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A broad range of physical treatments have been used to help with major depression.

Medication

Antidepressants in general are as effective as psychotherapy; their benefits increase with the severity of the depression,[1][2] although more patients cease treatment than psychotherapy, likely because of the side effects of antidepressants.[1] A large 2008 meta-analysis of past studies reported that the response to antidepressant treatment in moderate depression were not shown to exceed that of placebo;[1] this interpretation was questioned in an editorial of the British Medical Journal, and a positive but small effect was not ruled out.[3] A black box warning has been introduced in the United States in 2007 on SSRI and other antidepressant medications due to increased risk of suicidality in patients younger than 24.[4]

Selective serotonin reuptake inhibitors (SSRIs), such as sertraline, escitalopram, fluoxetine, paroxetine, and citalopram are the primary medications considered owing to their effectiveness, relatively mild side effects, and because they are less toxic in overdose than other antidepressants.[5] Those who do not respond to one SSRI can be switched to another, which results in improvement in almost 50% of cases.[6] Another option is to switch to the atypical antidepressant bupropion.[7][8][9] It is not uncommon for SSRIs to cause or worsen insomnia; the sedating antidepressant mirtazapine can be used in such cases.[10][11][12] Venlafaxine, and other serotonin-norepinephrine reuptake inhibitors, may be modestly more effective than SSRIs;[13] however, venlafaxine is not recommended as a first-line treatment because of evidence suggesting its risks may outweigh benefits.[14][15] Its use is specifically discouraged in children and adolescents.[16] Fluoxetine is the only antidepressant recommended for people under the age of 18 years.[16]

Amitriptyline-2D-skeletal

Amitriptyline is a tricyclic antidepressant, so called because there are three rings in its molecular structure.

Tricyclic antidepressants have more side effects than SSRIs and are usually reserved for the treatment of inpatients, for whom the tricyclic antidepressant amitriptyline, in particular, appears to be more effective.[17][18] A different class of antidepressants, the monoamine oxidase inhibitors, have historically been plagued by life-threatening adverse effects. They are still used only rarely, although newer and better tolerated agents of this class have been developed.[19]

To find the most effective antidepressant medication with tolerable or fewest side effects, the dosages can be adjusted, and, if necessary, combinations of different classes of antidepressants can be tried. Response rates to the first antidepressant administered may be as low as 50%,[20] and it can take at least six to eight weeks from the start of medication to remission, when the patient is back to their normal self.[21] Antidepressant medication treatment is usually continued for 16 to 20 weeks after remission, to minimise the chance of recurrence.[21] People with chronic depression usually need to take medication for the rest of their lives.[22] The terms refractory depression or treatment-resistant depression are used to describe cases that do not respond to adequate courses of least two antidepressants.[23]

A doctor may add a medication with a different mode of action to bolster the effect of an antidepressant in cases of treatment resistance.[24] Medication with lithium salts has been used to augment antidepressant therapy in those who have failed to respond to antidepressants alone.[25] Furthermore, lithium dramatically decreases the suicide risk in recurrent depression.[26] Addition of a thyroid hormone, triiodothyronine may work as well as lithium, even in patients with normal thyroid function.[27] Addition of atypical antipsychotics when the patient has not responded to an antidepressant is also known to increase the effectiveness of antidepressant drugs, albeit offset by increased side effects.[28]

