Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A representative sample of 117 patients with definite multiple sclerosis (MS) was interviewed on pain syndromes. Chronic syndromes lasting more than one month included dysaestesthesia, low back pain, spasms, tonic seizures, tightening and painful sensations in the extremities. Acute syndromes included neuralgia, L'Hermitte's sign and pain associated with optic neuritis. Thirty-five per cent were pain-free. Of the remaining patients had 45% pain at the time of the examination, 32% indicated pain among the most severe symptoms of MS and 23% had pain at the onset of MS. The number of patients with pain at the time of the examination increased with age and duration of disease. Patients with pain were significantly more often spastic and significantly more often sought alternative treatment forms. No difference was found for mean age, sex, physical impairment, duration of disease from onset of MS, depressive score and score of delayed verbal memory.
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PMID:Acute and chronic pain syndromes in multiple sclerosis. 195 Apr 60

Carbamazepine, a first-line drug for the treatment of epilepsy and neuralgia, may exert hazardous effects on the cardiac conduction system. Standard ECG and long-term ECG monitoring and invasive electrophysiologic testing were carried out in 10 patients who required this drug for neurologic disorders, but in whom its safe use had been questioned because of symptoms of ECG abnormalities. We observed depression of sinus node function and an atrioventricular conduction delay with a significant prolongation of the PQ interval of 16 msec (9%; 95% confidence interval: 1.9% to 16.5%; p less than 0.05), of which the HV interval was significantly prolonged but not the PA and AH intervals. These effects are in accordance with previously shown class 1A properties. However, the lack of effects on QRS, JT, and QT intervals at normal heart rates is a class 1B characteristic. Thus carbamazepine seems to have composite electropharmacologic actions. A cause effect relationship between carbamazepine treatment and significant arrhythmias was established in five patients. Thus the negative chronotropic and dromotropic effects of carbamazepine may, at least in predisposed patients, induce symptoms confusingly similar to the epileptic seizures it is used to prevent.
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PMID:Electrophysiologic effects and clinical hazards of carbamazepine treatment for neurologic disorders in patients with abnormalities of the cardiac conduction system. 201 74

Medical records for 572 patients in two extended care facilities were reviewed to study seizure disorders and antiepileptic drug use. Seventy patients (12.2 percent) were receiving antiepileptic drugs. Of this group, 43 patients (61.4 percent) had a diagnosis of epilepsy or documented seizures, 2 were being treated for neuralgia, and 25 (35.7 percent) had no reason given for antiepileptic use. The most common cause was cerebrovascular accident (38.9 percent), and no associated etiology was found in 29.2 percent. Phenytoin was the most commonly used agent. Thirty-two (45.7 percent) were taking two or more antiepileptic drugs. Thirteen patients had had no serum concentration monitoring in the last year. Thirty-seven patients (52.9 percent) had had at least one serum concentration outside of the therapeutic range.
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PMID:Use of antiepileptic drugs in the elderly population. 310 51

In the case described, electroencephalography (EEG) proved valuable for determining the nature of spells of loss of consciousness with brief clonic jerks associated with ear and throat pain. A 70-year-old woman had a history of episodic brief attacks of pain below the right ear and deep in the neck that had started three years previously. The spells became more severe and progressed to loss of awareness associated with clonic jerks of the extremities. Because of a concern that the spells represented seizures, an EEG was performed, with electrocardiographic monitoring. Multiple spells were recorded; they began with profound bradycardia followed by generalized slow-wave activity and then by suppression of all EEG activity correlating with loss of consciousness and clonic jerking. The spells were thought to represent syncopal attacks associated with glossopharyngeal neuralgia.
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PMID:An electroencephalographic study of glossopharyngeal neuralgia with syncope. 335 4

A case of glossopharyngeal neuralgia associated with episodic cardiac arrest and syncope is presented. Posterior fossa exploration showed that the left glossopharyngeal and vagus nerves were compressed by the posterior inferior cerebellar artery. Microvascular decompression resulted in complete relief of glossopharyngeal neuralgia, cardiac syncope, and seizure. The mechanism of glossopharyngeal neuralgia associated with cardiac syncope is discussed.
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PMID:Glossopharyngeal neuralgia with cardiac syncope. A case successfully treated by microvascular decompression. 402 9

