To the Editor: In animal studies, transcranial magnetic stimulation is reported to have some properties similar to ECT and to have therapeutic properties in depression. Therefore, we hypothesized that transcranial magnetic stimulation might be effective in treating catatonia. We report a case of catatonia treated with transcranial magnetic stimulation.
Ms. A, a 24-year-old Bedouin woman with a history of an acute psychotic episode 1 year earlier, was admitted in a severe catatonic state. Three days before admission, she had stopped eating, drinking, and speaking. On admission, she was stuporous, automatically obeying simple orders. She had psychotic mutism and negativism with a remarkable waxy flexibility and rigidity. She could not walk. Ms. A was in this state throughout the day, except for brief periods of time. After 15 days’ treatment with the maximal dose of haloperidol (3 mg daily) that she could tolerate, a dose that had resolved her previous psychosis, there was no change in Ms. A’s catatonic state; in addition, she showed a worrisome weight loss. We considered ECT treatment.
We obtained informed consent from both parents of Ms. A, a compassionate use permit from the Ministry of Health, and written consent from Ms. A during a brief period of cooperativeness in the presence of both her parents.
Repetitive transcranial magnetic stimulation was delivered by a Cadwell High Speed Magnetic Stimulator device with a 90-mm planar coil. Stimulation was given over the right prefrontal cortex. The stimulus was 20 Hz (train duration: 2 seconds; intertrain interval: 58 seconds) 20 times per daily session for 10 working days. The intensity of the stimulus was 80% of patient motor threshold. To establish the patient motor threshold, we routinely increase the stimulus strength by 5% when stimulating the motor cortex until a visible motor response can be observed in the contralateral hand. For the first time in our experience, we increased stimulus strength to 100%, and no motor response was observed. The procedure was repeated three times. Arbitrarily, we decided to proceed with 65% machine capacity for treatment, since this is the average patient motor threshold in our experience.
A small improvement was noticed within the first 24 hours of the first treatment. For the first time since her admission, Ms. A woke up in the morning, walked to the bathroom, and talked to another patient in her room about her fears of aliens. Ms. A participated in group therapy that morning, but she did not talk. During continued daily transcranial magnetic stimulation, Ms. A’s stupor, automatism, and rigidity gradually disappeared. She became able to tend to personal hygiene, to participate in ward activities, and to cooperate with both the staff and her family. Ms. A was willing to spend a day at home, and her family reported a significant improvement. She performed daily activities and smiled occasionally, although she remained mute for another month while taking haloperidol (3 mg daily) before full remission of psychosis.
This case appears to illustrate an ECT-like effect of right prefrontal transcranial magnetic stimulation in catatonic schizophrenia. The extremely high motor threshold to transcranial magnetic stimulation in this catatonic patient should be investigated in other patients.