al-Azhar University ECT workshop


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The presentation part of a two-day workshop on ECT held at al-Hussain University Hospital of al-Azhar Univeristy. It was accompanied by one-to-one training on the Thymatron system IV machine in the ECT suite of al-Hussain hospital.

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  • There is no evidence to suggest that the mortality associated with ECT is greater than that associated with minor procedures involving general anesthetics,• There is no evidence to suggest that ECT causes brain damage
  • Immediately post-ECT: acute effects within 24 hours of ECT seizure termination,• Subacute effects: greater than 24 hours to less than two weeks after receiving a course of ECT,• Medium-term effects: two weeks to less than three months after receiving a course of ECT,• Longer-term effects: three months to less than six months after receiving a course ECT,• Long term effects: six months or greater after ECT.
  • Limited evidence from controlled clinical trials suggests that the effects on memory and cognitive function may not last beyond 6 months• Subjective reports of memory loss may be more persistent (> 6 months post-ECT) than findings examining objective measures (up to 6 months)
  • Little evidence exists supporting the long-term effectiveness of ECT
  • These results suggest that ECT is an effective and safe treatment for agitation and aggression in dementia.
  • Effects of increasing treatment number on the relationship between stimulus intensity and seizure duration:As shown in Figure 5–1, when the stimulus is barely suprathreshold, increasing stimulus intensity will be associated with a longer seizure duration.However, when the stimulus greatly exceeds seizure threshold, seizure duration can be expected to fall rather than increase. In addition, as the numberof index ECT treatments increases, seizure threshold rises and seizure duration falls, resulting in a shift to the right and downward of the curve depictingthe relationship between stimulus intensity and seizure duration. What this means is that some seizures that appear very brief may actually be associatedwith a higher relative stimulus intensity than longer seizures, particularly toward the end of an index ECT course. In practical terms, if increasing stimulusintensity is seen to lead to a decrease in seizure duration, that effect is evidence that the stimulus was well above seizure threshold.
  • The half-age (HA) method estimates the stimulating dose according to the patient's chronological age, using half this age in “percent of charge” for the Thymatron device or the equivalent in milicoulombs for the MECTA device as starting point at the first session.Our data indicates that in most patients the HA method can be used as a starting point of treatment without concerns of over-stimulation. For the few patients who would not seize at their HA method level, treatment could be performed with restimulation at a higher point.Petrides, 2009 PubMed PMID: 19972637
  • In CORE study: Subsequent treatments were performed at a dose level 50% higher than the ST estimated at treatment 1
  • CORE: Seizure threshold was defined as the lowest stimulation level required to elicit an adequate seizure, defined as at least 25 seconds of EEG duration and at least 20 seconds of motor duration. 
  • The optimal dose of muscle relaxant for ECT reduces muscle contractions without inducing complete paralysis.
  • Factors that have been described as lowering butyrylcholinesterase activity are liver disease, advanced age, malnutrition, pregnancy, burns, oral contraceptives, monoamine oxidase inhibitors, echothiophate, cytotoxic drugs, neoplastic disease, anticholinesterase drugs, tetrahydroaminacrine, hexafluorenium, and metoclopramide. The histamine type 2 receptor antagonists have no effect on butyrylcholinesterase activity or the duration of succinylcholine's effect. Bambuterol, a prodrug of terbutaline, produces marked inhibition of butyrylcholinesterase activity and causes prolongation of succinylcholine-induced blockade. The β-blocker esmolol inhibits butyrylcholinesterase but causes only minor prolongation of succinylcholine blockade. Despite all the publications and efforts to identify situations in which normal butyrylcholinesterase enzyme activity may be low, this has not been a major concern in clinical practice because even large decreases in butyrylcholinesterase activity result in only moderate increases in the duration of action of succinylcholine. When butyrylcholinesterase activity is reduced to 20% of normal by severe liver disease, the duration of apnea after the administration of succinylcholine increases from a normal duration of 3 minutes to just 9 minutes. Even when treatment of glaucoma with echothiophate decreased butyrylcholinesterase activity from 49% of control to no activity, the increase in duration of neuromuscular blockade varied from 2 to 14 minutes. In no patient did the total duration of neuromuscular blockade exceed 23 minutes. Millers, 2009
