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

Physiological and pharmacological studies of more than 150 patients with movement disorders are reported. Particular attention is paid to the differentiation of various types of tremor on the basis of rate, rhythm, and pattern of EMG activity in antagonistic muscles. The typical 'tremor-at-rest' of Parkinson's disease--3-7 Hz activity which alternates between antagonistic muscles--is suppressed, at least briefly, during voluntary activity, at which time typical 8--12 Hz 'physiological tremor' may be seen. Essential tremor and its familial or senile variants also have a characteristic EMG pattern during voluntary activity--5-8 Hz bursts of activity which are synchronous in antagonistic muscles. This type of tremor may also be present in patients with Parkinson's disease and in certain kinships with a Charcot-Marie-Tooth polyneuropathy. Other tremors in association with polyneuropathy ('neuropathic tremor') have different physiological characteristics. Myoclonus is of essentially two types ('positive' with EMG bursts and 'negative' with brief pauses in ongoing activity, as with asterixis) and may, at times, mimic tremor. Certain specific tremors respond predictably to specific pharmacological therapy.
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PMID:Physiological and pharmacological aids in the differential diagnosis of tremor. 0 92

Clinical and pathological findings in two cases of degenerative progressive myoclonic epilepsy (PME) are described. The clinically difficult task of differentiating a "cerebellar" tremor from an action myoclonus is emphasized. Simultaneous electroencephalography and electrokymography was done, using capacity to ground transients for recording hand movements. This method was found useful in corroborating the cerebellar nature of the remaining disorder, after successful treatment of the myoclonic element with anticonvulsants.
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PMID:Degenerative progressive myoclonic epilepsy electrokymographic observations. 12 41

This review covers recent advances in a variety of dyskinesias. Introduction of new drugs for the treatment of myoclonus and sensory biofeedback therapy for focal dystonia are expanding our concepts of these types of movement disorders. Progress in the treatment of action myoclonus is especially noteworthy and has led to the implication of serotonin deficit in the pathophysiology of this syndrome. Knowledge of the biochemical pathology of Huntington's chorea has outpaced therapy for this disorder, but new forms of therapy have been proposed based on the chemical findings. Basic pharmacologic studies suggest pathophysiologic mechanisms for the syndrome known as tardive dyskinesia, but treatment is still far from ideal for this disorder. Other movement disorders with recent therapeutic advances include essential tremor and hemiballism. This review will cover only those dyskinesias in which new therapies have been advanced in the last few years. Aside from parkinsonism, which will not be discussed here, progress in the treatment of movement disorders has been slow, but steady. New drugs are being tested constantly, and the purpose of this review is to call attention to the ongoing evaluation in this field. Descriptions and etiologies for these dyskinesias are covered elsewhere (Fahn, 1976a) and therefore are not repeated here.
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PMID:New approaches in the management of hyperkinetic movement disorders. 30 60

Intracisternal injection of 5,7-dihydroxytryptamine (5,7-DHT) following treatment with desmethylimipramine induced development of behavioral supersensitivity to the intraperitoneally administered serotonin precursor 5-hydroxytryptophan (5-HTP) in the mouse. This behavioral syndrome, characterized by tremor and muscle twitches (myoclonus), showed a clear dose-response relationship with 5,7-DHT as well as with 5-HTP. Mice lesioned with a low dose of 5,7-DHT (20 micrograms) or a placebo were treated repeatedly with a protein synthesis inhibitor, sycloheximide (45 mg/kg, s.c., every 12 h for up to 10 days). This treatment resulted in a reversible decrease of cerebral protein synthesis varying between 70 and 20% with time between treatments. The myoclonic response to 5-HTP in animals pretreated with 5,7-DHT and by cycloheximide showed a decrease in intensity within 24 h when evaluated quantitatively by an electronic activity monitor, the results of which were confirmed by direct observation. Cycloheximide also exerted a similar, though smaller, effect following full development of sensitivity to 5-HTP over 10 days. These effects may de mediated by inhibition of rapidly turning over serotonin receptor proteins, although their interpretation is somewhat obscured by possible toxic effects of cycloheximide.
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PMID:Inhibition of 5,7-dihydroxytryptamine-induced supersensitivity to 5-hydroxytryptophan in mice by treatment with cycloheximide. 31 Mar 31

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

An extrapyramidal disorder occurring in three generations of a family (only males) is described The clinical features were progressive dementia and extrapyramidal signs without choreiform hyperkinesia. The youngest patient (onset of disease at the age of 22 years) showed tremor, rigidity, ataxia, convulsions, and myoclonus. The neuropathologic findings were characterized by isolated symmetrical degeneration of the corpus striatum and diffuse cortical atrophy without affecting other cerebrospinal neuronal systems. The clinical features of this familial disorder and its relation to other types of familial striatal degeneration and to the juvenile form of Huntington's chorea are discussed.
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PMID:[Familial striatal degeneration (author's transl)]. 54 75

