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)

Eighty-two schizophrenic outpatients receiving maintenance antipsychotic medication were assessed for akathisia and tardive dyskinesia. Thirty-nine (48%) manifested patterns of nondyskinetic, restless movement characteristic of akathisia. On the basis of their clinical features, these patients were divided into three groups: "acute" akathisia (recent onset, related to an increase in antipsychotic drug dose); "pseudoakathisia" (motor signs but no subjective symptoms); and "chronic" akathisia (a mixed category including persistent acute akathisia and "tardive" akathisia with the pharmacologic characteristics of tardive dyskinesia). Coarse, jerky foot tremor was observed as an invariable accompaniment of acute akathisia. A significant association was found between choreoathetoid limb dyskinesias, orofacial dyskinesias, and the presence of chronic akathisia. Also, the findings suggested a possible relationship between pseudoakathisia, orofacial and limb dyskinesia, and the severity of negative schizophrenic symptoms.
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PMID:Akathisia variants and tardive dyskinesia. 286 31

There are a number of different relationships among aging, psychosis and movement disorders, most of which have been proposed to involve the neurotransmitter dopamine. Dopamine content and dopamine receptors have been shown to decrease with age, which may relate to the time of onset of different motor and psychotic disorders, as well as to the appearance of these disorders. For example, some so-called senile movement disorders, such as senile tremor and senile chorea, may relate to alterations in dopaminergic transmission with age, as might the general findings of increased slowing of movements and mildly increased rigidity with age, although it is not clear how common some of these changes are in the medically healthy elderly. Decrease in dopamine with age may also be associated with the findings that choreiform and psychotic disorders (which have been proposed to be related to excess dopaminergic activity) tend to predominate at younger ages, whereas parkinsonism is more common at later ages. Certain findings support this notion, such as the appearance of both dyskinesia and psychosis in patients treated with L-dopa, the finding that psychosis may be less common in patients with later-onset Huntington's disease, and the fact that neuroleptic-induced parkinsonism is often more severe in the elderly. However, the situation is more complicated than this, because there are a number of phenomena that do not fit the pattern, including the observation of an increased incidence of tardive dyskinesia in the elderly. Age-related changes in other transmitters are undoubtedly important in both movements disorders and psychosis, and even dopamine has been proposed to have both trophic and toxic properties over the aging process. In general, care is warranted in the use of any psychotropic medications in the elderly, because there can be widespread and often unpredictable effects of these drugs on both motor and mental function.
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PMID:Association of psychosis and movement disorders in the elderly. 289 37

Tardive dyskinesia (TD); abnormal involuntary movements appearing late in neuroleptic treatment) was described shortly after introduction of chlorpromazine and other antipsychotic agents in the 1950s. Consideration of this disorder as a common, progressive, and relentless problem of major public-health and medicolegal concern in the 1970s now appears to have been somewhat exaggerated. Several symptom patterns associated with neuroleptic treatment may or may not appropriately be lumped with the concept of TD (acute and withdrawal-emergent dyskinesias, dystonias, and akathisia, in particular); parkinsonism (with bradykinesia, rigidity, and tremor, including perioral tremor of the "rabbit syndrome") should be differentiated from TD, even though elements of both may occur together. Dyskinesias, more or less similar to TD, can occur in chronically ill neuropsychiatric patients not exposed to neuroleptics. Some may represent stereotyped behaviors of schizophrenia or undiagnosed neurological disorders, but a risk of spontaneous dyskinesias indistinguishable from TD averages about 5% (probably less in young patients). Mean prevalence rates for TD, corrected for spontaneous dyskinesias, average about 15-20% with higher risks at advancing ages. Incidence rates are less certain, but estimates average about 5% a year for at least several years in young patients, with higher rates within the first two years of treatment of elderly patients. Risk factors most clearly defined are advancing age, use of neuroleptic agents at relatively high daily doses for more than six months, and perhaps the diagnosis of a major affective disorder. Female gender and relatively high plasma levels of neuroleptic agents are less significant risk factors and other metabolic or neuroradiological indicators of risk remain unproved. The etiology of TD remains obscure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A summary of current knowledge of tardive dyskinesia. 290 54

The role of D1 and D2 dopaminergic receptors in the occurrence of dyskinesia, particularly that of tics, is discussed. Observation of neuroleptic-induced oral movements in rats strongly suggests that stimulation of D1 receptors triggers or increases dyskinesia. Such distinction between the action of D1 and D2 dopamine agonists is not yet possible in humans. Experiments on the resting finger tremor in man or women enable to suspect and interaction between D1 and D2 receptors. Prenatal neuroleptic exposure during vulnerable periods of pregnancy decreases the density of dopaminergic D2 receptors in rat.
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PMID:Insights into the pathophysiology and pathogenesis of Gilles de la Tourette syndrome. 295 May 84

One hundred two patients with recurrent, drug-refractory tachyarrhythmias were treated with amiodarone for nine +/- eight months (mean +/- SD) (range, one to 50 months). Forty-five patients exhibited some form of neurotoxic reaction that was severe enough in nine patients to require discontinuation of treatment or reduction in dosage of the drug. The most frequent neurotoxic findings were tremor (44 patients), peripheral neuropathy (ten patients), and ataxia (seven patients). Five patients developed unusual neurotoxic manifestations: brainstem dysfunction characterized by downbeat nystagmus, hemisensory loss and ataxia, severe dyskinesia, jaw tremor, and proximal myopathy. Neurophysiologic studies revealed varying degrees of predominantly demyelinating peripheral neuropathy. Neurotoxic symptoms improved after discontinuing treatment or decreasing the dosage of the drug. Age of the patient and total cumulative dose did not seem to be risk factors for development of neurotoxicity. These neurotoxic findings suggest that amiodarone-induced neurotoxic reactions are not only confined to the peripheral nervous system, but also that parts of the central nervous system (eg, basal ganglia, brain stem, or their connections) may also be involved.
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PMID:Unusual neurotoxicity associated with amiodarone therapy. 303 78

