The pervasive fear of ECT, a product of poor treatment practices and inaccurate portrayals by the media, has been a stumbling block that has hindered people from pursuing the treatment. The fear of serious medical and psychiatric consequences and the stigma attached to ECT seem counterintuitive given its demonstrated efficacy and safety,120
and the documented successful treatment of well-known entertainers, authors, musicians, and politicians.121
The notion that ECT causes brain damage or “fries the brain” has been promulgated since the inception of this treatment. However, there are no data to support this idea and research, in fact, refutes it. For example, in 1994, Devanand et al. published a systematic review of virtually all of the research and general literature regarding this question, reviewing cognitive effects, imaging, autopsies on former ECT patients, human epilepsy studies, and over 20 animal studies, and found no evidence that ECT produces any damage to the brain on a structural or cellular level.122
Serious Medical Outcomes and Counterindications
Serious medical outcomes associated with ECT are quite rare. The Texas Department of Mental Health, due to its stringent reporting requirements, provides data on this subject. Shiwach et al.123
reviewed this database, which contains information on 8,148 patients who received 49,048 ECT treatments over a 5-year period. The database describes causes of death for the 30 patients who died within 14 days of ECT. No deaths occurred during ECT treatment. Of the 30 patients who died within 14 days of ECT, 10 died from cardiac complications, 8 by suicide, 4 by automobile accident. Three patients died from sepsis, which was unlikely to be related to ECT (1 from peritonitis due to a burst diverticulum, 1 from generalized organ failure, while the cause was not reported for the third). Three additional patients died from neurological problems (supranuclear palsy, stroke, and ruptured aneurism) unrelated to ECT. One patient died from laryngospasm, likely related to intubation required in this case for anesthesia. Another patient died of pneumonitis secondary to the aspiration of vomitus, which may have been indirectly related to ECT. One patient died from cancer, and two from unknown causes.123
Of interest is that death rates from cardiac disease are higher among people suffering from severe depression, regardless of treatment type.124
Special considerations arise in using ECT to treat patients with coexisting medical conditions, particularly certain cardiovascular disorders such as recent myocardial infarction, congestive heart failure, or valvular heart disease. Other conditions of concern are neurological disorders such as space-occupying lesions or venous malformations, diabetes, obstructive pulmonary disease, and osteoporosis. Pre-ECT medical evaluation should identify coexisting medical illnesses and evaluate their potential interaction with and impact on ECT treatment. Issues related to using ECT in patients with coexisting medical conditions are reviewed comprehensively in Prudic8
and in the American Psychiatric Association's recommendations concerning ECT treatment.5
As mentioned above, Shiwach et al.123
reported one death that occurred on the day of ECT, which was due to laryngospasm that was attributable to anesthesia. The deaths that occurred within 48 hours of ECT included 5 from cardiac complications, 3 from sepsis, 1 by suicide, and 1 from unknown causes. It is not possible to know definitively whether or not these deaths were due directly to complications from ECT; however, with these broad inclusion criteria, a mortality rate of 2 to 10 in 100,000 is obtained. It is generally estimated that this death rate is comparable to that for anesthesia alone, about 3.3 to 3.7 deaths in 100,000.123
Cognitive Side Effects: Four Types of Memory Disturbance
Memory disturbances remain the most problematic effect of ECT. Since the introduction of ECT in 1938, patients who have received the treatment have reported cognitive side effects.125
These effects remain a source of concern. Numerous neurobiological, technical and patient-related factors can contribute to the cognitive side effects associated with ECT, and profound variations can occur among patients both in objective effects and subjective reactions. Clarifying the neurobiology of ECT's amnestic effects has posed significant challenges, and remains a goal for continuing research 8,126
. Although a detailed review of this work is beyond the scope of this paper, it is important to note here that ECT is known to produce physiologic effects on brain regions which may be integrally involved in short- and long-term declarative memory. For example, ECT affects memory systems associated with the medial temporal lobe, which contains the hippocampus, implicated in the consolidation of new information (anterograde memory).126-128
ECS in animal models has been shown to interfere with hippocampal long-term potentiation (LTP), proposed as mechanism that may subserve the neural substrates of new learning.127,128
A salient finding here is that the duration of the reduction in hippocampal LTP mirrors the duration of anmestic effects following ECT.127
