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)

We describe the clinical characteristics, causes and response to treatment in 6 patients with AIDS who presented with abnormal movement disorders between January 1987 and July 1993 in our hospital, 3 with hemiballismus-hemichorea, 1 with athetosis, 1 myoclonia and 1 with "rubric" tremor. Brain imaging showed lesions in the corpus striatum in all the patients. Suspected diagnoses were cerebral toxoplasmosis in 4, cerebral lymphoma in 1 and progressive multifocal leukoencephalopathy in 1. The toxoplasmosis patients showed improvement (2 cases) or disappearance (2 cases) of movements with antiparasitic therapy. Treatment provided no benefit to the patients with leukoencephalopathy and lymphoma. Hemiballismus-hemichorea was the most common movement disorder in AIDS patients. The underlying cause is usually lesions in the basal ganglia arising from toxoplasmosis. If the lesions are so caused, movements may improve with antiparasitic therapy.
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PMID:[Movement disorders and AIDS]. 865 95

Chronic acquired hepatocerebral degeneration (CAHD) is a heterogeneous disorder that can occur with a primary neurologic, hepatic, or combined presentation. Little has been added to the understanding of this disorder since the detailed, early clinical and pathological descriptions. The spectrum of clinical presentations can be neuropsychiatric (apathy, lethargy, excessive somnolence), a movement disorder (ataxia, tremor, chorea, parkinsonism, myoclonus, dystonia), or both. Cortical laminar necrosis and polymicrocavitation in the cortex and basal ganglia are combined with cerebral and cerebellar atrophy. Microscopically, Alzheimer type II astrocytes and cytoplasmic glycogen granules are characteristic. Recent neuroradiological observations in patients with liver failure have shown a specific magnetic resonance (MR) imaging appearance with a hyperintense T1 signal in the pallidum, putamen, and, rarely, mesencephalon. Using clues from a similar MR appearance in patients receiving total parenteral nutrition as well as animals given parenteral manganese, and the knowledge that manganese is cleared by the hepatobiliary system, deposition of manganese in the brain is postulated in patients with CAHD. In this review we describe three cases of CAHD with detailed clinical and radiological documentation and discuss the aforementioned pathogenetic mechanisms.
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PMID:Chronic acquired hepatocerebral degeneration: case reports and new insights. 886 9

Levodopa-induced psychotic symptoms frequently complicate the management of patients with Parkinson's disease (PD). We examined the efficacy and tolerability of a novel antipsychotic, remoxipride, in this population. This was a 7-week, open-label pilot evaluation of patients with moderate to severe PD and levodopa-induced psychotic symptoms of at least 2 months' duration. The patients were recruited at the Movement Disorders Clinic, The Toronto Hospital, a tertiary referral center. After 1 week of baseline observation, the patients received remoxipride, 25 mg, three times a day orally, with the dose increasing by 25 to 50 mg each week as tolerated. The outcome measures included the Brief Psychiatric Rating Scale (BPRS), the Clinical Global Impressions (CGI) scale, and the United Parkinson's Disease Rating Scale. Adverse symptoms were elicited by an open-ended questionnaire and a symptom checklist. Six men and three women aged 69.3 +/- 9 years received remoxipride 147 +/- 57 mg/day. Total BPRS score decreased modestly in eight of nine subjects, and there was a statistically significant improvement of mental status as indicated by the CGI scale score, which decreased from 3.8 +/- 0.4 at baseline to 2.4 +/- 1.3 at last rating (p < 0.05; Wilcoxon signed rank test). The motor performance deteriorated somewhat in two subjects, whereas the rest showed no appreciable change. The most common adverse effects included tremor, rigidity, akathisia, and hypersalivation. Remoxipride treatment reduced psychotic symptoms in eight of nine subjects while having no appreciable effect on the parkinsonian status of seven of nine subjects.
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PMID:Remoxipride in the treatment of levodopa-induced psychosis. 888 13

Developmental regression is the presenting symptom of most infants with cobalamin (Vitamin B12) deficiency. We present a report of three infants with cobalamin deficiency in which the infants also developed a movement disorder. In each case the mother was a vegetarian and the infant was exclusively breast-fed. In two of the infants, a striking movement disorder consisting of a combination of tremor and myoclonus particularly involving face, tongue, and pharynx appeared 48 h after the initiation of treatment with intramuscular cobalamin. This was associated with marked changes in plasma amino acid levels. Paradoxically, the onset of the movement disorder coincided with overall neurological improvement. The third infant had a persistent focal tremor, which appeared before the commencement of treatment. The movements slowly abated during a 3-6 week period. The presence of a movement disorder in cobalamin deficiency has received less attention than other features, but in a mild form is probably common. It may offer an early clue to the diagnosis before the onset of profound neurological deterioration. The cause of the severe movement disorder that can appear after treatment is not known.
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PMID:The neurological syndrome of infantile cobalamin deficiency: developmental regression and involuntary movements. 899 52

Parkinsonism, tremor, chorea-ballismus, dystonia, tardive dyskinesia, myoclonus, tics and akathisia can be induced by many drugs. The drugs that are most frequently implicated in movement disorders are antipsychotics, calcium antagonists, orthopramides and substituted benzamides (e.g. metoclopramide, sulpiride, clebopride, domperidone), CNS stimulants, antidepressants, anticonvulsants, antiparkinsonian drugs and lithium. It is possible for a single drug to induce 2 or more types of movement disorders in the same patient. Movement disorders are not always reversible after drug withdrawal.
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PMID:Drug-induced movement disorders. 909 56

