Convulsions tricyclic antidepressants causing

Among the many toxicants that cause convulsions are chlorinated hydrocarbons, amphetamines, lead, organophosphates, and strychnine. There are several levels of coma, the term used to describe a lowered level of consciousness. At level 0, the subject may be awakened and will respond to questions. At level 1, withdrawal from painful stimuli is observed and all reflexes function. A subject at level 2 does not withdraw from painful stimuli, although most reflexes still function. Levels 3 and 4 are characterized by the absence of reflexes at level 4, respiratory action is depressed and the cardiovascular system fails. Among the many toxicants that cause coma are narcotic analgesics, alcohols, organophosphates, carbamates, lead, hydrocarbons, hydrogen sulfide, benzodiazepines, tricyclic antidepressants, isoniazid, phenothiazines, and opiates. 

Tricyclic antidepressant overdose includes cardiotoxicity, convulsions, and symptoms of muscarinic receptor blockade. The antidote for the quinidine-Uke cardiotoxicity of tricyclic antidepressants is sodium bicarbonate. Although physostigmine does effectively reverse anticholinergic symptoms, it can aggravate depression of cardiac conduction and can cause seizures. The answer is (J). 

Tranylcypromine (Parnate) Blocks metabolisni of biogenic amines (norepinephrine, serotonin, dopamine) increasing the synaptic concentration of these transmiTters. Suppresses REM sleep. Used tu tiedt depression if tricyclic antidepressants fail and when electroconvulsive therapy fails or is refused. Also used to treat narcolepsy, phobic/anxiety states and Parkinson s disease. Hepatotoxicity, excessive CNS stimulation, orthostatic hypoten -sion. Overdose may cause agitation, hallucinations, hyperreflexia, hyperpyrexia, convulsions, altered blood pressure. ... 

The aetiology is unknown in 60-70% ol cases, but heredity is an important factor. Damage to the brain (e.g. tumours, asphyxia, infections or head injury) may subsequently cause epilepsy. Convulsions may be precipitated in epileptics by several groups of drugs, including pheno-ihiazines. tricyclic antidepressants and many antihistamines. 

Detailed information about adverse interactions between nefopam and other drugs does not seem to be available. The manufacturer advises caution if nefopam is given with a tricyclic antidepressant because they lower the convulsive threshold convulsions have been seen in some patients taking nefopam. In addition, the antimuscarinic adverse effects of nefopam may be additive with those of tricyclics and other drugs with antimuscarinic effects. For example, the CSM in the UK has a number of reports of urinary retention caused by nefopam, which would be expected to be worsened by drugs with antimuscarinic activity. Nefopam appears to have sympathomimetic activity and the manufacturer therefore says it should not be given with the MAOIs (see MAOIs or RIMAs + Sym-pathomimetics Indirectly-acting , p.l 147). 

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. 

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