Electroconvulsive therapy (ECT)-- perhaps more commonly known as electric shock therapy--is a medical procedure that has been used since the 1930s to successfully treat the most severe forms of depression in adults. However, during the 20th century, many celebrity critics and fiction authors have cast ECT in a very negative light.
Definition
Electroconvulsive eherapy (ECT) is a psychiatric treatment whereby doctors administer brief yet potent electrical currents across specific regions of an anesthetized patient's skull/brain in order to induce a seizure. Lasting between 15 seconds and 1 minute, this seizure generally results in improved quality of life (both over the short and long term) for victims of severe depression and catatonia who are unresponsive to drug therapy.
History
As early as the 1500s, European physicians began experimenting with seizure-inducing chemical agents, using it specifically on patients with psychiatric afflictions. In 1934, Hungarian psychiatrist Ladislas Meduna became the first doctor to promote a regimen of convulsive therapy as a treatment for schizophrenia and epilepsy, using camphor and metrazol to induce the seizures. Use of metrazol-based convulsive therapy spread quickly, culminating with Switzerland hosting the first-ever international conference on the procedure in 1937.
Meanwhile, Italian psychiatrists Ugo Cerletti and Lucio Bini were running experiments on animals to induce seizures via electricity. In 1937, encouraged by the growing popularity of convulsive therapy, they conducted an experiment wherein they successfully caused a metrazol-like seizure in a human patient using electricity. Cheaper, more convenient and less disorienting for patients, electricity soon became the preferred convulsive therapy. Hence, ECT was born.
ECT has changed only slightly over the years, mainly to mitigate side effects like memory loss and muscle strains. For memory, the "shock" changed from a sinusoidal, direct-current trigger to a brief-pulse, alternating-current trigger. For the skeletal-muscular injuries, doctor began treating patients with muscle relaxers before the treatment to minimize the violence of the convulsions, although the drugs tended to relax the diaphragm muscle as well, leading to a feeling of suffocation, despite a breathing tube. Doctors addressed this discomfort by administering a gentle anesthetic.
Today, almost 1 million people receive ECT each year for severe depression.
Procedure
A psychiatrist will prescribe ECT to patients with severe major depression or severe mania who either (a) aren't responding to antidepressant medication, (b) are pregnant (the effects of ECT are limited to the mother's brain) or (c) have demonstrated good responsiveness to ECT before. In most cases, the choice to undergo treatment is left completely to the patient. However, for a patient in a catatonic depression or one who is actively set on suicide, a psychiatrist can administer ECT without consent. In both cases, the doctor is acting in the interest of time, as prolonged catatonic depression can result in permanent brain damage and a suicidal patient can do serious harm to himself during the 2 to 3 weeks it takes for medication to start to work.
Before ECT, an electroencephalogram (EEG) is attached to the patient to monitor brain wave activity and an electrocardiogram (EKG) is attached to monitor pulse and vital signs. The procedure begins with a short-acting anesthetic--such as methohexital, propofol, etomidate or thiopental--designed to put the patient to sleep. A nurse then injects him with the muscle relaxant succinycholine. Some treatments also use the drug atropine to stop saliva production during ECT, to prevent choking. The patient breaths pure oxygen through a mask or tubing.
There are two kinds of ECT: unilateral and bilateral. For unilateral ECT, one electrode is placed on the temple of the nondominant side of the brain (i.e. left temple for right-handed and vice versa) and the other is placed in the middle of the forehead. For bilateral ECT, one electrode is placed on each temple.
Next, a brief-pulse current, consisting of about 800 milliamps (0.8 amps), flows across the brain for 1 to 6 seconds. Immediately, a clonic seizure lasting between 30 and 60 seconds occurs. Ten to 15 minutes later, the patient awakens and may feel confusion, headaches or stiffness. However, this passes after about 30 minutes to an hour.
Mechanism
While clinical researchers agree that ECT is an effective treatment, their understanding of its physiological mechanism is limited by their tools for studying the brain. Currently, EEG measurements of delta brain waves show that, after the initial seizure spikes, brain waves slow to a reduced frequency, similar to that observed during of sleep.
On the cellular level, studies have reported that ECT significantly increases the sensitivity of post-synaptic serotonin receptors, one of the most important neurotransmitter systems in depressive illness. Studies have also found that ECT increases the sensitivity of serotonin receptors in the hippocampus part of the brain, triggering an increased release of the neurotransmitters glutamate and gamma-aminobutyric acid. Meanwhile, ECT deadens the receptors in the noradrenaline and dopamine negative feedback loop, thus increasing their levels in the blood.
Finally, in 2006 Bocchio-Chiavetto et al. found that ECT increases the levels of the brain-derived neurotrophic factor (BDNF) in the blood of severely depressed patients. BDNF is a nerve growth factor that encourages the survival and growth of new neurons, especially in the areas of the brain controlling long-term memory. Previous research has found that BDNF levels are significantly lower in patients with severe depression, schizophrenia and other serious mental disorders. That said, it's not clear whether BDNF levels are the cause or merely the symptom of these conditions.
Side Effects
Aside from the 20 to 60 minutes of temporary confusion and memory loss immediately following ECT, some patients report memory loss for events weeks or months before the treatment ("retrograde amnesia") and/or after it ("anterograde amnesia"). This tends to be more common in patients who receive bilateral ECT. Unfortunately, studies also suggest the bilateral ECT is more effective at treating depression than the unilateral method.
A poor memory is also a symptom of severe depression, so it is often difficult to discern whether ECT caused retrograde amnesia or the severe depression leading up to ECT interfered with the initial formation of memories.
A 1999 report by the U.S. Surgeon General reviewed the existing body of research on ECT (including autopsies, CAT scans and MRIs) and concluded that the procedure did not cause "gross structural brain pathology," Today, severe and permanent memory loss only effect 0.05% of patients (1 in every 2,000).
Tags: severe depression, convulsive therapy, memory loss, patients with, found that, BDNF levels, before treatment