Clinical depression medical therapy
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
The treatment of depression is highly individualized to the patient, based on the patient's unique combination of biological, psychological and social health factors and the severity of their condition.[1] The three most conventional treatments for depression include medication, psychotherapy, and Electroconvulsive therapy, however new treatments and less conventional options are also available, including self help, life style changes, and vagus nerve stimulation.[1] If there is an imminent threat of suicide or the patient is a danger to others, hospitalization is employed as an intervention method to keep at-risk individuals safe until they cease to be a danger to themselves or others. At-risk individuals may also be placed in a partial hospitalization therapy, in which the patient sleeps at home but spends most of the day in a psychiatric hospital setting. This intensive treatment usually involves group therapy, individual therapy, medication management, and is used often in the case of children and adolescents.
Medical Therapy
Antidepressant drugs include selective serotonin reuptake inhibitors, such as escitalopram oxalate (Lexapro), citalopram (Celexa), fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft), are the primary medications considered for patients, having fewer side effects than the older monoamine oxidase inhibitors (MAOIs).
The effect size is very small for moderate depression but increased with severity reaching the NICE criteria for 'clinical significance' for very severe depression.[2] This result is consistent with the earlier clinical studies where only patients with severe depression benefited from the treatment with a tricyclic antidepressant imipramine or from psychotherapy more than from the placebo treatment.[3][4][5] According to the STAR*D randomized controlled trial, about 50% of patients with major depression have a response and about 30% of have remission of symptoms with usage of citalopram.[6]
Bupropion (Wellbutrin, Zyban), an atypical antidepressant that acts as a norepinephrine and dopamine reuptake inhibitor, is also considered to be effective in the treatment of depression,[7] without sexual dysfunction or sexual side effects[8] and without weight gain. Bupropion has also been shown to be more effective than SSRIs at improving symptoms such as hypersomnia and fatigue in depressed patients.[9]
Measurement-based care, which guides mediation based on serial measurement of psychometric testing, improves outcomes according to randomized controlled trials[6][10].
Predictors of a response to treatment
Severity of depression
The effectiveness is antidepressants may[11] or may not[12][13] depend on the severity of a patient's depression. This relationship may be due to the declining effect of placebo among more severely depressed patients.
| American Psychiatric Association classification of severity[14] |
Hamilton Depression Rating Scale (HDRS) |
Number needed to treat[11] | Clinical significance (NICE)[15] |
|---|---|---|---|
| Mild to moderate | < 19 | 16 | No |
| Severe | 19 - 22 | 11 | No |
| Very severe | > 22 | 4 | Yes |
Genetic variations
Variations in the GRIK4 (glutamate receptor, ionotropic, kainate 4 protein) and HTR2A (5-hydroxytryptamine receptor) genes predict response to citalopram.[16]
Treatment failure
| Intervention | Outcome | ||
|---|---|---|---|
| Medication | Mode final dose | Remission % | Quit 2˚ ADRs (%) |
| Switch medications | |||
| Bupropion SR | 200 mg twice daily | 22.3% | 10% |
| Augment medications | |||
| Aripiprazole | 10 mg | 29% | 5% |
| Bupropion SR | 300 mg daily | 27% | 7% |
After starting medications, treatment should be switched if there is no response within one month.[18]
When treated with monotherapy for depression, approximately 30% of patients have remission of symptoms while 50% have a response to medications.[6]
For patients with inadequate response, randomized controlled trials provide guidance.[17][19]
- The original VAST-D trial, that did not include aripiprazole, confirms that augmenting with bupropion is the most effective of options other than augmentation with aripiprazole. In this trial, either adding sustained-release bupropion ("bupropion was 200 mg per day during weeks 1 and 2, increasing to 300 mg per day by week 4 and to 400 mg per day (the final dose) during week 6") or buspirone (up to 60 mg per day) for augmentation as a second drug can cause remission in approximately 30% of patients (bupropion may be more effective than buspirone)[19], while switching medications can achieve remission in about 25% of patients[20]. Alternatively, "extended-release venlafaxine, the starting daily dose of 37.5 mg for 7 days was increased to 75 mg from day 8 to 14, to 150 mg from day 15 to 27, to 225 mg from day 28 to 41, to 300 mg from day 42 to 62, and to 375 mg from day 63 onward."[20]
- The PReDICT trial found that among patients who initially were treated with either an SSRI or CBT, remission was increased when the opposite treatment (CBT or SSRI) was added to non-remitters[21].
- The newer VAST-D trial found that augmentation with aripiprazole is effective.[17] The dose of aripiprazole was 2 mg of with titration to 5, 10, or 15 mg daily as guided by measurement-based care using the PHQ-9.[17] However, aripiprazole led to more adverse drug reactions including somnolence, akathisia, and weight gain. The second most effective was augmentation with buproprion starting at 150 mg sustained release to 300 mg or 400 mg daily as guided by measurement-based care using the PHQ-9.
