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Convulsion carbamazepine

This peripheral activity may be a rational basis for the use of systemic local anaesthetics in neuropathic states since ectopic activity in damaged nerves has been shown to be highly sensitive to systemic sodium channel blockers. This too is probably part of the basis for the analgesic effects of established effective anti-convulsants that block sodium channels such as carbamazepine, although central actions are important and may even predominate. The precise actions of excitability blockers therefore remains hazy as does any clear basis for the effectiveness of antidepressants and other adrenergic agents in the treatment of neuropathic pain as both central and peripheral actions, including sympathetic effects are possible. [Pg.460]

Rifampicin, the anti-convulsants phenytoin, phe-nobarbitone and carbamazepine, and the steroid dex-amethasone, are amongst the best recognized inducers of enzyme function, and their action nearly... [Pg.152]

Carbamazepine has been shown to be better tolerated as long-term monotherapy than DVP in children with epilepsy or febrile convulsions (Herranz et ah, 1988). Nevertheless, a comparison of the adverse effect profile in the Kowatch sample (Kowatch et ah, 2000) shows that nausea (46%), rash (8%), and dizziness (8%) were more prevalent in youngsters taking CBZ, compared to children on DVP, who experienced overall less nausea (20%), rash (0%), and dizziness (0%). [Pg.315]

Mebendazole is teratogenic in animals and therefore contraindicated in pregnancy. It should be used with caution in children younger than 2 years of age because of limited experience and rare reports of convulsions in this age group. Plasma levels may be decreased by concomitant use of carbamazepine or phenytoin and increased by cimetidine. Mebendazole should be used with caution in patients with cirrhosis. [Pg.1152]

Mebendazole Accidental mebendazole poisoning in infants is associated with convulsions, respiratory arrest, and tachyarrhythmia.181 If administered concomitantly, mebendazole interacts with phenytoin, carbamazepine, and cimetidine. [Pg.357]

Isoniazid can cause convulsions and therefore should be prescribed with caution in patients with epilepsy. Isoniazid is an enzyme inhibitor and may increase carbamazepine levels. Rifampicin is an enzyme inducer and may decrease carbamazepine levels. [Pg.352]

Use with caution in patients with mixed seizure disorders that include atypical absence seizures because carbamazepine has been associated with increased frequency of generalized convulsions in such patients... [Pg.50]

Tricyclics and SSRIs can lower the convulsion threshold making epilepsy more difficult to control by anti-epilepsy drugs and lengthening seizure time in electroconvulsive therapy. The situation is further complicated by the ability of carbamazepine to accelerate (induce) the metabolism of antidepressants and inhibition of carbamazepine metabolism by certain antidepressants (below). [Pg.377]

Adverse effects of phenytoin, many of which can be very slow to develop, include impairment of cognitive function, which has led many physicians to prefer carbamazepine and valproate. Other nervous system effects range from sedation to delirium to acute cerebellar disorder to convulsions. Peripheral neuropathy also occurs. Cutaneous reactions include rashes (dose related), coarsening of facial features and hirsutism. Gum hyperplasia (due to inhibition of collagen catabolism) may develop and is more marked in children and when there is poor gum hygiene. [Pg.420]

In a 65-year-woman, carbamazepine-induced hyponatremia (127-130 mmoFl) led to serial tonic-clonic seizures, somnolence, confusion, and an electroence-phalographic misdiagnosis of non-convulsive status. [Pg.630]

Carbamazepine is contraindicated in patients taking monoamine oxidase inhibitors (101,102). The combination can cause sudden high body temperature, extremely high blood pressure, and severe convulsions at least 14 days should be allowed between stopping treatment with one medicine and starting the other. [Pg.634]

Vogt H. Non-convulsive status epileptics or metabolic encephalopathy due to carbamazepine induced hyponatremia Epilepsia 1999 40(Suppl 2) 254. [Pg.636]

A 47-year-old man developed 30-second episodes of facial contortions, aphasia, garbled speech, neologism, nocturnal episodes of deep breathing, swallowing, and incomprehensible speech after taking trazodone 150 mg/day for 3 weeks. On withdrawal of trazodone, his symptoms abated, but an electroencephalogram showed a left anterior lobe spike. He was treated with carbamazepine and within 6 months was not depressed and had no further convulsive symptoms. [Pg.3482]

Place in Therapy. Carbamazepine should be considered a first-line therapy for patients with newly diagnosed partial seizmes and for patients with primary generalized convulsive seizures who are not in an emergent situation. [Pg.1037]

