April 17, 1995

Testimony to Texas State Legislature regarding House Bill 2452.
Peter Sterling, Ph.D.

As a neuroscientist I have studied the structure and function of the mammalian brain for more than 30 years. I teach this subject to medical and graduate students at the University of Pennsylvania where I also conduct an active research program on this subject. I became concerned abut the effects of electroconvulsive shock (ECS) on the brain more than 20 years ago after reading in the public press of a bright, professional woman whose memory was destroyed by a series of “therapeutic” ECS treatments. This led me to study the literature on ECS, both the clinical literature regarding possible efficacy and negative side -effects and also the experimental literature - - the application of ECS to animals in order to study the basis for the possible efficacy and side effects. I have continued to follow this literature over several decades and here summarize my main conclusions.
ECS unquestionably damages the brain. The damage is due to a variety of known mechanisms:

1. ECS is designed to evoke a grand mal epileptic seizure involving massive excitation of cortical neurons that also deliver excitation to lower brain structures. The seizure causes an acute rise in blood pressure well into the hypertensive range, and this frequently causes small hemorrhages in the brain. Wherever a hemorrhage occurs in the brain, nerve cells die - and nerve cells are not replaced. 2. ECS ruptures the “blood -brain barrier.” This barrier normally prevents many substances in the blood from reaching the brain. This protects the brain, which is our most chemically sensitive organ, from a variety of potential insults. Where this barrier is breached, nerve cells are exposed to insult and may also die. Rupture of this barrier also leads to brain edema (swelling), which, since the brain is enclosed by the rigid skull, leads to local arrest of blood supply, anoxia and neuron death. 3. Compromised neurons tend to release the neurotransmitter, glutamate, into the surrounding milieu. This chemical excites further neuronal activity which releases more glutamate, leading to “excito-toxicity” - - neurons literally die due to overactivity. Such excito -toxicity has been recognized relatively recently and is now a major topic of research. It is known to accompany seizures and over repeated episodes of ECS may be a significant contributor to accumulated brain damage. The degree of damage consequent to ECS varies between individuals. It can be catastrophic in response to a single series, or it can appear more gradually following repeated series. This is much like the damage to boxers - who may occasionally die in the ring due to massive cerebral hemorrhage, or more commonly accumulate damage until the impairment becomes obvious. Since any positive therapeutic effect of ECS is temporary, the treatment is commonly repeated, so chronic brain damage is inevitable.

The key manifestation of this damage is memory loss. This is disturbing enough, but there are probably other losses as well, such as the ability to think clearly, to learn new facts and so on. It must be particularly incapacitating to individuals who are already impaired by a mental illness. So, one would expect physicians to weigh carefully the possible benefits of the therapy against the cumulative damage that it causes. However, rather than weigh gain vs. loss, psychiatrists deny the obvious, that there is cumulative damage.

The reason that psychiatrists can remain unaware of accumulating memory loss is that they do not routinely test for it. Testing is required when patients take certain drugs, such as lithium. high blood levels of lithium can be toxic; and lithium can damage the blood-forming cells in the bone marrow. Therefore, blood levels of the drug and the state of the bone marrow are monitored. Memory loss could be monitored just as easily, by asking patients before ECS about early events in their lives and then questioning the patients following each series of ECS. When this was done by Janis (almost 50 years ago), losses were marked and prolonged. However, no effort has been made since then to do this simple test.

The physician’s first injunction is “Do no harm.” Because this treatment clearly does harm, I believe it to be misguided. Where the treatment is applied without investigating the degree of harm and monitoring its accumulation, I believe it to be irresponsible and therefore requiring of regulation.

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Dr. Peter Sterling is Associate Professor of Neurobiology in the School of Medicine at University of Pennsylvania.

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