Addressing safety concerns
In addition to changes to waveforms, dosing, and electrode placement, using anesthesia, muscle relaxants, and other medications has dramatically reduced adverse effects of ECT.8,10,13 See the Box10,14,15 for the specific agents used and their purposes. Before these medications and electroencephalography and electrocardiography (ECG) monitoring were used during ECT, the mortality rate was approximately 0.1%.13 Today, ECT is considered a low-risk medical intervention, with a mortality rate of approximately 0.002%.1,16 Before beginning an acute course of ECT, patients undergo laboratory testing, including a complete blood count, basic metabolic panel, and ECG. Spinal radiography and neuroimaging studies can be obtained to rule out preexisting vertebral injuries or neurologic disorders.1,8
Hemodynamic changes in response to ECT-induced seizures can exacerbate preexisting cardiac conditions. Normal physiologic response to ECT consists of a brief parasympathetic outflow, inducing bradycardia for 10 to 15 seconds, followed by a prominent sympathetic response characterized by hypertension and tachycardia for approximately 5 minutes. Although these changes can induce myocardial ischemia or infarction,14 the most common cardiac disturbances caused by ECT are arrhythmias, primarily in patients with preexisting cardiac abnormalities.17
Memory impairment. The most prevalent adverse reaction to ECT is memory loss, although not all aspects of recall are impaired to the same degree.18 Memory impairment varies based on factors such as electrode placement,9 stimulus waveform,19 site of seizure initiation, and pattern of activation.20 The risk of experiencing memory loss or other cognitive side effects following ECT can be decreased by using RUL electrode placement, brief pulses, and lower stimulus charge relative to seizure threshold.21 Memory deficits incurred by ECT usually are transient. In a study of 21 patients who received BT ECT for severe MDD, Meeter et al22 found that memory was stable and possibly improved at 3-month follow-up.
Procedural memory—memories of learned motor skills or mechanical tasks—often are left intact compared with semantic memory, which is general, declarative information recalled without context.18 The subsets of memory collectively regarded as declarative memory—the recollection of facts and events—may be most severely affected because this type of memory relies upon median temporal lobe structures, which are affected by ECT.21
Anterograde amnesia—the inability to form new memories—often is limited to the immediate posttreatment period and has been shown to become less pronounced at follow-up visits.22 Many clinicians and patients consider retrograde amnesia—forgetting memories that were formed before ECT—to be the most serious adverse effect of ECT. However, Mini-Mental State Examination scores tend to improve for patients who undergo ECT.1,16 Retrograde amnesia usually improves within weeks to months after ECT.12 Evidence suggests that retrograde amnesia mostly lifts during the recovery period and typically is not evident after 3 months.22 The best indicators of possible retrograde amnesic effects are preexisting cognitive deficits12 and duration of disorientation after ECT.1 Therefore, retrograde amnesia is more common among older adults, in whom age-related changes predispose patients to ECT’s adverse effects.24
The conventionally accepted mechanism for memory deficits after ECT is excitotoxic damage in the pyramidal cell layer of neurons in the hippocampus that induces calcium influx, which damages cells and causes neuronal atrophy.12 However, in animal studies, Dwork et al25 found an absence of neuronal or glial loss in regions subserving memory or cognitive functions (ie, the hippocampus or frontal cortex). Even in regions exquisitely sensitive to neuronal damage—such as CA1 of the hippocampus—neither cell number or volume or density of neuronal or glial cells were detected at statistically significant levels.25 Therefore, it is unlikely that ECT causes cell damage or atrophy in hippocampal neurons.
Medications used during electroconvulsive therapy
Anesthesia increases patients’ comfort during electroconvulsive therapy (ECT) by making them unaware of and unable to recall the procedure. The most commonly used anesthetic for ECT is methohexital, 0.5 to 1 mg/kg.14 Etomidate can be used in patients with contraindications to methohexital15; however, this medication can lengthen ictal duration.14 After the initial ECT treatment, clinicians can adjust the anesthetic dose based on the patient’s previous response.14
Using muscle relaxants during ECT has virtually eliminated bone fractures resulting from the procedure.10 The most common muscle relaxant is succinylcholine,15 which also reduces delirium in patients with post-ECT agitation.14 Mask ventilation and standard, noninvasive monitoring of cardiac parameters and oxygen saturation are necessary.14
Tachycardia and hypertension associated with ECT can be countered with beta blockers such as esmolol or labetalol as well as calcium channel blockers such as nicardipine.14 In addition, most patients are treated with the anticholinergic glycopyrrolate before the procedure to avoid bradycardia14 and reduce secretions, which may cause aspiration.15 Patients who experience headache or muscle pain after ECT can be treated with ibuprofen or acetaminophen before ECT sessions; patients with more severe complaints can be treated with IV ketorolac, 15 to 30 mg, before stimulus administration.15