- More recently, mirtazapine, was found not to add to SSRIs[22].
| Intervention | Outcome | ||
|---|---|---|---|
| Medication | Mean final dose | Remission % | Quit 2˚ ADRs (%) |
| Switch meds (NEJM 2006; PMID: 16554525[20]) | |||
| Bupropion SR | 283 mg | 21% | 27% |
| Sertraline (SSR) | 136 mg | 18% | 21% |
| Venlafaxine ER (SNRI) | 194 mg | 25% | 21% |
| Augment meds (NEJM 2006; PMID: 16554526[19]) | |||
| Bupropion SR | 268 mg | 30% | 13% |
| Buspirone | 41 mg | 30% | 21% |
The STAR*D trial has reported the frequency of re-emergence of suicidality for different second levels of treatment.[23]
In level 3 of the STAR*D trials, patients who had failed two trials of a second-generation antidepressant, tended to better with nortriptyline than mirtazapine.[24]
Aripiprazole, originally introduced as an atypical antipsychotic agent, is approved as an adjunct to other antidepressants.[25]
Stopping medications
Patients are generally advised not to stop taking an antidepressant suddenly and to continue its use for at least four to months to prevent the chance of recurrence.[18] For patients that have chronic depression, medication may need to be continued for the remainder of their life.
Patients should be treated indefinitely if they have "three or more prior major depressive episodes or who have chronic major depressive disorder should proceed to the maintenance phase of treatment after completing the continuation phase."[18]
References
- ↑ 1.0 1.1 Mayo Clinic Staff (2006-03-06). "Depression Treatment Guide". Mayo Clinic. Retrieved 2007-10-20.
- ↑ Kirsch I, Deacon BJ, Huedo-Medina TB, Scoboria A, Moore TJ, Johnson BT (February 2008). "Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration" (htm). PLoS Medicine. Retrieved 2008-02-26.
- ↑ Elkin I, Shea MT, Watkins JT, Imber SD, Sotsky SM, Collins JF, Glass DR, Pilkonis PA, Leber WR, Docherty JP (1989). "National Institute of Mental Health Treatment of Depression Collaborative Research Program. General effectiveness of treatments". Arch. Gen. Psychiatry. 46 (11): 971–82, discussion 983. PMID 2684085.
- ↑ Elkin I, Gibbons RD, Shea MT, Sotsky SM, Watkins JT, Pilkonis PA, Hedeker D (1995). "Initial severity and differential treatment outcome in the National Institute of Mental Health Treatment of Depression Collaborative Research Program". J Consult Clin Psychol. 63 (5): 841–7. PMID 7593878.
- ↑ Sotsky SM, Glass DR, Shea MT, Pilkonis PA, Collins JF, Elkin I, Watkins JT, Imber SD, Leber WR, Moyer J (1991). "Patient predictors of response to psychotherapy and pharmacotherapy: findings in the NIMH Treatment of Depression Collaborative Research Program". Am J Psychiatry. 148 (8): 997–1008. PMID 1853989.
- ↑ 6.0 6.1 6.2 Trivedi MH, Rush AJ, Wisniewski SR, Nierenberg AA, Warden D, Ritz L; et al. (2006). "Evaluation of outcomes with citalopram for depression using measurement-based care in STAR*D: implications for clinical practice". Am J Psychiatry. 163 (1): 28–40. doi:10.1176/appi.ajp.163.1.28. PMID 16390886.
- ↑ Fava M, Rush AJ, Thase ME, Clayton A, Stahl SM, Pradko JF, Johnston JA. (2005). "15 years of clinical experience with bupropion HCl: from bupropion to bupropion SR to bupropion XL". Prim Care Companion J Clin Psychiatry. 7 (3): 106–113. PMID 16027765.
- ↑ For the review, see: Clayton AH (2003). "Antidepressant-Associated Sexual Dysfunction: A Potentially Avoidable Therapeutic Challenge". Primary Psychiatry. 10 (1): 55–61.
- ↑ Baldwin DS, Papakostas GI (2006). "Symptoms of Fatigue and Sleepiness in Major Depressive Disorder". J Clin Psychiatry. 67 (suppl 6): 9–15. PMID 16848671.
- ↑ Yeung AS, Jing Y, Brenneman SK, Chang TE, Baer L, Hebden T; et al. (2012). "Clinical Outcomes in Measurement-based Treatment (Comet): a trial of depression monitoring and feedback to primary care physicians". Depress Anxiety. 29 (10): 865–73. doi:10.1002/da.21983. PMID 22807244.