However, medial temporal lobe changes do not explain ECT-related long term (retrograde) memory deficits, which may be associated with physiologic changes in the prefrontal cortex caused by ECT.9
A resolution of these issues may change conceptions of, and translate into alterations in, the technical aspects of treatment.126
Generally speaking, technical aspects of treatment such as stimulus waveform, electrode placement, stimulus intensity, dosage relative to threshold, and number and spacing of treatments can significantly affect the nature and extent of cognitive deficits following a course of ECT.5,11,86,96-99
Patient-related factors such as gender, age, cognitive functioning at baseline, and concomitant psychotropic medications may also play a role. As discussed above, in the prospective longitudinal study by Sackeim et al.99
that investigated clinical and cognitive outcomes at seven facilities, significant differences in treatment technique were found to be associated with differences in patients' short- and long-term cognitive deficits. However, these investigators also found that specific patient factors (the covariates age and premorbid IQ) increased the likelihood that patients would experience more severe cognitive deficits when assessed immediately after and 6 months after ECT. Specifically, they found that older patients and patients with lower estimated premorbid IQ evidenced the most significant deficits in functioning. In addition, gender had quite strong effects on the assessment of autobiographical memory, with women showing marked deficits on this measure that persisted over time. These findings indicate that adverse cognitive effects following ECT are associated with a multitude of factors related not only to treatment parameters but also to certain patient characteristics and that, under very specific circumstances, these adverse effects may persist over time.
Common cognitive side effects fall into four basic categories. The first type of cognitive effect is the stereotypical and transient postictal disorientation
that patients experience immediately after ECT treatment, which is a function of the seizure itself and of the anesthesia that was administered. This can range from mild, clearing within minutes to a few hours, to severe organic syndromes in rare cases. Factors in the administration of ECT, including electrode placement and number of treatments, can affect recovery time.96
However, patients subjectively experience this period quite differently. Some patients awaken rapidly and are able to resume their regular activities. Others may sleep for several hours, following which they are able to eat and resume their day. However, there are patients who experience notable disorientation, and these effects can produce greater subjective distress. This is demonstrated in the following case.
Ms. C., a 43-year-old woman with recurrent major depression, received her first course of ECT treatment in our hospital during 2005. She experienced considerable disorientation following her first and second treatments. After 1 hour spent in the post-ECT recovery area, she found she was unable to return to her room in our inpatient unit without assistance and had to use a wheelchair. This made her feel very personally vulnerable; she considered stopping treatment unless she could be escorted through the nursing area so that she could avoid being seen by other patients. Her request was granted and she continued her course; the disorientation attenuated over time.
A second type of cognitive effect is anterograde amnesia, the inability to retain information learned during and shortly after a course of ECT treatment, which also varies in severity. Anterograde amnesia can contribute significantly to a patient's inability to retain important information, both in general and specifically about the treatment. Patients may feel that clinicians are prevaricating or simply not providing information, when, in fact, they may not have retained it. The use of a daily log or diary is highly recommended for this reason, as illustrated in the following case.
Mr. D. experienced a profound melancholic depression, which was treated with ECT. He responded after 10 treatments but then quickly relapsed; he was then provided with 6 additional bilateral treatments. He eventually remitted fully; however, he experienced notable difficulties with memory retention. It was suggested that Mr. D. try keeping a diary, but he resisted, stating that he was “not much of a writer.” Toward the end of his treatment, Mr. D. would ask staff members the same questions about his treatment multiple times a day, even on days when he did not receive treatment. With considerable support, he was eventually able to use a diary and began recording the results of meetings with clinical staff, visits and calls from family, and proposals for discharge plans. He began reviewing these each day and stated that this activity did make him feel more empowered about his treatment. Mr. D. was discharged to his home, family, and job. His cognitive problems cleared within about 2 months of his ECT course.
