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

Industrial overexposure to chlordecone, an organochlorine insecticide, caused tremor in 76 of 148 exposed workers. Chlordecone was absorbed through oral, respiratory, and dermal routes, the last possibly the most significant. Epidemiology of this incident disclosed low-level, widespread environmental exposure of man to chlordecone. In 23 workers with chronic chlordecone intoxication, tremor was associated with opsoclonus, pleuritic pain and arthralgia. No seizures were reported. The site of action of chlordecone on the central nervous system is unknown. It concentrates in human adipose and hepatic tissue but is not biodegradable, either in humans or elsewhere in nature.
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PMID:Chlordecone intoxication in man. I. Clinical observations. 7 55

Chronic bipolar electrodes were implanted in cortical, limbic, diencephalic and mesencephalic regions of the rat. Following recovery from surgery the rats were maintained for 14--26 days on a liquid diet in which 35--42% of total calories were provided by ethanol. Following ethanol withdrawal, electrographic and behavioral monitoring was continued for 8--10 h. The withdrawal of ethanol resulted in the time-dependent appearance of a variety of withdrawal signs including tail arching, ataxia, rigidity, tremor and spontaneous and audiogenic convulsions. These behavioral signs were accompanied by the development of epileptiform abnormalities across wide-spread brain regions. Analysis of preconvulsive spike activity revealed a greater spike frequency in limbic, mesencephalic and non-specific diencephalic regions, as compared to those in cortex and specific diencephalon. Seizure discharge during the tonic-clonic phase of the primary audiogenic convulsion was initiated in the mesencephalon or amygdala, but spread rather extensively to the remainder of the brain. In those instances, however, where multiple convulsions occurred following the audiogenic convulsions, there was a marked decline in spread of seizure discharge to the cortex. These results were interpreted to support the notion that some degree of neuroanatomical specificity exists in the genesis of epileptiform abnormalities during ethanol withdrawal. A comparison of these results with those studying the neural mechanisms underlying other forms of generalized epilepsy was made. It is hypothesized that central pacemaking regions such as medial thalamus or reticular formation may serve to organize isolated epileptiform activity into coherent patterns of paroxysmal activity throughout the brain during the ethanol withdrawal syndrome.
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PMID:Ethanol dependence in the rat: role of non-specific and limbic regions in the withdrawal reaction. 8 50

Rats with complete spinal transections were compressed in helium-oxygen to 120 bars. Tremors and increased EMG activity in limbs rostral as well as caudal to the lesions were observed beginning at 30 bars. Spinal seizures occurred at 95 bars, similar to cortical seizure thresholds of intact rats. Denervated limbs remained flaccid throughout the dives. No rostro-caudal progression of symptoms was evident in normal animals, but fluctuation of symptoms with increasing pressure was frequently observed. These findings are consistent with the hypothesis that the effects of pressure on aggregates of neurons exceed those on isolated components.
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PMID:Spinal cord seizures elicited by high pressures of helium. 8 59

Alcohol withdrawal syndromes in humans lie on a continuum of increasing severity, from the acute hangover to delirium tremens. Early mild reactions consist primarily of hyperexcitability phenomena such as tremor, insomnia, hyperreflexia and hyperventilation. In more severe degree, the same process gives rise to hallucinations and seizures. These early reactions are mimicked closely by alcohol withdrawal signs in experimental animals. Late reactions in humans are characterized by marked sympathetic nervous system overactivity, profound disorientation and hallucinations. Analogous reactions have not yet been observed clearly in other species. The problem may be one of finding appropriate techniques for detecting such changes, rather than a true species difference in their occurrence.
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PMID:Alcohol withdrawal syndromes in the human: comparison with animal models. 33 82

Periodic brain stimulation, particularly in the limbic system, at stimulus intensities initially too low to produce any behavioural or EEG effects, progressively produces EEG changes, motor automatisms, and eventually convulsions, an effect called kindling. Data are presented and reviewed that suggest that the severity of alcohol withdrawal symptoms progressively increases over years of alcohol abuse in a stepwise fashion similar to the kindling process. The model is presented that the limbic system hyperirritability which accompanies each alcohol withdrawal serves over time to kindle increasingly widespread subcortical structures. These long-term changes in neuronal excitability might relate to the progression of alcohol withdrawal symptoms from tremor to seizures and delirium tremens, as well as the alcoholic personality changes between episodes of withdrawal.
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PMID:Kindling as a model for alcohol withdrawal syndromes. 35 67

Sodium valproate (Epilim) has been used in the management of 100 patients with previously uncontrolled epilepsy for periods up to 2 years. If all manifestations of epilepsy are considered together, 75% to 100% control of seizures was achieved in 43% of patients, 25% to 74% control in 26%, and no improvement occurred in 31% of patients. Control of 75% to 100% was achieved in 57% of patients with a spike and wave electroencephalogram (EEG) disturbance but only in 35% of those with focal abnormalities, excessive slow activity, or normal records. When the various manifestations of epilepsy were considered individually, the greatest improvement was found among the patients with the minor forms of generalized epilepsy (petit mal absences, myoclonus and atonic attacks) in whom 75% to 100% control was obtained in 67%, compared with 43% of those with major generalized seizures (grand mal) and 30% of those with temporal lobe attacks and other forms of focal epilepsy. Gastrointestinal disturbances and drowsiness were noted as side effects in the early stages of treatment, but the majority of patients tolerated the drug well and many commented on increased mental alertness while taking it. Two patients were over-stimulated and some noticed tremor or twitching as side effects. Some minor abnormalities in blood coagulation studies were noted, but these were transient and did not appear to be of clinical significance. Regular blood counts and biochemical studies have not shown any significant changes. Sodium valproate appears to be a safe and useful anticonvulsant with the advantage that it usually makes patients brighter rather than drowsier. Abnormalities of platelet function have been described in some overseas reports, so that any unexplained bruising or bleeding in a patient taking valproate is an indication for a platelet count and coagulation studies.
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PMID:The anticonvulsant action of sodium valproate (Epilim) in 100 patients with various forms of epilepsy. 40 31

