A bend in the river:

The version of ECT that debuted in 1937 is every bit deserving of its shocking reputation. Although the idea of inducing seizures, rather than treating them, seems odd and counterintuitive, a Hungarian psychiatrist called Ladislas Joseph von Meduna hit upon it as a possible treatment for schizophrenia. Beginning in January 1934, von Meduna first used camphor and then a drug called metrazol to induce seizures in people with schizophrenia. His remarkable success — he claimed that 95 percent of individuals with acute schizophrenia recovered — inspired Italian researchers Ugo Cerletti and Lucio Bini three years later to pursue electric shock as a safer and more effective way to induce seizures.

In those early years, the patients were neither anesthetized nor sedated and their grand mal seizures sometimes broke their bones. But by the mid-1950s, the routine use of general anesthesia and muscle relaxants had made ECT much safer. And by the 1970s, doctors began triggering the seizure with a brief square-wave electric pulse rather than the harsher sine wave currents that emerge from an electrical socket.

At the same time, antipathy to ECT rose apace. During World War II, many psychiatrists in the U.S. were acolytes of Sigmund Freud and held up psychotherapy and psychoanalysis as the gold standard treatments for psychiatric illness. They published statements opposing ECT, which they said damages the brain. Among the general public, there were waves of protest against ECT in general and its use in children in particular. “It just became inconceivable that one would pump electricity into the developing child’s brain,” says Edward Shorter, Jason A. Hannah Professor of the History of Medicine at the University of Toronto. “ECT in children became very badly stigmatized.”

Part of ECT’s image problem is that nobody knows how it works: The idea that shocking the brain would somehow restore its health seems so profoundly paradoxical as to be disturbing. The stigma against it only intensified with “One Flew Over the Cuckoo’s Nest.” The scene in which Jack Nicholson is forcibly held down and zapped with electricity as he screams became etched in the minds of everyone who saw it. ECT became second only to abortion in its vilified public image.

At least partly in response, several states enacted laws around the procedure — mandating the consent of two psychiatrists, or forbidding it altogether in children under 14 or 16. “As though it was the role of the state legislators to practice medicine and to protect the children from psychiatrists,” says Shorter.

In the late 1990s, after the hubbub over antidepressants had subsided, there was a resurgence in interest in ECT to treat severe depression and other conditions. But the damage to its reputation had endured. It wasn’t until 2008 that Wachtel, along with Reti and others, reported that ECT can treat self-injury associated with autism. The case study describes a young woman called “J” who had autism and ‘psychomotor retardation,’ meaning she was slow-moving — “except that sometimes she would pound herself into oblivion,” says Wachtel.

J’s slow movements were the manifestation of catatonia, which can overlie many conditions across the psychiatric spectrum, from deep depression to tic disorders such as Tourette syndrome. But the classic idea of a mute, motionless person is just one side of catatonia; the flip side is ‘psychomotor agitation’ — repetitive, uncontrolled and purposeless movements, as if driven by a motor gone awry.

What Wachtel and other experts say now is that the self-injury seen in some people with autism is an expression of catatonia’s agitated side. (Some children can show both aspects of catatonia at once: In one video of Kyle, one of his arms is wooden like a tree branch, and the other is repeatedly whacking his head.)

The experts owe this theory to Max Fink, a psychiatrist who has, formally or informally, served as a mentor to most of them. Fink, 93, lives in Nissequogue, New York, in a rambling old house by the water, with exactly the kind of ornate rugs and book-lined shelves you would expect to see in a learned psychiatrist’s home. Over the course of an hours-long conversation, Fink details the long and troubled history of ECT, replete with dates, occasionally shuffling in his bent gait to his formidable library to bring out a relevant manuscript or a book.

Fink is the world’s leading expert on catatonia and ECT, and many of his ideas have become mainstream. Psychiatric diagnostic manuals now describe both kinds of catatonia, as well as the idea that catatonia can accompany any number of other conditions. Case studies suggest that both sides of catatonia are exquisitely responsive to ECT. If the therapy — which Fink prefers to call “induced seizures” — helps some children with autism, he says, it’s because it relieves their catatonic self-injurious behaviors.

One of Fink’s protégées, a Belgian researcher called Dirk Dhossche, deserves the credit for solidifying this link between autism and catatonia. Dhossche trained with Fink at Stony Brook University in the 1990s. “At that time, there was very little talk about catatonia in children; we didn’t even talk about autism much, for that matter,” recalls Dhossche. When working in the Netherlands, he had seen two adolescents, one with autism and the other with Prader-Willi syndrome, an autism-related condition. Both boys had catatonia and responded to lorazepam — a benzodiazepine that is the standard first-line therapy for catatonia. (In fact, ‘the lorazepam challenge test,’ or response to the drug, has come to be known as proof of catatonia.) Dhossche set out to search the literature for more reports of children with catatonia and found about 30.

In 2001, Dhossche moved to the University of Mississippi, where he is now medical director of the child psychiatry inpatient unit. Shortly after his move, he saw a 9-year-old boy who had for months stayed mute and bedridden, and was not eating or drinking — all criteria for catatonia. After exhausting various treatment options, including benzodiazepines, Dhossche suggested using ECT. The response was nothing short of “spectacular,” Dhossche says. “This boy started speaking again, eating again, walking again.”

Even though the boy didn’t have autism, some of his characteristics even prior to the catatonia reminded Dhossche of autism. “This was my first realization that actually, autism and catatonia, they seem to overlap at some point,” he says. Repetition is a hallmark of catatonia; by that token, the echolalic speech and repetitive movements — including self-injurious behavior — characteristic of autism could be seen as catatonic. Dhossche’s publications on this topic prompted Wachtel to contact him, and eventually led to the 2008 case report. Since that success, Wachtel has referred about 20 children with autism who seemed to meet the criteria for catatonia to clinics that offer ECT, including the one at Johns Hopkins. Like Kyle, these children were a danger to themselves. Like him, they are doing well, some still receiving ECT as maintenance therapy, others on lithium or antipsychotic drugs to keep their self-injury in check.

“The reward of diagnosing catatonia is that it’s treatable,” says Dhossche. “Not with the easiest type of treatment, not the most popular one, but that’s just unfortunate at this point.”

Because of his publications on the topic, parents come to Dhossche from as far away as California or Texas — two states that have banned ECT in children under a certain age. But the numbers are still vanishingly small. In total, he says, he has treated perhaps 10 children with autism.

One thing Dhossche has noticed among the children he has treated is that the catatonia seems to appear after a stressful event of some sort. One 14-year-old boy with autism from Texas, for example, developed unusual finger movements and grimacing expressions after a particularly severe episode of bullying at his school. “It often starts with an incident, with an event, and then it gets worse,” says Dhossche.