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)

Double Blind comparative trial of a new dibenzodiazepine derivative Clozapine (Leponex) with Chlorpromazine was conducted in the treatment of acute schizophrenic illness over a 6 week period. Factor Analysis of ratings in 9 matched pairs indicates that Clozapine, at 300 mg. per day, is comparable in efficacy to Chlorpromazine in all factors except "Irritability" for which Clozapine appears to be superior. Illness severity and Global Change ratings in all patients showed that Clozapine is more effective in producting a shift towards improvement at the end of 6 weeks. Major side effects reported in Clozapine confirmed sedation and hypersalivation as consistent problems and presence of rigidity and tremor (extra-pyramidal) being at variance with other studies.
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PMID:Double-blind comparison of clozapine with chlorpromazine in acute schizophrenic illness. 79 82

The clinical and pathological features of 19 neonatal Holstein-Friesian calves affected with moderate to severe neurological disease are presented. Most calves were recumbent from birth, and many developed variable neurological signs including hyperaesthesia or depression, limb extension, head tremor, nystagmus, apparent blindness, and opisthotonos when stimulated. Consistent lesions of moderate to severe, diffuse, axonal swelling and loss, with Wallerian-type degeneration and myelin depletion in the spinal cord and brainstem, and occasionally in the midbrain and peripheral nerve roots, were observed. The lesions indicated a pre-natal insult affecting mainly motor areas of the foetal neuraxis, however the aetiology of the disorder remains undetermined. It is suggested that the calves may have been affected by a hitherto unrecognised disease entity for which we propose the term, degenerative axonopathy.
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PMID:Neurological disease associated with degenerative axonopathy of neonatal Holstein-Friesian calves. 273 93

The records of 37 patients with systemic lupus erythematosus (SLE) followed at The Children's Hospital of Philadelphia between 1968 and 1978 were reviewed for evidence of central nervous system (CNS) involvement. Criteria for CNS involvement included evidence of organic brain syndrome, electroencephalographic abnormalities with symptoms referable to CNS, or objective neurologic signs. Sixteen of 37 children had CNS involvement (43%). Thirteen patients had CNS involvement at the onset of SLE. Three patients had late onset CNS manifestations 1 to 2 years after the diagnosis of SLE. The most frequently observed symptoms were headache, behavior disorder, lethargy, diplopia, blurred vision, memory alteration, dizziness, and alteration of consciousness. The most frequently observed neurologic signs were seizures, cranial nerve palsy, ataxia, papilledema, nystagmus, meningitis, tremor, rigidity, cortical blindness, and coma. Neuropsychiatric manifestations included organic brain syndrome, functional psychosis, and personality disorder. Laboratory tests showed elevated cerebrospinal fluid opening pressure and protein, negative cultures, and abnormal electroencephalograms and computerized axial tomography scans. Fourteen of 16 children with CNS manifestations are alive. Thirteen had a mean IQ of 89 by the Wechsler Intelligence Tests. Twelve are in educational programs. One required long-term psychiatric care. A residual neurologic abnormality, a seizure disorder, was present in 3. CNS involvement with SLE in children carries a favorable prognosis.
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PMID:Central nervous system involvement in childhood systemic lupus erythematosus. 731 16

We report 2 survivors of severe methanol poisoning who developed, apart from blindness, a Parkinson-like extrapyramidal syndrome characterized by reduced initiative, poor voice volume, masked facies, mild tremor, rigidity, and bradykinesia. Both patients were mildly demented and 1 had hyperreflexia and bilateral Babinski responses. Computed tomographic scans in both patients demonstrated bilateral symmetrical infarction of the frontocentral white matter and putamen. Electromyography in 1 patient showed extensive denervation, mainly involving the legs, but normal motor conduction velocities. L-Dopa administered to the more severely affected patient had no effect on the parkinsonian features. Autopsy revealed cystic resorption of the putamen and the frontocentral subcortical white matter in additon to widespread neuronal damage throughout the cerebrum, cerebellum, brainstem, and spinal cord.
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PMID:Methanol poisoning: a clinical and pathological study. 742 69

Child abuse by whiplash-shaking can lead to severe injury in infants, including cerebral damage, neurological defects, blindness, and mental retardation. These findings are seen often without external evidence of head injury. Nurses should suspect shaken baby syndrome (SBS) in infants less than 1 year of age who present with apnea, seizures, lethargy or drowsiness, bradycardia, respiratory difficulty, coma, or death. Subdural and retinal hemorrhages accompanied by the absence of external signs of trauma are hallmarks of the syndrome.
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PMID:Shaken baby syndrome: a nursing perspective. 771 67

