Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Similar movement disorders developed in two 8-year-old retarded children while they were receiving phenytoin. Seizures subsequent to a diphtheria-pertussis-tetanus immunization had developed in each child at 1 to 2 months of age. A static encephalopathy ensued, characterized by mental retardation, ataxia, spasticity, and a mixed seizure disorder. Intermittent dystonia and choreoathetosis developed insidiously while serum phenytoin concentrations were in the therapeutic range. Sustained dystonia and choreoatheosis developed 2 hours after an oral provocation with phenytoin. The baseline abnormalities on the electroencephalogram remained unchanged during the choreoathetosis. Recognizable metabolic abnormalities known to be associated with similar movement disorders were excluded. It was concluded from these studies that the movement disorder is secondary to phenytoin and can occur at therapeutic serum concentrations. Phenytoin is a central anticholinergic agent and a central stimulant of serotonin, and may induce movement disorders as a result of altering these neurotransmitters in the brain. The variable expression of these movement disorders may relate to the nature of the preexisting striatal insult.
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PMID:Phenytoin-induced dystonia and choreoathetosis in two retarded epileptic children. 94 1

The relationship between phenytoin-induced ataxia and its concentration was characterized in rats who received i.v. infusions of the drug at either 0.52, 0.85 or 1.70 mg/min/rat until the onset of ataxia. Phenytoin dose to ataxia did not change with infusion rate but the total and unbound serum concentrations at onset of ataxia increased with increasing infusion (input) rate. Concentrations in cerebrospinal fluid, CSF, and in brain, at this end-point, were not affected by the infusion rate. Direct i.v. infusion of phenytoin major metabolite, p-HPPH, failed to produce ataxia. Thus phenytoin in CSF and brain, unlike serum phenytoin, equilibrates rapidly with site(s) of phenytoin neurotoxicity and represents appropriate sampling sites for identifying factors affecting phenytoin neurotoxicity.
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PMID:Pharmacodynamics of phenytoin-induced ataxia in rats. 230 25

Dilantin toxicity has been well described and has generally been noted to include signs and symptoms of nystagmus, ataxia, nausea, and vomiting. Dilantin's depressive effects are seldom mentioned. Two patients are presented who, although stable while on the rehabilitation unit, developed vegetative signs of depression soon after discharge. Both were found to have toxic levels of Dilantin. Neither revealed the classic neurologic or gastrointestinal complaints. Although one patient had documented family and social stressors, the other had a stable home life. Both patients recovered remarkably once their Dilantin dosages were adjusted. In such patients who present with change in mood, sleeping, and eating patterns, Dilantin toxicity should be suspected. Serum blood levels should be checked, and dosage adjusted before the addition of antidepressant medication. Possible causes for Dilantin-associated depression are discussed in detail.
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PMID:Dilantin toxicity and vegetative depression: a report of two cases. 224 39

Records of all patients admitted to an urban teaching hospital from 1977-1987 with a diagnosis of phenytoin toxicity were reviewed in order to determine indications for admission and discharge, and to assess the need for therapeutic intervention and monitoring. Of 94 patients identified, 57 were male and 37 were female. Ages ranged from 19 mo to 84 yr. Serum phenytoin levels ranged from 21.4-90 micrograms/ml, with a mean level 44.4 +/- 12.5 micrograms/ml. Ataxia was observed in 59/94 patients (63%), and of these 18 patients had fallen; 9 had suffered injury from falling sufficient to require medical care. No other factors were associated with morbidity. No hemodynamic instability was seen in any of the cases. Electrocardiographic records were available for 71/94 cases (76%). There were no abnormalities due to phenytoin. Symptoms of toxicity resolved with supportive care. There were no deaths in this series. Phenytoin is a relatively safe medication even in the toxic range as determined by baseline phenytoin levels. Hospital admission is indicated in symptomatic cases until a declining serum phenytoin level is observed and ataxia resolves. The data in this series do not support routine electrocardiographic monitoring in cases of phenytoin toxicity.
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PMID:Phenytoin toxicity: a review of 94 cases. 292 27

CT findings in three female epileptic patients are presented. The patients were treated with toxic doses of the anticonvulsant diphenylhydantoin, leading to irreversible ataxia of varying severity. CT shows cerebellar atrophy, including discernible sulci, a dilated 4th ventricle, basal cisterns, and subarachnoid space. These effects of severe DPH toxicity are relevant in the differential diagnosis of 'idiopathic' and other toxic and systemic atrophies, as well as dysontogenetic lesions of the cerebellum.
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PMID:CT findings following diphenylhydantoin intoxication. 400 Jul 49

