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)

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

Four patients with an acute overdose of carbamazepine were examined with serial blood level determinations. The clinical spectrum consisted of coma, respiratory depression, seizures, myoclonus, nystagmus, hyperreflexia, hyporeflexia, delayed gastric emptying with cyclic coma, ataxia, sinus tachycardia, and atrioventricular conduction delay. Carbamazepine elimination half-lives varied from 10 to 29 hours, and in one case carbamazepine-10,11-epoxide was measured and had a half-life of 24 hours.
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PMID:Acute carbamazepine toxicity resulting from overdose. 719 79

Neuropathic pain, whether of peripheral or central origin, is characterized by a neuronal hyperexcitability in damaged areas of the nervous system. In peripheral neuropathic pain, damaged nerve endings exhibit abnormal spontaneous and increased evoked activity, partly due to an increased and novel expression of sodium channels. In central pain, although not explored in detail, the spontaneous pain and evoked allodynia are also best explained by a neuronal hyperexcitability. The peripheral hyperexcitability is due to a series of molecular changes at the level of the peripheral nociceptor, in dorsal root ganglia, in the dorsal horn of the spinal cord, and in the brain. These changes include abnormal expression of sodium channels, increased activity at glutamate receptor sites, changes in gamma-aminobutyric acid (GABA-ergic) inhibition, and an alteration of calcium influx into cells. The neuronal hyperexcitability and corresponding molecular changes in neuropathic pain have many features in common with the cellular changes in certain forms of epilepsy. This has led to the use of anticonvulsant drugs for the treatment of neuropathic pain. Carbamazepine and phenytoin were the first anticonvulsants to be used in controlled clinical trials. Studies have shown these agents to relieve painful diabetic neuropathy and paroxysmal attacks in trigeminal neuralgia. Subsequent studies have shown the anticonvulsant gabapentin to be effective in painful diabetic neuropathy, mixed neuropathies, and postherpetic neuralgia. Lamotrigine, a new anticonvulsant, is effective in trigeminal neuralgia, painful peripheral neuropathy, and post-stroke pain. Other anticonvulsants, both new and old, are currently undergoing controlled clinical testing. The most common adverse effects of anticonvulsants are sedation and cerebellar symptoms (nystagmus, tremor and incoordination). Less common side-effects include haematological changes and cardiac arrhythmia with phenytoin and carbamazepine. The introduction of a mechanism-based classification of neuropathic pain, together with new anticonvulsants with a more specific pharmacological action, may lead to more rational treatment for the individual patient with neuropathic pain.
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PMID:Anticonvulsants in neuropathic pain: rationale and clinical evidence. 1188 43

OBJECTIVE:: To describe nystagmus induced by cranial vibration in a case series of 8 patients with superior semicircular canal dehiscence. DESIGN:: Consecutive case series review. SETTING:: Tertiary vestibular center. PATIENTS:: Eight consecutive patients with computed tomographic confirmed superior semicircular canal dehiscence syndrome observed in the last 24 months. PROCEDURE:: Vertex, bilateral mastoid, and bilateral suboccipital cranial vibration were performed using 100 Hz. Vibration for 10 to 15 seconds on patients in the seated position during office evaluation for vestibular complaints. Nystagmus was monitored by infrared video oculography with digital recording. RESULTS:: All patients demonstrated distinct torsional/vertical vibration-induced nystagmus. Maximal recorded slow-phase velocity was 20 degrees/s. This was observed best with suboccipital vibration on the side of the dehiscence. CONCLUSION:: Vibration-induced torsional/vertical nystagmus, observed best with ipsilateral suboccipital cranial vibration in the seated position, seems to be a sensitive screening test in the office setting for the presence of superior semicircular canal dehiscence.
Otol Neurotol 2007 Oct
PMID:Vibration-Induced Nystagmus as an Office Procedure for the Diagnosis of Superior Semicircular Canal Dehiscence. 1770 4

Carbamazepine (CBZ) is a commonly used antiepileptic agent. Common toxic effects include neurological abnormalities; ataxia, seizures, coma, cardiorespiratory problems; dysrhythmias; conduction disorders; respiratory depression; and eye abnormalities, such as nystagmus and ophthalmoplegia. Carbamazepine is highly protein bound. There is no antidote for the medication. Carbamazepine is not removed effectively through conventional hemodialysis. Supportive measures and charcoal hemoperfusion have been regarded as efficient treatment methods. We herein report a 17-year old girl to whom continuous venovenous hemodiafiltration lacking the albumin-enhance after suicidal overdose of CBZ was performed. We suggest continuous venovenous hemodiafiltration lacking the albumin-enhance as an alternative emergency treatment modality for cases who had ingested CBZ in toxic levels.
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PMID:Management of a severe carbamazepine overdose with continuous venovenous hemodiafiltration. 2015 17

: The acute vestibular syndrome is a clinically defined entity consisting of vertigo or dizziness that develops acutely over minutes to hours and is accompanied by nausea/vomiting, gait instability, head motion intolerance, and nystagmus, while persisting over a day or more. When it is caused by a peripheral vestibular lesion and is not associated with clinically manifest auditory deficits, it is mostly labeled vestibular neuritis/neuronitis/neuropathy or sometimes peripheral vestibulopathy. Here, we propose hypotheses and discuss current research advances on viral or vascular factors in the pathogenesis, the recurrence, the site of lesion, old and new treatment options, contraindicated measures, the differential diagnosis, and the prognosis of vestibular neuritis/neuronitis/neuropathy or vestibulopathy. Possibly, other structures than the vestibular nerve are also involved in the pathogenetic process and the label peripheral vestibulopathy would be more apt.
Otol Neurotol 2017 06
PMID:Diagnosis and Treatment of Vestibular Neuritis/Neuronitis or Peripheral Vestibulopathy (PVP)? Open Questions and Possible Answers. 2834 94

Episodic ataxias (EAs) are characterized by recurrent, discrete episodes of vertigo and ataxia. EA1 and EA2 are the two most common forms. In the interictal interval, myokymia is typically present in EA1, whereas EA2 patients present with interictal nystagmus. Specific pharmacological therapies are available for EA1 and especially EA2. We briefly discuss the case of an Italian young man with EA2, with a novel de novo CACNA1A mutation, who in our opinion is particularly illustrative for introducing the therapeutic approach. Acetazolamide could fully suppress EA episodes in our patient. We also provide a perspective review of the topic. 4-Aminopyridine is another valid treatment option. For EA1 (and for rarer EAs), the therapeutic possibilities are more limited. Carbamazepine is probably the treatment of choice for EA1, but the optimal treatment plan is unknown. A better understanding of the molecular processes involved in the mediation of EAs will lead to more specific and efficacious therapies for this still elusive group of disorders.
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PMID:Therapy of episodic ataxias: case report and review of the literature. 3089 Oct 74

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