- ↑ 11.0 11.1 11.2 Fournier JC, DeRubeis RJ, Hollon SD, Dimidjian S, Amsterdam JD, Shelton RC; et al. (2010). "Antidepressant drug effects and depression severity: a patient-level meta-analysis". JAMA. 303 (1): 47–53. doi:10.1001/jama.2009.1943. PMID 20051569.
- ↑ Hieronymus F, Lisinski A, Nilsson S, Eriksson E (2019). "Influence of baseline severity on the effects of SSRIs in depression: an item-based, patient-level post-hoc analysis". Lancet Psychiatry. doi:10.1016/S2215-0366(19)30216-0. PMID 31303567.
- ↑ Gibbons RD, Hur K, Brown CH, Davis JM, Mann JJ (2012). "Benefits From Antidepressants: Synthesis of 6-Week Patient-Level Outcomes From Double-blind Placebo-Controlled Randomized Trials of Fluoxetine and Venlafaxine". Arch Gen Psychiatry. doi:10.1001/archgenpsychiatry.2011.2044. PMID 22393205.
- ↑ First, Michael B. (2007). Handbook of Psychiatric Measures, Second Edition. American Psychiatric Publishing, Inc. ISBN 1-58562-218-4.
- ↑ National Institute for Clinical Excellence. Depression: Management of Depression in Primary and Secondary Care. London, England: National Institute for Clinical Excellence; 2009.
- ↑ Paddock S, Laje G, Charney D, Rush AJ, Wilson AF, Sorant AJ; et al. (2007). "Association of GRIK4 with outcome of antidepressant treatment in the STAR*D cohort". Am J Psychiatry. 164 (8): 1181–8. doi:10.1176/appi.ajp.2007.06111790. PMID 17671280.
- ↑ 17.0 17.1 17.2 17.3 Mohamed S, Johnson GR, Chen P, Hicks PB, Davis LL, Yoon J; et al. (2017). "Effect of Antidepressant Switching vs Augmentation on Remission Among Patients With Major Depressive Disorder Unresponsive to Antidepressant Treatment: The VAST-D Randomized Clinical Trial". JAMA. 318 (2): 132–145. doi:10.1001/jama.2017.8036. PMID 28697253.
- ↑ 18.0 18.1 18.2 American Psychiatric Association (APA). Practice guideline for the treatment of patients with major depressive disorder. 3rd ed. Arlington (VA): American Psychiatric Association (APA); 2010 Oct. 152 p. [1170 references]
- ↑ 19.0 19.1 19.2 Trivedi MH, Fava M, Wisniewski SR; et al. (2006). "Medication augmentation after the failure of SSRIs for depression". N. Engl. J. Med. 354 (12): 1243–52. doi:10.1056/NEJMoa052964. PMID 16554526.
- ↑ 20.0 20.1 20.2 Rush AJ, Trivedi MH, Wisniewski SR; et al. (2006). "Bupropion-SR, sertraline, or venlafaxine-XR after failure of SSRIs for depression". N. Engl. J. Med. 354 (12): 1231–42. doi:10.1056/NEJMoa052963. PMID 16554525.
- ↑ Dunlop BW, LoParo D, Kinkead B, Mletzko-Crowe T, Cole SP, Nemeroff CB; et al. (2019). "Benefits of Sequentially Adding Cognitive-Behavioral Therapy or Antidepressant Medication for Adults With Nonremitting Depression". Am J Psychiatry: appiajp201818091075. doi:10.1176/appi.ajp.2018.18091075. PMID 30764648.
- ↑ Kessler DS, MacNeill SJ, Tallon D, Lewis G, Peters TJ, Hollingworth W; et al. (2018). "Mirtazapine added to SSRIs or SNRIs for treatment resistant depression in primary care: phase III randomised placebo controlled trial (MIR)". BMJ. 363: k4218. doi:10.1136/bmj.k4218. PMC 6207929. PMID 30381374.
- ↑ http://dx.doi.org/10.4088/JCP.12m07777
- ↑ Fava M, Rush AJ, Wisniewski SR, Nierenberg AA, Alpert JE, McGrath PJ; et al. (2006). "A comparison of mirtazapine and nortriptyline following two consecutive failed medication treatments for depressed outpatients: a STAR*D report". Am J Psychiatry. 163 (7): 1161–72. doi:10.1176/appi.ajp.163.7.1161. PMID 16816220. Review in: Evid Based Ment Health. 2007 Feb;10(1):16
- ↑ Marianna Mazza, Maria Rosaria Squillacioti1, Riccardo Daniele Pecora, Luigi Janiri1 & Pietro Bria (December 2008), "Beneficial acute antidepressant effects of aripiprazole as an adjunctive treatment or monotherapy in bipolar patients unresponsive to mood stabilizers: results from a 16-week open-label trial", Expert Opinion on Pharmacotherapy, 9 (18): 3145–3149, doi:10.1517/14656560802504490