Electroconvulsive therapy (ECT)

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Electroconvulsive therapy (ECT)

Does electroconvulsive therapy cause brain damage: An update by Amal Joseph Jolly and Shubh Mohan Singh

—evidence suggests that ECT has a demonstrable impact on the structure and function of the brain. However, there is a lack of evidence at present to suggest that ECT causes brain damage—

—cognitive side effects, structural neuroimaging studies, neuropathologic studies of patients who had received ECT, autopsy studies of epileptic patients, and finally animal ECS studies—

3 groups: 1) 19 with MDD (major depressive disorder), 15 with BPD (borderline personality disorder); 2) 10 patients with 5 MDD + 5 BPD received ECT (electroconvulsive therapy) versus 3) 24 patients who did not receive ECT—

Neuroimaging studies in electroconvulsive therapy—

Neurochemical studies in electroconvulsive therapy—

Devanand et al. reviewed 16 structural neuroimaging studies on the effect of ECT on the brain. Of these, two were pneumoencephalography—

The different cognitive domains reviewed included processing speed, attention/working memory, verbal episodic memory, visual episodic memory, spatial problem-solving, executive functioning, and intellectual ability.—

The authors concluded that there was no evidence to show that ECT caused any structural damage to the brain—

Neuroanatomical changes associated with effective ECT can be better described as ECT-induced brain neuroplasticity or ECT-induced brain neuromodulation rather than ECT-induced brain damage—

The most important conclusion which emerged from this early series of studies was that there was no evidence of cortical atrophy, change in ventricle size, or increase in white matter hyperintensities. The next major conclusion was that there appeared to be an increase in the T1 and T2 relaxation time immediately following ECT, which returned to normal within 24 h. This supported the theory that immediately following ECT, there appears to be a temporary breakdown of the blood–brain barrier, leading to water influx into the brain tissue. The last significant observation by Coffey et al. in 1991 was that—

—indicates that ECT causes destruction or degeneration of neurons. Though cognitive impairment studies do show that there is objective impairment of certain functions – particularly memory immediately after ECT, these impairments are transient with full recovery within a span of 2 weeks—

imply that cognitive impairment is tied in with the mechanism of action of ECT and not an indicator of damage to the brain produced by ECT.—

Memory impairment following ECT can be analyzed broadly under two conceptual schemes – one that classifies memory impairment as objective memory impairment and subjective memory impairment and the other that classifies it as impairment in anterograde memory versus impairment in retrograde memory. Objective memory can be roughly defined as the ability to retrieve stored information and can be measured by various standardized neuropsychological tests. Subjective memory or meta-memory, on the other hand, refers to the ability to make judgments about one's ability to retrieve stored information. As described previously, it has been conclusively demonstrated that anterograde memory impairment does not persist beyond 2 weeks after ECT. However,—

Our titular question is whether ECT leads to brain damage, where damage indicates destruction or degeneration of nerves or nerve tracts in the brain, which leads to loss of function—

—these studies reveal is rather than damaging the brain, ECT has a neuromodulatory effect on the brain.



Current electroconvulsive therapy practice and research in the geriatric population by Nancy Kernerand Joan Prudic

Electroconvulsive therapy (ECT) is a biological treatment procedure involving a brief application of electric stimulus to produce a generalized seizure—

Research studies have shown that ECT is the most effective and rapid treatment available for elderly patients with—

Reducing the ECT pulse amplitude should be explored as a potential means of diminishing side effects—

Convulsive therapy was reintroduced in 1934 by the neuropsychiatrist Meduna, who, based on his theory of "a biological antagonism between epilepsy and schizophrenia",—

It is controversial whether the difference in anatomical positioning of electrode placement has a significant impact on the efficacy of ECT in bipolar mania—

— Lacking evidence of superiority of ECT over medication beyond an acute treatment phase, ECT is no longer used as a first-line treatment for chronic schizophrenia—

The stimulus dose is controlled by frequency of pulses, pulse width, duration of pulse train, and pulse amplitude. Each exerts unique neurobiological effects. Determining chronaxie is the standard method for determining optimal pulse width in neurostimualtion. Studies have shown the chronaxie for mammalian neuronal depolarization is 0.1–0.2 ms. Standard ECT stimulus has had a pulse width between 0.5 and 2 ms. Reduction of pulse width to physiologic range results in markedly reduced adverse effects while maintaining efficacy, except possibly BL electrode placement—

Traditionally, there was a widely held belief that the efficacy of ECT depended exclusively on whether or not a seizure was induced successfully; and stimulus dosing was responsible for cognitive side effects. However, data from the controlled trials—

ECT carries risks, similar to all other medical procedures and treatments. The most common somatic side effects of ECT are headaches (48%), muscle pain (15%), dry mouth (23%), nausea (23%) and tiredness (73%). The most common cognitive side effects are anterograde memory impairment (41%) and confusion (37%)—

Maximizing ECT efficacy & minimizing ECT side effects

Right unilateral ECT has fewer cognitive adverse effects than bilateral ECT while efficacy can be made equivalent to bilateral ECT with adequate dosing. Stimulus intensity for unilateral ECT should be 2.5- to 8-times of seizure threshold to yield the best ECT effectiveness. Right unilateral ECT appears to be optimal in elderly patients.

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