Free
Correspondence  |   November 1998
Sumatriptan Was Effective in Electroconvulsive Therapy (ECT) Headache 
Author Notes
  • (Oms)
  • Departments of Anesthetics and Psychiatry; Hospital de Bellvitge; Feixa Llarga, Barcelona, Spain (Miro, Rojo)
Article Information
Correspondence
Correspondence   |   November 1998
Sumatriptan Was Effective in Electroconvulsive Therapy (ECT) Headache 
Anesthesiology 11 1998, Vol.89, 1291-1292. doi:
Anesthesiology 11 1998, Vol.89, 1291-1292. doi:
To the Editor:-We would like to draw attention to the benefit of sumatriptan on a 35-yr-old woman with chronic depression who was schedule for a course of electroconvulsive therapy (ECT) during general anesthesia. We were able to find only one reference of this subject. [1] After her initial ECT sessions, the patient complained of severe headache. This appeared just after emergence from the anesthetic and lasted for several hours. After trying different analgesics with only partial or no relief, we decided to try 6 mg sumatriptan administered subcutaneously just after the ECT was performed. The patient had a history of migraine, and she described her ECT headache pain to be similar.
The patient was headache free after the first ECT in which she received sumatriptan. Except for one instance in which she experienced a pressure-tingling sensation, the patient continued to be headache free for the remainder of the final four ECT sessions of a 12-treatment series.
Sumatriptan is a selective 5-hydroxytryptamine (5-HT) receptor agonist [2] used for the acute treatment of migraine and cluster headache. The pain of migraine appears to involve the vessels of the pia and dura mater and the trigeminal nerve, which innervates these vessels. Specifically, activated trigeminovascular axons produce pain and result in the local release of vasoactive neuropeptides, which produce vasodilation. [3] This “neurogenic inflammation” is thought to be the mechanism underlying the pain of migraine. Sumatriptan appears to work via specific serotonin receptors (5-HT 1B and 5-HT 1D) to mediate selective vasoconstriction within the cranial vasculature and to prevent the release of inflammatory mediators from trigeminal nerve terminals. Headache is a well-known side effect of ECT. [4] Although the exact mechanism is not known, it is possible that 5-HT receptors are involved and also that the pain can take the form of migraine. [5] Electroconvulsive therapy acts as well on 5-HT receptors and also on postsynaptic 5-HT receptors. [6] 
Angel Oms, M.D., D.A., F.A., F.R.C.S.E.
Emilio Miro, M.D.
Jose-Emilio Rojo, M.D.
Departments of Anesthetics and Psychiatry; Hospital de Bellvitge; Feixa Llarga, Barcelona, Spain
(Accepted for publication April 24, 1998.)
REFERENCES
DeBattista C, et al: Sumatriptan prophylaxis for postelectroconvulsive therapy headaches. Headache 1995; 35(8):502-3
Buzzi MG, Moskowitz MA: The antimigraine drug, sumatriptan, selectively blocks neurogenic plasma extravasation from blood vessels in dura mater. Br J Pharmacol 1990; 99(1):202-6
Moskowitz MA: Neurogenic inflammation in the pathophysiology and treatment of migraine. Neurology 1993; 43(6 suppl 3):16-20
Weiner SJ, Ward TN, Ravaris CL: Headache and electroconvulsive therapy. Headache 1994; 34(3):155-9
Weinstein RM: Migraine occurring as sequela of electroconvulsive therapy (letter). Headache 1993; 33(1):45
Coppen A, Rama-Rao VA, Bishop M, et al: Neuroendocrine studies in affective disorders: Plasma prolactin response to THR in affective disorders. Effect of ECT. J Affect Dis 1980; 2:311-5