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Seizures antidepressants causing

Seizures, muscular hyperactivity, and rigidity may result in death. Seizures may cause pulmonary aspiration, hypoxia, and brain damage. Hyperthermia may result from sustained muscular hyperactivity and can lead to muscle breakdown and myoglobinuria, renal failure, lactic acidosis, and hyperkalemia. Drugs and poisons that often cause seizures include antidepressants, theophylline, isoniazid (INH), diphenhydramine, antipsychotics, cocaine, and amphetamines. [Pg.1397]

Which of the following antidepressants would be most likely to cause the patient to have a seizure ... [Pg.293]

Isolated seizures that are not epilepsy can be caused by stroke, central nervous system trauma, central nervous system infections, metabolic disturbances (e.g., hyponatremia and hypoglycemia), and hypoxia. If these underlying causes of seizures are not corrected, they may lead to the development of recurrent seizures I or epilepsy. Medications can also cause seizures. Some drugs that are commonly associated with seizures include tramadol, bupropion, theophylline, some antidepressants, some antipsy-chotics, amphetamines, cocaine, imipenem, lithium, excessive doses of penicillins or cephalosporins, and sympathomimetics or stimulants. [Pg.444]

For completeness, buproprion should be mentioned even though it is not widely registered as an antidepressant in Europe, partly because of its propensity to cause seizures in some patients. Buproprion, quite widely used in the USA as an antidepressant, appears to inhibit the reuptake of both dopamine and noradrenaline and therefore tends to have a slightly alerting action. In many European countries it has recently been introduced, at a lower than antidepressant dose, in the treatment of nicotine withdrawal in smoking cessation programmes. [Pg.176]

There is a large evidence base for the antidepressant efficacy of venlafaxine, but fewer studies have been carried out in anxiety disorders. The best evidence is for GAD (Allgulander et al. 2001) and anxiety symptoms associated with depression (Silverstone and Ravindran 1999). Side-effects on initiation of therapy are similar to those of SSRIs, with nausea being the most common. Higher doses can cause raised blood pressure. A discontinuation syndrome similar to that seen with SSRIs has been reported. Toxicity causes cardiac conduction problems, seizures and coma, and venlafax-... [Pg.483]

These facts must be kept in mind when evaluating the efficacy data with this antidepressant. The best evidence supporting this warning is the recent approval of the sustained release version of bupropion. Three double-blind studies were done to support the submission of this formulation for approval. The FDA concluded that all three of these studies failed to show that the sustained release version of bupropion in the doses used (i.e., less than 450 mg per day) was superior to placebo in the treatment of outpatients with major depression (bupropion summary basis of approval). As a result, this formulation was approved on the basis of bioequivalence with the immediate release formulation. The FDA in its approval documents did not specify why it chose to approve this formulation without efficacy data. One possibility is that there are reasons to believe that the sustained release formulation is less likely to cause seizures than is the immediate release version at comparable doses. In contrast to these failed studies, two relatively small studies published in 1983 reported that immediate release bupropion at doses up to 600 mg per day was superior to placebo in the treatment of inpatients hospitalized for major depression (165, 166). [Pg.123]

Adverse effects of flumazenil include agitation, confusion, dizziness, and nausea. Flumazenil may cause a severe precipitated abstinence syndrome in patients who have developed physiologic benzodiazepine dependence. In patients who have ingested benzodiazepines with tricyclic antidepressants, seizures and cardiac arrhythmias may follow flumazenil administration. [Pg.481]

Physostigmine Suggested for antimuscarinic anticholinergic agents not for tricyclic antidepressants Adult dose is 0.5-1 mg IV slowly. The effects are transient (30-60 minutes), and the lowest effective dose may be repeated when symptoms return. May cause bradycardia, increased bronchial secretions, seizures. Have atropine ready to reverse excess effects. Do not use for tricyclic antidepressant overdose. [Pg.1255]

A large number of prescription and nonprescription drugs, as well as a variety of plants and mushrooms, can inhibit the effects of acetylcholine at muscarinic receptors. Some drugs used for other purposes (eg, antihistamines) also have anticholinergic effects. Many of them have other potentially toxic actions. For example, antihistamines such as diphenhydramine can cause seizures tricyclic antidepressants, which have anticholinergic, quinidine-like, and a-blocking effects, can cause severe cardiovascular toxicity. [Pg.1256]

Newer antidepressants (eg, fluoxetine, paroxetine, citalopram, venlafaxine) are mostly SSRIs and are generally safer than the tricyclic antidepressants and monoamine oxidase inhibitors, although they can cause seizures. Bupropion (not an SSRI) has caused seizures even in therapeutic doses. Some antidepressants have been associated with QT prolongation and torsade de pointes arrhythmia. SSRIs may interact with each other or especially with monoamine oxidase inhibitors to cause the serotonin syndrome, characterized by agitation, muscle hyperactivity, and hyperthermia (see Chapter 16). [Pg.1257]

Some of the tricyclic antidepressants also have the ability to block serotonin 2A receptors, which may contribute to the therapeutic actions of those agents with this property. Blockade of serotonin 2A receptors is discussed in Chapter 7. Tricyclic antidepressants also block sodium channels in the heart and brain, which can cause cardiac arrhythmias and cardiac arrest in overdose, as well as seizures. [Pg.220]

Because oxycodone may intensify the effects of other drugs that cause drowsiness, it should not be taken with antidepressants, antihistamines, anti-anxiety drugs, seizure medications, sedatives, sleeping pills, or muscle relaxants, except under the supervision of a doctor. Patients who may be prescribed oxycodone should tell their doctor if they are taking any of these medications. [Pg.405]

Meperidine Demerol 50-100 mg every 3 hours An effective pain reliever but potentially fatal if given in combination with antidepressants known as MAO (monoamine oxidase) inhibitors can also cause seizures... [Pg.44]

Antimuscarinic syndromes consist of tachycardia, dilated pupils, dry, flushed skin, urinary retention, decreased bowel sounds, mild elevation of body temperature, confusion, cardiac arrhythmias and seizures. They are commonly caused by antipsych-otics, tricyclic antidepressants, antihistamines, anti-spasmodics and many plants (see p. 160). [Pg.158]

Of 279 patients who presented to a hospital emergency service between 1994 and 1998 with a first tonic-clonic seizure, 17 (6.1%) had seizures that were thought to be drug-related (5). The most common drug-induced causes were cocaine intoxication (6/17) and benzodiazepine withdrawal (5/17) followed by amfebutamone use (4/17). While one amfebutamone-associated seizure occurred in a 26-year-old woman without any other risk factors, the three other patients (all women) had additional risk factors, such as concomitant treatment with antidepressants that also lower seizure threshold and a history of bulimia nervosa. These results suggest that amfebutamone is not an infrequent cause of de novo seizures. However, because of the time frame of the study, many of the patients would have been taking standard-release amfebutamone. It would be of interest to repeat the study now that modified-release amfebutamone is available. [Pg.108]


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