Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case histories of four patients who developed choreoathetoid movements during intoxication with phenytoin are presented. Drug intoxication was confirmed in each case by measuring the serum phenytoin concentration. Drug interactions were, in part, responsible for the occurrence of intoxication in three of them. Phenytoin intoxication is not always easy to recognize, particularly when nystagmus is minimal or absent, as in these four patients. The estimation of the serum phenytoin concentration is invaluable in this situation.
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PMID:Involuntary movements caused by phenytoin intoxication in epileptic patients. 23 1

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.
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PMID:Choreoathetosis during phenytoin treatment. 40 43

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

Downbeat nystagmus is generally the result of a structural lesion at the craniocervical junction. It has rarely been reported as a manifestation of metabolic disease or drug intoxication. We observed two patients with downbeat nystagmus secondary to phenytoin (Dilantin) intoxication. Both individuals had other features of phenytoin-induced central nervous system dysfunction with toxic blood levels of the drug (greater than 20 micrograms/ml). Complete resolution of the downbeat nystagmus followed the return of phenytoin levels to the therapeutic range.
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PMID:Downbeat nystagmus with phenytoin. 621 26

Phenytoin plasma level and toxicity data were compared in a three-way crossover study performed in 18 patients at steady state. Formulations compared were a rapid and a slow release capsule and an oral solution. Plasma concentration-time integrals and maximum plasma phenytoin levels were significantly greater for the rapid release capsule and solution than for the slow release capsule. The incidence of nystagmus and toxicity did not differ for the three treatments, but the occurrence of mental symptoms was more frequent for the oral solution, possibly because of the solvent used in this formulation.
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PMID:Rapid and slow release phenytoin in epileptic patients at steady state: comparative plasma levels and toxicity. 715 70

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

Neonatal seizures are frequently manifested by subtle movements that are referable to brain stem structure, ie, nystagmus, conjugate eye movements, posturing, sucking movements, and so forth. Electroencephalogram (EEG) confirmation of abnormal movements is essential in diagnosing seizures in the neonate. Clinical seizure signs are often a clue to etiology. Metabolic abnormalities must always be considered, and blood gases, calcium, magnesium, glucose, and ammonia obtained. Neonatal seizures are an indication for cerebrospinal fluid examination. Specific metabolic abnormalities are treated with metabolic approaches, not conventional anticonvulsant drugs. Hypertensive encephalopathy is treated by controlling blood pressure, and not through anticonvulsant drugs. Critically ill infants bind anticonvulsants in an unpredictable fashion, and unbound or free anticonvulsant drug concentrations should be used to guide therapy. Phenobarbital is the most commonly used drug in treating nonmetabolic seizures. Doses to achieve free concentrations of at least 35 mg/L should be used. Use in vitro binding determinations with this formula to calculate loading doses. Dose is 25 mg/kg multiplied by volume and distribution (1 L/kg) divided by % free. Phenytoin is the second most commonly used agent, and doses should be calculated to achieve, but not exceed, 3 mg/L. Dose is 3 mg/kg multiplied by volume and distribution (1 L/kg) divided by % free. Benzodiazepines, notably lorazepam and diazepam are used at doses of 0.15 mg/kg and 0.3 mg/kg, respectively.
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PMID:Neonatal Seizures. 1128 39

Phenytoin is an effective anticonvulsant, but high serum phenytoin concentrations may be associated with serious toxicity. The upper limit for the therapeutic serum concentration of phenytoin is considered to be 80 micromol/L. However, in some situations higher serum concentrations are needed to control seizures. The authors describe a 9-year-old girl who needed concentrations twice the normal amount to control recurrent episodes of decreased levels of consciousness. Except for nystagmus, she had no other signs of phenytoin toxicity. This patient highlights the critical principle in therapeutic drug monitoring of individualizing drug therapy. Although some patients receiving phenytoin may achieve seizure control with "subtherapeutic" levels (i.e., <40 micromol/L), others may need supratherapeutic levels, as was the case with this patient. Clinicians should be careful not to treat "numbers" (i.e., serum concentrations), but rather the patient's clinical condition, with a careful balance between therapeutic advantage and adverse effects.
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PMID:How high can we go with phenytoin? 1202 30

Phenytoin toxicity may result from intentional overdose, dosage adjustments, drug interactions, or alterations in physiology. Intoxication manifests predominantly as nausea, central nervous system dysfunction (particularly confusion, nystagmus, and ataxia), with depressed conscious state, coma, and seizures occurring in more severe cases. Cardiac complications such as arrhythmias and hypotension are rare in cases of phenytoin ingestion, but they may be seen in parenteral administration of phenytoin or fosphenytoin. Deaths are unlikely after phenytoin intoxication alone. A greatly increased half-life in overdose due to zero-order pharmacokinetics can result in a prolonged duration of symptoms and thus prolonged hospitalization with its attendant complications. The mainstay of therapy for a patient with phenytoin intoxication is supportive care. Treatment includes attention to vital functions, management of nausea and vomiting, and prevention of injuries due to confusion and ataxia. There is no antidote, and there is no evidence that any method of gastrointestinal decontamination or enhanced elimination improves outcome. Activated charcoal should be considered if the patient presents early; however, the role of multiple-dose activated charcoal is controversial. Experimental studies have proven increased clearance rates, but this effect has not been translated into clinical benefit. There is no evidence that any invasive method of enhanced elimination (such as plasmapheresis, hemodialysis, or hemoperfusion) provides any benefit. This article provides an overview of phenytoin pharmacokinetics and the clinical manifestations of toxicity, followed by a detailed review of the various treatment modalities.
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PMID:Phenytoin poisoning. 1617 88

Phenytoin is an anti-convulsant drug commonly used to prevent seizures in patients with cerebral metastases. Phenytoin has complicated non-linear kinetics, is highly protein bound and has a small window between its therapeutic and toxic dose. This combination of factors means that small increases in dosage can all too quickly result in high plasma levels and toxic symptoms. Symptoms of phenytoin toxicity include: confusion, nystagmus, agitation, abnormal gait and hallucinations. This case report describes phenytoin toxicity in a patient receiving phenytoin 300 mg three times a day for a number of weeks. The patient was admitted to the unit for terminal care, where his phenytoin levels were found to be very high. Phenytoin was withheld until levels returned to within the normal range. During this time the patient became orientated and many of his symptoms resolved.
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PMID:A case of phenytoin toxicity in a patient with advanced lung cancer. 1716 67


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