Antidepressants history

The miscellaneous anticonvulsants are used cautiously in patients with glaucoma or increased intraocular pressure a history of cardiac, renal or liver dysfunction and psychiatric disorders. When the miscellaneous anticonvulsants are used with other CNS depressants (eg, alcohol, narcotic analgesics, and antidepressants), an additive CNS depressant effect may occur. 

As with all antidepressants, the TCAs are used cautiously in patients witii hepatic or renal impairment. The tricyclics are used cautiously in patients witii heart disease, angina, paroxysmal tachycardia, increased intraocular pressure, prostatic hypertrophy, or a history of seizures. 

The MAOI antidepressant drag s are contraindicated in patients widi known hypersensitivity to die drug s, liver and kidney disease, cerebrovascular disease, hypertension, or congestive heart failure and in die elderly. These drag s are given cautiously to patients witii impaired liver function, history of seizures, parkinsonian symptoms, diabetes, or hyperthyroidism. 

Ciraulo DA, Jaffe JH Tricyclic antidepressants in the treatment of depression associated with alcoholism. Clin Psychopharmacol 1 146—150, 1981 Ciraulo DA, Nace E Benzodiazepine treatment of anxiety or insomnia in substance abuse patients. Am J Addict 9 276—284, 2000 Ciraulo DA, Barnhill JG, Jaffe JH, et al Intravenous pharmacokinetics of 2-hydroxy-imipramine in alcoholics and normal controls. J StudAlcohol 51 366-372, 1990 Ciraulo DA, Knapp CM, LoCastro J, et al A benzodiazepine mood effect scale reliability and validity determined for alcohol-dependent subjects and adults with a parental history of alcoholism. Am J Drug Alcohol Abuse 27 339—347, 2001 Collins MA Tetrahydropapaveroline in Parkinson s disease and alcoholism a look back in honor of Merton Sandler. Neurotoxicology 25 117-120, 2004 COMBINE Study Research Group Testing combined pharmacotherapies and behavioral interventions in alcohol dependence rationale and methods. Alcohol Clin Exp Res 27 1107-1122, 2003a... 

Nortriptyline. Nortriptyhne, a tricychc antidepressant, has been shown in double-blind, placebo-controlled randomized trials to be superior to placebo for smoking cessation (Prochazka et al. 1998). Nortriptyline appears to have efficacy comparable to that of bupropion for smoking cessation (Hall et al. 2002). The efficacy of this agent may be improved with more intensive behavioral therapies (Hall et al. 1998). Nortriptyline s mechanism of action is thought to relate to its noradrenergic and serotonergic reuptake blockade, because these two neurotransmitters have been implicated in the neurobiology of nicotine dependence. Side effects of nortiptyline are typical of tricyclic antidepressants and include dry mouth, blurred vision, constipation, and orthostatic hypotension. Nortriptyline appears to have some utility for smokers with a past history of major depression, and it can be recommended as a second-... 

Hall SM, Reus VI, Munoz RF, et al Nortriptyline and cognitive-behavioral therapy in the treatment of cigarette smoking. Arch Gen Psychiatry 55 683-690, 1998 Hall SM, Humfleet GL, Reus VI, et al Psychological intervention and antidepressant treatment in smoking cessation. Arch Gen Psychiatry 59 930-936, 2002 Hayford KE, Patten CA, Rummans TA, et al Efficacy of bupropion for smoking cessation in smokers with a former history of major depression or alcoholism. Br J Psychiatry 174 173-178, 1999... 

Psychiatric adverse effects occur frequently and may include irritability, depression, and rarely, suicidal ideation. Individuals with a history of uncontrolled psychiatric disorders must weigh the risk versus benefit of treatment, as interferon may exacerbate or worsen the psychiatric condition. Patients who develop mild to moderate symptoms may require antidepressants or anxiolytics. Those with severe symptoms including suicidal ideation should have the treatment discontinued immediately.43... 

Patients with bipolar disorder have a high risk of suicide. Factors that increase that risk are early age at disease onset, high number of depressive episodes, comorbid alcohol abuse, personal history of antidepressant-induced mania, and family history of suicidal behavior.15 In those with bipolar disorder, 1 of 5 suicide attempts are lethal, in contrast to 1 of 10 to 1 of 20 in the general population. 

Benzodiazepines are used commonly in SAD however, there are limited data supporting their use. Clonazepam has been effective for social anxiety, fear, and phobic avoidance, and it reduced social and work disability during acute treatment.58 Long-term treatment is not desirable for many SAD patients owing to the risk of withdrawal and difficulty with discontinuation, cognitive side effects, and lack of effect on depressive symptoms. Benzodiazepines may be useful for acute relief of physiologic symptoms of anxiety when used concomitantly with antidepressants or psychotherapy. Benzodiazepines are contraindicated in SAD patients with alcohol or substance abuse or history of such. 

The most interesting aspect of the results of the study by Lee etal (2004) is that they also differ from those in a Caucasian population (Smeraldi, Benedetti Zanardi, 2002). The authors reported a more favorable natural history in those with the s/s genotype than in 1-allele carriers, which also differs from acute antidepressant responses in Caucasian populations. The frequencies of the s and 1 alleles among the Korean sample were approximately 86% and 14%, respectively, while the corresponding figures for Caucasians are 43% and 57% (Lesch etal, 1996). 

Domino, E. F. (1999). History of modern psychopharmacology a personal view with an emphasis on antidepressants. Psychosom. Med., 61(5), 591-8. 

