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Tricyclic antidepressant-induced

Preskorn SH, Fast GA. Tricyclic antidepressant induced seizures and plasma drug concentration. J Clin Psychiatry 1992 53 160-162. [Pg.44]

Brown TC, Barker GA, Dunlop ME, Loughnan PM. The use of sodium bicarbonate in the treatment of tricyclic antidepressant-induced arrhythmias. Anaesth Intensive Care 1973 1(3) 203-10. [Pg.25]

Yeragani VK, Pohl R, Balon R, Kulkarni A, Keshavan M. Low serum iron levels and tricyclic antidepressant-induced jitteriness. J Clin Psychopharmacol 1989 9(6) 447-8. [Pg.25]

Xia, Z., E-L. Appelkvist, J. W. Depierre, and L. Nassberger. 1997. Tricyclic antidepressant-induced lipidosis in human monocytes in vitro as well as monocyte derived cell line, as monitored by spectrofluorimetry and flow cytometry after staining with Nile red. Biochemical Pharmacology 53 1521-1532. [Pg.199]

Hayward D, Luff B. Lithium and tricyclic antidepressant-induced delirium presenting with prominent dyspraxia case report. Ther Adv Psychopharmacol 2012 2(4) 147-8. [Pg.36]

If excessive noradrenergic transmission is a causal factor in anxiety, then it would be predicted that a lesion of central noradrenergic neurons would have an anti-anxiety effect in behavioural models of this condition. Unfortunately, the behavioural effects of such lesions are notoriously inconsistent and there are many reports of negative findings (e.g. Salmon, Tsaltas and Gray 1989). One study has even shown that a lesion of central noradrenergic neurons, induced by the selective neurotoxin, DSP-4, abolishes the anti-anxiety effects of tricyclic antidepressants and MAO inhibitors, but not those of the benzodiazepine, alprazolam, or the barbiturate, phenobarbitone (Fontana,... [Pg.412]

The linkage of uptake to the Na+ gradient may be of physiological significance since transport temporarily ceases at the time of depolarization-induced release of catecholamines. The transport of catecholamines can be inhibited selectively by such drugs as tricyclic antidepressants and cocaine. In addition, a variety of phenylethyl-amines, such as amphetamine, are substrates for carrier thus, they can be concentrated within catecholamine-containing neurons and can compete with the catecholamines for transport. [Pg.217]

The atypical tricyclic antidepressant amineptine (Survector) is an indirect dopamine agonist, which selectively inhibits dopamine uptake and induces its release, with additional stimulation of the adrenergic system. Its antidepressant effects are similar to those of other tricyclic antidepressant drugs. However, it acts more rapidly, is better... [Pg.4]

Dmg-induced serotonin syndrome is generally mild and resolves when the offending drugs are stopped. However, it can be severe and deaths have occurred. A large number of drugs have been implicated including tricyclic antidepressants, monoamine oxidase inhibitors (MAOIs), selective serotonin re-uptake inhibitors (SSRIs), pethidine, lithium, and dextromethorphan. The most severe type of reaction has occurred with the combination of selective serotonin re-uptake inhibitors and monoamine oxidase inhibitors. Both non-selective MAOIs such as phenelzine and selective MAOIs such as moclobemide and selegiline have been implicated. [Pg.259]

Clonidine is an agonist at a - and o 2-adreno-ceptor subtypes. It reduce the sympathetic tonus and is thereby a useful antihypertensive drug. Clonidine can induce sedation, depression and peripheral side effects like a dry mouth. Unspecific a-adrenoceptor blocking agents like tricyclic antidepressants can reduce the antihypertensice effect of clonidine. [Pg.309]

Tricyclic antidepressants are cardiotoxic, inducing tachycardias and an increased tendency for ventricular arrhythmias with high doses. This dose dependent cardiotoxicity gives these agents a low therapeutic index. Overdoses are characterized by cardiac conduction disturbances, hyperpyrexia, hypertension, confusion, hallucinations, seizures and coma and there is a high mortality rate in suicide attempts. Depressed patients should therefore not be given more than one week supply of these drugs. [Pg.353]

