Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 74-year-old female who complained of severe attacks of pain in the throat and neck on the left side was first admitted to our hospital in 1971. Carbamazepine was effective at this time, and so she could be discharged. She was readmitted to the hospital in 1974 because of severe stabbing paroxysms of pain in the left throat, radiating into the auricular region as frequent as more than ten times a day. Paroxysms could not be alleviated by large doses of Carbamazepine, and side effects of the drug ensued. The pain could be easily elicited by talking, laughing, swallowing, pulling the left ear and pushing the left tragus. Block of the left 9th nerve with xylocaine produced complete relief of pain for 30 minutes to 1 hour; Plain skull X-rays and veretebral angiograms were normal. The patient was operated under general anesthesia in the sitting position. With the left suboccipital craniectomy, the left 9th nerve was cut without any change on ECG. Pulse rate, and blood pressure. Upon touching vagus nerve, the ventricular extrasystole and hypotension occurred. After the blood pressure restored to normal level and the extrasystole disappeared with administration of atropine and carnigen, the uppermost rootlet of the vagus nerve was cut. The blood pressure dropped abruptly again followed by the right bundle-branch block on ECG for approximately 20 minutes. Postoperatively, she was lethargic and had disorientation, delusion and disorientation. We attributed these symptoms to the hypoxia in operative procedure. The symptoms completely disappeared on the fifth postoperative day. The patient has been perfectly free from pain at the 15 month's follow-up without neurological or mental deficit except diminished gag reflex on the left side. We reported this our experienced case and discussed about the mechanism of the hypotension on sectioning a rootlet of the vagus nerve with literatures.
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PMID:[Glossopharyngeal neuralgia associated with the right-bundle branch block and hypotension on sectioning a rootlet of the vagus nerve--case report (author's transl)]. 55 84

Carbamazepine is being used more frequently in the U.S. as an initial agent of choice to treat generalized tonic-clonic, mixed, and partial seizures with complex symptomatology. Carbamazepine is extensively metabolized in the liver; however, there is little information available on its pharmacokinetics in patients following surgery or myocardial infarction, or in those with liver disease. We report a case of a patient who attained toxic carbamazepine serum concentrations (ranging from 18.2 to 21.5 micrograms/mL) two days after cardiothoracic surgery and an intraoperative myocardial infarction, and experienced lethargy, diplopia, dysarthria, diaphoresis, and horizontal and downgaze nystagmus. These alterations in serum carbamazepine concentration normalized ten days after surgery. They may have been due to a combination of changes in protein binding and decreased elimination due to altered intrinsic hepatic clearance. With carbamazepine achieving a more prominent place in anticonvulsant therapy, the influence of various procedures and disease processes on the pharmacokinetics and pharmacodynamics of carbamazepine, as well as the clinical consequences of such changes, need further investigation.
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PMID:Toxic carbamazepine concentrations following cardiothoracic surgery and myocardial infarction. 226 Mar 36

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