Electroconvulsive therapy

Main article: Electroconvulsive therapy

Electroconvulsive therapy (ECT) is a procedure where pulses of electricity are sent through the brain via two electrodes, usually one on each temple, to induce a seizure while the patient is under a short general anaesthetic. Hospital psychiatrists may recommend ECT for cases of severe major depression which have not responded to antidepressant medication or, less often, psychotherapy or supportive interventions.[29] ECT can have a quicker effect than antidepressant therapy and thus may be the treatment of choice in emergencies such as catatonic depression where the patient has stopped eating and drinking, or where a patient is severely suicidal.[29] ECT is probably more effective than pharmacotherapy for depression in the immediate short-term,[30] although a landmark community-based study found much lower remission rates in routine practice.[31] Used on its own the relapse rate within the first six months is very high; early studies put the rate at around 50%,[32] while a more recent controlled trial found rates of 84% even with placebos.[33] The early relapse rate may be reduced by the use of psychiatric medications or further ECT[34][35] (although the latter is not recommended by some authorities[36]) but remains high.[37] Common initial adverse effects from ECT include short and long-term memory loss, disorientation and headache.[38] Although objective psychological testing shows anterograde memory has mostly returned to baseline by one month post treatment, ECT remains a controversial treatment, and debate on the extent of cognitive effects and safety continues.[39][40]

Repetitive transcranial magnetic stimulation

Repetitive transcranial magnetic stimulation utilizes powerful magnetic fields which applied to the brain from outside the head. Multiple controlled studies support the use of this method in treatment-resistant depression; it has been approved for this indication in Europe, Canada, Australia, and the US.[41][42][43] It was inferior to ECT in a side-by-side randomized trial.[44]

Depression - vagus nerve stimulation|Vagus nerve stimulation

Main article: Depression - Vagus nerve stimulation

Vagus nerve stimulation (VNS) has recently been approved for treating drug-resistant cases of clinical depression.[45] A convenient, non-invasive VNS device that stimulates an afferent branch of the vagus nerve is also being developed and will soon undergo trials.

Phototherapy

File:Bright light lamp.jpg

Bright light therapy, a form of phototherapy has been found to be an effective treatment for the winter depression produced by seasonal affective disorder. There has been some conflicting evidence as to its effectiveness for non-seasonal depression.[46][47] Physical exercise has been proposed as an alternative form of treatment, and is recommended by U.K. health authorities,[48] but systematic review has not been conclusive on its effectiveness in symptom reduction.[49] Vagus nerve stimulation was approved by the FDA in the United States in 2005 for use in treatment-resistant depression,[50] although it failed to show short-term benefit in the only large double-blind trial when used as an adjunct on treatment-resistant patients.[51]

Depresssion - Rest cures

Depression - Water treatments

Depression - Diets

Depression - Herbal remedies

Two products, St John's wort and S-Adenosyl methionine, are available as prescription antidepressants in several European countries, and are classified as herbal supplements and sold over-the-counter in the UK[5] and US. There is inconsistent evidence on the effect of St John's wort extract on major depression. The pharmaceutical quality of the extract has an effect on the safety and efficacy for the treatment of any type of depression,[52][53] and the quantity of active ingredient varies between different preparations.[5] St John's wort interacts with a number of prescribed medicines including other antidepressants, oestrogens and progesterones, and can reduce the effectiveness of oral contraceptive pills.[54]

Clinical trials of S-Adenosyl methionine have shown that it is equivalent to tricyclic antidepressants in effectiveness, although the safety and efficacy of over-the-counter versions is unknown.[55][56] Other supplements such as omega-3 fatty acids,[57] tryptophan, and 5-hydroxytryptophan,[58] have shown no effect beyond those of placebo.

Exercise

New evidence suggests that aerobic exercise eases depression nearly as well as commonly prescribed antidepressant medications do.[59] The results described are for patients with mild or moderate depression in a study conducted by Dr. James Blumenthal of Duke University Medical Center in Durham, North Carolina, United States. The study included 202 patients randomly assigned to one of four settings: supervised group-exercise, a home exercise program, antidperessant treatment with Sertraline (Zoloft), or a placebo-pill treatment. After four months, depression largely cleared up in 45% of the group exercise patients, 40% of the home group, 47% of the medication group, and 31% of the placebo group.