A patient with trigeminal neuralgia experienced a generalized seizure and a prolonged syncopal episode. He was found to be asystolic during the syncopal episode. There was no recurrence of loss of consciousness after implantation of a pacemaker. Mechanical stimulation of the trigeminal nerve during craniotomy for microvascular decompression of the trigeminal nerve resulted in bradycardia. Since vascular decompression of the trigeminal nerve, there has been no recurrent facial pain, and no further syncope, seizures, or bradycardia. Syncope and seizures have not been previously reported in association with trigeminal neuralgia, although they are well described with glossopharyngeal neuralgia.
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PMID:Trigeminal neuralgia associated with seizure and syncope. Case report. 674 98

A case of glossopharyngeal neuralgia associated with seizures, syncope, bradycardia, and hypotension is presented. Intracranial section of the 9th cranial nerve and the upper filaments of the 10th cranial nerve resulted in the resolution of all symptoms. The literature is reviewed and the pathogenesis and treatment of the condition are discussed.
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PMID:Glossopharyngeal neuralgia associated with syncope and seizures. 707 Jun 39

Carbamazepine is a major antiepileptic drug which is primarily used to treat epileptic patients suffering from partial seizures with or without secondary generalization, but which also has applications in those suffering from primary generalized tonic-clonic seizures. Besides its antiepileptic effect, carbamazepine is also indicated in the treatment of trigeminal and occipital neuralgia, and in manic depressive disorders. Because of its minimal unwanted effects on cognition and behaviour, carbamazepine is an excellent drug for the treatment of people with intellectual disability and epilepsy. Carbamazepine is still one of the most commonly prescribed medications in the treatment of epileptic disorders.
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PMID:Carbamazepine in the treatment of epilepsy in people with intellectual disability. 1003 Apr 30

An adolescent girl presented with severe, lancinating tonsillar pain exacerbated by swallowing 6 weeks after initiation of left vagus nerve stimulation for intractable epilepsy. Her symptoms mimicked those seen in glossopharyngeal neuralgia and were relieved by temporary cessation of stimulation. Gradual reinstitution of therapy with alteration in stimulus parameters resulted in improved seizure control as well as cessation of pain symptoms. Direct stimulation of the vagus nerve may result in vagoglossopharyngeal neuralgia, which, in this case, was amenable to stimulus modification.
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PMID:Tonsillar pain mimicking glossopharyngeal neuralgia as a complication of vagus nerve stimulation: case report. 1089 65

Between 10%-28% of patients who receive the immunosuppressant cyclosporine (CsA) experience some form of neurotoxic adverse event. Both sensorial motoric functions may be adversely affected, and thus patients present with a wide range of neurological and psychiatrical disorders. Mild symptoms are common and include tremor, neuralgia, and peripheral neuropathy. Severe symptoms affect up to 5 % of patients and include psychoses, hallucinations, blindness, seizures, cerebellar ataxia, motoric weakness, or leukoencephalopathy. Tacrolimus is associated with similar neurotoxic adverse events. Neurotoxicity may result in serious complications for some patients, particularly recipients of orthotopic liver transplants. Factors that may promote the development of serious complications include advanced liver failure, hypertension, hypocholesterolemia, elevated CsA or tacrolimus blood levels, hypomagnesemia, and methylprednisolone. Occipital white matter appears to be uniquely susceptible to the neurotoxic effects of CsA; injury to both the major and minor vasculature may cause hypoperfusion or ischemia and local secondary toxicity in the white matter. Calcineurin inhibition by CsA and tacrolimus alters sympathetic outflow, which may play a role in the mediation of neurotoxic and hypertensive adverse events. The symptoms of CsA- and tacrolimus-associated neurotoxicity may be reversed in most patients by substantially reducing the dosage of immunosuppressant or discontinuing these drugs. However, some patients have experienced permanent or even fatal neurological damage even after dose reduction or discontinuation. CsA-sparing and tacroli-mus-sparing drug regimens that use the immunosuppressant mycophenolate mofetil, which has no neurotoxic effects, may reduce the incidence and severity of neurotoxic adverse events while maintaining an adequate level of immunoisuppression.
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PMID:Neurotoxicity of calcineurin inhibitors: impact and clinical management. 1105 66


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