A single dose of p-chloroamphetamine, 10 mg per kilogram, produced postural abnormalities, tremor, myoclonus, and autonomic signs in rats 5 minutes after intraperitoneal injection. This syndrome lasted 60 to 90 minutes, and its intensity was directly proportional to the amount of p-chloroamphetamine given over a 2 to 10 mg per kilogram range. Whole-brain levels of serotonin and 5-hydroxyindoleacetic acid were not altered during this interval, although both were reduced significantly 1 day later. Pretreatment with drugs that interfere with the uptake of p-chloroamphetamine into terminals of serotonergic neurons (fluoxetine), depress brain serotonin levels (p-chlorophenylalanine), or block serotonin receptors (methiothepin or methergoline) suppressed this syndrome, whereas drugs that antagonize the effects of dopamine, norepinephrine, and acetylcholine did not. These observations implicate serotonergic mechanisms and provide behavioral evidence of p-chloroamphetamine's immediate actions on serotonergic neurons in the central nervous system.
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PMID:Postural changes, tremor, and myoclonus in the rat immediately following injections of p-chloromaphetamine. 56 3

A 10 1/2 years old boy fell brutally ill with a fit followed by confusion, and then by deep coma, with 40 degrees C fever and morbilliform rash. Consciousnesse came back within ten days, with transient Parkinson-like tremor. Myoclonus persisted for about six months. Complete recovery was followed up for six years. A diagnosis of encephalitis was considered on early EEG evidence (stereotyped repetitive sharp wave bursts) and was confirmed by isolation of ECHO 5 virus from brain specimen, and ultrastructural observation of characteristic cytopathic effect (disappearance of organelles, proliferation of smooth membranes) and of probable viral particules in astrocytes, without any inflammatory process.
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PMID:[Curable ECHO 5 virus encephalitis. Clinical, electroencephalographic, virologic and ultrastructural study]. 88 30

A myoclonic syndrome consisting of tremor, myoclonus, and seizures was produced following the systemic administration of 5-hydroxytryptophan to adult rats previously given intracisternal injections of 5,7-dihydroxytryptamine and systemic desmethylimipramine, but not in their controls. This behavioral response was blocked by pretreatment with the putative serotonin receptor blocking agents methysergide, lysergic acid diethylamide, and bromolysergic and diethylamide, as well as centrally effective doses of the aromatic amino acid decarboxylase inhibitor Ro4-4602. Blockers of receptors of other neurotransmitters had little effect. This neurologic response in the adult rat may be relevant to some forms of clinical myoclonus and may be useful in testing potential agonists and antagonists of serotonin receptors in the mammalian central nervous system.
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PMID:Myoclonus after 5-hydroxytryptophan in rats with lesions of indoleamine neurons in the central nervous system. 108 96

Two postmortem case of multiple sclerosis treated by sterotactic operations for the intention shaking of limbs, trunk, and head, and for the action myoclonus are analyzed to determine the location of the substrate of myoclonic and ballistic movements, the location of the coagulations for relief of these movements, and whether fresh demyelinating foci are elicited by intracerebral interventions. In the first case of a clinically typical multiple sclerosis, the foci responsible for the severe action myoclonus and intention ataxia of the trunk are demyelinations in the right and left red nucleus resulting in nerve cell damage and loss and an almost complete destruction of myelinated fibers. The restricted foci in the white matter of the cerebellum which do not involve the cerebellar nuclei are not extensive enough or old enough to be the cause of the action myoclonus but may, perhaps, sustain the pathogenesis. - In the second case of cerebral palsy and combined multiple sclerosis (detected post mortem), the combination of the severe damage of putamen and caudate nucleus by status marmoratus and the extensive nerve cell and fiber damage due to demyelinating foci in the substantia nigra are probably the substrate of the jactitation and intention myoclonus of the left limbs. The stereotactic coagulation of the dentatothalamic and pallidothalamic fibers in the base of V. o.p. and V.o.a. at the point where they pass through the zona incerta (location confirmed post mortem) resulted in a nearly complete relief of hyperkinetic movements. In the first case, fresh demyelinating foci are present in both hemispheres with stereotactic interventions; these foci are located, amongother places, around the coagulation and the electrode track. In the second case, post mortem serial brain sections demonstrate that stereotactic operations even in subacute multiple sclerosis can be carried out without eliciting any exacerbation of demyelination foci. Therefore, the danger exists that stereotactic intervention in cases of multiple sclerosis may precipitate fresh demyelinating foci. As our clinical experience [Riechert and Richter, 1972a, b] indicates, however, this occurred in markedly less than 10% of the cases.
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PMID:Pathologic-anatomical findings and cerebral localization in stereotactic treatment of extrapyramidal motor disturbances in multiple sclerosis. 109 87


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