A third type of cognitive effect is short-term retrograde amnesia
, which involves memory gaps for events that occurred within a few weeks or possibly months before the course of ECT
. Retrograde amnesia usually improves during the first few months after the acute ECT course, but recovery can be incomplete for some patients. This can be upsetting, particularly if patients place particular value on their personal memories and experiences. Lisanby et al. investigated whether memory for personal, autobiographical events or public, impersonal events is more vulnerable to the effects of ECT.129
In a randomized controlled trial involving 55 patients with major depression who received RUL ECT or BL ECT at two different stimulus intensities, they found that patients' recall was more acute for autobiographical memories, particularly the most salient of those memories. At 2-month follow up, patients treated with RUL ECT returned to baseline levels for impersonal memory, while those who received BL ECT maintained deficits for recent impersonal events. However, it is the value placed on memories versus the subjective experience of wellness that seems to determine patients' views of these deficits, as illustrated in the following case.
Mr. E., a 35-year-old patient with a history of intermittent depressive episodes and anxiety, developed a severe agitated depression. He received ECT and remitted after 14 treatments, relapsed quickly, and was provided with 8 bilateral treatments after which he experienced a full and lasting remission. Mr. E. thoroughly enjoyed “feeling like himself again” and “getting his personality back.” However, he had taken a work-related trip to China about 8 months before receiving the course of ECT. He noted that he was unable to recall much of this trip, but stated that he “didn't care because he had not felt this well in years.” During the next 6 months of post-discharge follow-up, Mr. E. stated that his recall was indeed improving for the trip and other events, and that he remained unconcerned as his wellness took precedence.
In some cases, however, short-term retrograde amnesia is not just a nuisance, but can have deleterious effects, as illustrated in the following case.
Ms. F. was treated for a severe melancholic depression with profound retardation. As she began to improve with ECT, she discussed her work and boasted acute recall of all her clients' medical information prior to her depression. She experienced a remission after receiving 20 treatments, and her Ham-D score dropped from a 42 before ECT to a 9 1 week after treatment. At that point, she began thinking about returning to work. Ms. F. was experiencing difficulty with recall in general and realized that she had not written down the password for a grant on which she had been working, nor had she given it to anyone else; the information was thus irrevocably lost. This led the staff to develop an ECT Pre-Treatment Information Log for patients, particularly those who, like Ms. F., have few if any friends or family members involved in their treatment (See Part II of this series for a more detailed discussion of this tool).
The fourth type of cognitive impairment, which is fortunately rare, involves more extensive retrograde memory loss
in which the patient experiences severe, persistent memory deficits dating back several months or even years.126
This phenomenon was described in an article by Anne Donahue,130
Representative from 2002 to the present in the Vermont State House of Representatives,. Ms. Donahue had ECT in the fall of 1995 and spring of 1996 for a total of 33 treatments, involving a switch from unilateral to bilateral delivery. She stated that the treatment saved her mental health and possibly her life, and that, if necessary, she would elect to undergo another course of ECT. However, in her personal account of her post-ECT experience, she reported subjectively significant loss of specific personal memories. While expecting her memory deficits to clear within 6 months, as she had been told, she experienced profound memory loss that extended back at least 5 years. She added that her deficits “exceeded anything the doctors anticipated” or that she was advised about. For example, she reported having the following conversation with a friend. After informing the woman that she had had “a treatment which affected her memory,” the conversation went roughly as follows:
Anne: Well, it's great to run into you here. What brings you to Burlington?
Friend: I live in Burlington, remember?
Anne: No, actually I never knew that.
Friend: Well actually, you did know that. We've had lunch together here several times over the past few years, and I've been out to visit you. It must be that treatment you mentioned. (p. 139).130
While acknowledging that patients who experience such pronounced effects are in the minority, Ms. Donahue felt the need to conduct her own investigation into the gap between anecdotal evidence of significant memory loss and the scientific community's official position. She concluded that patients deserve more complete explanations of possible long-term cognitive effects, and that the scientific community had not expressed adequate support for controlled research to determine which patients may be particularly at risk for such adverse effects and for providing definitive explanations for such effects.