Tricyclic antidepressants are notorious for their risk to be involved in drug-drug interactions. Additive anticholinergic effects can be expected in combination with antihistamines, antipsychotics and anticholinergic-type anti-Parkinson agents. Hepatic enzyme-inducing agents increase their hepatic metabolism while enzyme inhibitors may potentiate the effects of tricyclics. Concomitant use with monoamine oxidase inhibitors will produce hypertension, hyperpyrexia and convulsions. [Pg.353]

Phenytoin Adjunct in treatment of tricyclic antidepressant toxicity, muscle relaxant in treatment of muscle hyperirritability, treatment of digoxin-induced arrhythmias and trigeminal neuralgia... [Pg.984]

Tricyclic antidepressants are still prescribed today, but some patients experience side effects such as dry mouth, blurry vision, constipation, and other uncomfortable conditions. Other antidepressants have since been found that induce fewer side effects. One of the most popular is fluoxetine, which is marketed under the trade name Prozac. This drug, along with Zoloft and other antidepressants, are known to inhibit reuptake proteins specifically for serotonin. As a result, these drugs are called selective serotonin reuptake inhibitors, or SSRIs. Although some concerns have appeared because of a possible risk of suicide in young patients who take Prozac, these drugs are commonly prescribed and have proved highly effective in millions of patients. [Pg.86]

SRls are currently the most prevalent pharmacological treatment used for panic disorder [see Westenberg and Den Boer, Chapter 24, in this volume], even though tricyclic antidepressants, monoamine oxidase inhibitors [MAOls], and benzodiazepines are also effective. The efficacy of the SRI antidepressants and the observation that initially they may induce deterioration of symptoms [which is usually not the case with treatment of depressed patients with the same medications] raise issues related to the pathobiology of anxiety and its comorbidity with depression. [Pg.8]

This case report (Figures 6-4Ato 6-4C) (McDermut et al. 1995) of selective response to dihydropyridine CCBs but not a phenylalkylamine CCB is of considerable interest in relationship to the patient s history of nonre-sponsivity to multiple tricyclic antidepressants, the selective serotonin reuptake inhibitors, lithium, carbamazepine (the patient developed drug-induced hepatitis on carbamazepine and was unable to be evaluated), alprazolam, trazodone, and phenelzine. This suggests that patients with refractory mood disorders may have differential responses to various CCBs and that nonresponse to one CCB does not preclude response to another CCB, particularly if the other CCB is from a different category (Table 6-3). [Pg.95]

In clinical practice, a number of patients with SRI-resistant OCD receive simultaneous treatment with two potent SRls. Apart from encouraging case reports of coadministering fluoxetine and clomipramine in adolescents [Simeon et al. 1990] and adults [Browne et al. 1993] with OCD, the efficacy and safety of this approach have not been subjected to rigorous examination. Because of the risks associated with fluoxetine-induced elevations in plasma levels of tricyclic antidepressants, caution should be exercised when these drugs are used concurrently [Rosenstein et al. 1991]. Clomipramine s potential for lowering seizure threshold is of particular concern, making it advisable to measure clomipramine plasma levels before and after addition of another SRI. [Pg.490]

Chuang DM, Gao X-M, Paul SM N-methyl-D-aspartate exposure blocks glutamate toxicity in cultured cerebellar granule cells. Mol Pharmacol 42 210-216, 1992 Chugh Y, Saha N, Sankaranarayanan A, et al Enhancement of memory retrieval and attenuation of scopolamine-induced amnesia following administration of S-HTj antagonist ICS 205-930. Pharmacol Toxicol 69 105-106, 1991 Ciraulo DA, Jaffe JH Tricyclic antidepressants in the treatment of depression associated with alcoholism. Clin Psychopharmacol 1 146, 1981 Ciraulo DA, Barnhill JG, Jaffe JH Clinical pharmacokinetics of imipramine and desipramine in alcoholics and normal volunteers. Pharmacol Ther 43 539-548, 1988... [Pg.612]


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Antidepressants, tricyclic

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