I Place in Therapy. Oxcarbazepine is indicated for use as monotherapy or adjunctive therapy in the treatment of partial seizures in adults and as monotherapy and adjunctive therapy in the treatment of partial seizures in patients as young as 4 years of age with epilepsy. It is also a potential first-fine drug for patients with primary generalized convulsive seizures. Oxcarbazepine may be effective in patients not demonstrating a response to carbamazepine. [Pg.1041]

Carbamazepine (brand name Tegretol) Originally developed as an anticonvulsant medication. It is used along with other medications such as valproic acid (Depakote or Depakene) to treat individuals suffering from some type of mood disorder (acute mania and bipolar disorders). It is thought to retard the electrochemical process in the nervous system that can set off either convulsions or manic episodes. Also used to treat alcohol withdrawal, cocaine addiction, and emotional disorders. [Pg.298]

TOXICITY Acute intoxication with carbamazepine can result in stupor or coma, hyperirritability, convulsions, and respiratory depression. During long-term therapy, untoward effects include drowsiness, vertigo, ataxia, diplopia, and blurred vision. The frequency of seizures may... [Pg.326]

There appear to be no reports of adverse reactions during the concurrent use of MAOIs and carbamazepine. However, the manufacturers of carbamazepine say that concurrent use should be avoided because of the close structural similarity between carbamazepine and the tricyclic antidepressants (and therefore the theoretical risk of an adverse interaction). They suggest that MAOIs should be discontinued at least 2 weeks before carbamazepine is started. Several reports describe successful use of carbamazepine and MAOIs, namely tranylcypromine, phenelzine, and moclobemide. Bearing in mind that the MAOIs and the tricyclics can be given together under certain well controlled conditions (see MAOIs or RIMAs + Tricyclic and related antidepressants , p.ll49), the warning about the risks may possibly prove to be overcautious. Note that, rarely, the MAOIs have been seen to cause convulsions. [Pg.533]

The reduction in the serum levels of amitriptyline, desipramine, doxepin, imipramine and nortriptyline caused by the interaction with carbamazepine appears to be established but the clinical importance is very much less certain. Evidence from one study, that achieved a beneficial response in patients taking tricyclics and carbamazepine suggests that it is possibly not necessary to increase the tricyclic dosage to accommodate this interaction. The fact that a retrospective study found that increased imipramine doses were being given to those taking carbamazepine suggests that this interaction will be naturally accounted for. If carbamazepine is added to treatment with any of these tricyclics, be aware that the dose of the tricyclic may need to be titrated up to achieve the desired therapeutic response. Remember too that the tricyclics can lower the convulsive threshold and should therefore be used with caution in patients with epilepsy. [Pg.1234]

Epilepsy is a disorder characterized by recurrent spontaneous electrical discharges within the brain which are manifested by clinical seizures. Four million patients in the United States are afflicted with this ailment 20% of these have seizures that cannot be controlled sufficiently with existing medications to permit normal activities of everyday life. The market for anticonvulsants is substantial a historical growth rate of 10 to 12% is expected to be sustained thereafter. Epileptic seizures can be classified as primary epilepsies (35%) or partial epilepsies (65%). Primary epilepsies (generalized convulsions) can be controlled with valproate (Depakote), carbamazepine (Tegretol), phenytoin (Dilantin), or phenobarbi-tol. Most partial epilepsies have resisted control with chemotherapeutic agents. [Pg.279]

Drugs implicated 3-Lactams other antibacterials NMBDs some NSAIDs quinolones mAbs proton pump inhib s P-Lactams quinine quinidine sulfonamides NSAIDs procainamide gold carbamazepine propylthiouracil ticlopidine P-Lactams ciprofloxacin sulfonamides lincomycin tetracycline NSAIDs carbamazepine allopurinol gold methyldopa mAbs NSAIDs p-lactams othCT antibiotics anti-convulsants antimalarials local anesthetics barbiturates quinolones dapsone... [Pg.27]


See other pages where Convulsion carbamazepine is mentioned: [Pg.478]    [Pg.590]    [Pg.478]    [Pg.590]    [Pg.339]    [Pg.127]    [Pg.85]    [Pg.181]    [Pg.673]    [Pg.720]    [Pg.53]    [Pg.83]    [Pg.87]    [Pg.85]    [Pg.300]    [Pg.111]    [Pg.723]    [Pg.30]    [Pg.302]    [Pg.390]    [Pg.72]    [Pg.85]    [Pg.17]    [Pg.46]    [Pg.46]    [Pg.235]    [Pg.250]    [Pg.844]    [Pg.267]   
See also in sourсe #XX -- [ Pg.53 ]




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