The experience that the supplementation of depleted dopamine in the nigro-striatal system of parkinsonian patients with L-dopa improves the clinical triad, akinesia, rigidity and tremor, mainly applies to long-term treatment in the early phase of Parkinson's disease. Complications in motor performance, like on-off response, wearing-off phenomena, peak-dose dyskinesia, biphasic dyskinesia, off-period dystonia and others, after more than 3 to 5 years following the onset of treatment indicate fluctuations in the dopaminergic feedback control system. It is suggested that these complications are due to progressive presynaptic degeneration and late changes in postsynaptic receptor amplification. However, as fluctuations are not imperative in all patients, an important additional aspect seems to be the topography of denervation, which involves different portions of the striatum to varying degrees. Location and extent of denervation are criteria which appear to have predictive value for the malignancy of the disease, the therapeutic response of drugs and complications in long-term treatment.
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PMID:Factors contributing to fluctuations of the dopaminergic nigro-striatal feedback system in Parkinson's disease. 316 34

Precise radiographical measurement of the third ventricle in the first and essential procedure in stereotaxic surgery in order to determine the target point. This is done while referring to an available standard brain atlas such as Schaltenbrand & Bailey. However there have been no criteria established for determining the deviation of the coordinates of the thalamic nuclei, especially in their lateral coordinates when the third ventricle is highly dilated. Therefore, in 109 cases encountered recently (81 parkinsonism, 11 essential tremor, 10 cerebral palsy, 3 thalamic pain, 1 Benedikt's syndrome, 1 torticollis, 1 oral dyskinesia, 1 striato-nigral degeneration), we studied the correlation between the width of the third ventricle and the lateral coordinate of the thalamic point where kinesthetic neurons or tremor-synchronously discharging neurons were detected. These neurons were especially related to the arm. According to the width of the third ventricle, we classified the cases into three types: 18 cases with large ventricles (more than 10 mm), 37 cases with medium-sized ventricles (4-10 mm) and 16 cases with small ventricles (less than 4 mm). By plotting the lateral coordinate of the thalamic point where kinesthetic neuron of the upper extremity was recorded in reference to the radiogram of anteroposterior view, we found that the lateral coordinates of large ventricular cases generally tended to show more lateral displacement than cases where the ventricles were narrower. Their mean lateral coordinate was 16.9 mm from midline in contrast ot 14.0 mm in cases with small ventricular width. There was a linear correlation between the width of the third ventricle and the lateral coordinate of the kinesthetic neuron of the Vim nucleus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Lateral coordinate of the thalamic Vim neurons in the cases with dilated third ventricle]. 320 65

Long-term observation over 3-8 postoperative years of cases of Parkinson disease operated by stereotactic thalamotomy using a microelectrode recording technique is reported. The procedure is specifically useful in the following four groups: (1) tremor-dominant cases, (2) hemiparkinsonism, (3) cases with marked asymmetry in motor symptoms and (4) juvenile parkinsonism presenting levodopa-induced dyskinesia.
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PMID:Long-term follow-up study of nucleus ventralis intermedius and ventrolateralis thalamotomy using a microelectrode technique in parkinsonism. 332 71

We compared 46 patients having onset of Parkinson's disease before age 45 years with 52 having onset after age 70. Young-onset cases more often presented with muscular stiffness (43%) and old-onset with difficulty walking (33%). One-third of young-onset cases had off-period dystonia, mostly affecting the legs, but no dystonia was recorded in old-onset cases. Presentation with rest tremor occurred in 41% of young-onset and 63% of old-onset. There were no differences in the number of affected relatives, endocrine disease, personality characteristics, dementia, or dyskinesia. A pathological study of 12 young-onset and 22 old-onset cases showed 24% greater nigral cell loss in the young, but no differences in the basic Lewy body pathology. Median disease duration in young cases was 5 years longer in the clinical study and 12 years longer in the pathological study. These studies show that the Parkinson's disease process is similar in young- and old-onset cases.
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PMID:A comparison of clinical and pathological features of young- and old-onset Parkinson's disease. 341 87

Chronic alcoholics who maintain abstinence often demonstrate remarkable improvement of neurological and mental dysfunction. This paper presents an overview of the clinical and laboratory work of our group. Reversible clinical manifestations include psychometric scores, ataxia, tremor, Parkinsonism, dyskinesia, cerebral atrophy, EEG parameters, and a CSF acidosis. Electrophysiological investigations showed that in the in vitro hippocampus of rats fed ethanol for several months there was evidence for diminished long-term potentiation, impaired neuronal inhibitory mechanisms (diminished inhibitory post-synaptic potentials and post-spike after hyperpolarisations), decreased neuronal specific membrane capacitance and increased specific membrane resistance. Golgi stains showed attenuation of hippocampal CA1 neuronal dendrites in rats fed ethanol for five months, which reverted to control size in rats permitted two months of alcohol withdrawal.
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PMID:Reversibility of alcohol-related brain damage: clinical and experimental observations. 347 66


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