To the Editor: ECT is an effective treatment for various depressive disorders. Evidence has indicated that ECT is not associated with structural brain lesions when administered in the treatment of acute depression (1, 2). However, we know of no studies of the effects of long-term treatment with ECT on the metabolism of the central nervous system. Here we report on a patient who was studied with 18F-labeled fluorodeoxyglucose (FDG) positron emission tomography (PET) during a severe major depressive episode after receiving a total of 60 brief-pulse unilateral ECT treatments over the past 5 years.
Ms. A, a physically healthy 42-year-old woman, was admitted to our hospital with a diagnosis of a severe major depressive episode (according to DSM-IV criteria) and an initial score on the Hamilton Depression Rating Scale (17-item version) of 36. She had suffered from at least nine severe major depressive episodes (intermittently with psychotic features) since 1987. Relapses occurred despite consequent pharmacological continuation treatment. Ms. A had been treated with high doses of tranylcypromine (80 mg/day) during the last few years, but she had not recovered. The addition of newer antidepressant drugs (e.g., mirtazapine, 30 mg/day) and different augmentation strategies (e.g., with lithium) over long periods of time had been ineffective.
A trial of ECT (three times a week, a total of nine sessions) had been conducted in 1995; Ms. A had good results after three applications. Because of the high risk of relapse, maintenance treatment with ECT in combination with tranylcypromine was administered for 6 months, during which Ms. A did well. Treatment was of short duration because of the lack of controlled studies combining long-term ECT with tranylcypromine. Continuation treatment remained an issue; Ms. A had periods of remission lasting only 10–12 months during the next several years. Nevertheless, ECT continued to be a highly efficacious and tolerable treatment option during acute depression owing to its short latency of action.
After we performed cerebral magnetic resonance imaging, which showed no abnormalities, we performed an FDG PET scan while Ms. A was still severely depressed, to exclude metabolic abnormalities possibly associated with the high number of previous ECT treatments. The scanning was performed under standard resting conditions, and the data were compared to data from an age-matched comparison group (N=20) on a pixelwise basis by means of an observer-independent analytical approach (3). This statistical subtraction analysis did not identify any areas with differences in glucose metabolism of more than two standard deviations from those in the normal database. This method has been proven to be extremely sensitive in detecting abnormalities. Thus, Ms. A’s glucose metabolism was regarded as normal. ECT was reinstituted. After nine sessions of brief-pulse unilateral ECT treatments, Ms. A had completely recovered and was discharged with a Hamilton depression scale score of 4.
In comparison with healthy volunteers, no pathological change could be determined by means of FDG PET scans in a patient with a long history of severe depression that was resistant to drug treatment who had undergone more than 60 ECT sessions in 5 years. Although no one knows what a "normal" PET scan is, our result provides hope that no irreversible damage is caused by the efficacious use of ECT.