A boy with mild hand tremor since age 2 1/2 was found at 4 to have cherry-red spots and mild trucal ataxia without seizures or dementia. Biochemically, he had striking hexosaminidase deficiency (serum: 4.6 percent of normal, 88.9 percent heat-labile; leukocyte: 2.2 percent of normal, 84.6 percent heat-labile; fibroblast 12.8 percent normal, 93.1 percent heat-labile). The residual hexosaminidase activity migrated electrophoretically in two bands. The major band comigrated with hexosaminidase A, the minor with hexosaminidase S. Hexosaminidase B was totally absent. The parents had partially reduced hexosaminidase with a decreased heat-stabile fraction. This disorder may result from a new mutation closely related to that causing Sandhoff-Jatzkewitz disease.
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PMID:A new juvenile hexosaminidase deficiency disease presenting as cerebellar ataxia. Clinical and biochemical studies. 56 95

The ethanol withdrawal syndrome in man and animals is characterized by signs of CNS hyperactivity although a direct measurement of a physiological variable reflecting this CNS hyperactivity has never been performed in untreated man or in animals. We induced ethanol dependence in the rat by means of intragastric intubation with a 20% w/v ethanol solution, thus keeping the animals in a state of continuous severe intoxication for 3--4 days; during the subsequent state of withdrawal characterized by tremor, rigidity, stereotyped movements and general seizures a 25% increase in cerebral oxygen consumption (CMRO2) could be measured; this increase was not due to catecholamines originating from adrenal medulla as adrenomedullectomized animals showed a similar increase in CMRO2 (28%); the withdrawing animals showed a corresponding cerebral blood flow (CBF) increase. The elevated CMRO2 and CBF could be reduced to normal by administration of a beta-adrenergic receptor blocker (propranolol 2 mg/kg i.v.), and hence the increased CMRO2 during ethanol withdrawal could be related to catecholaminergic systems in the brain, e.g. the noradrenergic locus coeruleus system which is anatomically well suited as a general activating system. This interpretation is supported by the earlier neurochemical finding of an increased cerebral noradrenaline turnover during ethanol withdrawal. The exact mechanism underlying the increased cerebral oxygen consumption during ethanol withdrawal and the effect of propranolol on cerebral function during this condition remains to be clarified.
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PMID:Cerebral blood flow and oxygen consumption during ethanol withdrawal in the rat. 57 52

Electroencephalographic activity of the frontal cortex, cerebellar vermis, and superior vestibular nucleus was recorded in awake rats during the high pressure nervous syndrome (HPNS) by means of permanently implanted electrodes. Power-spectrum analysis revealed a decline in the faster frequencies and an increase in the slow frequences as the seizure end-point was approached. Effects of compression to 4500 fsw varied from severe tremor and myoclonic jerks to status epilepticus, with seizures occurring at an average depth of 3560 fsw. In all animals, multifocal-spiking activity progressed in severity with increasing depth. The predominant seizure pattern observed was a spike and slow-wave pattern reminiscent of absence seizures. Initial evidence of generalized seizure activity was equally divided between the cerebellum and cortex. It is concluded that the cerebellum participates in HPNS seizures. Possible evolution of the syndrome by loss of Purkinje cell inhibitory influence on subcortical sites that modulate cortical excitability is discussed.
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PMID:Cerebellar and cerebral electroencephalogram during the high pressure nervous syndrome (HPNS) in rats. 60 10

Modification of cocaine's stimulant and local anesthetic behavioral effects as a function of chronic treatment was evaluated in seven female cats. Video tape of behavior pre- and post-cocaine (iv) on days 1, 4, 7, 10, and 13 in seven cats, and in addition, on days 21, 28, and 35 for s subset of four cats, was rated for several scales of the Behavioral Rating Inventory for Drug-Generated Effects (BRIDGE), developed to quantify stimulant-induced behaviors. Preseizure events were measured using scales for Tremor Intensity and Preseizure-Seizure Intensity (PSI), developed to quantify local anesthetic-induced behaviors. Behaviors associated with cocaine's local anesthetic effects, i.e., Tremor Intensity and PSI levels, showed tolerance over the treatment period, while behaviors associated with cocaine's psychomotor stimulant effects, i.e., the BRIDGE measures, showed augmentation, or reverse tolerance. These data are discussed in terms of catecholamine supersensitivity, kindling mechanisms, and stimulant models of psychosis.
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PMID:Behavioral analysis of chronic cocaine intoxication in the cat. 66 28


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