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Late life depression - Treatment

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Ttreatment in Late life depression 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.[1][2]

PsychotherapyEdit

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.[3]

PharmacotherapyEdit

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. 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. Although antidepressants may not cure depression, they can lead to remission, which is the disappearance or nearly complete reduction of depression symptoms.[4][5][6]

Selective Serotonin Reuptake InhibitorsEdit

Selective serotonin reuptake inhibitors (SSRIs) are a popular class of antidepressant medications. The first drug in this class was fluoxetine (Prozac), which hit the U.S. market in 1987. Precisely how SSRIs affect depression isn't clear. Certain brain chemicals called neurotransmitters are associated with depression, including the neurotransmitter serotonin (ser-oh-TOE-nin). Some research suggests that abnormalities in neurotransmitter activity affect mood and behavior. SSRIs seem to relieve symptoms of depression by blocking the reabsorption (reuptake) of serotonin by certain nerve cells in the brain. This leaves more serotonin available in the brain. Increased serotonin enhances neurotransmission, the sending of nerve impulses, and improves mood. SSRIs are called selective because they seem to affect only serotonin, not other neurotransmitters.

Tricyclic AntidepressantsEdit

Tricyclic antidepressants (TCAs) are a class of psychoactive drugs used primarily as antidepressants, which were first discovered in the early 1950s, and subsequently introduced later in the decade. They are named after their chemical structure, which contains three rings of atoms, and are closely related to the tetracyclic antidepressants (TeCAs), which contain four rings of atoms.

Monoamine Oxidase Inhibitors (MAOIs)Edit

Researchers believe MAOIs relieve depression by preventing the enzyme monoamine oxidase from metabolizing the neurotransmitters norepinephrine (nor-ep-ih-NEF-rin), serotonin (ser-oh-TOE-nin) and dopamine (DOE-puh-mene) in the brain. As a result, these levels remain high in the brain, boosting mood.

Other AntidepressantsEdit

Other antidepressants exist that have different ways of working than the SSRIs, tricyclics, and MAOIs. Commonly used ones are venlafaxine, nefazadone, bupropion, mirtazapine and trazodone.

Electroconvulsive Therapy (ECT)Edit

Electroconvulsive therapy (ECT) is a first-line option in patients with depression and psychotic features who have not responded to antipsychotic and antidepressant medications,and patients with severe nonpsychotic depression who have not responded to adequate trials of two antidepressants.

ECT is a procedure in which electric currents are passed through the brain, deliberately triggering a brief seizure. This seizure releases many chemicals in the brain. These chemicals, called neurotransmitters, deliver messages from one brain cell to another. The release of these chemicals makes the brain cells work better. A person's mood will improve when his or her brain cells and chemical messengers work better. Although electroconvulsive therapy can still cause side effects and complications, it now uses precisely calculated electrical currents administered in a controlled setting to achieve the most benefit with the fewest possible risks.[7]

Deep Brain Stimulation (DBS)Edit

Deep brain stimulation (DBS) is a surgical treatment involving the implantation of a medical device called a brain pacemaker, which sends electrical impulses to specific parts of the brain. DBS in select brain regions has provided remarkable therapeutic benefits for otherwise treatment-resistant movement and affective disorders such as chronic pain, Parkinson’s disease, tremor and dystonia. Despite the long history of DBS, its underlying principles and mechanisms are still not clear. DBS directly changes brain activity in a controlled manner, its effects are reversible (unlike those of lesioning techniques) and is one of only a few neurosurgical methods that allows blinded studies.[8][9][10]

Transcranial Magnetic Stimulation (TMS)Edit

Transcranial magnetic stimulation (TMS) is a procedure that uses magnetic fields to stimulate nerve cells in the brain to improve symptoms of depression. Transcranial magnetic stimulation is one of the newer types of brain-stimulation methods designed to treat depression when standard treatment hasn't worked. There are different ways to perform transcranial magnetic stimulation. But in general, a large electromagnetic coil is placed against the scalp near the forehead. The electromagnet creates painless electric currents that stimulate nerve cells in the region of your brain involved in mood regulation and depression.[11]

Vagus Nerve Stimulation (VNS)Edit

Vagus nerve stimulation (VNS) is a neurological procedure that sends electrical impulses into the brain in an effort to improve chronic depression symptoms. Vagus nerve stimulation is one of several newer types of brain stimulation methods designed to treat depression when standard treatment hasn't worked. Vagus nerve stimulation is sometimes called vagal nerve stimulation. With vagus nerve stimulation, a device called a pulse generator is surgically implanted in the chest. A wire threaded under the skin connects the pulse generator to the left vagus nerve in the neck. The pulse generator sends out electrical signals along the vagus nerve to the brain. These signals affect mood centers in the brain, possibly improving depression symptoms. Vagus nerve stimulation is recommended only for certain cases of severe or chronic depression.[12]

See alsoEdit

ReferencesEdit

  1. Cathy J. Frazer, Helen christensen, and Katheleen M. Griffiths (2005). Effectiveness of treatments for depression in older people. Medical Journal of Australia 182 (12): 627–632.
  2. Smith GS, Alexopoulos GS. (2009). Neuroimaging in geriatric psychiatry. Int J Geriatr Psychiatry 24 (8): 783–7.
  3. 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.
  4. Taylor WD, Kuchibhatla M, Payne ME, Macfall JR, Sheline YI, Krishnan KR, Doraiswamy PM. (2008). Frontal white matter anisotropy and antidepressant remission in late-life depression. PLoS ONE 3 (9): 24.
  5. Murphy GM Jr, Kremer C, Rodrigues HE, Schatzberg AF. (2003). Pharmacogenetics of antidepressant medication intolerance. Am J Psychiatry 160 (10): 1830–5.
  6. Serafeim A et al. (2003). Selective serotonin reuptake inhibitors directly signal for apoptosis in biopsy-like Burkitt lymphoma cells. Blood 101 (8): 3212–3219.
  7. Lisanby, S.H. (2008). Electroconvulsive Therapy for Depression. N Engl J Med 358 (19): 1939–1945.
  8. Gunning FM, Cheng J, Murphy CF, Kanellopoulos D, Acuna J, Hoptman MJ, Klimstra S, Morimoto S, Weinberg J, Alexopoulos GS. (2009). Anterior cingulate cortical volumes and treatment remission of geriatric depression. Int J Geriatr Psychiatry 24 (8): 829–36.
  9. Jamie Talan, "Deep brain stimulation", Dana Press, 2008
  10. Kerry J Ressler, Helen S Mayberg (2007). Targeting abnormal neural circuits in mood and anxiety disorders: from the laboratory to the clinic. Nature Neuroscience 10 (9): 1116–1124.
  11. Paul B. Fitzgerald, Sarah Fountain, Zafiris J. Daskalakis (2006). A comprehensive review of the effects of rTMS on motor cortical excitability and inhibition. Clinical Neurophysiology 117 (12): 2584–96.
  12. Lauren B. Marangell, A. John Rush, Mark S. George, Danae Georges, and Harold A. Sackeim (2001). A Review of Vagus Nerve Stimulation for Treatment-Resistant Depression. Epilepsy & Behavior 2 (3): 6–10.

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