Antidepressants in depression

Geddes JR, Freemantle N, Mason J, Eccles MP, Boynton J (1999). SSRIs versus alternative antidepressants in depressive disorder (Cochrane Review). In Cochrane Library, Issue 4. Oxford Update Software. 

Electroencephalogram (EEG) sleep studies on the use of antidepressants in depressed patients have not produced clear evidence of the involvement of REM or non-REM sleep in the mechanisms underlying clinical change. Furthermore, the role of the physiological mechanisms of sleep during treatment with antidepressants is still unclear. Further basic sleep research is necessary (Gillin 1983) to interpret the effects of antidepressants on EEG sleep in terms of the physiological processes of sleep. 

Goa and Ward 1986 Pecknold et al. 1989 Rickels et al. 1982]. In contradistinction to benzodiazepines, the therapeutic effect of buspirone has a lag period similar to that of antidepressants in depression, suggesting that its therapeutic benefits derive from receptor modulation. In addition, buspirone seems to act preferentially in those patients who are not responsive to benzodiazepines, suggesting a possible subgrouping of generalized anxiety disorders. 

Mindham RHS, Howland C, Shepherd M. An evaluation of continuation therapy with tricyclic antidepressants in depressive illness. Psychol Med 1973 3 5-17. 

Roose SP, Glassman AH, Giardina EGV, et al. Tricyclic antidepressants in depressed patients with cardiac conduction disease. Arch Gen Psychiatry 1987 44 273-275. 

MacGillivray S, Arroll B, Hatcher S, et al. Efficacy and tolerability of selective serotonin reuptake inhibitors compared with tricyclic antidepressants in depression treated in primary care systematic review and metaanalysis. BMJ. 2003 326 1014. 

Avery, D., Winokur, G. (1977). The efficacy of electroconvulsive therapy and antidepressants in depression. Biological Psychiatry, 12, 507-523. 

Rifkin, A. (1988). ECT versus tricyclic antidepressants in depression A review of evidence. Journal of Clinical Psychiatry, 49, 3—7. 

Veith RC, Raskind MA, Caldwell JH, Barnes RF, Gumbrecht G, Ritchie JL. Cardiovascular effects of tricyclic antidepressants in depressed patients with chronic heart disease. N Engl J Med 1982 306(16) 954-9. 

Leucht S, Hackl HJ, Steimer W, Angersbach D, Zimmer R. Effect of adjunctive paroxetine on serum levels and side-effects of tricyclic antidepressants in depressive inpatients. Psychopharmacology (Berl) 2000 147(4) 378-83. 

Dencker SJ, Hopfner Petersen HE. Side effect profile of citalopram and reference antidepressants in depression. In Montgomery SA, editor. Citalopram—The New Antidepressant from Lundbeck Research. Amsterdam Excerpta Medica, 1989 31. 

The 1 allele occurs at a frequency of 20% to 26% in Asian populations and about 53% to 55% in Caucasians [83-86]. In Caucasians and Chinese, the 1/1 genotype has been associated with a significantly better and faster SSRI response, while the s/s allele is associated with poor response [83,84,87-97]. In two studies in Japanese and Korean patients, one found that neither the 1 nor s allele had an effect on treatment response the other observed only a slight improved response among s allele carriers [98,99]. The 1 allele has been associated with improved response to paroxetine, fluoxetine, sertraline, and tricyclic antidepressants in depressed patients, while the s allele has been associated with both poorer response and greater incidence... 

Future Outlook for Antidepressants. Third-generation antidepressants are expected to combine superior efficacy and improved safety, but are unlikely to reduce the onset of therapeutic action in depressed patients (179). Many dmgs in clinical development as antidepressive agents focus on estabhshed properties such as inhibition of serotonin, dopamine, and/or noradrenaline reuptake, agonistic or antagonistic action at various serotonin receptor subtypes, presynaptic tt2-adrenoceptor antagonism, or specific monoamine—oxidase type A inhibition. Examples include buspirone (3) (only... 

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... 

In summary, research on the use of antidepressants to treat cannabis dependence, particularly among individuals with comorbid major depressive disorder, although limited, offers a promising avenue for the development of pharmacological aids to assist in the treatment of cannabis withdrawal. There are clear parallels between this literature and the existing research on the use of antidepressants in the treatment of alcohol dependence comorbid with major depressive disorder (see Chapter 1, Medications to Treat Co-occurring Psychiatric Symptoms or Disorders in Alcoholic Patients). 

Anderson IM, Tomenson BM (1994). The efficacy of selective serotonin reuptake inhibitors in depression a meta-analysis of studies against tricyclic antidepressants. / Psychopharmacol 8, 238 9. 

Donoghue JM, Tylee A (1996). The treatment of depression prescribing patterns of antidepressants in primary care in the United Kingdom. Br JPsychiatry 168, 164—8. 

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). 

Drawing all this evidence together, Schildkraut (1965) concluded that depression was caused by a functional deficit of noradrenergic transmission in the brain. He also thought that the rebound depression and fatigue, which are experienced after the arousing effects of amphetamine have worn off, were due to depletion of neuronal stores of noradrenaline. However, Schildkraut made a clear distinction between the effects of antidepressants and the arousal induced by amphetamine, describing the latter as stimulation and excitement . To this day, there is controversy over whether or not amphetamine has a beneficial effect in depression. 

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