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)

Plasma phenytoin and phenobarbitone levels were estimated in 123 adult Ethiopian epileptics by gas-liquid chromatography. Thirty four (38.2%) of the patients on phenytoin, and 52 (52%) of those on phenobarbitone, had plasma levels in the conventional therapeutic ranges of 10-20 micrograms/ml and 10-30 micrograms/ml respectively. Of the 89 patients who were taking phenytoin either singly or combined with phenobarbitone, motor disturbances (ataxia and nystagmus) were seen in 31 (34.8%) and dysmorphic and idiosyncratic side effects including gum hypertrophy, hirsutism, acne and skin rash in 37 (41.6%). Subnormal serum calcium levels were noted in 15 (30.6%) and high alkaline phosphatase was found in 13 (26.5%). Phenobarbitone was found to be an effective anticonvulsant (78.1% seizure control rate), with adverse effects of sedation and intellectual depression. Seizure control was achieved in 77.1% of patients on a single drug as opposed to 55.6% on combination of phenytoin and phenobarbitone (p less than 0.05). The overall seizure control rate was 66%.
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PMID:Plasma level distribution, effect and toxicity of antiepileptic drugs among Ethiopian epileptics. 230 55

Although intravenous phenobarbital loading is effective in barbiturate withdrawal, controlled infusions of a drug are inconvenient. To develop a practical and more widely applicable method, oral loading doses of phenobarbital were given to 21 barbiturate addicts, whose estimated mean daily intake of barbiturates was 1 gm (range 0.5 to 4 gm). Twelve had a past or present history of barbiturate withdrawal seizures. Phenobarbital was given orally at a rate of 120 mg/hr until a predetermined clinical end point of phenobarbital effect was achieved. This end point was the presence of at least three of the following: nystagmus, drowsiness, ataxia, dysarthria, or emotional lability. The total phenobarbital loading dose (mean +/- SD) was 23.4 +/- 7.1 mg/kg, median phenobarbital concentration after loading was 35.9 mg/l (range 13.2 to 71.6 mg/l), and median half-life (t 1/2) of phenobarbital was 90 hr (range 38 to 240 hr). One patient with t 1/2 = 38 hr was given supplemental doses of phenobarbital. None developed seizures or other evidence of barbiturate withdrawal.
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PMID:Barbiturate and hypnosedative withdrawal by a multiple oral phenobarbital loading dose technique. 723 1

Phenobarbital, diazepam, lorazepam, and phenytoin are all currently used for the treatment of acute seizures, including status epilepticus. None of these drugs is considered ideal. Fosphenytoin is a new phenytoin prodrug that fulfills many of the properties of an ideal anticonvulsant drug. The safety, tolerance, and pharmacokinetics of intramuscularly administered fosphenytoin have been evaluated in three clinical trials involving patients requiring loading or maintenance doses of phenytoin. These investigations demonstrated that fosphenytoin is rapidly and completely absorbed after injection into muscle and is quickly converted to produce therapeutic phenytoin plasma concentrations within 30 min of administration. Plasma concentrations of phenytoin achieved with i.m. fosphenytoin exceeded those associated with an equimolar dose of oral phenytoin. i.m. fosphenytoin was well tolerated both locally and systemically. Only mild and transient reactions occurred at the injection site. The most common systemic adverse events reported--somnolence, nystagmus, dizziness, and ataxia--are side effects commonly seen with phenytoin and tended to be mild. Preexisting seizure disorders remained stable. Combination treatment with i.v. diazepam or lorazepam to attain rapid seizure control and i.m. fosphenytoin to maintain the anticonvulsant effect theoretically offers many advantages for control of acute seizures and should be studied.
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PMID:Intramuscular use of fosphenytoin: an overview. 864 11

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

Antiepileptics include various groups of drugs that have different mechanisms of actions and adverse effects. They are often also used to treat other disorders such as psychosis, chronic pain, and migraine. The most common drugs implicated in overdose include phenytoin, sodium valproate, carbamazepine, and phenobarbital. Common signs of toxicity of these drugs are central nervous system manifestations such as altered sensorium, lethargy, ataxia, and nystagmus. Some ingestions can paradoxically precipitate seizures and even status epilepticus. Sodium valproate can cause hyperammonemic encephalopathy and cerebral edema. Carbamazepine is implicated in cardiac arrhythmias and hyponatremia. Phenobarbital causes sedation, respiratory depression, and hypotension. In suspected overdose, apart from the routine laboratory tests, serum levels of the drug should be sent. Serial levels should be measured, as drug toxicity can be prolonged. Treatment of all these overdoses begins with stabilization of airway, breathing, and circulation, and endotracheal intubation being performed to protect the airway in patients with altered mental status. For decontamination, a single dose of activated charcoal should be given. Multidose of activated charcoal may be useful in phenytoin, carbamazepine, and phenobarbital overdose. Naloxone and carnitine are indicated in valproate overdose. Carbamazepine overdose can cause a widened QRS complex and arrhythmias, which can be treated with sodium bicarbonate. Forced alkaline diuresis is no longer advocated for phenobarbital poisoning. The Extracorporeal Treatments in Poisoning (EXTRIP) workgroup have formulated guidelines for extracorporeal removal of all these drugs. In most cases, hemodialysis is preferred. Other modalities include charcoal hemoperfusion (especially for carbamazepine) or continuous venovenous hemodialysis. Patients who ingest long-acting preparations should be monitored for longer periods.
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PMID:Antiepileptic Overdose. 3202 Oct 7