Electroconvulsive Therapy As A Treatment Option For Intractable

Epilepsy, A Case ReportAmany H Ragab*, MD(1), Ahmed Elaghoury, MD(2)

(1) Neurologist at Cairo University, Neurology Department, (2) Psychiatrist at Abbassia Mental Hospital, Cairo, Egypt

Introduction• During the electroconvulsive therapy (ECT) there is a cumulative increase in the seizure

threshold (ST), which in turn requires an increase in electrical stimulus intensities toinduce a seizure in the subsequent sessions (1-4).

• It was postulated that the therapeutic effect of ECT is related to this anticonvulsant effect(5, 7, 9, 21, 25).

• The American Psychiatric Association has considered the presence of intractable seizuresas an indication for ECT (1).

• It was documented that ECT reduces the frequency of seizures in patients with epilepsy(2, 9).

• Recently, evidence suggested an improvement in seizure control with ECT for patientswith refractory status epilepticus (11, 12, 18).

• The largest published group of patients with epilepsy comorbid with mental disordersreceived ECT (n=43) showed improvement regarding both seizure frequency andpsychiatric manifestations (10). Similar results were documented in several case series(13).

• Recently, cases of temporal lobe epilepsy (n=5) following maintenance ECT werepublished (14), but without clear etiologic relation to ECT.

• Previously, cases of new-onset epilepsy (n=4) during a maintenance ECT course werepublished with shown safety of continuing ECT (15).

• Old reviews attributed this to multiple factors of patients’ medical conditions (16).• A large-scale retrospective study of patients with epilepsy (n=619) has concluded that ECT

did not cause seizures (17).

ECT technique

• ECT machine: MECTA spECTrum M (200J)• Dose parameters: Current intensity was constant at 800 mAmp, pulse width (Ultrabrief):

0.3 ms, duration was variable between 4 – 8 sec, and frequency was variable between 40-80 Hz

• Seizure threshold (ST): defined clinically as bilateral motor generalized tonic-clonicseizures for at least 20 sec. EEG monitoring during the sessions is not available at ourfacility. No prolonged seizures (>60 sec) were observed during the course.

• Initial ST was easily induced at 23 mC; then the patient was put on a moderate dose (2.5 xST = 58mC) RUL electrode, with biweekly sessions for two months (n= 15 sessions).

• ECT sessions were tapered along another two months (n= 6, as follows 1/wk×2, 1/10 ds×2,1/ 2 wks×2). This long taper protocol was adopted after an ECT facility at EmoryUniversity, Atlanta, GA as an abbreviated continuation ECT (26, 27).

• ST was noticed to increase along the course to reach the range between 184 mC (8x ST) -230 mC (10x ST).

Conclusion and recommendations1) RUL ultrabrief ECT was preferred in our patient to easily induce seizures, avoid seizure

threshold variations and to reduce ECT memory impairment (22). Though ST hasincreased, and the patient got the benefit of this as regards his epileptic seizurefrequency.

2) Safety and efficacy of ECT in adolescents with comorbid epilepsy and mental disordershave repeatedly been documented in previous case reports and our case (19, 20, 21).

3) The rise of ST during the ECT course is still not observed in all cases (23-25), but whenpresent it may provide a crossover period for patients with epilepsy to modify theirmaintenance AEDs during the breakthrough seizures.

4) As we did not find any controlled studies about the use of ECT in patients with epilepsy,we are suggesting from our experience with psychiatric patients that this anticonvulsanteffect is a short-term effect, so it may be beneficial to abort refractory statusepilepticus.

References1. The Practice of Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging: A. Washington, DC: American Psychiatric

Association; 2001. Task Force Report of the American Psychiatric Association.2. Krishnamoorthy E. Ch 17: The use of ECT in neuropsychiatric disorders. In: Waite J, Easton A. The ECT handbook. RCPsych Publications; 2013. 3. Swartz CM (editor): Electroconvulsive and Neuromodulation Therapies. Cambridge University Press. 2009.4. Abrams R: Electroconvulsive Therapy, 4th ed, 2002. Oxford University Press.5. Sackeim HA, Decina P, Prohovnik I, Malitz S, Resor SR. Anticonvulsant and antidepressant properties of electroconvulsive therapy: a proposed

mechanism of action. Biological psychiatry. 1983 Nov.6. Sackeim HA, Decina P, Portnoy S, Neeley P,Maltiz S. Studies of dosage, seizure threshold, and seizure duration in ECT. Biol Psychiato1987,

22:249-268.7. Sackeim HA. The anticonvulsant hypothesis of the mechanisms of action of ECT: current status. The journal of ECT. 1999 Mar 1;15(1):5-26.8. Nobler MS, Oquendo MA, Kegeles LS, Malone KM, Campbell C, Sackeim HA, Mann JJ. Decreased regional brain metabolism after ECT.

American Journal of Psychiatry. 2001 Feb 1;158(2):305-308.9. Coffey CE, Lucke J, Weiner RD, Krystal AD, Aque M. Seizure threshold in electroconvulsive therapy (ECT) II. The anticonvulsant effect of ECT.