We describe a patient who developed right arm dystonia following an electrical injury. The patient's arm remained adducted, and flexed at the elbow and wrist, with all movement resulting in pain and tremor. Surface electromyographic evaluation revealed constant tonic activity of multiple upper and lower arm muscles at rest, that was not distractible. Voluntary and passive movement of the elbow or wrist resulted in high amplitude EMG activity, with motor grouping at 11 Hz at the elbow and 8 Hz at the wrist. Although a diagnosis of psychogenic dystonia was entertained, the stereotyped nature of the movement disorder and lack of variability on clinical and surface EMG evaluation support an organic disorder that was temporally-related to an electrical injury.
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PMID:Dystonia secondary to electrical injury: surface electromyographic evaluation and implications for the organicity of the condition. 912 15

We describe four patients who developed asymmetrical, rhythmic, stereotyped, and repetitive movements of the upper and lower limbs hours to days after infarction that involved the thalamus and/or basal ganglia. The movements appeared to occur spontaneously and were initially labeled as focal motor seizures, ballism, or tremor; they could however, be induced by passive movement of the limbs. The movements most commonly observed were scratching or rubbing movements of the hands that were of such persistence as to cause trauma to the skin; in the lower limbs, the heel was run up and down the bed sheet, often until it bled. The movements were part of a syndrome characterised initially by a reduced level of consciousness and followed by aspontaneity, usually with mutism and frontal release signs. One patient who had relatively preserved cognition and language repeated words or phrases again and again when encouraged to speak, but had no difficulty changing responses appropriately to different cues. In drawing, he overwrote each figure but could change the figure on command. The distinctive movement disorder in these patients was due to clonic perseveration. We suggest that clonic perseveration results from disconnection of prefrontal cortico-basal ganglia-thalamo-cortical loops that are important for the termination of motor plans. Clonic perseveration should be recognised as a movement disorder following thalamic lesions.
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PMID:Clonic perseveration following thalamofrontal disconnection: a distinctive movement disorder. 915 33

We examined the occurrence of posttraumatic movement disorders after moderate or mild head injury with a three-level follow-up study including questionnaires, telephone interviews, and personal examinations 4-6 years after the trauma (mean 5.2 years). Sixteen of 158 patients (10.1%) for whom a detailed follow-up was available had developed movement disorders most probably related to craniocerebral trauma. The most frequent finding was a low-amplitude postural/intention tremor that appeared to resemble enhanced physiological or essential tremor. Twelve patients reported transient tremor, two patients had persistent tremor, one patient had transient tremor and persistent hyperekplexia, and another patient had mild persistent cervical myoclonic twitches. Overall, the movement disorder was transient in 12 patients (7.6%) and persisted in only 4 patients (2.6%). These movement disorders were not disabling and did not require medical therapy. Taking into account possible bias by selection of the sample group, the frequency of movement disorders secondary to moderate or mild head trauma might be lower than 10.1%. Posttraumatic movement disorders occurred significantly more often in the group of patients with Glasgow Coma Scores between 9 and 14 than in those with a score of 15. Severe movement disorders such as low-frequency kinetic tremor or hemidystonia were not identified in this survey.
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PMID:Posttraumatic movement disorders after moderate or mild head injury. 915 42

Movement disorders in Japanese encephalitis (JE), although reported, have not been analyzed systematically. In this study, we report an analysis of movement disorders in 14 out of 17 JE patients, correlated with the radiological findings. All patients had at least a four fold rise of IgG antibodies against JE in a haemagglutination inhibition test. The patients' ages ranged between 2 and 54 years and 4 of them were women. Extrapyramidal signs, such as hypokinesia, hypophonia and masking of the face, were present in all patients by the first month as the patients came out of the coma-except for 1 patient. Eight patients had axial and 3 tongue dyskinesia; rigidity was present in 6 and tremor in 2 patients. At 3 months, these symptoms improved considerably in 6 patients. Cranial CT scan revealed thalamic involvement in 10, which was bilateral in 9 patients. Two patients had brain stem and one had cerebellar involvement. Cranial MRI was carried out in 9 patients and revealed additional findings in lentiform nucleus, midbrain and pons in 3 each and cerebellum in 4 patients. Bilateral thalamic involvement on MRI was seen in all the patients, including two patients whose CT scans were normal. SPECT studies using 99mTc-ECD revealed bilateral thalamic hypoperfusion in all (n = 7) and frontal hypoperfusion in 3 patients. In JE, movement disorders are common and may be due to thalamic involvement in isolation or in combination with basal ganglia or midbrain or both.
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PMID:Movement disorders in Japanese encephalitis. 917 54

We report three members of a single family with an apparently autosomal dominant, nonparoxysmal, hyperkinetic movement disorder with onset in adolescence. The proband, a 56-year-old woman, manifested dystonia, tremor and myoclonus; one of her daughters exhibited myoclonus with tremor, and the other demonstrated myoclonus with chorea later accompanied by tremor and dystonia. The slowly progressive but not debilitating symptoms were restricted to the head, arms and hands and were only moderately affected by alcohol. Laboratory investigations failed to identify any abnormality, and linkage analysis excluded the region containing the DYT1 locus, indicating that the gene responsible for idiopathic torsion dystonia was not implicated in this family. While this disorder shares manifestations with myoclonic dystonia, essential myoclonus and benign chorea, the marked intrafamilial heterogeneity and the sex-limited phenotype expressed only in females of two generations appear to be unique.
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PMID:Intrafamilial heterogeneity of movement disorders: report of three cases in one family. 926 60


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