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)

Stroke-related nonepileptic transient dyskinesias are rare, and the site of ischemia remains often undetermined. Five cases out of 47 consecutive thalamic infarcts (10.6 per cent) are reported. Patients presented with monochorea (1 case), hemiballism-hemichorea (2 cases), choreoathetosis (1 case with subsequent arm painful dystonia and hand tremor), and asterixis (1 case). Magnetic resonance imaging demonstrated that the subthalamic nucleus was spared in all cases. Transient dyskinesias occurred at any time in the course of infarction (as a warning sign in 1 case, as an associated symptom in 3 cases, or during recovery in 1 case). Moreover, this study suggests that: 1) transient dyskinesias are mainly related to thalamic ischemic injury, and 2) small vessels disease is the main etiology.
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PMID:[Transient involuntary movement disorders and thalamic infarction]. 830 59

This article focuses on the current knowledge about movement disorders associated with alcohol and drug abuse. Chronic alcohol use can produce a wide spectrum of movement disorders including tremor, withdrawal parkinsonism and dyskinesias, cerebellar ataxia, and asterixis. MPTP, a neurotoxin first reported to cause parkinsonism in a group of drug abusers, has provided important insights into the pathogenesis of Parkinson's disease. There is a growing body of literature providing evidence that dyskinesias such as tics and dystonia may be precipitated or exacerbated by cocaine. Amphetamines have been implicated in the production of stereotypies and exacerbation of tics.
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PMID:Movement disorders. 837 47

Asterixis (flapping tremor) can be induced by treatment with psychopharmacologic agents. We observed 10 cases of asterixis in psychiatric inpatients, most with affective spectrum disorders being treated with combination therapy. The drugs most often used were clozapine (eight cases), lithium (seven cases), and carbamazepine (seven cases). There were neither metabolic disorders nor structural brain lesions that might explain the occurrence of asterixis. Because dosage in general was moderate and serum levels were within therapeutic boundaries in most cases, the symptom seemed to have been caused by an interaction of drugs rather than by a single agent. Therefore clozapine, carbamazepine, and lithium should be combined with each other only with great care.
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PMID:Asterixis induced by psychotropic drug treatment. 882 98

Negative myoclonus (NM) is a motor phenomenon characterized by involuntary jerky movements due to a brief, sudden interruption of muscular activity. This motor disturbance can be observed in a variety of clinical conditions, that can range from physiological NM, occurring when falling asleep or after prolonged exercise, to asterixis, a form of NM observed in patients with toxic-metabolic encephalopathies or with focal brain lesions, or, as a paroxysmal phenomenon, labelled as epileptic negative myoclonus, in epileptic patients. Neurophysiological investigations are essential to diagnose NM and to distinguish it from other motor disorders, such as tremor or positive myoclonus. Furthermore, neurophysiological findings can provide useful information supporting a subcortical or cortical origin of NM. In cortical NM, recent data suggest a role of cortical active inhibitory areas in the generation of this motor phenomenon.
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PMID:Negative myoclonus. 889 93

Involuntary movements are an infrequent complication of treatment with phenytoin and include tremor, asterixis, myoclonus, parkinsonism, and dyskinesias. The mechanism by which phenytoin exerts its actions is unclear. Phenytoin has been observed to exert variable effects on dopamine metabolites and also may induce changes in serotonergic activity. In this report, we discuss the available experimental evidence concerning the possible mechanisms of involuntary movements induced by phenytoin. We describe a case of postural myoclonus during treatment with phenytoin.
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PMID:Postural myoclonus induced by phenytoin. 893 94

Instrumental tremorgrams have been used to improve the diagnostic accuracy of various movement disorders, including tardive akathisia. The aim of the present work was to evaluate their place in the diagnosis of neuroleptic-induced tremor and to determine whether they can help to differentiate this disorder from other neuroleptic-induced movement disorders and from other types of tremor. Fourteen psychiatric patients treated with various neuroleptic medications were diagnosed as having neuroleptic-induced tremor on the basis of clinical criteria. They underwent accelerometric recordings following diagnosis. All patients demonstrated upper-limb tremor; four also had involvement of the lower limbs, jaw or tongue. Most demonstrated both resting and postural tremor, the latter being the more prominent. The tremor was mainly rhythmic, regular and sinusoidal. It did not significantly interfere with activities of daily living in the majority of patients, but four did exhibit some degree of impairment. Repeated accelerometric recordings showed constant and regular waveforms and frequencies (between 4 and 7 Hz) in each patient. We conclude that the presence of repeated constant waveforms and frequencies on accelerometric tracings may serve as confirmation of the diagnosis of neuroleptic-induced tremor. In light of the findings of this and other studies, we suggest that tremorgrams may be helpful in differentiating neuroleptic-induced tremor from other neuroleptic-induced movement disorders (e.g., tardive dyskinesia and tardive akathisia) and from psychogenic tremor. Although these techniques may also assist in the differentiation of neuroleptic-induced tremor from some tremor disorders (e.g., asterixis or ataxic tremor), their overall potential to distinguish it from other types of organic tremor is more limited.
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PMID:Clinico-tremorgraphic features of neuroleptic-induced tremor. 969 Sep 78