  • continuing administration of the anticonvulsant sodium valproate does neither adversely affect nor enhance the efficacy of ECT inpatients with manic episodes. Jahangard et al Journal of ECT & Volume 00, Number 00, Month 2012 (PAP): Iran
  • al-Azhar University ECT workshop

    1. 1. ELECTROCONVULSIVE THERAPY(ECT)Ahmed Eid el-AghouryBoard-certified, MScMed, MBChBECT Fellowship, Emory University School of Medicine, USAClinical instructor & trainer at ATPAbbassia Hospital for Mental Health, MOHCairo, Egypt
    2. 2. ECT: history and state-of-art More than 70 years of continuous practice. Epilepsy & Dementia Praecox Meduna: Camphor oil, 1934 Cerletti & Bini: ECT, 1938 Still a controversial practice! Anti-ECT movements On the other hand: Ia level of evidence in treatment of depression! Specialized ECT centers, certifications and medical journals. Not the only electrical therapy in medicine: Cardiac defibrillation. Convulsive therapy: now magnetic and NO gas al-Azhar University, May 2012 2
    3. 3. “Efficacy has not, and has never been, theproblem with ECT. ECT remains, indisputably, thesingle most efficacious treatment for seriousdepression. The problem with ECT has been, andremains, the need to diminish adverse cognitiveeffects.”Kellner CH. (2000): High-dose right unilateral ECT [editorial]. J ECT 76:209-210 al-Azhar University, May 2012 3
    4. 4. ECT amnestic syndrome  Transient / permanent ?  Objective / subjective?  Electrode placement / electrical dosage :No significant evidence-base that their predictive value regarding cognitive outcome following brief- pulse ECT after the subacute period.M. Semkovska, O. Babalola, D. Keane, D.M. McLoughlin, P.1.g.008 Cognitive effects ofelectrode placement and stimulus dose in brief-pulse electroconvulsive therapy fordepression, European Neuropsychopharmacology, Volume 20, Supplement 3, August 2010,Pages S312-S313, al-Azhar University, May 2012 4
    5. 5. FDA executive summary, 2011  Disorientation: acute NOT long term, BL > UL  Executive function: no effect, may improve  Anterograde memory: improves  Retrograde memory: decline in subacute phase EXCEPT with ultrabrief waves  Autobiographical memory: decline inFDA executive summary: Prepared for the January 27-28, 2011 meeting of the NeurologicalDevices subacute phase EXCEPT with Panel. Meeting to Discuss the Classification of Electroconvulsive Therapy Devices(ECT) al-Azhar University, May 2012 5
    6. 6. Factors may increase cognitive side effectsMankad WV, et al (eds): Clinical manual of electroconvulsive therapy. American Psychiatric Publishing, VA 22209-3901. 2010 al-Azhar University, May 2012 6
    7. 7. Tools of neurostimulationSwartz CM (editor): Electroconvulsive and Neuromodulation Therapies. Cambridge University Press. 2009 al-Azhar University, May 2012 7
    8. 8. ECT helps brain to work: few seconds with long effects !Swartz CM (editor): Electroconvulsive and Neuromodulation Therapies. Cambridge University Press. 2009 al-Azhar University, May 2012 8
    9. 9. Hypotheses of mechanisms ofaction al-Azhar University, May 2012 9
    10. 10. ECT works at multiple levels ofbrain function al-Azhar University, May 2012 10
    11. 11. ECT induces neuronalreorganization al-Azhar University, May 2012 11
    12. 12. ECT and neuronal circuits al-Azhar University, May 2012 12
    13. 13. The centrencephalic theory of seizure generalization  Regional cerebral blood flow (rCBF): increases extensively, particularly in the centrencephalic structures in generalized seizures.Differences in cerebral blood flow between missed and generalized seizures withelectroconvulsive therapy: A positron emission tomographic study Harumasa Takano,Nobutaka Motohashi, Takeshi Uema, Ken‟ichi Ogawa, Takashi Ohnishi, Masami Nishikawa,Hiroshi Matsuda Epilepsy research 1 November 2011 (volume 97 issue 1 Pages 225-228 al-Azhar University, May 2012 13
    14. 14. al-Azhar University, May 2012 14
    15. 15. al-Azhar University, May 2012 15
    16. 16. EEG  Relative alpha activity (8.5 12.0 Hz) increased in occipital lobe after a course (qEEG analysis)Y. Kitaura, K. Nishida, R. Hama, Y. Takekita, M. Yoshimura, A. Tajika, T. Kinoshita,P27-6 Quantitative EEG analysis of electroconvulsive therapy response for senile depression: acase report, Clinical Neurophysiology, Volume 121, Supplement 1, October 2010, Page S264 al-Azhar University, May 2012 16
    17. 17. Vagal system stimulation  ECT increases vagal activity which might be associated with the beneficial effect seen following ECTBär KJ, Ebert A, Boettger MK, Merz S, Kiehntopf M, Jochum T, Juckel G, Agelink MW.Is successful electroconvulsive therapy related to stimulation of the vagal system?J Affect Disord. 2010 Sep;125(1-3):323-9. al-Azhar University, May 2012 17
    18. 18. ECT and BRAIN DAMAGE:fiction of antipsychiatrists ! al-Azhar University, May 2012 18
