitude of a single tremor. The spectrum of a tremor whose frequency or amplitude vary and are independent has the recognisable pattern of a central carrier frequency with sidebands of equal amplitudes distributed symmetrically around the carrier. However, if tremor amplitude and frequency fluctuate and are not independent, (frequency proportional to amplitude or frequency inversely proportional to amplitude), the spectrum has a pattern of sidebands which are asymmetrical in amplitudes and may resemble the spectrum of the combined signal from different independent oscillators. The investigation of sidebands in spectra has been neglected in tremor studies and multiple irregular peaks on a tremor spectrum have sometimes been used wrongly as evidence for the coexistence of multiple tremor mechanisms or frequency components assumed to be concurrent.
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PMID:Spectral analysis of tremor: understanding the results. 228 29

The parkinsonian syndrome rests on the clinical tripod: akinesia, rigidity, tremor. Akinesia is the key symptom, broadly defined as a difficulty in initiating and performing movements in proportion to their complexity (sophisticated, simultaneous movements) and their duration (repetitive movements). The most frequent cause of the syndrome is Parkinson's disease. Although this diagnosis needs to be confirmed in pathological terms by the loss of neurons and the presence of Lewy's bodies in the substantia nigra, some clinical data enable it to be envisaged with a minimum of errors; these are pure parkinsonian triad, good response to dopatherapy and asymmetrical symptoms. The other causes of parkinsonian syndrome are usually related to the administration of neuroleptic drugs and to degenerative diseases with lesions that are more diffuse than those of Parkinson's disease. In Steele-Richardson-Olzewski disease a parkinsonian syndrome is associated with supranuclear ophthalmoplegia. Multiple systematized atrophy presents under three different clinical aspects: a parkinsonian syndrome without tremor and resistant to L-dopa, suggesting atrophy of the strionigral tract; a parkinsonian syndrome associated with a cerebellar syndrome, suggesting olivo-cerebellar-pontine atrophy, and Shy-Drager disease which includes primary dysautonomy and other neurological syndromes.
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PMID:[Parkinson's disease and parkinsonian syndromes]. 272 71

Six divers were compressed on heliox to 350 m. Repeated neuropsychological and neurological tests were conducted during the dive. Averaged increased tremor during the compression was found. Two divers had major EEG changes, while two divers had a completely normal EEG. Memory was most impaired among the cognitive variables. At 350 m there was some normalization in the EEG, and the tremor levels returned to normal. Memory impairment, however, was sustained. Three months later nine divers performed an open sea dive to 300 m. Whereas minor fatigue effects were found for the experimental dive, examinations after the open sea dive indicated more specific cerebral after effects. An increased tremor, reduced hand grip strength and foot tapping speed, lowered autonomic reactivity, and memory problems were found. Some divers had unequivocal asymmetrical plantar responses and unilateral weak abdominal reflexes, accompanied by EEG changes with corresponding laterality. In three of the divers these signs were not present 1 month later.
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PMID:Differential neuropsychological effects of diving to 350 meters. 382 92

RX 336-M (7,8-dihydro-5',6'-dimethylcyclohex-5'-eno-1',2',8',14 codeinone) and four other chemically-diverse agents--AG-3-5 (1-[2-hydroxyphenyl]-4-[3-nitrophenyl]-1,2,3,6-tetrahydropyrimidine-2-one), Sgd 8473 (alpha-[4-chlorobenzylideneamino)-oxy]-isobutyric acid), thyrotropin releasing hormone (TRH), and sodium valproate--each induce signs of withdrawal, most notably 'wet-dog' shaking, after acute i.p. administration in drug-naive rats. They are therefore additions to a recently recognized and, as yet, ill-defined class of behaviorally active compounds. The pharmacological baselines that link these disparate agents together have been studied in the present work, using 'wet-dog' shaking as the behavioral measure and RX 336-M as the reference shake-inducing compound. Peripheral administration of clonidine, haloperidol, d-lysergic acid diethylamide, or morphine suppressed chemically induced shaking: naloxone had no marked effect. Reverse tolerance was associated with TRH-induced shaking whereas tolerance occurred with the other four compounds. Cross-tolerance interactions were asymmetrical. Thus, rats rendered tolerant to RX 336-M were cross-tolerant to AG-3-5, TRH, and sodium valproate but not to Sgd 8473; in contrast, RX 336-M-induced shaking was only significantly reduced in rats made tolerant to Sgd 8473. In view of the unidirectional nature of the cross-tolerance relationships studied, it is concluded that AG-3-5, Sgd 8473, sodium valproate, and TRH initiate 'wet-dog' shaking through neural substrates that differ from the one(s) associated with RX 336-M. Nevertheless, all five compounds may eventually trigger a common shake-inducing mechanism.
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PMID:RX 336-M, a new chemical tool in the analysis of the quasi-morphine withdrawal syndrome. 678 43