Biological Psychiatry. 1995 Jun 1;37(11):777-788.10. Lunde ME, Lee EK, Rasmussen KG. Electroconvulsive therapy in patients with epilepsy. Epilepsy & Behavior. 2006 Sep 30;9(2):355-359.11. Bayrlee A, Ganeshalingam N, Kurczewski L, Brophy GM. Treatment of super-refractory status epilepticus. Current neurology and neuroscience

reports. 2015 Oct 1;15(10):66.12. Zeiler FA, Matuszczak M, Teitelbaum J, Gillman LM, Kazina CJ. Electroconvulsive therapy for refractory status epilepticus: A systematic review.

Seizure. 2016;35:23–32.13. Shah N, Pande N, Bhat T, Murke M, Andrade C. Maintenance ECT as a therapeutic approach to medication-refractory epilepsy in an adult with

mental retardation: case report and review of literature. The journal of ECT. 2012 Jun 1;28(2):136-140.14. Bryson A, Gardner H, Wilson I, Rolfe T, Archer J. Temporal lobe epilepsy following maintenance electroconvulsive therapy—Electrical kindling in

the human brain? Epilepsia. 2016 Nov 1;57(11).15. Rasmussen KG & Lunde ME. Patients who develop epilepsy during extended treatment with electroconvulsive therapy. Seizure. 2007 Apr

30;16(3):266-270.16. Devinsky O & Duchowny MS. Seizures after convulsive therapy A retrospective case survey. Neurology. 1983 Jul 1;33(7):921-925.17. Ray AK. Does Electroconvulsive Therapy Cause Epilepsy? J ECT. 2013;29:201-205.18. Yang X & Wang X. Potential mechanisms and clinical applications of mild hypothermia and electroconvulsive therapy on refractory status

epilepticus. Expert Rev Neurother. 2015;15(2):135–144.19. Griesemer DA, Kellner CH, Beale MD, Smith GM. Electroconvulsive therapy for treatment of intractable seizures Initial findings in two children.

Neurology. 1997 Nov 1;49(5):1389-1392.20. Shin HW, O’Donovan CA, Boggs JG, Grefe A, Harper A, Bell WL, McCall WV, Rosenquist P. Successful ECT treatment for medically refractory

nonconvulsive status epilepticus in pediatric patient. Seizure. 2011 Jun 30;20(5):433-436.21. Maixner DF: Ch 6 ECT in Youth with Comorbid Medical and Neurological Disorders. In: Ghaziuddin N, Walter G, editors. Electroconvulsive

therapy in children and adolescents. Oxford University Press; 2013.22. Sackeim HA, Prudic J, Nobler MS, Fitzsimons L, Lisanby SH, Payne N, Berman RM, Brakemeier EL, Perera T, Devanand DP. Effects of pulse width

and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. Brain stimulation. 2008 Apr 30;1(2):71-83.23. Tharyan P &Adams CE. Electroconvulsive therapy for schizophrenia. The Cochrane Library. 2005 Apr.24. Fink M, Petrides G, Kellner C, Mueller M, Knapp R, Husain MM, Rasmussen K, Rummans T, O'connor K, CORE Group. Change in seizure

threshold during electroconvulsive therapy. The journal of ECT. 2008 Jun 1;24(2):114-116.25. Duthie AC, Perrin JS, Bennett DM, Currie J, Reid IC. Anticonvulsant mechanisms of electroconvulsive therapy and relation to therapeutic

efficacy. J ECT. 2015;31(3):173–178.26. McDonald WM, et al: Electroconvulsive therapy. In: Schatzberg AF & Nemeroff CB (editors): The American Psychiatric Publishing textbook of

psychopharmacology. 3rd ed. 200427. McDonald WM, Director of Geriatric Psychiatry / Fuqua Center for Late Life Depression / ECT and Neuromodulation Services: personal

communication in Nov, 2010

• A 17-year-old boy working at an ironing shop started to develop complex partial seizures(CPS) during sleep since the age of 12 yrs.

• He has a history of delayed intellectual and motor milestones, with a family history ofepilepsy.

• Semiology of CPS was in the form of mouth automatism and staring look, which occurredonce per week then became once per month after starting carbamazepine 1200 mg/day.

• Later, he developed a skin rash, so shifted to oxcarbazepine 2400 mg/day.• Baseline EEG and MRI were unremarkable.• During the follow-up, his platelet count was found to be 145000/mm3. So, he was shifted

to levetiracetam 1000 mg/day, and seizures became controlled.• Two months later, he developed behavioral disturbances in the form of agitation,

irritability, aggression and suicidal attempts, which required starting of an ECT course.• Consequently, the psychiatric manifestations were controlled, alongside with the epileptic

seizures; but at lower doses of oxcarbazepine to 1200 mg/day, plus levetiracetam 1000mg/day.

Case report Authors contacts:Dr. Amany Ragab: Dr.ahmajd@kasralainy.edu.egDr.Ahmed Elaghoury: Dr.aghoury@gmail.com

Anticonvulsant properties of ECT (7, 8)o Increase in ST over the courseo Decrease in seizure duration over the courseo Ictal and immediate postictal EEG inhibitory signso Reduction of regional blood flow and hypometabolic stateo Increase and persistent of slow-wave activity in EEGo Anticonvulsant effects in animal models of epilepsyo Anticonvulsant effect in intractable seizure and status epilepticus in humano GABAergic transmission enhancement