Late life depression

From Wikipedia, the free encyclopedia
Jump to navigation Jump to search

Late life depression refers to a major depressive episode occurring for the first time in an older person (usually over 50 or 60 years of age). Concurrent medical problems and lower functional expectations of elderly patients often obscure the degree of impairment. Typically, elderly patients with depression do not report depressed mood, but instead present with less specific symptoms such as insomnia, anorexia, and fatigue. Elderly persons sometimes dismiss less severe depression as an acceptable response to life stress or a normal part of aging.[1][2][3][4][5][6]


To meet criteria for a major depressive episode, a patient must have 5 of these 9 symptoms nearly every day for at least 2 weeks.[7]

  1. Depressed or sad mood
  2. Anhedonia (loss of interest in pleasurable activities)
  3. Sleep disturbance (increased or decreased sleep)
  4. Appetite disturbance (increased or decreased appetite) typically with weight change
  5. Energy disturbance (increased or decreased energy/activity level), usually fatigue
  6. Poor memory and/or concentration
  7. Feelings of guilt or worthlessness
  8. Psychomotor retardation or agitation (a change in mental and physical speed perceived by other people)
  9. Thoughts of wishing you were dead; suicidal ideation or suicide attempts


The exact changes in brain chemistry and function that cause either late life or earlier-onset depression are unknown. It is known, however, that brain changes can be triggered by the stresses of certain life events such as illness, childbirth, death of a loved one, life transitions (such as retirement), interpersonal conflicts, or social isolation. Risk factors for depression in elderly persons include a history of depression, chronic medical illness, female sex, being single or divorced, brain disease, alcohol abuse, use of certain medications, and stressful life events.


Treatment is effective in about 80% of identified cases, when treatment is provided. Effective management requires a biopsychosocial approach, combining pharmacotherapy and psychotherapy. Therapy generally results in improved quality of life, enhanced functional capacity, possible improvement in medical health status, increased longevity, and lower health care costs. Improvement should be evident as early as two weeks after the start of therapy, but full therapeutic effects may require several months of treatment. Psychotherapy and medication are the two primary treatment approaches.Therapy for older patients should be continued for longer periods than are typically used in younger patients.[8][9]


Psychologic therapies are recommended for elderly patients with depression because of this group’s vulnerability to adverse effects and high rates of medical problems and medication use. Psychotherapeutic approaches include cognitive behavioral therapy, supportive psychotherapy, problem-solving therapy, and interpersonal therapy. The potential benefit of psychotherapy is not diminished by increasing age. Older adults often have better treatment compliance, lower dropout rates, and more positive responses to psychotherapy than younger patients.[10] Consultation with a clinical geropsychologist is useful.


Pharmacotherapy for acute episodes of depression usually is effective and free of complications. Underuse or misuse of antidepressants and prescribing inadequate dosages are the most common mistakes physicians make when treating elderly patients for depression. Only 10 to 40 percent of depressed elderly patients are given medication. Different types of antidepressants may by used such as TCAs(Tricyclic antidepressants), SSRIs, and MAOIs, but more studies are still needed about TCAs recommendations.[11] Antidepressants, in general, may also work by playing a neuroprotective role in how they relieve anxiety and depression. It's thought that antidepressants may increase the effects of brain receptors that help nerve cells keep sensitivity to glutamate which is an organic compound of a nonessential amino acid. This increased support of nerve cells lowers glutamate sensitivity, providing protection against the glutamate overwhelming and exciting key brain areas related to depression. Antidepressant medications are often the first treatment choice for adults with moderate or severe depression, sometimes along with psychotherapy. The most promising therapeutic effect is achieved when the treatment continues for at least 6 weeks.[11] Although antidepressants may not cure depression, they can lead to remission, which is the disappearance or nearly complete reduction of depression symptoms.[12][13][14]


Major Depression is a mental disorder characterized by an all-encompassing low mood accompanied by low self-esteem, and loss of interest or pleasure in normally enjoyable activities.Nearly 5 million of the 31 million Americans who are 65 years or older are clinically depressed, and 1 million have major depression. Approximately 3 percent of healthy elderly persons living in the community have major depression. Recurrence may be as high as 40 percent. Suicide rates are nearly twice as high in depressed patients as in the general population. Major depression is more common in medically ill patients who are older than 70 years and hospitalized or institutionalized. Severe or chronic diseases associated with high rates of depression include stroke (30 to 60 percent), coronary heart disease (8 to 44 percent), cancer (1 to 40 percent), Parkinson's disease (40 percent), Alzheimer's disease (20 to 40 percent), and dementia (17 to 31 percent).[15]

