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

Electroencephalographic (EEG) activity was continuously monitored from the hippocampus, amygdala, reticular formation and frontal cortex in freely moving Sprague-Dawley rats exposed to 91 atmospheres absolute pressure (ATA) using compression rates of 1 or 3 ATA/min. Videotape recordings were made for subsequent behavioural analysis. Tremor, myoclonic jerks and tonic extensions of the tail were observed in all animals but did not appear to correlate with epileptiform activity. Convulsions occurred between 66.5 and 91 ATA in all subjects compressed at 3 ATA/min, but in only 1 rat (at 91 ATA) in the 1 ATA/min group. Tonic-clonic motor seizures developed explosively and involved the entire body. EEG records showed continuous spiking at all sites during the generalized convulsive state. There was no evidence of differential susceptibility of the various brain regions examined to the epileptogenic effects of high pressure. The behavioural and EEG data indicate that hyperbarically induced seizures differ from the classical limbic type.
Epilepsy Res
PMID:Electroencephalographic and behavioural correlates of seizure development in rats in response to hyperbaric exposure. 229 48

The spontaneously epileptic rat (SER), a mutant homozygous for both zitter and tremor genes, exhibits absence-like seizures and tonic convulsions without external stimulation from 7 to 8 weeks of age. Histopathological studies of the central nervous system revealed the following abnormalities. The 35-day-old SERs which exhibit body tremor, and which have never shown seizures, had marked vacuolation and hypomyelination in the brainstem and cerebellum. The vacuoles were produced by splitting of the myelin sheaths and swelling of the dendrites and were related to primary swelling of the astrocytes. The 2- to 3-month-old SERs with staggering gait and seizures showed focal axonal swelling ('torpedo') and advanced vacuolation in the granular cell layer of the cerebellum in addition to the abnormalities observed at 35 days of age. Degenerative neurons and spheroidal bodies were observed in the substantia nigra and ventral tegmental nucleus. These brain areas are known to be related to tonic convulsions in the several experimental models. The SER is believed to be a useful tool for the investigation of the relationship between the structure and function of the central nervous system in epilepsy. It is probable that the more severe changes in the cerebellum are responsible for the staggering gait.
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PMID:The spontaneously epileptic rat (SER), a zitter*tremor double mutant rat: histopathological findings in the central nervous system. 237 85

From 1986 till 1988, 88 patients received sodium valproate for the first time as a therapy for epilepsy. One of them developed a fine tremor, three a coarse tremor with a cogwheel phenomenon, two developed a full parkinsonian syndrome. All these symptoms in these six patients disappeared completely or nearly completely after changing to another anti-epileptic drug or reducing the dose.
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PMID:[Transient Parkinson syndrome and tremor caused by the use of sodium valproate]. 250 90

Movement disorders are well-known presenting signs of metabolic disorders. Focal motor abnormalities may be the chief initial presentation of diabetes mellitus in the nonketotic hyperglycemic state in 6% of patients. Nonketotic hyperglycemia (NKH), in particular, may manifest any of a wide variety of movement disorders. These have been described as focal seizures, epilepsia partialis continua, myoclonus, and opsoclonia. There are descriptions of movement disorders in hyperglycemia that are similar to the coarse flapping tremor of asterixis, the posturing of paroxysmal kinetogenic choreoathetosis, and of "fencing (stance) seizures." Disorders of facial motor function including aphasia, facial muscle twitching and jerking, and disorders of muscular tone have been described. These may include hemiparesis and hemiplegias as well as increased tone, in some cases mimicking the nuchal rigidity of meningitis. The movement disorders in NKH may mimic cerebral vascular accidents, meningitis, or psychiatric disorders, as well as various types of seizures. Clinicians may be able to avoid expensive and time-consuming diagnostic evaluations to rule out NKH in patients with movement disorders. We present two patients with focal motor abnormalities associated with nonketonic hyperglycemia and review the pertinent literature.
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PMID:Movement disorders as a manifestation of nonketotic hyperglycemia. 260 Mar 93

High-dose treatment with pilocarpine hydrochloride, a cholinergic muscarinic agonist, induces seizures in rodents following systemic or intracerebral administration. Pilocarpine seizures are characterized by a sequential development of behavioral patterns and electrographic activity. Hypoactivity, tremor, scratching, head bobbing, and myoclonic movements of the limbs progress to recurrent myoclonic convulsions with rearing, salivation, and falling, and status epilepticus. The sustained convulsions induced by pilocarpine are followed by widespread damage to the forebrain. The amygdala, thalamus, olfactory cortex, hippocampus, neocortex, and substantia nigra are the most sensitive regions to epilepsy-related damage following convulsions produced by pilocarpine. Spontaneous seizures are observed in the long-term period following the administration of convulsant doses of pilocarpine. Developmental studies show age-dependent differences in the response of rats to pilocarpine. Seizures are first noted in 7-12 day-old rats, and the adult pattern of behavioral and electroencephalographic sequelae of pilocarpine is seen in 15-21-day-old rats. During the third week of life the rats show an increased susceptibility to the convulsant action of pilocarpine relative to older and younger animals. The developmental progress of the convulsive response to pilocarpine does not correlate with evolution of the brain damage. The adult pattern of the damage is seen after a delay of 1-2 weeks in comparison with the evolution of seizures and status epilepticus. The susceptibility to seizures induced by pilocarpine increases in rats aged over 4 months. The basal ganglia curtail the generation and spread of seizures induced by pilocarpine. The caudate putamen, the substantia nigra, and the entopeduncular nucleus govern the propagation of pilocarpine-induced seizures. The antiepileptic drugs diazepam, clonazepam, phenobarbital, valproate, and trimethadione protect against pilocarpine-induced convulsions, while diphenylhydantoin and carbamazepine are ineffective. Ethosuximide and acetazolamide increase the susceptibility to convulsant action of pilocarpine. Lithium, morphine, and aminophylline also increase the susceptibility of rats to pilocarpine seizures. The pilocarpine seizure model may be of value in designing new therapeutic approaches to epilepsy.
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PMID:Review: cholinergic mechanisms and epileptogenesis. The seizures induced by pilocarpine: a novel experimental model of intractable epilepsy. 264 33