    19. 19. ECT - responsive syndromes There are no diagnoses that should automatically lead to treatment with ECT. APA Task Force 2001 Syndromic view offers more homogeneous pts, eg; acute psychosis Vs acute mood disorders. Primary (1st line) Vs Secondary ( last resort) use of ECT. *Fink M: Electroconvulsive therapy. In: Gelder M, Andreasen N, Lopez-Ibor J, and Geddes J (Editors). New Oxford Textbook of Psychiatry. 2nd ed. 2009. Oxford University Press al-Azhar University, May 2012 19
    20. 20. Primary Use ECT (APA 2001)1. A need for RAPID, DEFINITIVE RESPONSE because of the severity of a psychiatric or medical condition (e.g., when illness is characterized by stupor, marked psychomotor retardation, depressive delusions or hallucinations, or life– threatening physical exhaustion associated with mania)2. When the risks of other treatments OUTWEIGH the risks of ECT3. A history of POOR MEDICATION RESPONSE or GOOD ECT RESPONSE in one or more previous episodes of illness4. The patient‟s PREFERENCE al-Azhar University, May 2012 20
    21. 21. ECT - responsive syndromes*  DEPRESSIVE MOOD DISORDERS: Melancholia, Delusional, Post-partum, Pseudodementia, Catatonia, Suicide & Intractable.  MANIC MOOD DISORDERS: excited, delirious, catatonic & mixed.  PSYCHOSES: acute, abrupt episode ± mood, OC Schiz, atypical psychosis, post- partum, catatonic & Intractable.  CATATONIA: retarded, excited, malignant, NMS, medical, CNS etc.  SUICIDE.  NEUROLOGICAL*Fink M: Electroconvulsive therapy. In: Gelder M, Andreasen N, Lopez-Ibor J, and Geddes J (Editors). New OxfordTextbook of Psychiatry. 2nd ed. 2009. Oxford University Press al-Azhar University, May 2012 21
    22. 22. Last resort ECT, FDA 2011  Treatment resistance: ◦ For depression, after one or more antidepressant trials ◦ For mania, after one or more mood stabilizer trials with adjunctive atypical antipsychotic treatment ◦ For clozapine resistant schizophrenia ◦ For lorazepam resistant catatonia  Intolerance to or adverse effects with pharmacotherapy that are deemed less likely or less severe with ECT  Deterioration of the patient‟s psychiatric or medical condition creating a need for a rapid, definitive response.FDA executive summary: Prepared for the January 27-28, 2011 meeting of the NeurologicalDevices Panel. Meeting to Discuss the Classification of Electroconvulsive Therapy Devices(ECT) al-Azhar University, May 2012 22
    23. 23. Pseudodementia Cognitive disorders resulting from functional disorders Common: depression, Ganser syndrome Suspect when: dementia syndrome appears suddenly in an adult, especially an elderly adult. Remarkable response to ECT Fink M. Electroconvulsive therapy: a guide for professionals and their patients. Oxford, 2009 al-Azhar University, May 2012 23
    24. 24. Unresponsive pt Stupor vs Coma Stupor: varying degrees of unresponsiveness due to an apparent decreased level of consciousness Stupor / not Catatonic signs / not Psychiatric / Neurologic ds BZD then ECTHurwitz TA. Psychogenic unresponsiveness. Neurol Clin. 2011 Nov;29(4):995-1006. al-Azhar University, May 2012 24
    25. 25. Super-refractory status epilepticus  SE that continues or recurs 24 h or more after the onset of anesthetic therapy, including those cases where SE recurs on the reduction or withdrawal of anaesthesia.  ECT as an option was used since 1943  After pharmacologic coma failsShorvon S, Ferlisi M. The treatment of super-refractory status epilepticus: a critical review ofavailable therapies and a clinical treatment protocol. Brain. Oct; (Pt - al-Azhar University, May 2012 25
    26. 26. Parkinson‟s Disease (PD)  Psychotic symptoms in Parkinsons disease (PDP) are relatively common  In a recent Japanese case series of 8 quetiapine-resistant PDP pts: ◦ significant ↑ in rCBF in the right middle frontal gyrus after ECT ◦ notable improvements not only in PDP but also in the severity of PDUsui C, Hatta K, Doi N, Kubo S, Kamigaichi R, Nakanishi A, Nakamura H, Hattori N, Arai H.Improvements in both psychosis and motor signs in Parkinsons disease, and changesin regional cerebral blood flow after electroconvulsive therapy. Prog Neuropsychopharmacol BiolPsychiatry. 2011 Aug 15;35(7):1704-8. al-Azhar University, May 2012 26
    27. 27. Dementia with Lewy bodies  Psychiatric Sx: ◦ Psychosis is an intrinsic part of DLB: 75% have hallucinations and >50% have delusions ◦ Depression: 20 – 65 %  „Neuroleptic sensitivity‟ phenomenon  ECT has antidepressant, antipsychotic, and dopamine- enhancing effectsBurgut FT, Kellner CH. Electroconvulsive therapy (ECT) for dementia with Lewy bodies.Med Hypotheses. 2010 Aug;75(2):139-40. al-Azhar University, May 2012 27
    28. 28. Multiple sclerosis Depression: up to 25 %, may be delusional Mania: up to 14 % Suicide: 5 x other population Recurrent catatonia / psychosis: rarePontikes TK, Dinwiddie SH. Electroconvulsive therapy in a patient with multiple sclerosis and recurrent catatonia. J ECT. 2010 Dec;26(4):270-1. University, May 2012 al-Azhar 28
