__________________________________________________ Management of Treatment-Resistant Depression Adverse effects are higher in combination pharmacotherapy, and combining antidepressants at treatment initiation is not recommended unless the MDD is characterized as severe (i.e., PHQ-0 >20); chronic (duration longer than two years); and recurrent (three or more episodes) [23].
ELECTROCONVULSIVE THERAPY ECT remains established as a potent and rapidly acting treat- ment for severe or refractory MDD and is considered unrivaled among standard options for rapidly inducing antidepressant effects. ECT is effective as acute treatment, but multiple treatments are required and many who respond experience symptoms again within six months [20]. ECT generates electri- cal stimuli for seizure induction through electrodes applied to the scalp, with the patient under general anesthesia and pre- medicated with a muscle relaxant. Clinical outcomes are highly influenced by electrode placements, electrical intensity, and pulse width [21]. Seizure-induced changes in neurotransmitter activity, neuroplasticity, and functional connectivity account for its effects. ECT also increases brain-derived neurotrophic factor, which may promote neuroplasticity and contribute to the antidepressant effect [21; 22]. As first-line treatment, ECT is used for severe melancholic, catatonic, psychotic, or refractory depression and for patients who refuse to eat or drink, have very high suicide risk or severe distress, pregnant women with severe depression, or who have a previous positive ECT response [20; 23; 24]. A large study reported 95% remission in study completers [25]. Full ECT response requires at least four to six sessions deliv- ered two to three times per week. Twice weekly ECT requires longer treatment duration, but more than three treatments per week is not recommended due to the greater cognitive side effect risk [21]. Relapse rates are greatest in the first six months post-ECT (37.7%). Even patients with maintenance ECT show high relapse rates at one year (51.1%) [26]. Severity of treatment resistance predicts poor ECT response [27; 28]. Adverse Effects Headaches (45%), muscle soreness (20%), and nausea (1% to 25%) during ECT are transient and treated symptomatically; 7% of patients with MDD switch into a manic or mixed state [21]. Cognitive impairment includes transient post-ECT disorientation, retrograde amnesia (i.e., difficulty recalling information learned pre-ECT), and anterograde amnesia (i.e., difficulty retaining information learned post-ECT). Mild, short-term memory and cognitive impairments are common during, and just after, ECT [24]. Within two to four weeks, impaired anterograde memory usually returns to normal or may improve from pre-ECT levels [29]. Retrograde impairment can persist for prolonged periods [30]. Most distressing to some patients is loss of autobiographic memory recall, infrequently reported to persist beyond six months [24]. ECT lacks absolute contraindication, but increased safety risk is associated with space-occupying cerebral lesion, increased intracranial pressure, recent cerebral hemorrhage, or aneurysm [21; 22].
The optimal duration of add-on therapy is not known, but it seems prudent that patients who are tolerating treatment and achieving therapeutic objectives should continue for at least 6 to 12 months with ongoing reassessment, with indefinite continuation for many [75]. BRIGHT-LIGHT THERAPY Use of bright-light therapy for treatment of major depression with a seasonal specifier (seasonal affective disorder) is well established [10; 11]. There is also evidence supporting its use for additional types of depressive symptom patterns, including non-seasonal depression, milder variations of seasonal depres- sive patterns, and depression in pregnant and postpartum women [12; 13; 14]. Bright-light therapy may quicken and enhance the effects of antidepressants [15]. The interaction between light intensity and duration of exposure requires two hours daily with 2,500 lux, one hour with 5,000 lux, and 30 minutes daily with 10,000 lux for efficacy [16]. Light therapy must also use equipment that eliminates ultraviolet frequencies. NEUROSTIMULATION THERAPIES The limitations of standard antidepressants, frequent treat- ment resistance, and the paradigm shift in psychiatry away from specific neurotransmitter focus and toward an integrative neural network perspective has prompted the development of novel depression treatment approaches, such as neurostimula- tion therapy. Neurostimulation therapies include a range of techniques that deliver electrical or magnetic stimulation to specific brain region targets for the treatment of refractory psychiatric and pain conditions. Neurostimulation efficacy in neurologic disorders led to their introduction in psychiatry. In addition to electroconvulsive therapy (ECT), several others are now FDA-approved for use in MDD and related disorders. The dorsolateral prefrontal cortex is a common brain stimula- tion target in patients with MDD. Its normal regulatory func- tion of control over stress and emotion reactivity is thought to be hypoactive in MDD. The dorsolateral prefrontal cortex and rostral anterior cingulate cortex areas are closely inter- connected; decreased activity in these frontal areas accounts for apathy, psychomotor slowness, and impaired executive functioning common in patients with MDD [17; 18; 19].
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