Cyclosporin A (CsA) has been shown to be useful in the prophylaxis of acute graft-versus-host-disease (GVHD). However, this immunosuppressive agent produces multiple side-effects including nephrotoxicity, hypertension, hypertricosis, gum hyperplasia, infections, and neurotoxicity. We report a retrospective analysis of neurotoxicity in 625 recipients transplanted for thalassemia and given CsA as part of GVHD prophylaxis. Neurotoxicity consisted in mental status changes, tremor, headache (grade 1), visual disturbance and cortical blindness (grade 2) and seizures and coma (grade 3). The overall toxicity was 28.8% and the incidence of convulsions was 10.1%. Neurological findings were reversible after temporary reduction or discontinuation of CsA. Class 3 patients, when prepared with protocol 6 (Bu 14 + Cy 200 and CsA for GVHD) or when they developed acute GVHD, had the highest risk of convulsions. Age, sex, different conditioning regimens, different anticonvulsive prophylaxis, liver damage due to iron-overload and/or to chronic inflammation did not influence the occurrence of CsA-related CNS toxicity. The occurrence of acute GVHD with concomitant use of high-dose corticosteroids is the single significant predisposing factor in the occurrence of convulsions. Grades 1 and 2 of neurotoxicity occurred earlier and were not influenced even by acute GVHD.
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PMID:CsA-associated neurotoxicity and ineffective prophylaxis with clonazepam in patients transplanted for thalassemia major: analysis of risk factors. 883 9

Cyclosporine has been associated with various neurological side-effects including postural tremor, seizures, headaches, encephalopathy, cortical blindness, and visual hallucinations. We describe here two patients who developed parkinsonism, with rest tremor and bradykinesia, after receiving cyclosporin A following allogeneic bone marrow transplantation. The patients did not have pre-existing neurological disorders, and had not received significant amounts of dopamine-blocking drugs. One patient improved markedly with Sinemet (carbidopa-levodopa), while the other (who did not tolerate Sinemet) improved with decrease in cyclosporine dosage. The relation of the parkinsonian symptoms to cyclosporine therapy and lack of other evident causes for the symptoms, suggests that parkinsonism may be an occasional consequence of cyclosporine.
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PMID:Parkinsonism during cyclosporine treatment. 887 34

Leber's congenital amaurosis (LCA), a type of congenital blindness, is clinically and genetically heterogeneous and often associated with systemic anomalies. We report on two sisters who were born to a consanguineous couple and had retinitis pigmentosa-like pigmented retinal lesions, alternating exotropia, bilateral cataracts, and anomalous coarse facies characterized by deformed skull with narrow forehead, low anterior hairline, hypertelorism, short philtrum, thin upper lip, and prominent jaw; cerebellar vermis hypoplasia; dilatation of the fourth ventricle; severe mental retardation; tremor; brisk deep tendon reflexes and abnormal behavior; and skeletal abnormalities such as limited extension of elbow and/ or finger joints and talipes equinovalgus. Skin defect and renal anomalies were seen in only one patient. Our patients are the first familial LCA associated with cerebellar vermis hypoplasia, and the disease involving particular multiple systemic anomalies may represent a distinct clinical entity.
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PMID:Two sib cases of Leber congenital amaurosis with cerebellar vermis hypoplasia and multiple systemic anomalies. 971 9

Shaken baby syndrome is a serious form of physical child abuse, which is frequently overlooked. It should be suspected in all children younger than one year of age, who present with drowsiness, coma, seizures or apnoea. A combination of subdural haematomas and retinal haemorrhages with minimal or no trauma and no coagulopathy is almost pathognomonic of the syndrome. The findings are caused by shaking with or without impact. Physical signs of violence are often absent and the syndrome may easily be mistaken for serious infection or seizure disorder. Many cases are fatal or lead to severe disability including blindness, cerebral palsy, mental retardation or epilepsy in about 60% of the children. There are many unresolved problems regarding diagnosis, pathophysiology, treatment, prognosis, prophylaxis and legal actions. We discuss these problems and in addition present eleven children with shaken baby syndrome.
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PMID:[Shaken baby syndrome]. 982 79

Cyclosporin A (CsA) induces neurological side effects in up to 40% of patients. A reversible posterior leukoencephalopathy syndrome is the most serious complication. Symptoms include headache, altered mental functioning, seizures, cortical blindness, and other visual disturbances, with hypertension. Neuroimaging studies show white matter changes in the posterior regions of the brain. Other neurological side effects of CsA include tremor, diffuse encephalopathy, cerebellar syndrome, extrapyramidal syndrome, pyramidal weakness, and peripheral neuropathy. Hypertension, hypomagnesemia, hypocholesteremia, and the vasoactive agent endothelin may all play a role in the pathogenesis of CsA neurotoxicty. Neurotoxicity is more frequent with high CsA blood levels, but levels may be within the therapeutic range. Dose reduction or withdrawal of CsA usually results in resolution of clinical symptoms and of neuroimaging abnormalities.
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PMID:Cyclosporine neurotoxicity: a review. 1039 63


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