    29. 29. Other movement disorders Successful case reports: ◦ NMS ◦ TD ◦ HD ◦ TSScott A. The ECT Handbook. 2nd Ed. The Third Report of the Royal College of Psychiatrists‟ Special Committee on ECT. 2005 al-Azhar University, May 2012 29
    30. 30. ECT as a drug: 10 actions at thesame time1. Antipsychotic2. Antidepressant3. Antimanic4. Mood stabilizer5. Antisuicidal6. Anticatatonic7. Alerting (anti-stupor): ↑ α activity in EEG8. Vegetative: eating after session9. Antiepileptic: ↑ ST10. Dopaminergic: ↓ Dyskinesia al-Azhar University, May 2012 30
    31. 31. ECT Non-responsive syndromes*  Poor previous response to ECT course  Neuroses.  Personality disorders.  Drug dependence & related disorders.  Maladjustment problems: dissociation / conversion  Lifelong intellectual & emotional dysfunction.  Dementia.  Impulse disorders.  Sexual dysfunctions.  Sleep disorders.  Factitious / Somatoform disorders.*Fink M: Electroconvulsive therapy. In: Gelder M, Andreasen N, Lopez-Ibor J, and Geddes J (Editors). NewOxford Textbook of Psychiatry. 2nd ed. 2009. Oxford University Press al-Azhar University, May 2012 31
    32. 32. Sine Vs Pulse squared waveMankad WV, et al (eds): Clinical manual of electroconvulsive therapy. American Psychiatric Publishing, VA 22209-3901. 2010 al-Azhar University, May 2012 32
    33. 33. Electrical waveforms of ECT Waveform: the “shape” of the stimulus as a function of time. Sine wave ECT: 1930s Cerletti and Bini, wall outlets, continuous, neurotoxic! Brief pulse ECT: 0.5 – 2 ms, late 1970s Ultra-brief pulse ECT: < 0.5 ms, late 1990s al-Azhar University, May 2012 33
    34. 34. Related Electricity principles V=I×R “Ohm‟s Law”V: voltage in volts, I: current intensity in milliamperes, R: resistance (impedance) in ohms U=Q×I×RU: energy in joules, Q: charge in millicoulombs, I: current intensity in milliamperes, R: resistance (impedance) in ohms Q = I × PW × 2F × DQ: charge in millicoulombs, I: current intensity in milliamperes, PW: pulse width, F: frequency in hertz (cycles pairs per second), D: duration of stimulus train in seconds• 1 mC = 1 mA / 1 sec• Constant current devices: safe• Summary metric: J / mC?• Energy (J): unpredictable Ohm‟s law triangle al-Azhar University, May 2012 34
    35. 35. Specs of common ECTdevices al-Azhar University, May 2012 35
    36. 36. Seizure Threshold (ST) The total amount of electricity necessary to induce a seizure ie CONVULSIVE THRESHOLD. ST variance: up to 50 folds, a lot of factors, strong evidence for age, gender and electrode placement, so NOT a constant measure Therapeutic stimulus is NOT equal to the ST stimulus al-Azhar University, May 2012 36
    37. 37. Factors influencing STMankad WV, et al (eds): Clinical manual of electroconvulsive therapy. American Psychiatric Publishing, VA 22209-3901. 2010 al-Azhar University, May 2012 37
    38. 38. Impedance IMPEDANCE: static (200 – 3000 Ω) and dynamic (120 – 350 Ω). Electrodes, scalp and skull. IMPEDANCE: automatic self-test in MECTA devices ◦ Females > Males ◦ RUL > BT > BF Scalp SHUNTING of current: a lower proportion of current entering the brain. It is a short-circuit So, INVERSE RELATION for constant- current devices between ST and dynamic impedance al-Azhar University, May 2012 38
    39. 39. Cause of variations in impedanceMankad WV, et al (eds): Clinical manual of electroconvulsive therapy. American Psychiatric Publishing, VA 22209-3901. 2010 al-Azhar University, May 2012 39
    40. 40. Is seizure duration enough?Mankad WV, et al (eds): Clinical manual of electroconvulsive therapy. American Psychiatric Publishing, VA 22209-3901. 2010 al-Azhar University, May 2012 40
    41. 41. STIMULUS DOSING Why? ◦ Cerebral generalization: more effective ◦ Barely suprathreshold (just above ST): ineffective ◦ Markedly suprathreshold (far beyond ST): hazardous ◦ ST is increasing along index ECT course: fixed dosing is inappropriate EMPERICAL TITRATION: most precise PRE SELECTED (FORMULA-BASED) METHOD: pts do not tolerate titration, eg cardiac, severely suicidal. etc FIXED DOSING: may be a malpractice, esp if randomly assigned. al-Azhar University, May 2012 41
    42. 42. Where to start dosing? RUL BT / BF1- Female 2- Female 2- Male 3- Male al-Azhar University, May 2012 42
    43. 43. STIMULUS DOSING RULES Stimulus 1: RUL, Female Stimulus 2: BT/BF Female, RUL Male Stimulus 3: BT/BF Male After 3rd failed stimulus (uncommon): jump 2 levels for 4th one Preselected stimulus: calculated dose ◦ Stimulus 3: RUL, Female ◦ Stimulus 4: All others Dial the device knob: 1 / 2 – 1 × pt age (poor method with no evidence) al-Azhar University, May 2012 43
    44. 44. Example: Dose titration technique forSomatics Thymatron System IV model al-Azhar University, May 2012 44
    45. 45. The final rules Titration session : up to 4-5 restimualtions with 20 seconds apart THERAPEUTIC STIMULUS INTENSITY is moderately suprathreshold for next sessions: ◦ 1.5 – 2.5 × ST in BT/BF, ◦ 2.5 – 6 × ST in RUL Restimulate increasing 50 – 100 % of the previous stimulus when needed al-Azhar University, May 2012 45
