To the Editor: ECT has been used effectively to treat major depression associated with multiple sclerosis (1, 2). However, concerns remain that ECT might exacerbate multiple sclerosis by increasing the size and number of plaques and/or periplaque edema (1, 2).
Ms. A, a 51-year-old woman, had her first multiple sclerosis symptoms 7 years ago. A magnetic resonance imaging (MRI) proton-density-weighted axial brain scan performed 1 year later at a specialized center for multiple sclerosis showed ventricular enlargement and several multiple white matter lesions in the right part of the brainstem and bilaterally in the periventricular and subcortical areas.
Five years after the onset of multiple sclerosis, Ms. A was first hospitalized in the psychiatric ward for major depression and responded well to sertraline, 100 mg/day. One year later, a significant deterioration required hospitalization in the neurology ward followed by hospitalization in the psychiatric ward for severe catatonic delusional major depression (DSM-IV-TR) necessitating tube feeding.
ECT was required to obtain rapid improvement in this life-threatening situation. A pre-ECT brain computerized tomography scan showed moderate cortical and subcortical atrophy. ECT stimuli were delivered bilaterally by a Thymatron Tm, DG-100%=504 microcoulomb (brief-pulse) device. Anesthesia was induced with intravenous methohexital (1 mg/kg) followed by intravenous succinylcholine (1 mg/kg) and oxygenation with 100% oxygen. Improvement was seen after the third session and persisted during the subsequent 11 consolidation ECT pulse sessions. Ms. A’s total score on the 17-Item Hamilton Depression Rating Scale was 26 before ECT and 10 after ECT. Haloperidol (15 mg/day) was also prescribed.
Neither significant confusion nor memory impairment suggesting the encephalopathic effect of ECT was observed, and there was neither clinical evidence of exacerbation nor remission of neurological multiple sclerosis symptoms. Brain MRI after ECT showed no change compared to the first MRI performed before ECT. Three months later, Ms. A was still in remission while being treated with venlafaxine, 100 mg/day, and haloperidol, 5 mg/day.
This case report shows rapid significant improvement after ECT for severe life-threatening catatonic delusional major depression in a patient with multiple sclerosis. No neurological deterioration was shown after ECT.
To our knowledge, only four case reports have been published regarding patients with multiple sclerosis treated with ECT for depression and with MRIs before and after ECT. Three reports, one with six right unilateral pulse (1), a second with nine right unilateral pulse, and a third with 10 bilateral pulse (2), reported efficacy without any neurological adverse effects, while one (six with a right unilateral pulse) (2) reported significant neurological deterioration.
In conclusion, a high bilateral ECT pulse rate was not found to be associated with a greater risk of neurological deterioration in the treatment of major depression with multiple sclerosis when it is well tolerated by the patient.