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Milton J. Foust, Jr., MD Director, ECT Service Assistant Professor of Psychiatry Medical University of South Carolina
(Pre-)History of Convulsive Therapies
1933 ± Manfred Sakel develops insulin coma therapy (Insulin-shock behandlung) ± treated opioid dependent pt¶s first, later schizophrenia. Txs were occasionally, but not always, accompanied by seizures. (Sakel later claimed to have invented convulsive therapy, but this is disputed)
History of Convulsive Therapies
1934 ± Ladislas Meduna induces seizures using SC camphor in oil initially and later, IV Metrazol (pentylenetetrazol, pentamethylenetetrazol):
Tx was based upon a theory of opposition beween epilepsy and schizophrenia.
(Drawing by Renato Sabattini, PhD)
History of Convulsive Therapies 1938 ± Ugo Cerletti and Lucio Bini induce seizures in Rome using electrical stimuli 1940 ± Renato Almansi and David Impasto administer ECT at Columbus Hospital in NYC.A. Bennett uses curare for muscle relaxation with Metrazol convulsive therapy 1952 ± Holmberg uses succinylcholine as a muscle relaxant with ECT 5 . Lothar Kalinowsky starts giving ECT at Psychiatric Institute 1940 .E.
6 (Image provided courtesy of Renato Sabattini. PhD) .
Integrated ECT Instrument (Reproduced with permission from: Somatics.Thymatron System IV . LLC) 7 .
8 sec Charge 25 .2 msec Duration 0.Electrical Stimulus Brief-pulse square-wave AC Voltage approx.5 .70Hz Pulsewidth 0.99J) impedance) 8 .1 .504mC (5 .9A Frequency 30 . 200V (based upon 220 Current 0.
Less effective clinically despite adequate seizure duration Down-regulation of beta receptors Up-regulation of 5HT2 receptors GABA (anti-convulsant theory of ECT) BDNF (reversal of hippocampal atrophy) 9 .15 to 180 sec (by EEG) Low-dose RUL ECT .How does it work? Seizure .
Anticonvulsant theory of ECT Increasing seizure threshold during a course of ECT is associated with clinical response Hypothesis: linked anticonvulsant and antidepressant response to ECT 10 .
ECT induced seizure Discharge of neuronal population which is: ± Paroxysmal ± Synchronous ± Repetitive Post-ictal suppression follows seizure ± Inhibitory interneurons ± GABA (as detected by MRS) 11 .
(Image provided courtesy of Conrad Swartz. MD) 12 .
MD) 13 .(Image provided courtesy of Conrad Swartz.
MD) 14 .(Image provided courtesy of Conrad Swartz.
14(3):181-193. 5HT cAMP PKA CREB BDNF Duman RS and Vaidya VA. 1998. 15 .ECS (ECT) induced depolarization NE. JECT.
mivacurium 0.4mg) Oxygen/ventilation by mask Continuous cardiac and EEG monitoring (Other pre.15mg/kg. atropine 0. sumatriptan.15mg/kg)) Anticholinergic (glycopyrrolate 0. methohexital 1mg/kg)) Muscle relaxant (succinylcholine 1mg/kg. etomidate 0.and post-medications as indicated ± NTG. sodium amytal) 16 . promethazine. Beta-blockers.2mg. midazolam.Modern (Modified) ECT General anesthesia (propofol 1mg/kg. ketorolac.
Electroshock revisited. March-April 2000.) 17 . American Scientist.(Fink M.
Indications for ECT Treatment-refractory conditions Severe or life-threatening psychiatric illness Most often used for the treatment of medication-resistant depression (MDD) 18 .
SAFD) Catatonia NMS PD Delirium 21 .Diagnostic Indications MDD BPAD Psychosis (Schizophrenia.
Reasons to consider ECT first Severe sucidality Catatonia/NMS Patient preference (usually previous ECT) Pregnancy and severe psychiatric illness 22 .
stable Elderly Adolescents Children 24 .Patient categories: Healthy young adults Pregnant Medical complicated .
unstable arrhythmias. malignant hyperthermia Death: 1:80. laryngospasm.000 patients) 25 . prolonged apnea. aspiration.000 Txs (1:10. fractures. retrograde and anterograde amnesia Uncommon: cardiac arrest. severe hypertension or hypotension. prolonged seizures (status). headache. ischemia. stroke. myalgia.Risks/Side Effects Common: transient confusion. nausea.