See also

References & Bibliography

  1. 1.0 1.1 1.2 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. PLoS Med. 5 (2): e45.
  2. Turner EH, Matthews AM, Linardatos E, Tell RA, Rosenthal R (January 2008). Selective publication of antidepressant trials and its influence on apparent efficacy. New England Journal of Medicine 358 (3): 252–60.
  3. Turner EH, Rosenthal R (March 2008). Efficacy of antidepressants. British Medical Journal 336 (7643): 516–17.
  4. FDA Proposes New Warnings About Suicidal Thinking, Behavior in Young Adults Who Take Antidepressant Medications. (htm) FDA. URL accessed on 2008-05-29.
  5. 5.0 5.1 5.2 Royal Pharmaceutical Society of Great Britain 2008, p. 204
  6. Whooley MA, Simon GE (2000). (abstract) Managing Depression in Medical Outpatients. New England Journal of Medicine 343: 1942–50.
  7. Zisook S, Rush AJ, Haight BR, Clines DC, Rockett CB (2006). Use of bupropion in combination with serotonin reuptake inhibitors. Biological Psychiatry 59 (3): 203–10.
  8. Rush AJ, Trivedi MH, Wisniewski SR, et al. (2006). Bupropion-SR, sertraline, or venlafaxine-XR after failure of SSRIs for depression. New England Journal of Medicine 354 (12): 1231–42.
  9. Trivedi MH, Fava M, Wisniewski SR, Thase ME, Quitkin F, Warden D, Ritz L, Nierenberg AA, Lebowitz BD, Biggs MM, Luther JF, Shores-Wilson K, Rush AJ (2006). Medication augmentation after the failure of SSRIs for depression. New England Journal of Medicine 354 (12): 1243–52.
  10. Mayers AG, Baldwin DS (December 2005). Antidepressants and their effect on sleep. Human Psychopharmacology 20 (8): 533–59.
  11. Winokur A, DeMartinis NA, McNally DP, Gary EM, Cormier JL, Gary KA (October 2003). Comparative effects of mirtazapine and fluoxetine on sleep physiology measures in patients with major depression and insomnia. Journal of Clinical Psychiatry 64 (10): 1224–29.
  12. Lawrence RW (August 2004). Effect of mirtazapine versus fluoxetine on "sleep quality". Journal of Clinical Psychiatry 65 (8): 1149–50.
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  14. Cipriani A, Geddes JR, Barbui C (2007). Venlafaxine for major depression. British Medical Journal 334: 215 (editorial).
  15. Prof Gordon Duff. The Medicines and Healthcare products Regulatory Agency (MHRA).
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  18. Anderson IM (April 2000). Selective serotonin reuptake inhibitors versus tricyclic antidepressants: A meta-analysis of efficacy and tolerability. Journal of Affective Disorders 58 (1): 19–36.
  19. Krishnan KR (2007). Revisiting monoamine oxidase inhibitors. Journal of Clinical Psychiatry 68 Suppl 8: 35–41.
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  21. 21.0 21.1 Karasu TB, Gelenberg A, Merriam A, Wang P (Arpil 2000). Practice Guideline for the Treatment of Patients With Major Depressive Disorder (Second Edition): 1–78.
  22. Cite error: Invalid <ref> tag; no text was provided for refs named NIMHPub
  23. Wijeratne, Chanaka, Sachdev, Perminder (2008). Treatment-resistant depression: Critique of current approaches. Australian and New Zealand Journal of Psychiatry 42: 751–62.
  24. Valenstein M, McCarthy JF, Austin KL, Greden JF, Young EA, Blow FC (2006). What happened to lithium? Antidepressant augmentation in clinical settings. American Journal of Psychiatry 163 (7): 1219–25.
  25. Bauer M, Dopfmer S (1999). Lithium augmentation in treatment-resistant depression: Meta-analysis of placebo-controlled studies. Journal of Clinical Psychopharmacology 19 (5): 427–34.
