Antidepressants augmentation

Sussman N. (1998). Anxiolytic antidepressant augmentation. J Clin Psychiatry. 59(suppl 5) 42-48. Tadokoro C, Kiuchi Y, Yamazaki Y, Oguchi K, Kamijima K. (1998). Effects of imipramine and sertraline on protein kinase activity in rat frontal cortex. Eur J Pharmacol. 342(1) 51-4. 

Ryan, N., Meyer, V, Dachille, S., Mazzie, D., and Puig-Antich, J. (1988a) Lithium antidepressant augmentation in TCA-refractory depression in adolescents. J Am Acad Child Adolesc Psychiatry 27 371-376. 

The serotonin 1A partial agonist buspirone, whose primary use is in generalized anxiety disorder, is also used as a popular augmenting agent for treatment-resistant depression, particularly in North America (serotonin 1A combo in Fig. 7—30). Its potential mechanism of action as an antidepressant augmenting agent is shown in Figures 7—31 to 7—33. 

Estrogen and Reproductive Hormones as Antidepressant Augmenting Agents... 

We have reviewed antidepressant augmentation strategies, including the principles and several specific examples. Finally, we have touched on the use of electroconvulsive therapy and psychotherapy for the treatment of depression. 

Bipolar patients with so-called breakthrough major depressive episodes, despite adequate treatment, were placed in a randomized doubleblind 10-week study and treated with bupropion, sertraline, or venlafaxine augmentation (Post et al., 2001). Switches to hypomania or mania occurred in 14% of the patients. Those who responded positively to the treatment were continued for 1 year in a blinded maintenance trial, and 33% switched into hypomania or mania. In a second phase of their antidepressant augmentation studies, 18.2% switched into hypomania or... 

Carpenter, L.L., Yasmin, S., and Price, L.H. 2002. A double-blind, placebo-controUed study of antidepressant augmentation with mirtazapine. Biol. Psychiatry 51 183-188. 

Attempts to find the cause(s) of depression have adopted two main approaches. One is to look for the neurobiological basis of depression in human subjects and animal models of this condition. The second is to investigate the pharmacology of established antidepressant agents to see whether they consistently augment some, and ideally the same, neurobiological targets in the brain. 

However, experience proves that depression can be reversed by drugs that augment serotonergic and noradrenergic transmission (and reinstated by a deficit in the synthesis of these monoamines). These, then seem to be crucial targets that ultimately determine mood. This would explain why, despite numerous neurochemical options for the causes of depression, all antidepressants developed so far (and even those discovered by chance) target these neuronal systems. Whatever the cause of depression, therefore, its relief seems to rest on appropriate secretion of these monoamines. This would be entirely... 

Hypothyroidism can precipitate a depression and be a risk factor for rapid cycling thyroid supplementation can be used for refractory rapid cycling and augmentation of antidepressants in unipolar depression. 

Lamotrigine is effective for the maintenance treatment of bipolar I disorder in adults. It has both antidepressant and mood-stabilizing effects, and it may have augmenting properties when combined with lithium or valproate. It has low rates of switching patients to mania. Although it is less effective for acute mania compared to lithium and valproate, it may be beneficial for the maintenance therapy of treatment-resistant bipolar I and II disorders, rapidcycling, and mixed states. It is often used for bipolar II patients. 

Lithium augmentation of antidepressants, carbamazepine, lamotrigine, and valproate can improve response, but it may increase the risk of sedation, weight gain, GI complaints, and tremor. 

Alternatively, the current antidepressant may be augmented (potentiated) by the addition of another agent (e.g., lithium, T3), or an atypical antipsychotic (e.g., risperidone). Risperidone has been shown to be effective in combination with fluvoxamine, paroxetine, or citalopram in treatment-resistant depression. Olanzapine and fluoxetine have been found to be safe and effective in treatment-resistant depression. 

The practice guideline of the American Psychiatric Association recommends that after 6 to 8 weeks of antidepressant treatment, partial responders should consider changing the dose, augmenting the antidepressant, or adding psychotherapy or ECT. For those with no response, options include changing to another antidepressant or the addition of psychotherapy or ECT. 

Consider augmentation ) (non-SSRI antidepressant, lithium, thyroid hormone,... 

Considerable effort in the field of monoamine reuptake inhibitors is focused on improving antidepressant efficacy since 30-40% of patients do not respond to treatment with currently available agents [6,7], An additional major objective is to enhance the onset of action. Current antidepressants typically require 2-6 weeks of treatment before clinical efficacy is seen [6]. Clinical trials exploring augmentation strategies, in which a DA reuptake inhibitor or a dual NE/DA reuptake inhibitor is combined with an SSRI, have resulted in improved efficacy in depressed patients refractory to SSRI treatment alone [4,5]. The improved results from clinical trials such as these serve to justify the considerable focus on the development of inhibitors that simultaneously block the reuptake of 5-HT, NE and DA. 

AS 1990). Several 5-HTlA agonists have been found to produce anxiolytic effects in animal models and in human clinical trials (File et al. 1996 Krummel and Kathol 1987 Goldberg and Finnerty 1979). Furthermore, they have antidepressant effects they augment the antidepressant effects of serotonin reuptake inhibitors, and they decrease the therapeutic latency (Bouwer and Stein 1997 Artigas et al. 1996 Sussman 1998 Rickels et al. 1991 Wieland and Lucki 1990 Jenkins et al. 1990 Fabre 1990). However, results have not been uniformly positive, such as in refractory severe depression (Sussman 1998 Fischer et al. 1998)... 

Fischer P, Tauscher J, Kufferle B, Kasper S. (1998). Weak antidepressant response after buspirone augmentation of serotonin reuptake inhibitors in refractory severe depression. Int Clin Psychopharmacol. 13(2) 83-86. 

In summary, stimulants can still be helpful to augment antidepressants in a medically ill patient. However, you must bear in mind that the stimulants can be abused. 

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