Seven epileptic patients with permanent ataxic dysfunction following DPH treatment are described. The ataxia correlates with cerebellar atrophy, though the extents of clinical and structural lesions are not necessarily proportional. Cerebellar atrophy is demonstrated by CT scans, the vermal region seems to be predominantly affected.--The tentatively increased susceptibility of female patients and of patients with pre-existing brain lesions, as well as the possible consequences pertaining to the course of the epilepsy are discussed.
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PMID:Cerebellar atrophy following diphenylhydantoin intoxication. 673 20

Diphenylhydantoin (DFH) is known to yield cerebellar ataxia in chronically treated epileptic patient due to cerebellar atrophy with loss of Purkinje cells. Little attention has been paid in the literature to the acute DFH intoxication bearing cerebellar symptoms. We report a patient afflicted with complex partial seizures due to a left temporal cyst, who has been treated during the last two years with DFH 100 mg/day. Due to the refractory characteristics of his seizures he was put on DFH 400 mg daily, and developed a pancerebellar syndrome. After surgical removal of the cyst his seizures entirely faded away and his cerebellar signs improved. Nevertheless his neurological examination still showed trunkal and lower limbs ataxia. After one year of follow up his neurological picture did not change, while he was seizures free. TC and MRI did not show cerebellar atrophy.
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PMID:[Persistent cerebellar ataxia after toxic administration of diphenylhydantoin]. 761 55

Mild overdosage of phenytoin produces reversible cerebellar symptoms (nystagmus, double vision, dysarthria and ataxia). Several case reports suggest that relatively mild and relatively short intoxication can lead to cerebellar degeneration. We observed 11 patients who had episodes of abnormally increased serum levels, most of which developed clinical signs of cerebellar dysfunction. All of these patients were examined with a 1.5-tesla whole-body system (Magnetom, Siemens). Five patients had normal cerebellar structures, although 3 of them had a history of clinical intoxication and all had at least one episode of increased serum level of diphenylhydantoin. The remaining 5 had moderate to severe cerebellar atrophy. Two of them never experienced signs of clinical intoxication. There was no correlation between degree of atrophy and severity of clinical symptoms and elevation of serum DPH levels. There was no correlation between cerebellar atrophy, duration of epilepsy and frequency of seizures.
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PMID:Phenytoin overdosage and cerebellar atrophy in epileptic patients: clinical and MRI findings. 800 16

Phenytoin toxicity is an uncommon problem seen in clinical practice. The predisposing factors for toxicity are hypoalbuminemia, chronic renal failure, hepatic dysfunction and drugs which interfere with phenytoin metabolism. Common manifestations of toxicity, like confusion and ataxia, are well known. A less well known phenomenon is paradoxical seizures. In this condition, seizures develop as the serum phenytoin level rises and decrease in frequency as levels drop. It may or may not be accompanied by other features of toxicity. We present three patients with paradoxical seizures; their serum phenytoin levels were 43.5 mcg/mL, 46.5 mcg/mL and 38.3 mcg/mL. In all cases, seizures were controlled by withdrawal of phenytoin and reduction of drug levels.
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PMID:Paradoxical seizures in phenytoin toxicity. 1048 84

Neurologic manifestations of HIV infection are quite diverse and can develop into seizures. Because new drug therapies have been developed, it is important to know the interactions between antiretroviral and antiepileptic agents. A 36-year-old patient with HIV developed a set of progressive left hemiparesis and secondarily generalized partial seizures related to progressive multifocal leukoencephalopathy. Phenytoin and carbamazepine were necessary to control the seizures. Instead of diverse antiretroviral therapies, the viral load was increased. Protease inhibitors (ritonavir and saquinavir) were added to the treatment and the patient developed progressive ataxia related to carbamazepine toxicity. Carbamazepine was discontinued and the patient remained asymptomatic. The patient was diagnosed with carbamazepine toxicity related to the introduction of ritonavir. Ritonavir is a potent inhibitor of hepatic cytochrome P450, mainly the CYP3A4 isoform. Carbamazepine is metabolized by this subsystem. Ritonavir acted as a CYP3A4 inhibitor, diminishing carbamazepine metabolism and provoking an increase in serum levels and clinical toxicity. We present a case of interaction between ritonavir and carbamazepine. Interaction between antiepileptic and antiretroviral agents is an emergent problem caused by the increasing association of the two therapies. We recommend strict monitoring of serum antiepileptic drug (AED) levels to avoid toxicity and inadequate seizure control.
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PMID:Protease inhibitor-induced carbamazepine toxicity. 1102 Jan 27


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