  26. Guzzetta F, Tondo L, Centorrino F, Baldessarini RJ (March 2007). Lithium treatment reduces suicide risk in recurrent major depressive disorder. Journal of Clinical Psychiatry 68 (3): 380–83.
  27. Nierenberg AA, Fava M, Trivedi MH, Wisniewski SR, Thase ME, McGrath PJ, Alpert JE, Warden D, Luther JF, Niederehe G, Lebowitz B, Shores-Wilson K, Rush AJ (2006). A comparison of lithium and T(3) augmentation following two failed medication treatments for depression: A STAR*D report. American Journal of Psychiatry 163 (9): 1519–30.
  28. includeonly>Bender KJ. "Evidence Grows for Value of Antipsychotics as Antidepressant Adjuncts - Psychiatric Times", Psychiatric Times, 2008-02-01. Retrieved on 2008-08-06.
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  31. Prudic J, Olfson M, Marcus SC, Fuller RB, Sackeim HA (2004). Effectiveness of electroconvulsive therapy in community settings. Biological Psychiatry 55 (3): 301–12.
  32. Bourgon LN, Kellner CH (March 2000). Relapse of depression after ECT: a review. The journal of ECT 16 (1): 19–31.
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  34. Tew JD, Mulsant BH, Haskett RF, Joan P, Begley AE, Sackeim HA (2007). Relapse during continuation pharmacotherapy after acute response to ECT: A comparison of usual care versus protocolized treatment. Annals of Clinical Psychiatry 19 (1): 1–4.
  35. Frederikse M, Petrides G, Kellner C (March 2006). Continuation and maintenance electroconvulsive therapy for the treatment of depressive illness: a response to the National Institute for Clinical Excellence report. The journal of ECT 22 (1): 13–7.
  36. National Institute for Clinical Excellence (2003). Guidance on the use of electroconvulsive therapy (PDF), London: National Institute for Health and Clinical Excellence.
  37. Kellner CH, Knapp RG, Petrides G, et al. (December 2006). Continuation electroconvulsive therapy vs pharmacotherapy for relapse prevention in major depression: A multisite study from the Consortium for Research in Electroconvulsive Therapy (CORE). Archives of General Psychiatry 63 (12): 1337–44.
  38. Barlow 2005, p. 239
  39. Ingram A, Saling MM, Schweitzer I (March 2008). Cognitive Side Effects of Brief Pulse Electroconvulsive Therapy: A Review. Journal of ECT 24 (1): 3–9.
  40. Reisner AD (December 2003). The electroconvulsive therapy controversy: evidence and ethics. Neuropsychology review 13 (4): 199–219.
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  43. DeNoon, Daniel J. FDA OKs TMS Depression Device: Brain-Stimulating Device Cleared for Depression Treatment After 1 Drug Failure. WebMD. WebMD. URL accessed on 10 November 2008.
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  53. St. John's Wort and Depression. NCCAM Health Information. URL accessed on 2008-10-13.
  54. Royal Pharmaceutical Society of Great Britain 2008, p. 764
  55. Mischoulon D, Fava M (November 2002). Role of S-adenosyl-L-methionine in the treatment of depression: A review of the evidence. American Journal of Clinical Nutrition 76 (5): 1158S–61S.
  56. Bressa GM (1994). S-adenosyl-l-methionine (SAMe) as antidepressant: Meta-analysis of clinical studies. Acta Neurologica Scandinavica, Suppl. 154: 7–14.
  57. Appleton KM, Hayward RC, Gunnell D, et al. (December 2006). Effects of n-3 long-chain polyunsaturated fatty acids on depressed mood: Systematic review of published trials. The American journal of clinical nutrition 84 (6): 1308–16.
  58. Shaw K, Turner J, Del Mar C (2002). Tryptophan and 5-hydroxytryptophan for depression. Cochrane Database of Systematic Reviews (1): CD003198.
  59. Science News, October 13, 2007, 172, #25, p. 237.

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