The Mind and the Brain by Jeffrey M. Schwartz, Sharon Begley Page A

psychiatric and psychological professions deemed OCD treatment-intractable : nothing could be done to release patients from its grip. “People didn’t know what to do with OCD,” says the clinical psychologist Michael Kozak, who spent nineteen years at MCP Hahnemann Hospital in Philadelphia studying the disease and its treatments. “They tried all sorts of things that didn’t work very well, from electroshock and psychosurgery to any available drug and classical talk therapy.” In the late 1960s and early 1970s, however, psychiatrists got a hand from serendipity: they noticed that when patients suffering from clinical depression were put on the tricyclic antidepressant clomipramine hydrochloride (Anafranil), some of them experienced relief from one or more of their OCD symptoms. Since clomipramine, among its many biochemical actions, strongly inhibits inactivation of the neurotransmitter serotonin (much as Prozac does), researchers suspected that amplifying the brain’s serotonin levels might alleviate OCD.
    There was at least one problem with this approach, however. Though clearly effective, clomipramine is a “dirty” drug, one with numerous pharmacological actions; as a result, it is associated with many unpleasant side effects. This problem led to the development of so-called selective serotonin reuptake inhibitors (SSRIs), such as Prozac, Paxil, Zoloft, Luvox, and Celexa, all of which specifically block the same mechanism that clomipramine acts on nonspecifically: the molecular pump that moves serotonin back into the neurons from which it was released, thus allowing more of the chemical to remain in the synapse. All of these SSRIs seem to be equally effective in treating OCD symptoms. For each of them, studies since the 1980s have shown, about 60 percent of patients respond at least somewhat, “and of those there’s about a 30 to 40 percent reduction in symptoms,” says Kozak. “So there’s something real going on with the drugs. But when about half of the people aren’t helped significantly and those who are helped are still left with 60 percent of their symptoms, we have a ways to go.”
    At about the same time that researchers stumbled onto clomipramine for OCD, Victor Meyer, a psychologist at Middlesex Hospital in London, began to develop what would emerge as the first effective behavioral therapy for the disease. In 1966 he tried out, on five patients in an inpatient psychiatric ward, what would become the most widely used psychological treatment for the nexttwenty-five years. Called exposure and response prevention (ERP), it consisted of exposing patients to the trigger that called forth obsessional thoughts and the compulsion to engage in a distress-relieving behavior. Meyer would tell a patient to leave her house, for instance, but prevent her from returning to check whether she had left the stove on. Or he would have her touch all the doorknobs in a public building but not allow her to wash her hands afterward. Or he would tell the patient to touch dried bird droppings but not allow her to wash (at least not right away). Meyer reported significant improvement in the patients he treated with exposure and response prevention. Edna Foa, who adopted the technique and added a detailed questionnaire to allow therapists to get at the patient’s so-called fear structure—the layers of emotions that underlie the obsessions—introduced it into the United States.
    Typically, the first exposure during therapy uses a trigger that the patient has assigned a low score on a scale of “subjective units of distress,” or SUDs. The therapist (during in-office sessions) then prevents the patient from responding as he usually does—dashing to a sink to wash, for instance. Prevents can mean many things, from gentle coercion to physical restraint of the patient; from carefully explaining that if the patient complies he is likely to get better, to turning off the water in the bathroom of his room in a mental