Antidepressants available drugs

Lastly, nomifensine was an interesting antidepressant that also had noradrenaline, dopamine and, due to its 4-hydroxy metabolite, serotonin reuptake properties. It was withdrawn some years ago because of the occurrence of haemolytic anaemia in a small number of patients. It was a particularly effective drug in the treatment of depression in patients with epilepsy as, unlike many antidepressants available at that time, it did not affect the seizure threshold. 

Modern psychopharmacology is about 50 years old. Few doctors and nurses survive to relate how clinical and ambulatory psychiatry looked and felt before the first neuroleptic and antidepressant medications became available. Drug treatment is routine in today s psychiatric practice, and even some of the most severe mental disorders are no longer fatal In view of the dramatic therapeutic advances brought about by psychopharmaceuticals it is of interest to ask how the introduction of these drugs has affected psychiatry as a science and what impact psychopharmacology has had on psychology. 

Paradoxically, ECT is equally useful in both the acute manic and depressive phases of bipolar disorder, constituting the only truly bimodal therapy presently available. For example, in their literature review, Mukherjee et al. ( 51) found that ECT was associated with marked clinical improvement or remission in 80% of patients undergoing treatment for an acute manic episode. This is not the case for lithium, valproate, or CBZ, which, at best, have relatively weak acute antidepressant effects. Drug therapies may also induce a switch from a depressed to a manic phase, whereas ECT can control both phases of the illness. 

Before 1980, the term anxiety neurosis was used to describe a syndrome that included both chronic generalized anxiety and panic attacks. GAD and panic were first listed as discrete diagnoses in the DSM-III, in part because of observed differences in their response to available drug treatments (i.e., the former to benzodiazepines, the latter to antidepressants for a more detailed discussion of panic disorder, see Chapter 13). 

The sale of tryptophan as dietary supplements for man is now illegal. Dietary supplements to animal stock feed is OK. Tryptophan is available to hospitals for use in critical situations. Tryptophan is available as a prescription drug. But it is not available in the health food stores and so cannot be explored by the lay researcher. The world of inquiring into the action on normals, schizophrenics, alcoholics, people who are overweight, people who are depressed, is denied both to the private individual and to the clinical researcher. There are commercially available drugs, all approved, that can play the same role. Within four days of the announced ban of tryptophan (after the problem had been resolved and corrected) a broad promotion of Prozac (an antidepressant similar in action to Tryptophan) appeared in Newsweek (March 26, 1990). Prozac is still widely promoted. Tryptophan is still not available to the private individual. Both can play the role of being an effective sedative. 

The antidepressants available in the United States are classified by either their chemical structure (e.g., the tricyclics, TCAs) or their actions on neurotransmitters (e.g., SSRIs and MAOIs) or simply as other (e.g., Wellbutrin). In the future, the classification of the antidepressants may become more confusing as new drugs are developed that are neither TCAs, SSRIs, or MAOIs. 

Mirtazapine, a drug derived from mianserin—an antidepressant available outside the USA—is a... 

The principal groups of antidepressants available today are all presumed to exert their action via alteration of brain monoamine metabolism. These amines include norepinephrine, dopamine, and serotonin. The involvement of catecholamines in the pathogenesis of depression was invoked as early as 1965. A deficiency in brain serotonin was theorized in 1967, while a role for dopamine in depression was formally proposed in 1975. The drugs that are used to treat depression basically act to increase neurotransmitter concentration in the synaptic cleft either by (1) decreasing neurotransmitter degradation or (2) inhibiting neurotransmitter reuptake. 

Among the tricylic antidepressants, imipramine, 54, was the first commercially available drug, which was introduced in 1960 [9],... 

Mental depression may be the result of an underlying schizophrenic disorder, and pure antidepressant therapy may merely unleash a full-blown psychotic attack with which an available drug may be powerless to cope. A useful agent must, therfore, have both antidepressant and antipsychotic properties. 

Post-traumatic stress disorder (PTSD) is a severe condition with a lifetime prevalence of about 12.5% in women and 6.2% in men (Pigott, 1999). About one in four individuals exposed to trauma develop the syndrome. Drug treatments are still being developed, mostly using antidepressants. Few systematic data are available on the pharmacoeconomics of the condition. 

The pharmacoeconomics of the anxiety disorders has received litde attention. In the past drug costs were largely incurred by use of benzodiazepines, most of which are available in generic forms and are cheap. They are effective and acceptable in the short term. Long-term use is associated with the risk of physical dependence, with an adverse risk—benefit ratio and high cost terms to facilitate withdrawal. There is now a trend towards the use of antidepressants in the anxiety disorders. Clinical experience has been followed by formal trial evaluation. 

In contrast, iproniazid, introduced in 1951 for treatment of tuberculosis, induced euphoria and was described as a psychic energiser . In fact, these patients, when given iproniazid, could become quite disruptive and this action was regarded as an undesirable side-effect However, its beneficial effects in depression were soon recognised and it was regarded as the first effective antidepressant drug. Studies of peripheral sympathetic neurons, later extended to noradrenergic neurons in the brain, showed that iproniazid irreversibly inhibits the catalytic enzyme, monoamine oxidase (MAO). Because only cytoplasmic monoamines are accessible to MAO, inhibition of this enzyme first increases the concentration of the pool of soluble transmitter but this leads to a secondary increase in the stores of vesicle-bound transmitter i.e. the pool available for impulse-evoked release (Fillenz and Stanford 1981). 

When the chemical-imbalance theory was introduced more than 40 years ago, the main evidence in favour of it was the contention that antidepressants, which were thought to increase the availability of serotonin and/or other neurotransmitters in the brain, seemed to be effective in the treatment of depression. As Alec Coppen wrote in 1967, one of the most cogent reasons for believing that there is a biochemical basis for depression or mania is the astonishing success of physical methods of treatment of these conditions. 26 The situation has not changed very much since then. People still cite the supposed effectiveness of antidepressants as fundamental support for the chemical-imbalance hypothesis. This theory, they say, is supported by the indisputable therapeutic efficacy of these drugs .27... 

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