A mother and son suffer from hemiplegic migraine with onset in childhood. Both have nystagmus which has not changed for many years, but the date of onset is uncertain. They have an asymmetrical tremor, clinically indistinguishable from essential tremor. Neuroophthalmological examination revealed inability to produce smooth pursuit, gaze-paretic nystagmus, rebound nystagmus, failure of fixation suppression of the vestibuloocular reflex both horizontally and vertically, and low gain of the optokinetic system. These abnormalities, confirmed by electrooculography, are commonly seen in disease of the cerebellum and brainstem. Treatment with propranolol and pizotyline lessened the number of episodes of hemiplegia and improved the tremor. Hemiplegic migraine has been reported in association with nystagmus, retinal degeneration, deafness, and ataxia in varying combinations in three other families with autosomal dominant inheritance. These associated neurological manifestations likely represent system degenerations rather than the effect of repeated ischemia imputable to the migraine itself. The syndrome of hemiplegic migraine, tremor, and ocular smooth pursuit system disorder seen in this family appears to be inherited as a single autosomal dominant trait, although more than one autosomal dominant gene may be involved.
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PMID:An autosomal dominant syndrome of hemiplegic migraine, nystagmus, and tremor. 743 78

Tremor (Tr) is an involuntary rhythmic movement disorder. Its causes are multifold. The physiopathogenesis is complex and only partially understood. The classification, based on clinical grounds distinguishes: 1) Physiological Tr at 8-12 Hz, postural, involving the limbs; 2) Essential Tr at 8 Hz, often familial, postural, involving the limbs; 3) Parkinsonian Tr at 4-6 Hz, present at rest, rarely isolated, often asymmetrical, involving the limbs, sometimes the jaw; 4) Cerebellar Tr at 3-4 Hz, maximal at the end of limb movements. Therapy is based on this classification. The main points for the diagnosis are age of onset, associated signs, toxic factors and heredity.
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PMID:[Tremors]. 793 1

'Arteriosclerotic' parkinsonism is still a subject of debate. The aim of this study was to investigate whether parkinsonism associated with basal ganglia lacunes possesses peculiar clinical features and a clinical course which enables its distinction from idiopathic Parkinson's disease (IPD). 106 consecutive ambulatory patients with the clinical diagnosis of parkinsonism were referred for CT examination. Patients in whom isolated basal ganglia lacunes were found were interviewed and examined, and their clinical characteristics were compared to those of patients suffering from IPD without lacunes (controls). In 20 patients, isolated basal ganglia lacunes were detected; all had risk factors for stroke (significantly more than controls) and 7 of them had had clinically diagnosed strokes. The extrapyramidal disability evolved slowly in all. The clinical picture was indistinguishable from IPD in individual patients. However, tremor was significantly less frequent in this group. Lower body parkinsonism was not observed. Extra-pyramidal signs were frequently asymmetrical (55%), with no consistent relationship to the side of the lacune. Asymmetrical pyramidal signs were present in 30% of those with unilateral lacunes, always on the appropriate side. Only 1 patient was an L-dopa nonresponder. Patients with parkinsonism associated with basal ganglia lacunes showed tremor less frequently than other IPD patients; otherwise, clinical features and course of the disease were indistinguishable from IPD. In these cases, parkinsonism and basal ganglia lacunes might have occurred independently of each other and tremor might have been prevented by ischemic events.
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PMID:Basal ganglia lacunes and parkinsonism. 801 63


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