The inadvertent deposition of 20 tons of aluminum sulfate in a reservoir downstream from the local water purification plant in 1988 gave the villagers in the small town of Camelford, in southeastern England, discolored acid-tasting drinking water for 3 days.1,2 Nausea, vomiting, rashes, and mouth ulcers were quickly reported. Hair, skin, and fingernails were stained brown. Rumors of shoals of dead fish in local rivers, widespread sickness in farm animals, and disruptive behavior in schoolchildren soon spread on local and national television and radio. Many complained that the water company was slow to respond, and when it did, that it gave false reassurances.
After the cleanup, official reports found the health risks from aluminum in the water to be esthetic, not toxic, because aluminum is not absorbed and aluminum poisonings are rare. Rather than assuaging anxiety, the reports encouraged people's fears. Adding insult to injury, newspapers misquoted the official report as claiming the residents' complaints were due to hysteria. Although the water standards were now excellent, litigation was under way as potential claimants formed a pressure group.
Academic reports that aluminum in drinking water was a risk factor for Alzheimer disease (AD) further inflamed indignation. Could the hazard of exposure lead to AD several years later? The thought was mixed in with reports that mad cow disease was characterized by a delayed onset of dementia. Soon, complaints of memory loss, poor concentration, and mental and physical fatigue dominated the community clinical picture with tie-ins to Camelford.
The cascade of events continued. Another commission assessed the evidence of long-term effects and despite the best evidence that there were none, the complaints persisted. These were finally quelled, in part, by out-of-court settlements. For the next decade, claimants related poor work performance, decline in memory, and symptoms of anxiety and depression to their Camelford exposure. The British Medical Journal recently reported that investigators have linked the death of a woman with a rare form of AD to the poisoning of the drinking water.3
In discussing these events, British neuropsychiatrists David and Wessely1 see little evidence of biologic (toxic) consequence. Instead, psychiatric morbidity was encouraged by the normal levels of somatic symptoms in any community, by the focused anxiety for environmental events following a publicized incident, and by the opportunity for litigation. Professional acceptance of the possibility that exposure might have persistent long-term effects, despite the lack of objective evidence, contributed strongly to the beliefs.
An application to memory loss in ECT?
Does this experience shed light on the claims that electroconvulsive therapy (ECT) causes persistent deficits in memory? Effects on memory, common in ECT, come in 2 flavors--an immediate transient delirium and a rare persistent impairment in personal memory.4,5 Delirium is common with each seizure and is well documented by immediate measurable changes in brain chemistry and physiology. Its occurrence is anticipated and managed with the same skill as the blood loss in surgery.
The second complaint is of a persistent loss of personal memories. Despite any benefits of ECT on the mental disorder, the patient complains that work is no longer possible because the treatments damaged the brain. Personal memories of experiences with family and friends are hazy, and patients are surprised when they meet people whose names and past relationships they cannot appreciate. They do not recall the names of their children, family holidays, or personal events. They are, however, able to carry on normal daily activities, read and write, make shopping lists, travel, and work about their home.
Their complaints cast a public shadow on ECT practice. That the complaints have a biologic basis in the treatment is widely accepted by the public and by many professionals. Compensation is demanded through litigation, with psychologists and psychoanalysts serving as experts for the plaintiffs. The persistent complaint of personal memory loss has stigmatized ECT and discouraged its use despite its proven efficacy and safety.
A disabled economist
In a 1974 New Yorker, the medical science writer Berton Roueché described the travails of the economist, Marilyn Rice, who, after extended complaints of dental pain that was not relieved by extraction of all her teeth and replacement by dentures, "fell into a deep depression," lost her appetite, and experienced a 20% loss in weight.6 During psychotherapy, she ruminated about her mouth and gums and her belief that she had become ugly. A 9-week stay in a psychiatric hospital, although uneventful, left her no better. "I am on a rest cure with do-it-yourself treatment." On another occasion, she wrote: "After being turned into a monster by the orthodontist, I must adjust to life as a damned ugly woman."
When her therapist despaired of success with psychotherapy, she was hospitalized for a course of ECT after which she wrote: "I felt just fine, perfectly relaxed and comfortable and also very hungry, as if I were making up for lost time."
Although she had been playing bridge throughout the hospital course, she now felt that she could no longer recall the cards. She returned home and described "a deja-vu experience." She believed that her memory was altered: "I was puzzled--but only vaguely. I really felt too vague to care. Nothing really bothered me. . . . I felt physically very well . . . and calm. I didn't have enough memory to think, or even worry. . . . Work was just something that drifted across my mind from time to time. It didn't interest me. I was too comfortable doing nothing."
1. David AS, Wessely SC. The legend of Camelford: medical consequences of a water pollution accident. J Psychosom Res. 1995;39:1-9.
2. Trimble M. Somatoform Disorders: A Medicolegal Guide. Cambridge, UK: Cambridge University Press; 2004.
3. McIntosh K. Screen Camelford residents, researchers say, after woman's death linked to poisoned water supply. BMJ. 2006;332:992.
4. Abrams R. Electroconvulsive Therapy. New York: Oxford University Press; 2002.
5. Fink M. Electroshock: Restoring the Mind. New York: Oxford University Press; 1999.
6. Roueché B. As empty as Eve: annals of medicine. New Yorker. 1974;9:84-100.
7. Donahue AB. Electroconvulsive therapy and memory loss: a personal journey. J ECT. 2000;16:133-143.
8. Sackeim HA. The cognitive effects of electroconvulsive therapy. In: Thahl LJ, Moss WH, Gamzu ER, eds. Cognitive Disorders: Pathophysiology and Treatment. New York: Marcel Dekker; 1992.
9. Breggin P. Electroshock: Its Brain-Disabling Effects. New York: Springer Publishing Co; 1979.
10. Cauchon D. Patients often aren't informed of full danger. USA Today. Dec 6, 1995:1.
11. Vermont Protection and Advocacy. Position paper on ECT. April 11, 1996.
12. Anne B. Donahue: 2003 Welcome Back Award Honoree in the Lifetime Achievement Category. Available at: http://www.lilly.com/about/awards/wba/2003_ donahue_lifetime.pdf. Accessed August 28, 2006.
13. Smith CS. Abuse of electroshock found in Turkish mental hospitals. New York Times. September 29, 2005; sect A:3-13.
14. Sackeim HA. Memory and ECT: from polarization to reconciliation. J ECT. 2000;16:87-96.
15. Prudic J, Peyser S, Sackeim HA. Subjective memory complaints: a review of patient self-assessment of memory after electroconvulsive therapy. J ECT. 2000;16: 121-132.
16. Shorter E. From Paralysis to Fatigue: A History of Psychosomatic Illness in the Modern Era. New York: The Free Press; 1992.