Repetitive Transcranial Magnetic Stimulation for the Treatment of Catatonia: an Alternative Treatment to Electroconvulsive Therapy?

To the Editor: Four catatonic patients have been successfully treated with repetitive transcranial magnetic stimulation (rTMS) (Table 1).^1–4 In each of these patients, the authors reported that stimulation of the dorso-lateral prefrontal cortex (DLPFC) led to a spectacular improvement after only seven to 10 high-frequency sessions. It has, therefore, been suggested that rTMS may be a therapeutic alternative for the treatment of catatonic disorders.²

Our results, however, are in sharp contrast. We report here the case of a patient who usually recovered from his catatonic disorders with ECT, but failed to improve significantly with rTMS even though the stimulations were delivered in optimal conditions.

Case Report

A 45-year-old man suffering from schizophrenia since the age of 20 was admitted to hospital in a catatonic state. He had a history of six benzodiazepine-resistant episodes of acute catatonia, each time successfully treated with ECT.

As before, the catatonic features of this seventh episode included immobility, mutism, fixed gaze, automatic obedience, and autonomic abnormalities (hypotension, tachycardia). He refused to eat or drink and required nasogastric feeding. When he was given ECT, he immediately presented a transient cardiac arrest (40 seconds), probably related to left bundle branch block. Although this cardiac event resolved without sequelae, the anesthetist decided that ECT should not be given again.

The patient was, thus, referred to our department for rTMS therapy as this treatment does not require anesthesia. His pharmacological treatment started several months beforehand was kept unchanged (clozapine, 400 mg/day, amisulpride, 150 mg/day, and escitalopram, 20 mg/day). We used a figure-8 coil and MRI-based neuronavigation to perform the rTMS therapy. The response was monitored with the Bush-Francis Catatonia Rating Scale (BFCRS).

The patient was first treated with 10-Hz rTMS daily from Monday to Friday (2000 pulses per session, at 110% of the motor threshold) to the right DLPFC for 4 weeks and then to the left DLPFC for 4 weeks with no significant improvement (BFCRS: 23 to 20).

Because treatment with rTMS targeted on the DLPFC failed, we performed an 18F-fluorodeoxyglucose-positron emission tomography/computed tomography (18F-FDG-PET/CT), which revealed impaired perfusion in the medial orbitofrontal cortex (OFC), the cortical area most often mentioned in the neurobiological explanation for catatonia syndrome.⁵ We, therefore, decided to deliver rTMS to the OFC using the same protocol as above. We stopped rTMS after 40 sessions to the OFC. There was a slight but not sufficient improvement (BFCRS: ranging from 13 to 15), and no change in a control 18F-FDG-PET/CT.

Discussion

In the light of the present case, it is difficult to advocate the use of rTMS instead of ECT for the treatment of catatonic disorders. Indeed, for our patient, we made every effort to maximize the efficacy of the rTMS therapy, but we failed to obtain a clinical response as quick and as robust as that achieved with ECT.

Nevertheless, we believe that rTMS therapy can be useful especially when ECT cannot be given, as was the case in our patient. Further studies are now necessary to determine parameters that could make rTMS effective in catatonic disorders.