Minor depression is a clinically significant depressive disorder that does not fulfill the duration criterion or the number of symptoms necessary for the diagnosis of major depression. Minor depression, which is more common than major depression in elderly patients, may follow a major depressive episode. It also can be a reaction to routine stressors in older populations. Fifteen to 50 percent of patients with minor depression develop major depression within two years.[16]


Brain imaging (functional/structural MRI) may help direct the search for microscopic abnormalities in brain structure and function responsible for late life depression. Ultimately, imaging technologies may serve as tools for early diagnosis and subtyping of depression.[17]

See also[edit]


  1. ^ George S. Alexopoulos; Robert E. Kelly (2009). "Research advances in geriatric depression". World Psychiatry. 8 (3): 140–149. PMC 2755271Freely accessible. PMID 19812743. 
  2. ^ D. C. Steffens; G. G. Potter (2008). "Geriatric depression and cognitive impairment". Psychological Medicine. 38 (2): 163–175. doi:10.1017/S003329170700102X. PMID 17588275. 
  3. ^ Alex J. Mitchell; Hari Subramaniam (2005). "Prognosis of Depression in Old age compared to Middle age: A systematic Review of Comparative Studies". Am J Psychiatry. 162 (9): 1588–1601. doi:10.1176/appi.ajp.162.9.1588. PMID 16135616. 
  4. ^ Yohannes AM, Baldwin RC (2008). "Medical Comorbidities in Late-Life Depression". Psychiatric Times. 25 (14). 
  5. ^ Krishnan KR. (2007). "Concept of disease in geriatric psychiatry". Am J Geriatr Psychiatry. 15 (1): 1–11. doi:10.1097/01.JGP.0000224600.37387.4b. PMID 17095750. 
  6. ^ Alexopoulos GS. (2005). "Depression in the elderly". Lancet. 365 (9475): 1961–70. doi:10.1016/S0140-6736(05)66665-2. PMID 15936426. 
  7. ^ Richard B. Birrer; Satahta P. Vemuri (2004). "Depression in Later Life:A Diagnostic and Therapeutic Challenge". American Family Physician. 69 (10): 2375–2382. PMID 15168957. 
  8. ^ Cathy J. Frazer; Helen christensen; Katheleen M. Griffiths (2005). "Effectiveness of treatments for depression in older people". Medical Journal of Australia. 182 (12): 627–632. PMID 15963019. 
  9. ^ Smith GS, Alexopoulos GS (2009). "Neuroimaging in geriatric psychiatry". Int J Geriatr Psychiatry. 24 (8): 783–7. doi:10.1002/gps.2335. PMID 19593778. 
  10. ^ Alexopoulos GS, Raue PJ, Kanellopoulos D, Mackin S, Arean PA (2008). "Problem solving therapy for the depression-executive dysfunction syndrome of late life". Int J Geriatr Psychiatry. 23 (8): 782–8. doi:10.1002/gps.1988. PMID 18213605. 
  11. ^ a b Wilson, K; Mottram, P; Sivanranthan, A; Nightingale, A (2001). "Antidepressant versus placebo for depressed elderly". The Cochrane Database of Systematic Reviews (2): CD000561. doi:10.1002/14651858.CD000561. PMID 11405969. 
  12. ^ Taylor WD, Kuchibhatla M, Payne ME, Macfall JR, Sheline YI, Krishnan KR, Doraiswamy PM. (2008). García, Antonio Verdejo, ed. "Frontal white matter anisotropy and antidepressant remission in late-life depression". PLoS ONE. 3 (9): 24. doi:10.1371/journal.pone.0003267. PMC 2533397Freely accessible. PMID 18813343. 
  13. ^ Murphy GM Jr; Kremer C; Rodrigues HE; Schatzberg AF. (2003). "Pharmacogenetics of antidepressant medication intolerance". Am J Psychiatry. 160 (10): 1830–5. doi:10.1176/appi.ajp.160.10.1830. PMID 14514498. 
  14. ^ Serafeim A, et al. (2003). "Selective serotonin reuptake inhibitors directly signal for apoptosis in biopsy-like Burkitt lymphoma cells". Blood. 101 (8): 3212–3219. doi:10.1182/blood-2002-07-2044. PMID 12515726. 
  15. ^ American Psychiatric Association 2000a, p. 354
  16. ^ Rapaport MH, Judd LL, Schettler PJ, Yonkers KA, Thase ME, Kupfer DJ, Frank E, Plewes JM, Tollefson GD, Rush AJ (2002). "A descriptive analysis of minor depression". Am J Psychiatry. 159 (4): 637–43. doi:10.1176/appi.ajp.159.4.637. PMID 11925303. 
  17. ^ Soares JC, Mann JJ (1997). "The anatomy of mood disorders--review of structural neuroimaging studies". Biol Psychiatry. 41 (1): 86–106. doi:10.1016/S0006-3223(96)00006-6. PMID 8988799.