Depression and Suicide _ ______________________________________________________________________
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 [278; 279; 280]. 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 treat- ments are required and many who respond experience symp- toms again within six months [281]. ECT generates electrical 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 [282]. 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 [282; 283]. 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 [64; 281; 284]. A large study reported 95% remission in study completers [285]. Full ECT response requires at least four to six sessions delivered 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 [282]. 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%) [286]. Severity of treatment resistance predicts poor ECT response [287; 288]. 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 [282]. 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 [284]. Within two to four weeks, impaired anterograde memory usually returns to normal or may improve from pre-ECT levels [289]. Retrograde impairment can persist for prolonged periods [290]. Most distressing to some patients is loss of autobiographic memory recall, infrequently reported to persist beyond six months [284]. ECT lacks absolute
contraindication, but increased safety risk is associated with space-occupying cerebral lesion, increased intracranial pressure, recent cerebral hemorrhage, or aneurysm [282; 283]. Vagus Nerve Stimulation Vagus nerve stimulation uses an implantable device to provide intermittent stimulation to the left vagus nerve (80% afferent to the CNS) [21]. It received FDA approval for treatment- resistant depression in 2005 due to the lack of approved drug treatments and concerns over the long-term efficacy and safety of ECT [291]. Controlled studies with follow-up six months or longer have found significant improvements in depressive symptoms that were often sustained over time, with relapse rates relatively low [292]. Long-term vagus nerve stimulation can lead to significant side effects, including decreases in airway flow and respiratory effort and laryngopharyngeal dysfunction [293]. Given the profound negative impact of treatment-resistant depression and lack of durable response in some patients, vagus nerve stimulation may be a useful option [294]. In a 2017 trial, patients with treatment-resistant MDD and four or more failed depression treatments (including ECT) received vagus nerve stimulation or treatment as usual and were fol- lowed five years. Response was a ≥50% decrease in MADRS score at any follow-up visit. Subjects who received vagus nerve stimulation (compared with usual treatment) had more severe treatment-resistant depression on several dimensions [295]. Vagus nerve stimulation led to greater five-year cumulative response (67.6%) and remission (43.3%) rates compared with usual treatment (40.9% and 25.7%, respectively). However, vagus nerve stimulation response often required 12 or more months to appear [295]. Guidelines recommend against the use of vagus nerve stimulation outside a research setting [64]. Deep Brain Stimulation With deep brain stimulation, an electrode is surgically implanted to stimulate the subgenual cingulate gyrus with high-frequency impulses to reduce depressive symptoms [21]. Deep brain stimulation is invasive and carries the risk of infection, hemorrhage, and other surgical complications. Stimulation-induced adverse effects such as facial contractions, facial paresthesias, olfactory phenomena, anxiety, and mood fluctuations have been reported, particularly at higher levels of stimulation [296]. Most clinical improvement shows delayed onset; one trial in patients with treatment-resistant depression reported remission rates of 27%, 24%, and 37% at three-month, six-month, and two-year follow-up, respectively [297]. Deep brain stimulation can increase the risk of suicide ideation, attempts, and death, strongly indicating that patients should be pre-screened for suicide risk and monitored closely for suicidal behavior pre- and postoperatively [298]. Deep brain stimulation is investigational for treatment-resistant depression and is reserved for use in patients with severe refractory psychiatric, neurologic, or chronic pain conditions [282; 296].
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