    46. 46. Electrode placementBT RUL BF d‟Elia Letemendia al-Azhar University, May 2012 46
    47. 47. SEIZURE ADEQUACY Pattern & Duration: motor & EEG Pattern: generalization both motor & EEG Duration: 20 – 60 sec motor, 30 – 120 sec EEG (CORE studies) MISSED: no activity both motor & EEG BRIEF (ABORTIVE): < 20 sec motor, < 30 sec EEG PROLONGED: > 60 sec motor, > 120 EEG Post-ictal suppression: a valid parameter Although: seizure adequacy parameters are still unclear, and lacking good al-Azhar University, May 2012 47
    48. 48. Seizure duration al-Azhar University, May 2012 48
    49. 49. How to manage inadequateseizure? MISSED / ABORTIVE: ◦ Check device and connections ◦ Restimulate: 20 sec apart, up to 5 times ( very rare), vary the duration and frequency, then pulse width ◦ Hyperventilate: 15 – 20 / min ◦ IV Flumazenil: if pt is on BZD ◦ DC / Taper drugs interfering: eg AEDs ◦ Decrease IV anesthetic dose / switch to less anticonvulsant one. Consider xanthines: Caffeine, theophylline, aminophylline. ◦ Space the schedule ◦ Check recent stimulus increase: paradoxical area of curve al-Azhar University, May 2012 49
    50. 50. PROLONGED / TARDIVEseizures More than 60 sec motor / 120 sec EEG (APA Task Report 2001: 180 sec both !) ◦ Abort with IV anesthetic (thiopental) / BZD (midazolam). If no response (rare): intubate, IV loading phenytoin and refer to ICU. ◦ Good ventilation ◦ Additional dose of muscle relaxant ◦ Decrease stimulus ◦ Check pt drugs: eg xanthines May 2012 al-Azhar University, 50
    51. 51. ECT seizure vs Epilepticseizure al-Azhar University, May 2012 51
    52. 52. ECT Prescribing Three items: electrode placement, schedule and number 2 / wk Vs 3 / wk: same at long term ie ( after 1 wk – 6 m) [More than 6 SR studies] It is not possible to predict reliably how many treatments will be required in a course of ECT. A set course of treatments SHOULD THEREFORE NOT BE PRESCRIBED. RCPsych, 2004 No sign of response: stop after BL 6 sessions Slight or temporary response: continue to BL 12 sessions al-Azhar University, May 2012 52
    53. 53. Anesthesia for ECT It is just a type of moderate sedation, NOT a full anesthesia. Adjusted per session. Suitable anesthetic drug: Ultra-brief not long duration, light not deep, weak antiepileptic & painless on injection. Typically: barbiturates. Thiopental is common in Egypt. Anticholinergics / Hyperventilation: are NOT routine. al-Azhar University, May 2012 53
    54. 54. Anesthesia for ECT Muscle relaxant: Short-acting to protect airway & decrease / minimize ictal motor activity. Full paralysis is not required in most cases. HYPERKALEMIA is a concern: Pts with catatonia / renal impairment / stroke / burn. Typically: succinylcholine (Suxamethonium): 9 – 13 min for recovery at dose 1 mg / Kg. The elimination half-life of succinylcholine is estimated to be 47 seconds al-Azhar University, May 2012 54
    55. 55. Muscle relaxants: 2 types al-Azhar University, May 2012 55
    56. 56. PChE deficiency • Enzyme produced by mainly the LIVER: hydrolyzes choline esters • Also known: plasma ChE, and BChE • Dibucaine number ( 70 – 90 %): NOT a routine test • Inherited / acquired (age / ds / drugs) • Very UNCOMMON, more rare in Africans • Next session: use Nondepolarizing ms relaxant eg atracuriumWilliams J, Rosenquist P, Arias L, McCall WV. Pseudocholinesterase deficiency and electroconvulsive therapy.J ECT. 2007 Sep;23(3):198-200. PubMed PMID: 17805000. Miller: Millers Anesthesia, 7th ed, 2009 al-Azhar University, May 2012 56
    57. 57. Drugs before ECT  Symptomatic improvement of patients who are ON AEDs during ECT is comparable to those who are NOT  AEDs + ECT (Vs ECT alone): ◦ Higher charge ◦ More sessions, esp titrations ◦ Delayed recovery ◦ Post ECT deliriumComparison of electroconvulsive therapy (ECT) with or without anti-epileptic drugs in bipolar disorder. Harve Shanmugam Virupaksha, Barki Shashidhara, Jagadisha Thirthalli, ChannaveerachariNaveen Kumar, Bangalore N. Gangadhar Journal of affective disorders 1 December 2010 (volume 127 issue 1 Pages 66-70 al-Azhar University, May 2012 57
    58. 58. Herbal drugs: must bestopped St John‟s wort (Hypericum) Ginkgo extracts Ginseng Kava ASA recommends stopping 2 wks before al-Azhar University, May 2012 58
    59. 59. Drugs delay recovery / prolongpost ECT delirium Anti-Ch TCA Li AEDs Anti ChE: esp rivastigmine al-Azhar University, May 2012 59
    60. 60. Egyptian MHA, 2009 Mandates: general anesthesia & muscle relaxation. Informed consent / agreement of 2 assessments from 2 registered specialists. National Accreditation Policy for ECT units and clinics was set in NMHC.MHA: mental health actNMHC: national mental health commission al-Azhar University, May 2012 60
    61. 61.    ◦ ◦  (1 (2 (3  al-Azhar University, May 2012 61
