Chapter 5. Adverse Effects - Objective Cognitive Side Effects
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.
Third, patients vary considerably in the extent and severity of cognitive side effects following ECT. There is limited information about the factors that contribute to these individual differences. There is evidence that among depressed patients without known neurological disease or insult, the extent of preECT global cognitive impairment, i.e., mini-Mental State Exam (MMSE) scores, predicts the magnitude of retrograde amnesia for autobiographical information at long-term follow-up. While ECT typically results in improvement in global cognitive status in these patients, as a function of symptomatic response, nonetheless, these same patients may have greater persistent amnesia for personal memories (Sobin et al. 1995). Similarly, there is evidence that the duration of disorientation immediately following the ECT treatment is independently predictive of the magnitude of retrograde amnesia for autobiographical information. Patients who require prolonged periods to recover orientation may be at greater risk for more profound and persistent retrograde amnesia (Sobin et al. 1995). Patients with pre-existing neurological disease or insult (e.g., Parkinson's disease, stroke) may also be at increased risk for ECT-induced delirium and memory deficits (Figiel et al. 1991). Magnetic resonance imaging (MRI) findings of basal ganglia lesions and severe white matter hyperintensities have also been linked to the development of an ECT-induced delirium (Figiel et al. 1990). Some medications may exacerbate ECT-induced cognitive side effects. These include lithium carbonate (Small et al. 1980; Weiner et al. 1980b), and medications with marked anticholinergic, properties, particularly in elderly patients.
Fourth, ECT results in highly characteristic cognitive changes. Across diagnostic groups, prior to receiving ECT, many patients have deficits in attention and concentration that limit their capacity information (Byrne 1977; Pogue-Geile and Oltmanns, 1980; Cornblatt et al. 1981; Sackeim and Steif, 1988). For example, patients with severe psychopathology often have deficient recall of information that was just presented to them (immediate memory). In depressed patients, these deficits are most marked for unstructured material that requires effortful processing in order to impose organization (Weingartner and Silberman 1984; Roy-Byrne et al. 1986). However, such patients are considerably less likely to have deficits in retaining the new information that they do learn (delayed memory) (Cronholm and Ottosson 1961; Sternberg and Jarvik 1976; Steif et al. 1986). With symptomatic response following ECT, the deficits in attention and concentration usually resolve. Consequently, measures of immediate memory are either unchanged or improved within a few days of ECT termination (Cronholm and Ottosson, 1961; Steif et al. 1986; Weiner et al. 1986b; Rossi et al. 1990; Sackeim et al. 1993). Since attention and concentration are essential to many aspects of cognitive function, it is not surprising that shortly following completion of the ECT course improvement may be observed in a wide variety of neuropsychological domains, including global cognitive status (Sackeim et al. 1991; Sobin et al. 1995) and measures of general intelligence (IQ) (Huston and Strother 1948; Stieper et al 1951; Squire et al. 1975; Malloy et al. 1981; Sackeim et al. 1992). There is no evidence that ECT results in impairments of executive functions (e.g., the capacity to shift mental sets), abstract reasoning, creativity, semantic memory, implicit memory, or skill acquisition or retention (Weeks et al. 1980; Frith et al. 1983; Squire et al. 1984; Taylor and Abrams 1985; Jones et al. 1988).
Against this background of unchanged or improved neuropsychological performance, ECT selectively results in anterograde and retrograde amnesia. The anterograde amnesia is characterized by rapid forgetting of newly-learned information (Cronholm and Ottosson 1961; Squire 1986; Steif et al. 1986; Weiner et al. 1986b; Frith et al. 1987; Sackeim et al. 1993). As noted, compared to preECT baseline, a few days following ECT patients may recall more items in a list that was just presented. However, recall after a delay will often be impaired (Korin et al. 1956; Cronholm and Ottosson 1961; Cronholm and Molander 1964; Squire and Miller 1974; Steif et al. 1986; Weiner et al. Squire and Chace 1975; d'Elia 1976; Robertson and Inglis 1978, 1986b; Calev et al. 1989b; Sackeim et al. 1993). The extent and persistence of this rapid forgetting of newly learned information varies among patients and should be taken into account when making recommendations regarding the postECT convalescence period. Until there is substantial resolution of the anterograde amnesia, returning to work, making important financial or personal decisions, or driving may be restricted. The anterograde amnesia rapidly resolves following the termination of ECT. Indeed, no study has documented anterograde amnestic effects of ECT more than a few weeks following the ECT course (Strain et al. 1968; Bidder et al. 1970; Heshe et al. 1978; Jackson, 1978; Fraser and Glass, 1980; Weeks et al. 1980; Gangadhar et al. 1982; Frith et al. 1983; Weiner et al. 1986b; Sackeim et al. 1993). It is unlikely that ECT has any long-term effect on the capacity to learn and retain new information.
reviewed by:
Harry Croft, MD (Psychiatrist)
Medical Director, HealthyPlace.com
Created on February 14, 2007 Last Updated on January 12, 2012
In Depression
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