How is it that the chemical-imbalance theory was proposed and so widely accepted, when the only controlled scientific study that had been done indicated that one could relieve depression, rather than induce it, by giving patients a drug that increases brain levels of monoamines David Healy, in his comprehensive treatise on the history of antidepressants, provides an answer to this question.19 The study was simply ignored, despite having been published in The Lancet, one of the world s most prestigious medical journals. 

I suppose that some ingenious minds will be able to find a way of accommodating the chemical-balance hypothesis to these data, but I suspect that the accommodation will require convoluted circumventions, like those used by the Flat Earth Society in their efforts to maintain their defunct theory in the face of photographic evidence from space. If depression can be equally affected by drugs that increase serotonin, drugs that decrease it and drugs that do not affect it at all, then the benefits of these drugs cannot be due to their specific chemical activity. And if the therapeutic benefits of antidepressants are not due to their chemical composition, then the widely proffered chemical-imbalance theory of depression is without foundation. It is an accident of history produced serendipitously by the placebo effect. 

If the chemical-imbalance theory is wrong, and if depression is not a brain disease, how is it produced and how can it be prevented and treated One way to look for clues is to examine the process by which we were misled into the realm of chemistry. There is a culprit hiding in the history of the chemical-imbalance theory - a culprit that is guilty of leading doctors and patients astray over and over again in the history of medicine. The culprit is the placebo effect, and its darker twin, the nocebo effect. Depressed people got better when given MAO and reuptake inhibitors as antidepressants, and this led researchers to conclude that depression must be caused by a chemical deficiency. But much (if not all) of that improvement turns out to be a placebo effect. So to understand depression and how it might be treated effectively, we need to examine the placebo effect more carefully. That is the topic of the next two chapters. 

Despite public misconceptions, there is little firm evidence that the typical and atypical antidepressants produce dependence in clinical users. A review of 21 case reports of antidepressant addiction revealed that 12 were associated with tranylcypromine, although 8 of these 12 had a previous history of substance misuse (Haddad, 1999). Tranylcypromine s structural similarity to amphetamine may account for the significant number of reports of its addictive potential, but even here the term (mild) discontinuation reaction rather than withdrawal reaction should be used to allay any concerns patients might have (Haddad, 1999). 

BZs are second-line agents except when rapid response is essential. They should not be used as monotherapy in panic disorder patients with a history of depression or alcohol or drug abuse. BZs are often used concomitantly with antidepressants in the first weeks to offset the delay in onset of antipanic effects. 

Lithium is effective for acute mania, but it may require 6 to 8 weeks to show antidepressant efficacy. It may be more effective for elated mania and less effective for mania with psychotic features, mixed episodes, rapid cycling, and when alcohol and drug abuse is present. Maintenance therapy is more effective in patients with fewer episodes, good functioning between episodes, and when there is a family history of good response to lithium. It produces a prophylactic response in up to two-thirds of patients and reduces suicide risk by eight- to 10-fold. 

Factors that influence the choice of antidepressant include the patient s history of response, history of familial response, concurrent medical conditions, presenting symptoms, potential for drug-drug interactions, comparative side-effect profiles of various drugs, patient preference, and drug cost. 

Herbal Antidepressants and Anxiolytics Saint-John s- Wort History and Botany... 

Drug Interactions. No modern discussion of the history of antidepressants would be complete without mention of the debate regarding potential drug interactions. As discussed more fully in Chapter 2, medications may interact in several ways, and their interactions may be helpful or harmful. The antidepressant debate has focused on the way these drugs influence the liver s ability to metabolize and thus deactivate other drugs. In particular, it is the impact of antidepressants on the liver s cytochrome P450 family of enzymes that has been so extensively discussed. 

Augmentation. Choosing an augmenting medication is much like choosing an antidepressant. The severity of the depression, the history of prior treatment, and the safety and side effects of the augmenting medication are all important considerations. 

Serotonin-boosting antidepressants or longer-acting benzodiazepines are also both suitable first-line treatments for APD. For APD patients who are also troubled by depression, an antidepressant is obviously preferable. We also prefer to use antidepressants rather than benzodiazepines to treat APD patients who have a history of substance abuse. The current data suggests that any of the SSRls as well as nefazodone, mirtazapine, and venlafaxine may be helpful. When these do not work, a MAOI is a reasonable alternative provided the patient is willing to commit to the dietary regimen. 

Usual effective dose range is 200 to 300 mg/day. If no response is seen at 300 mg, increase dosage, depending upon tolerance, to 400 mg/day. Hospitalized patients refractory to antidepressant therapy and who have no history of convulsive seizures may have dosage cautiously increased up to 600 mg/day in divided doses. 

Seizures Bupropion is associated with a dose-related risk of seizures. Discontinue bupropion and do not restart in patients who experience a seizure while on treatment. Use extreme caution when bupropion is administered to patients with a history of seizure, cranial trauma, or other predisposition(s) toward seizure, or prescribed with other agents (eg, antipsychotics, other antidepressants, theophylline, systemic steroids) that lower seizure threshold. 

AppetiteAA/eight changes Anorexia was reported for venlafaxine-treated patients. A dose-dependent weight loss often was noted in patients treated for several weeks. Manla/Hypomania During clinical trials, hypomania or mania occurred in 0.5% of patients treated with venlafaxine. As with all antidepressants, use venlafaxine cautiously in patients with a history of mania. 

Mania/Hypomania As with all antidepressants, use nefazodone cautiously in patients with a history of mania. 

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