    62. 62. Post-ictal suppression: the only biological marker for good response &prognosis of the session. Note cerebral seizure (72 sec) lags behindthe peripheral motor seizure ( around 30 sec). al-Azhar University, May 2012 62
    63. 63. Example for a titration session: High ST in a young man: 184.5mC! So, next session therapeutic dose was 2.5 x IST = 461 mC al-Azhar University, May 2012 63
    64. 64. Medical clearance There are no “absolute” medical contraindications for ECT. APA Task Force 2001 No routine Pre-ECT workup / evaluation, but tailored on individual base. Risk / Benefit analysis: ECT psychiatrist & Anesthetist. Medical consultation on demand. Increased risk: ASA level 4 / 5.* Special patients groups: Elderly, Pregnant women, Puerperium, Children and Adolescents. Medical comorbidities esp. cardiovascular. *ASA: American Society of Anesthesiology al-Azhar University, May 2012 64
    65. 65. al-Azhar University, May 2012 65
    66. 66. Medical illness & ECT ECT is often administered to patients with severe medical illness Risk/benefit analysis: ◦ Severity of psychiatric illness ◦ Therapeutic success with ECT ◦ Medical risks ◦ Alternative treatments or no ttt Medical consultation: optimize medical status / modification to ECT procedure al-Azhar University, May 2012 66
    67. 67. Pre ECT workup is tailored: anexample al-Azhar University, May 2012 67
    68. 68. CVS conditions Can be safely managed during ECT. APA Task Force 2001 Parasympathetic stim --- > Symapthetic stim HTN, IHD, VHD, CHD and arrhythmias Before ECT: ECG, CXR, electrolytes ± echo β –blockers: consider by case Antihypertensives: morning of session al-Azhar University, May 2012 68
    69. 69. CNS conditions Increased ICP: SOLs, may pre use steroids, diuretics, anti HTN & HV CVA: recent / not? Type? Dementia: esp DLB Epilepsy: refractory Parkinson ds: PDP Trauma: recent? Others: MS, Muscle ds, al-Azhar University, May 2012 69
    70. 70. Other medical conditions Pulmonary: COPD DM Hyperkalemia / Hypokalemia Hyponatremia / Dehydration GERD: aspiration. Treat by: metoclopramide, Ranitidine OR consider intubation Bone Teeth Urinary retention al-Azhar University, May 2012 70
    71. 71. ECT in Elderly The largest age group receiving ECT Why? ◦ Relative low risk, rapid, drug resistance, medical comorbidity People should not be denied access to ECT solely on the grounds of age. (RCPsych, 2005) Aging effect: improves therapeutic outcome Case report: A 100-year-old woman with severe aortic stenosis received ECT safely for 5 years. [OReardon JP, Cristancho MA, Ryley B, Patel KR, Haber HL. Electroconvulsive therapy for treatment of major depression in a 100-year-old patient with severe aortic stenosis: a 5-year follow-up report. J ECT. 2011 Sep;27(3):227-30.] Increased: ST Increased: cognitive SE al-Azhar University, May 2012 71
    72. 72. ECT during pregnancy  Risks of mental illness during pregnancy: ◦ Poor self-care, ◦ Poor prenatal care, ◦ Inadequate weight gain, ◦ Premature delivery, ◦ Substance abuse, ◦ Disengaged parenting behaviors, ◦ Neonaticide and suicideOReardon JP, Cristancho MA, von Andreae CV, Cristancho P, Weiss D. Acute and maintenance electroconvulsive therapy for treatment of severe major depression during thesecond and third trimesters of pregnancy with infant follow-up to 18 months: case report and review of theliterature. J ECT. 2011 Mar;27(1):e23-6. Review. PubMed PMID: 20562638. al-Azhar University, May 2012 72
    73. 73. ECT in pregnancy May be used in all 3 trimesters APA guidelines: Depression & BAD Relatively safe Obstetric consultation is a must IV Saline / Ringer Good pre oxygenation NOT hyperventilation Elevate Rt hip: separate uterus from IVC & aorta ASPIRATION: ……? Monitoring al-Azhar University, May 2012 73
    74. 74. ECT during pregnancy  A total of 300 case reports of ECT during pregnancy drawn from the literature from 1942 through 1991 were reviewed  Twenty-eight (28) of the 300 cases reported complications: transient, benign fetal arrhythmias; mild VAGINAL BLEEDING; abdominal pain; and self-limited uterine contractions.  Without proper preparation, there was also increased likelihood of ASPIRATION, aortocaval compression, and respiratory alkalosis.  ECT is a relatively safe and effective treatment during pregnancy if steps are taken to decreaseMiller LJ. Use of electroconvulsive therapy during pregnancy. Hosp Community Psychiatry. 1994 May;45(5):444-50. potential risks.Review. PubMed PMID: 8045538. al-Azhar University, May 2012 74
    75. 75. ECT during pregnancy  Among the 339 cases reviewed: ◦ 25 fetal or neonatal complications, but only 11 of these, which included two deaths, were likely related to ECT. ◦ 20 maternal complications reported and 18 were likely related to ECT.  Although there are limited available data in the literature, it seems that ECT is an effective treatment for severe mental illness during pregnancy and that the risks to fetus and mother are LOW.Anderson EL, Reti IM. ECT in pregnancy: a review of the literature from 1941 to 2007. Psychosom Med. 2009 Feb;71(2):235-42. Review. PubMed PMID: 19073751. al-Azhar University, May 2012 75