Conditions of increased risk Increased ICP (mass) Unstable angina Recent MI Recent stroke Pheochromocytoma Retinal detachment 26 .
may be synergistic Reserpine.taper and d/c or reduce (except in the case of seizure disorder) Stimulants .taper and d/c D/C Lithium 36-48 hrs prior to Tx Trazodone -d/c Others (SSRI¶s. anti-PD ) consider dose reduction or d/c Neuroleptics .Medications and ECT Anticonvulsants . MAOI's. chlopromazine . TCA¶s.adverse effects 27 .
ECT and Medications. cont. Mylanta. etc. Risperdal ± may be beneficial in combination with ECT 28 . Beneficial medications (Give before Tx) Anti-HTN (other than diuretics) Anti-GERD/reflux (not Carafate. Clozapine.) Pulmonary (brochodilators) Glaucoma meds Neuroleptics/Antipsychotics ± Haldol.
POA.two licensed physicians concur (SC Adult Health Care Consent Act ± SC Code of Laws Title 44.adequate mental capacity. benefits. side effects. understand procedure. Chapter 66) 29 .Consent Informed consent . alternatives Printed consent form Surrogate consent ± Guardian. NOK if patient is incapacitated . risks.
most cognitive dysfunction Right unilateral (RUL) . most effective.less cognitive effect.Electrode Placement Bilateral (BL) .most common. may be less clinically effective Bifrontal (BF) ± may be as effective as BL with less cognitive effect 30 .
Mayo Clin Proc. 2002:77:552-556 31 .Bilateral RUL Bifrontal Rasmussen KG et al.
RUL Response rates: Low-dose RUL . 1993. 328:839-846.43% Low-dose BL . NEJM. 32 . BL vs.65% High-dose BL .63% Sackheim HA et al.17% High-dose RUL .Electrode Placement.
Stimulus Dosing Stimulus titration Age-based Fixed high dose (RUL) 33 .
8 Txs 2 -5 Txs per week Tx until improvement plateaus Continuation/Maintenance ECT Prophylactic medication 34 .Course of ECT Index course 6 .
ECT Instructions/Orders Void on call to ECT in AM NPO after MN Hold BZ after 9pm Hold all current medications the morning of ECT except Anti-HTN (other than diuretics) Anti-GERD/reflux (not Carafate. etc. Mylanta.) Pulmonary (brochodilators) Glaucoma meds 35 .
CBT VNS (FDA approved) rTMS (experimental) Neurosurgery ± DBS (experimental) 36 . Lamictal Psychotherapy .Alternatives to ECT Pharmacologic Tx . venlafaxine. SSRI.TCA. MAOI. Atypical Neuroleptic.
RN (843) 792-5734 (843) 792-5697 (Fax) Kim Andrews. Foust. MD (843) 792-5907 Carol Burns.ECT Program staff Milton J. RN 40 .
41 . New York: Oxford University Press. 77:552-556. 141:1034-1041. 1984. Electroconvulsive therapy and newer modalities for the treatment of medicationretractory mental illness. Am J Psychiatry. Mayo Clin Proc. Electroconvulsive Therapy. 1997.References . Rasmussen KG et al. 2002.General Abrams R. Meduna and the origins of convulsive therapy. 3rd Edition. Fink M.
157:1960-1965.References . JAMA. Am J Psychiatry. 42 2001. Continuation pharmacotherapy in the prevention of relapse following electroconvulsive therapy: A randomized controlled trial. 285:1299-1307. Efficacy of continuation ECT and antidepressant drugs compared to long-term antidepressants alone in depressed patients. 2000. . Sackheim HA et al.Prophylaxis Gagne GG et al.
Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. 157:121-123. Bailine SH et al. 43 .References . 1993. Am J Psychiatry. 328:839-846. 2000. Comparison of bifrontal and bitemporal ECT for major depression.Electrode Placement Sackheim HA et al. NEJM.
1990. (DBS study) 44 . Lawson JS et al. 1993. 20:335-344. Psychological Medicine. Psychological Medicine. Mayberg HS et al. Electrode placement in ECT:cognitive effects. 45:651-60. 23:349-360.References . Deep brain stimulation for treatment-resistant depression. Neuron. Therapeutic advantage of bifrontal electrode placement in ECT.Electrode Placement Letemendia FJJ et al. 2005 Mar 3.
Duman RS and Vaidya VA. 14(3):153-171. Molecular and cellular actions of chronic electroconvulsive seizures.The Journal of ECT. 1998.References ± Neurochemistry Newman ME et al. Journal of ECT. 45 . Neurochemical mechanisms of action of ECT: evidence from in vivo studies. 1998. 14(3):181193.