1/9. Dyskinesia induced by phenytoin.phenytoin is an effective antiepileptic drug, although, it can be associated with many side effects, including dyskinesia. OBJECTIVE: To describe the clinical characteristics of phenytoin induced dyskinesia. methods: We investigated the occurrence of involuntary movements in patients followed at our adult and pediatric epilepsy clinics during the period of one year. RESULTS: Three patients presented with phenytoin-induced dyskinesia: one adult with axial and orofacial dyskinesia, and two children with choreoathetosis. They did not have other signs of phenytoin intoxication and had complete recovery after phenytoin withdrawal. CONCLUSION: phenytoin induced dyskinesia may occur during either chronic or initial treatment and with normal serum phenytoin levels. However, it occurs most often in patients on polytherapy, usually after increasing dosage and with toxic serum levels. Other signs of phenytoin intoxication may be present in these patients, but often the dyskinesia is the only side effect, which may delay the diagnosis and treatment. The clinical characteristics of the involuntary movements vary and may be focal or generalized, most often characterized by choreoathetosis and dyskinesias. These may last for hours, days or even years, but frequently disappear completely after phenytoin withdrawal.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
2/9. Organophosphate intoxication-related coital-like involuntary movements: report of A case.The neurologic manifestations of organophosphate intoxication are many, and different pathophysiologic mechanisms are responsible for the different presentations occurring at different stages of the disease process. movement disorders constitute one of the neurologic manifestations, which may include Parkinsonism or other dyskinetic movements. However, involuntary coital-like movements have not been reported as one of the organophosphate intoxication-related movement disorders. In this case report, we describe a 71-year-old man who developed involuntary coital-like movements about one and a half months after an event of organophosphate intoxication in an attempt to commit suicide. The involuntary movements were to-and-fro pelvic thrusting and back-rocking movements. The patient was able to suppress the involuntary movements for a short period of time, although they usually persisted all day long. The involuntary movements occurred in all postures including standing, sitting and in supine postures, resulting in great embarrassment. These involuntary movements also interfered with the initiation of sleep, although they discontinued while asleep. With clonazepam and piracetam therapy, the involuntary coital-like movements of this patient decreased in amplitude, although remaining to a degree even after one year of follow-up.- - - - - - - - - - ranking = 3.5keywords = intoxication (Clic here for more details about this article) |
3/9. dystonia and akinesia due to pallidoputaminal lesions after disulfiram intoxication.A case with segmental cranial plus crural dystonia of delayed onset and akinesia after acute intoxication with disulfiram is presented. Computed tomography showed bilateral pallidal lesions, whereas on magnetic resonance imaging additional small lesions of the putamen could be detected. Long-term observation with progression and a change of symptoms over a period of 10 years after the intoxication is demonstrated on videotape. Although other central side effects after intoxication with disulfiram are well known, movement disorders are uncommon. carbon disulfide, a disulfiram metabolite, may be important in the etiopathogenesis.- - - - - - - - - - ranking = 3.5keywords = intoxication (Clic here for more details about this article) |
4/9. High-dose pyridoxine in tardive dyskinesia.The clinical similarities of tardive dyskinesia and 1-dopa intoxication lend support to the post-synaptic hypersensitivity hypothesis in tardive dyskinesia. pyridoxine, a co-factor in the decarboxylation of dopa, reverses the movement disorder of l-dopa intoxication. Although early studies of pyridoxine in tardive dyskinesia have not been encouraging, the results of the present study suggest that high doses of pyridoxine may reduce the frequency and severity of involuntary movements in tardive dyskinesia.- - - - - - - - - - ranking = 1keywords = intoxication (Clic here for more details about this article) |
5/9. Choreoathetosis during phenytoin treatment.A patient with symptomatic epilepsy receiving only phenytoin developed choreoathetosis and orofacial dyskinesias. These movement disorders disappeared when the drug was stopped and reappeared when the patient was challenged. Throughout the period of treatment, concentrations of phenytoin in serum were consistently low within the therapeutic range. Interfering symptoms from the cardiovascular system and the absence of some classic symptoms of phenytoin intoxication (nystagmus and dysarthria) contributed to delay the diagnosis. The patient died in hospital and autopsy of the brain showed rather localized encephalomalacies of corpus striatum. The pathogenic action of phenytoin and the role of preexisting brain lesions are discussed. phenytoin must be suspected as the cause, when patients on this drug present with uncontrolllable epilepsy or neurological or mental deterioration.- - - - - - - - - - ranking = 0.5keywords = intoxication (Clic here for more details about this article) |
6/9. carbamazepine-induced orofacial dyskinesia.Extrapyramidal syndromes have been described after administration of phenytoin and primidone. Although asterixis, dystonia, and tremor have been described with carbamazepine (Tegretol), there is no report of orofacial dyskinesia. We report a case in which a dose-related lingual-facial-buccal extrapyramidal reaction occurred in association with carbamazepine intoxication.- - - - - - - - - - ranking = 0.5keywords = intoxication (Clic here for more details about this article) |
7/9. death due to benzhexol toxicity.A rare case of death due to benzhexol toxicity is reported in a 48-year-old schizophrenic male with a resolving empyema and underlying patchy, mild bronchopneumonia. Toxicological analysis revealed the benzhexol blood and liver concentrations to be 0.12 mg/l and 0.5 mg/kg, respectively. Gastric contents contained 0.4 mg of benzhexol. Other drugs were not detected. It is suggested that for fatalities to occur following benzhexol intoxication, secondary contributory factors, which probably further alter the patient's conscious state, are necessary.- - - - - - - - - - ranking = 0.5keywords = intoxication (Clic here for more details about this article) |
8/9. Dyskinesia from manganism in a hepatic dysfunction patient.A 14-year-old boy came to the neurological clinic because of involuntary movement. He represented a case of common variable hypogammaglobulinemia, with hepatosplenomegaly noted for 5 years and jaundice for 1 month. Neurological and laboratory examinations revealed choreoathetosis and hyperbilirubinemia, hypoalbuminemia, increased hepatic aminotransferase, and decreased indocyanine green clearance; as well as increased signal change over the globus pallidus, subthalamic area, internal capsule, tegmentum, brain stem and pituitary gland revealed by a brain magnetic resonance (T1-weighted) imaging study. A manganese study confirmed high body manganese loading. trihexyphenidyl administration ameliorated the dyskinesia; however, the patient died from hepatic failure later. Though rare in incidence, manganese intoxication should be considered in cases with dyskinesia and the characteristic brain MRI findings. Even if no environmental exposure is involved, total parenteral nutrition, porto-systemic shunt and chronic hepatic dysfunction could lead to a heavy manganese load resulting in symptomatic manifestation.- - - - - - - - - - ranking = 0.5keywords = intoxication (Clic here for more details about this article) |
9/9. delirium and persistent dyskinesia induced by a lithium-neuroleptic interaction.We report the case of a bipolar patient developing severe delirium and extrapyramidal signs shortly after initiation of a lithium-neuroleptic combination therapy. Clinical presentation, EEG changes and lithium plasma levels showed a close correlation. The delirium was reversible when all drugs were stopped; however, dyskinesia was found to be persistent after a period of 6 months. This rare syndrome is difficult to differentiate from lithium intoxication and neuroleptic malignant syndrome. Given the additional use of valproate and biperiden in this patient, valproate encephalopathy and anticholinergic delirium are further differential diagnoses. To avoid this serious pharmacodynamic drug interaction, patients should be closely monitored when lithium-neuroleptic comedication is started.- - - - - - - - - - ranking = 0.5keywords = intoxication (Clic here for more details about this article) |