    76. 76. al-Azhar University, May 2012 76
    77. 77. al-Azhar University, May 2012 77
    78. 78. ECT in Puerperium DO NOT stop breastfeeding How to decrease infantile exposure to anesthetic drugs? Delay / Bottle al-Azhar University, May 2012 78
    79. 79. Child and adolescent RARE indications Low ST: slow EMPERICAL titration Catatonia: CP, ID and autism Consent al-Azhar University, May 2012 79
    80. 80. Ideal ECT suite (Typical at Abbassia with lesser beds capacity) After Swartz Textbook, al-Azhar University, May 2012 80
    81. 81. Assessment after an index course  From start: target symptoms list & criteria of remission. Eg: Double depression & Schizoaffective  “Continuation treatment has become the rule in contemporary psychiatric practice”. APA 1993  Abruptly stopping ECT after improving is associated with high relapse rates (≥ 50%) ± C-Pharm, esp in the first 6 ms after an index ECT course.  Prophylactic (Preventive) ECT: Continuation / Maintenance ECT.  A controversial practice, no guidelines, few controlled studies and vague differences.*C-Pharm: Continuation pharmacotherapy al-Azhar University, May 2012 81
    82. 82. Assessment after an indexcourse Although psychotropic continuation therapy is the prevailing practice, few studies document the efficacy of such treatment after a course of ECT. APA Task Force 2001 Recurrent illness / Relapse on psychotropics / Intolerance to them: a viable option C-ECT: up to 6 ms, aiming at relapse prevention. M-ECT: more than 6 ms, aiming at recurrence prevention. al-Azhar University, May 2012 82
    83. 83. Key terms After Index ECT (2 – 4 wks) 1. Short -Taper ECT Abbreviated 2. Long - Taper ECT C-ECT Prophylactic ECT 3. C-ECT 4. M-ECT 5. Abruptly Stopping ECT: ± continuation pharmacotherapy. Ambulatory ECT (Outpatient) Vs Inpatient ECT? Procedure of prophylactic ECT: Same as Index / modified? al-Azhar University, May 2012 83
    84. 84. C-ECT Classically: up to 6 m. Abbreviated C-ECT (Tapering): short (1 m), long (2 ms). Try tapering before C-ECT. Most studied in depression: likened to antidepressants. Pt has a disorder known to be an acutely responsive to an index ECT: ± drug resistance. Relapse on drugs = partial resistance. Previously / Currently intolerant to drugs: AE / Medical comorbidities / Poor compliance. Poor response to an index ECT: re evaluate after 10 – 12 sessions. al-Azhar University, May 2012 84
    85. 85. C-ECT 2nd time relapse / ECT in 3 ms. Pt is severely ill: Taper / C – ECT, you cannot stop or depend on drugs alone. C-ECT Vs C-Pharmacotherapy: controversial esp in depression. CORE 2010: After improvement of a depressive episode: C-Pharm after Index ECT (TCA ± Lithium), nearly equal to C- ECT. (one of the strongest RCTs) Nortriptyline: the most studied C-Pharm, enhancing ECT response & tolerable in old age. al-Azhar University, May 2012 85
    86. 86. C-ECT  Recommendations according to EMORY UNIVERSITY ECT Facility, USA*:  Short- Taper: ◦ 1/wk × 1, 1/10 ds × 1, 1/ 2 wks × 1 Long-Taper: ( 2 × Short-Taper) ie 1/wk × 2, 1/10 ds × 2, 1/ 2 wks × 2 C-ECT: RUL: 1/wk × 4, 1/10 ds × 3, 1/ 2 wks × 4 ms BT/BF: 1/wk × 2, 1/10 ds × 2, 1/ 2 wks × 4 ms Inter treatment intervals may be decreased if pt relapses during spacing / tapering. Drugs: Last 2 wks of tapering*Hands-on training and personal communication in Nov, 2010 al-Azhar University, May 2012 86
    87. 87. M-ECT More than 6 ms, against recurrence. Controversial practice: NICE report 2003 questioned its empirical evidence ! While it is stated by the APA & RCPsych as a “viable option” in treatment of selected pts. Almost same indications like C-ECT, or if C- ECT cannot be tapered, “convulsive dependence”. Long practice in: Elderly & Medically ill pts who are intolerable to psychotropics. Best studied in: Depression & Schizophrenia. Again: no guidelines, and few RCTs. al-Azhar University, May 2012 87
    88. 88. M-ECT 1 / 3-4 wk for 1 y, then re assess. RUL is preferred at 6 – 7 × ST. Ambulatory: Outpatient. al-Azhar University, May 2012 88
    89. 89. Suggested readings & references TEXTBOOKS: 1. 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. Mankad WV, et al (eds): Clinical manual of electroconvulsive therapy. American Psychiatric Publishing, VA 22209-3901. 2010 3. Swartz CM (editor): Electroconvulsive and Neuromodulation Therapies. Cambridge University Press. 2009 4. Abrams R: Electroconvulsive Therapy, 4th ed, 2002. Oxford University Press. 5. McDonald WM, et al: Electroconvulsive therapy. In: Schatzberg AF & Nemeroff CB (editors): The American Psychiatric Publishing textbook of psychopharmacology. 3rd ed. 2004 6. Fink M. Electroconvulsive therapy: a guide for professionals and their patients. Oxford, 2009 7. Scott A. The ECT Handbook. 