This is a proposal of the Movement Disorder Society for a clinical classification of tremors. The classification is based on the distinction between rest, postural, simple kinetic, and intention tremor (tremor during target-directed movements). Additional data from a medical history and the results of a neurologic examination can be combined into one of the following clinical syndromes defined in this statement: enhanced physiologic tremor, classical essential tremor (ET), primary orthostatic tremor, task- and position-specific tremors, dystonic tremor, tremor in Parkinson's disease (PD), cerebellar tremor, Holmes' tremor, palatal tremor, drug-induced and toxic tremor, tremor in peripheral neuropathies, or psychogenic tremor. Conditions such as asterixis, epilepsia partialis continua, clonus, and rhythmic myoclonus can be misinterpreted as tremor. The features distinguishing these conditions from tremor are described. Controversial issues are outlined in a comment section for each item and thus reflect the open questions that at present cannot be answered on a scientific basis. We hope that this statement provides a basis for better communication among clinicians working in the field and stimulates tremor research.
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PMID:Consensus statement of the Movement Disorder Society on Tremor. Ad Hoc Scientific Committee. 982 89

We prospectively studied motor symptoms in 32 patients with CT- or MRI-proven acute pure parietal stroke. A transient, mild, 'pseudoparesis' of the hand (90%), was noted, improved by visual attention and prompting, associated with non-awareness of muscle power (53%), transient soft pyramidal signs (50%), unilateral akinesia (100%) and motor hemineglect (37%) in non-dominant lesions. Lower motoneurone-type atrophy was not observed in this acute phase. We called 'poikilotonia' the striking unpredictable variations in muscle tone, ranging from extreme hypertonia to hypotonia, found in all patients. When maintaining postures, patients showed large oscillations (100%), laterodeviation or levitation of the arm (60%), especially in the case of large or posterior lesions, or, occasionally (3%), motor persistence or even hemicatalepsy (3%). Limb kinetic and manipulatory apraxia, with inadequate organization and anticipation of motor sequences and synergies, motor arrests, perplexity, unrecognizable gestures and loss of bimanual coordination, was a constant finding (100%). Other apraxias (62%) and difficulty in copying intransitive gestures of the hand (84%) were associated with posterior lesions involving the supramarginal gyrus. When reaching towards objects, all patients showed abnormal anticipatory hand shaping, but visuomotor ataxia (3%) was only seen with bilateral posterior stroke. Sensory (70%) or pseudocerebellar (4%) ataxia, was seen in both anterior and posterior lesions. Avoidance behaviors (34%) were not uncommon, but had no localizing value. Of the dyskinesias, hand dystonia (84%) was frequent, but athetosis (16%), asterixis (15%), postural tremor (15%), myoclonus (9%) and stereotypia (9%), were uncommon. The abnormal eye movements were unilateral hypo-akinesia of exploratory saccades (43%), abnormal ipsilateral pursuit and contralateral optokinetic nystagmus in the case of posterior lesions, and oculomotor apraxia with bilateral posterior lesions. In conclusion, parietal motor syndrome can be recognized during bedside examination, and probably reflects the loss of multiple sensory feedback to motor programs, especially those directed to the extrapersonal space.
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PMID:Parietal motor syndrome: a clinical description in 32 patients in the acute phase of pure parietal strokes studied prospectively. 987 53

Portal-systemic encephalopathy may be seen with hyperammonemia that complicates chronic liver disease. We report an unusual case of reversible parkinsonism associated with hyperammonemia and portal vein thrombosis. An active 90-year-old male developed motor slowing and resting hand tremor over 6 months. Examination showed asterixis, bradykinesia, cogwheel rigidity, rest tremor, and a parkinsonian gait. Serum venous ammonia was elevated at 145 microM. The next day, the patient became comatose and serum ammonia was 178 microM. With lactulose therapy, serum ammonia level normalized and examination showed only minimal parkinsonism after 1 week. An abdominal CT scan identified portal vein thrombosis with porto-systemic shunting that reversed after 7 months of treatment. Examination 2 years later showed no signs of parkinsonism. Parkinsonism can dominate the clinical picture of patients with hyperammonemia before the onset of encephalopathy.
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PMID:Reversible parkinsonism and hyperammonemia associated with portal vein thrombosis. 1124 May 69

The authors investigated 12 patients with cirrhosis who had hepatic encephalopathy (HE): six with continuous mini-asterixis and six with subclinical HE without asterixis. They studied the coupling between hand-muscle electromyography (EMG) recordings and brain activity recorded by magnetoencephalography. On forearm elevation, patients with tremor developed excessive coupling between activity in the motor cortex (M1) and contralateral hand-muscle EMG recordings at the frequency of mini-asterixis, which was not found in controls. The corticomuscular coupling demonstrates the involvement of M1 in asterixis and may reflect a pathologically slowed and synchronized motor cortical drive.
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PMID:Cortical origin of mini-asterixis in hepatic encephalopathy. 1180 39


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