Sir,We read with great interest the case report of a chronic subdural hematoma (SDH) following electroconvulsive therapy (ECT) by Saha et al.[1] The incidence of SDH in patients receiving ECT is exceedingly rare, making this case report even more important, so it is essential that some points be clarified. Common factors which predispose patients to spontaneously develop a SDH include very young or very old age, anticoagulant therapy, long-term alcohol abuse, and dementia. The patient in this report appears to be an otherwise healthy young woman who has none of these risk-factors, so the assumption is that the SDH occurred as a result of the ECT. It would be helpful to know if the authors are aware of any unreported factors, which would have predisposed her to the development of SDH during treatment. If, indeed, she did not have any risk-factors for developing SDH during the peri-treatment period, then it makes sense to examine closely what, if anything, may have contributed to either the initial SDH or the worsening of an existing (but sub-clinical) hematoma during ECT. It is possible that the transient increase in blood pressure and intracranial pressure (ICP) experienced during the therapeutic seizure contributed to either the initial SDH or to the worsening of an existing SDH,[2] but patients with chronic SDH have been successfully treated with ECT without complication, so even that point is unclear.[3] Lacking hemodynamic data from this case, it is difficult to tell if increased blood pressure was involved. Was the patienthypertensive at any point before, during or after the treatment? Was the adverse advent likely the result of uncontrolled hypertension and subsequent increased ICP? Was she treated with anti-hypertensive agents, such as labetalol, to mitigate the effects of increased Blood Pressure and Heart Rate? These are important questions which remain unanswered. As well, we do not know what kind of anesthesia was administered, in what doses, if muscle relaxation was achieved with succinylcholine or some other agent, and if the patient was hyperventilated prior to stimulus. These procedural interventions all have the potential to significantly alter the ICP and blood pressure during the treatment. Since the authors suggest that SDH be considered in the differential diagnosis of an acute change in mental status after treatment it would be helpful to identify what factors put their patient, and others, at risk for developing SDH, so that this complication may be anticipated and avoided in the future.