2nd Ed. The Third Report of the Royal College of Psychiatrists‟ Special Committee on ECT. 2005 SELECTED JOURNAL ARTICLES: Trevino K, McClintock SM, Husain MM. A review of continuation electroconvulsive therapy: application, safety, and efficacy. J ECT. 2010 Sep;26(3):186-95. Electroconvulsive therapy stimulus parameters: rethinking dosage. Peterchev AV, Rosa MA, Deng ZD, Prudic J, Lisanby SH. J ECT. 2010 Sep;26(3):159-74. Effects of pulse width and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. Sackeim HA, Prudic J, Nobler MS,et al. Brain Stimul. 2008 Apr;1(2):71-83. Navarro V, Gastó C, Torres X, Masana G, Penadés R, Guarch J, Vázquez M, Serra M, Pujol N, Pintor L, Catalán R. Continuation/maintenance treatment with nortriptyline versus combined nortriptyline and ECT in late-life psychotic depression: a two-year randomized study. Am J Geriatr Psychiatry. 2008 Jun;16(6):498-505. Sienaert P, Vansteelandt K, Demyttenaere K, Peuskens J. Randomized comparison of ultra-brief bifrontal and unilateral electroconvulsive therapy for major depression: clinical efficacy. J Affect Disord. 2009 Jul;116(1- 2):106-12. al-Azhar University, May 2012 89
    90. 90.  Smith GE, Rasmussen KG Jr, Cullum CM, Felmlee-Devine MD, Petrides G, Rummans TA, Husain MM,Mueller M, Bernstein HJ, Knapp RG, OConnor MK, Fink M, Sampson S,Bailine SH , Kellner CH; COREInvestigators. A randomized controlled trial comparing the memory effects of continuation electroconvulsivetherapy versus continuation pharmacotherapy: results from the Consortium for Research in ECT (CORE) study. JClin Psychiatry. 2010 Feb;71(2):185-93. Rasmussen KG, Mueller M, Rummans TA, Husain MM, Petrides G, Knapp RG, Fink M, Sampson SM,Bailine SH, Kellner CH. Is baseline medication resistance associated with potential for relapse after successfulremission of a depressive episode with ECT? Data from the Consortium for Research on ElectroconvulsiveTherapy (CORE). J Clin Psychiatry. 2009 Feb;70(2):232-7. Kellner CH, Knapp RG, Petrides G, Rummans TA, Husain MM, Rasmussen K, Mueller M, Bernstein HJ,OConnor K, Smith G, Biggs M, Bailine SH, Malur C, Yim E, McClintock S, Sampson S, Fink M. Continuationelectroconvulsive therapy vs pharmacotherapy for relapse prevention in major depression: a multisite study fromthe Consortium for Research in Electroconvulsive Therapy (CORE). Arch Gen Psychiatry. 2006 Dec;63(12):1337-44. Kellner CH, Tobias KG, Wiegand J. Electrode placement in electroconvulsive therapy (ECT): A review of theliterature. J ECT. 2010 Kellner CH, Knapp R, Husain MM, Rasmussen K, Sampson S, Cullum M, McClintock SM, Tobias KG,Martino C, Mueller M, Bailine SH, Fink M, Petrides G. Bifrontal, bitemporal and right unilateral electrodeplacement in ECT: randomised trial. Br J Psychiatry. 2010 McDonald WM. Is ECT cost-effective? A critique of the National Institute of Health and Clinical Excellencesreport on the economic analysis of ECT. J ECT. 2006 Mar;22(1):25-9. Kellner CH, Fink M, Knapp R, Petrides G, Husain M, Rummans T, Mueller M, Bernstein H, Rasmussen K,Oconnor K, Smith G, Rush AJ, Biggs M, McClintock S, Bailine S, Malur C. Relief of expressed suicidal intent byECT: a consortium for research in ECT study. Am J Psychiatry. 2005 May;162(5):977-82. Tharyan P, Adams CE. Electroconvulsive therapy for schizophrenia. Cochrane Database Syst Rev. 2005 Apr18;(2):CD000076. Van der Wurff FB, Stek ML, Hoogendijk WL, Beekman AT. Electroconvulsive therapy for the depressedelderly. Cochrane Database Syst Rev. 2003;(2):CD003593. al-Azhar University, May 2012 90
    91. 91. Anti ECT Burstow B. Electroshock as a form of violence against women. Violence Against Women. 2006 Apr;12(4):372-92. [ECT functions and is experienced as a form of assault and social control, not unlike wife battery. Emergent themes include electroshock as life destroying, a sign of contempt for women, punishment, a means of enforcing sex roles, a way to silence women about other abuse, an assault, traumatizing for those who undergo it and those forced to witness it]. Canada Read J, Bentall R. The effectiveness of electroconvulsive therapy: a literature review. Epidemiol Psichiatr Soc. 2010 Oct-Dec;19(4):333-47. [The cost-benefit analysis for ECT is so poor that its use cannot be scientifically justified]. New Zeland McDonald A, Walter G. Hollywood and ECT. Int Rev Psychiatry. 2009 Jun;21(3):200-6. [Film depictions continue to exert a powerful and predominantly negative effect on public attitudes towards the treatment. From review of the 22 currently available films that directly refer to ECT the main themes identified are described. While initially portrayed as a dramatic but effective psychiatric intervention, ECT on film has come to stand for something quite different, representing the brutal and generally futile attempts of society to control and suppress the individual, gathering along the way a hackneyed cinematic grammar that emphasizes its inhumane and punitive nature.] UK al-Azhar University, May 2012 91
    92. 92. ATP Building at Abbassia al-Azhar University, May 2012 92