Chapter 5. Adverse Effects - ECT - Adverse Effects

Written by Juli Lawrence

Treatment of postECT headache is symptomatic. Aspirin, acetaminophen, or non-steroidal anti-inflammatory drugs (NSAIDs) typically are highly effective, particularly if given promptly after the onset of pain. Sumatriptan, a serotonin 5HTID receptor agonist, has also been effective at doses of 6 mg subcutaneously (DeBattista and Mueller 1995) or 25 - 100 mg orally (Fantz et al. in press). Some patients will require more potent analgesics (e.g. codeine), although narcotics may contribute to associated nausea. Most patients also benefit from bed rest in a quiet, darkened environment.

Post-ECT headache may occur after any ECT treatment in a course, irrespective of its occurrence at any prior treatment. Patients who experience frequent post-ECT headache may benefit from prophylactic treatment, such as aspirin, acetaminophen, or NSAIDs given as soon as possible after ECT, or even immediately prior to the ECT treatment. Subcutaneous sumatriptan 6 mg given several minutes prior to ECT was also found to provide effective prophylaxis in a patient with severe, refractory postECT headache (DeBattista and Mueller 1995).

Estimates of the prevalence of nausea following ECT vary from 1.4% - 23% of patients (Gomez 1975; Sackeim et al. 1987d), but the occurrence is difficult to quantify because of methodological issues noted above for headache. Nausea may occur secondary to headache or its treatment with narcotics, particularly in patients with vascular-type headache. It may also occur independently either as a side effect of anesthesia or via other unknown mechanisms. When nausea accompanies headache, the primary treatment should focus on the relief of headache as outlined above. PostECT nausea is otherwise typically well controlled with dopamine-blocking agents, such as phenothiazine derivatives (e.g. prochlorperazine and others), butyrophenones (haloperidol, droperidol), trimethabenzamide, or metoclopramide. If nausea is severe or accompanied by vomiting these agents should be administered parenterally or by suppository. All of these agents have the potential to cause hypotension and motoric side effects, and may lower seizure threshold. If nausea does not respond to these treatments or if side effects are problematic, the serotonin 5HT3 receptor antagonists ondansetron or dolasetron may be useful alternatives. These medications may be given in single intravenous doses of 4 mg and 12.5 mg respectively, several minutes before or after ECT. The greater expense of these medications and their lack of proven superiority over traditional anti-emetics in the setting, of ECT may limit their routine use. If problematic nausea routinely follows the use of a particular anesthetic, an alternative anesthetic may be considered.

5.3 ). Treatment Emergent Mania

As with pharmacological antidepressant treatments, a small minority of depressed patients or patients in mixed affective states switch into hypomania or mania during the ECT course (Devanand et al. 1988b; Andrade et al. 1988b, 1990; Angst et al. 1992; Devanand et al. 1992). In some patients, the severity of manic symptoms may worsen with further ECT treatments. In such cases, it is important to distinguish treatment emergent manic symptoms from delirium with euphoria (Devanand et al. 1988b). There are a number of phenomenological similarities between the two conditions. However, in delirium with euphoria patients are typically confused and have pronounced memory disturbance. The confusion or disorientation should be continuously present and evident from the period immediately following the treatment. In contrast, hypomanic or manic symptomatology may occur in the context of a clear sensorium. Therefore, evaluating cognitive status may be particularly helpful in distinguishing between these states. In addition, states of delirium with euphoric are often characterized by a giddiness in mood or "carefree" disposition. Classical features of hypomania, such as racing thoughts, hypersexuality, irritability, etc. may be absent. In cases of delirium with euphoria an increase in the time between treatments, a decrease in the stimulus intensity, or a change to unilateral from bilateral electrode placement may lead to resolution of the condition.

There is no established strategy on how to manage emergent manic symptoms during the ECT course. Some practitioners continue ECT to treat both the mania and any residual depressive symptomatology. Other practitioners postpone further ECT and observe the patient's course. At times, manic symptomatology will remit spontaneously without further intervention. Should the mania persist, or the patient relapse back into depression, reinstitution of ECT may be considered. Yet other practitioners terminate the ECT course and start pharmacotherapy, often with lithium carbonate or other mood stabilizer, to treat emergent manic symptomatology.

5.4. Objective Cognitive Side Effects

The cognitive side effects produced by ECT have been the subject of intense investigation (Squire 1986; Sackeim 1992; McElhiney et al. 1995) and are the major complications limiting its use. ECT psychiatrists should be familiar with the nature and variability of cognitive side effects, and this information should be conveyed during the consent process (see Chapter 8).

The cognitive side effects of ECT have four essential features. First, the nature and severity of cognitive alterations rapidly change with time from last treatment. The most severe cognitive side effects are observed in the postictal period. Immediately following seizure induction, patients experience a variable, but usually brief, period of disorientation, with impairments in attention, praxis, and memory (Sackeim 1986). These deficits recede at variable rates over time. Consequently, the magnitude of deficits observed during the course of ECT will be a function, in part, of the time of assessment relative to the last treatment and the number of treatments received (Daniel and Crovitz, 1983a; Squire et al. 1985).

Second, the methods used in ECT administration profoundly impact on the nature and magnitude of cognitive deficits. For example, the methods of ECT administration will strongly determine the percentage of patients that develop delirium, characterized by continuous disorientation (Miller et al. 1986; Daniel and Crovitz 1986; Sackeim et al. 1986, 1993). In general, as described in Table 1, bilateral electrode placement, sine wave stimulation, high electrical dosage relative to seizure threshold, closely spaced treatments, larger numbers of treatments, and high dosage of barbiturate anesthetic agents are each independently associated with more intense cognitive side effects compared to right unilateral electrode placement, brief pulse waveform, lower electrical intensity, more widely spaced treatments, fewer treatments, and lower dosage of barbiturate anesthesia (Miller et al. 1985; Sackeim et al. 1986; Weiner et al. 1986b: Sackeim et al. 1993; Lerer et al. 1995; McElhiney et al. 1995). Optimization of these parameters can minimize short-term cognitive side effects and likely reduce the magnitude of long-term changes (Sobin et al. 1995). In patients who develop severe cognitive side effects, such as delirium (Summers et al. 1979; Miller et al. 1986; Mulsant et al. 1991), the attending physician and ECT psychiatrist should review and adjust the treatment technique being used, such as switching to unilateral ECT, lowering the electrical dosage administered, and/or increasing the time interval between treatments, and decrease the dosage or discontinue any medications being administered that may exacerbate cognitive side effects.