This paper deals with the differential diagnosis of Hitler's Parkinsonian syndrome based upon our recently published results of an analysis of Hitler's motor functions in German news-reels, upon archived materials with notes and comments of Hitler's doctors, various memories, and our own interrogations of eye-witnesses of Hitler's nearest entourage. According to these sources, Hitler's Parkinsonian syndrome developing since mid-1941 cannot be attributed to any of the symptomatic forms of Parkinsonism. In light of family history, age of manifestation and clinical features the assumption of idiopathic Parkinson's disease seems somewhat more plausible than that of postencephalitic Parkinsonism; the genetic variant is less probable. Hitler's neurological pathography is further analysed in respect to an abuse with "Antigas pills" and to some statements in the literature presuming an amphetamine-dependence, a syphilitic manifestation, an epileptic seizure in 1932, and a tremor already present in 1923.
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PMID:[Hitler's neurologic disease--differential diagnosis of Parkinson syndrome]. 269 89

Venom was microinjected into the dorsal hippocampus of rats and electroencephalographic recordings were obtained from the hippocampus and occipital cortex. Behavioural alterations consisted of circling, wet shaking and scratching that evolved to head and body jerks and isolated clonic episodes and then to wild running followed by tonic-clonic generalized seizures and status epilepticus. Electroencephalographic alterations consisted of high frequency and high voltage spikes together with epileptiform seizures beginning in the hippocampus and evolving to the cortex. However there was only a poor electrographic-behavioural correlation between the generalized tonic-clonic seizures preceded by wild running and the electrical recordings from hippocampus and occipital cortex. Histology revealed lesions at the site of injection as well as at distant sites. Severity of neuronal damage was associated with seizure intensity. Damaged areas were almost the same as found within other models of epilepsy. Nevertheless a remarkable difference was the highly lesioned hypothalamus seen in this experiment. We discuss our results in relation to results obtained with other methods of inducing epilepsy. This venom may be a useful tool for studying the nervous system.
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PMID:Behavioural, electroencephalographic and neuropathological effects of the intrahippocampal injection of the venom of the South American rattlesnake (Crotalus durissus terrificus). 271 90

Clinical and electrical evidence of peripheral neuropathy may result from long term treatment with phenytoin or barbiturates, especially in combination, or after repeated exposure to toxic blood concentrations of either drug. Prolonged acute toxicity with phenytoin may rarely lead to permanent residual ataxia. Reversible dystonia may occasionally be precipitated by phenytoin or carbamazepine; asterixis by phenytoin, barbiturates or carbamazepine; and, more commonly, tremor by valproate. All the major anticonvulsant drugs, especially in combination, can produce occasional subacute cognitive or behavioural syndromes. In varying degrees, the drugs also impair attention, concentration, memory, mental speed or processing, or motor speed. Possible mechanisms of impaired mental function include neuronal damage, or disturbance of folic acid, monoamine or hormonal metabolism. The relative influence on neurological or psychological function is an important factor in the choice of anticonvulsant drug for the treatment of epilepsy.
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PMID:Adverse neuropsychiatric effects of anticonvulsant drugs. 286 Oct 75

The paper provides a survey of neuropharmacological fundamentals for the use of beta-adrenolytics in the treatment of psychiatric and neurological diseases. In particular there are discussed results of animal- and clinical-pharmacological experiments carried out in order to assess the influence of betaadrenolytics in disorders and diseases such as anxiety, psychoses, tremor, some kinds of addiction, migraine and epilepsy. The conclusion is that in spite of some ascertained clinical indications on the one hand and a variety of neuropharmacological results on the other the mode of action of betaadrenolytics at the level of the CNS remains still insufficiently explainable.
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PMID:[The neuropharmacology of beta adrenolytics]. 286 12

A mutant rat, which was found in a colony of Kyoto:Wistar rats and genetically defined as a tremor rat (tm/tm), developed tremor of the whole body at 2 weeks of age but the tremor gradually disappeared between 6 and 8 weeks of age. The electroencephalogram (EEG) recorded using chronically implanted electrodes showed a 5-7 Hz (mostly 6 Hz) spike and wave complex synchronously in the cerebral cortex and hippocampus accompanied by absence-like seizure in all six tremor rats examined. The spike and wave complex appeared 0.8-1.9 times per minute and lasted for 1-17 s. However, normal EEG activity was observed in the intervening periods, free of absence-like seizure. Thus the tremor rat is considered to be a possible model for studying the pathogenesis and therapy of petit mal epilepsy in humans.
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PMID:A new model of petit mal epilepsy: spontaneous spike and wave discharges in tremor rats. 310 69


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