How does ECT work? Is it dangerous? Is it scary? Does it work? What mental health conditions can be effectively treated by ECT? Is it true that ECT works better than prescription antidepressants? What are common side effects of ECT and how are this managed? Has the practice of ECT changed over time? What patient factors are the best predictors of positive and negative outcomes of ECT treatment? Come with me on a journey as I present my grand rounds lecture for the department of psychiatry as I complete my 4th year of psychiatry residency at UTHSC Memphis. These are exciting times. Recovery is definitely an option.

1. Lisa E Goldman, MD, MSW, R4
Department of Psychiatry Grand Rounds April 25, 2017
University of Tennessee Health Sciences Center,
Memphis

2. Disclosure
 Dr Goldman has no disclosures which need revealed (yet) and won’t be discussing any
off-label uses of products.

3. Learning Objectives
 By the end of this talk you will be able to:
 Compare effectiveness of ECT vs pharmacotherapy for
Treatment Resistant Depression, and outline current
indications for ECT use
 Understand the historical context of ECT
 Describe side effects that can accompany ECT use and how
these are mitigated.
 Describe factors in patient selection which make some
patients ideal candidates for ECT.

4. General Indications for ECT
 Major Depression
 Mania
 Schizophrenia with Catatonia
 Schizoaffective d/o
 Catatonia other
 NMS
 Other Illnesses

5. Indications for ECT in United States
 FDA lists 6 “cleared indications for use” for ECT devices (analogous to
on-label indications for a drug)
 Severe depression in MDD and bipolar d/o,
 Mania (uncommon, it is reserved for Tx resistant cases)
 Schizophrenia, schizoaffective, schizophreniform d/o’s
 Catatonia.
 In US, ECT is used mainly after Tx failure on multiple medications.
 Outside the US, ECT is used to Tx schizophrenia much more
commonly than it is used here.

6. Efficacy of ECT for Depression
 For comparison, rates of response and remission in STAR*D trial.
 STAR*D: 7 years, over 4,000 patients, 41 sites, diverse patients seeking Tx for MDD.
Medications included SSRI’s, SNRI’s, mirtazapine, buspirone, TCA’s, MAOI’s,
concluded that about half to 2/3 of patients can respond to something (get
somewhat better), a smaller number remit (Sx’s are gone) and most drop out of
study, stop taking medications within 1 – 2 years.
 People who are going to get better with a medication generally do so fairly quickly.
Those who do not may have treatment resistant depression (TRP) and for them,
multiple medications lead to fewer positive results.
 Note that ECT in US is mainly used for TRD patients. Many barriers exist.
 ECT is the most effective biological treatment for depression currently available.
Remission rates vary by study, in the range of 50 – 80%, associated with
improvement in quality of life.

8. ECT in current practice
 Apply electricity to scalp, induces seizure activity in
brain.
 Brain seizure is therapeutic element in treatment.
Theories exist, but exact mechanism not clearly
understood.
 Patient is under general anesthesia. Very short acting
muscle relaxant* is used to minimize discomfort,
potential injury. *succinylcholine

9. Agents that are used to mitigate
side effects….
 Anesthesia. Short acting. Brevital, or etomidate usually. –
nobody gets ECT without it
 Muscle relaxant (try not to say “paralytic”), also short acting,
succinylcholine aka anectine. No patient gets ECT without this.
 Optional meds- management of blood pressure:
 Labetolol – antihypertensive
 glycopyrrolate/Robinul to prevent bradycardia, manage secretions.
 Prevent headache: Toradol
 Prevent nausea: Zofran
 Suspend the anticonvulsant action of benzodiazepines: Flumazanil

10. The ECT experience
 Patients who receive ECT were satisfied with their
treatments and had more favorable attitudes about
ECT than patients who did not have ECT.
 85% pts who received ECT would agree to a second
course of ECT if needed .
Adriana Hermida, MD, Assistant professor, psychiatry,
Emory University

11. Mitigating cognitive side effects
 Minimize electricity dose, maximize benefits, targeted exposure:
 Square wave rather than sine wave
 brief and ultrabrief pulse ECT
 Placement of electrodes: unilateral vs bilateral
 Individualized treatment planning, individual assessment,
reassessment, monitoring. Weigh risks and benefits. Informed
consent.
 There is no “one size fits all”. Frequency and duration of treatments,
maintenance ECT
 Years of data, ongoing research, new developments.

12. History of ECT
 Ancient Greece, Galen et al: live fish as headache
treatment.
 Middle ages, pre-industrial revolution: Spirits, special
fluids, vibrations used to explain electric phenomena.
 1791, Galvani shows electricity from electric machines, can
be used to stimulate nerves. Nephew applies electricity to
decapitated heads, induces facial movements.
 1864, Fritsch: Stimulating injured soldiers’ brains causing
twitching (discovery of motor cortex).

13. History of ECT
 1930’s Penfield: Successfully treated epilepsy by locating
foci in brain tissue. Remove only damaged tissue.
 Early 20’th C: Discovery of brain regions and predictable
responses to stimulation, mapping of cortex by function,
Broca’s area, etc.
 Unexpected discovery….temporal lobe stimulation and
memory. 1937: Papez, MacLean, discovery of limbic
system… visceral brain, emotional circuitry..

14. Learning Objectives
 By the end of this talk you will be able to:
 Compare effectiveness of ECT vs pharmacotherapy for
Treatment Resistant Depression, and outline current
indications for ECT use
 Understand the historical context of ECT
 Describe side effects that can accompany ECT use and how
these are mitigated.
 Describe factors in patient selection which make some
patients ideal candidates for ECT.

15. History of ECT
 1954, McGill : Olds & Milner , alertness and learning in rats (reticular
activating system) … discover pleasure center…..better than food.
 1950’s, Tulane University: Heath, Tx depression, pain, homosexuality
with electrical stimulation of deep cortical structures, septal area ..
NOT successful.
 1950’s, Yale: Delgado stops charging bull by pressing button.
 1967: Goddard Tx of epilepsy, kindling, seizure production.
 1950’s: beginning of replacement of ECT with medications, some fairly
effective ones. Thorazine- 1954, Imipramine, iproniazid 1950’s,
(MAOI’s, TCA’s), later SSRI’s, Prozac 1988.

16. History of ECT…. some setbacks
 November 19, 1975 “One Flew Over the Cuckoo’s Nest”
released, ECT becomes subject misinformation.
 1982: L. Ron Hubbard, founder of scientology
pronounces that psychiatrists “constitute a special,
identifiable form of evil spirit”. ECT is particularly
reviled.

17. ECT renewed interest…
 1970’s: Brief pulse begins to replace sine wave as predominant format of
ECT. Nearly universal adoption of measures to improve comfort, safety
(anesthesia, muscle relaxant).
 1980’s, 90’s, 2000’s – growing recognition of limitations of medications
(STAR*D) trial, renewed interest in nonpharma Tx of depression other
mental health disorders.

18. How Does it Work?
 ECT increases cortical GABA, enhances serotonergic
function.
 ECT and hypothalamic-pituitary-adrenal axis,
normalizing dexamethasone suppression test,
(reversing brain toxic effects of cortisol, stress
indicator).
 Neuronal structure and synaptic plasticity, neurotropic
factors, cell proliferation.

19. The Procedure…Modern ECT
 General anesthesia
 Sz titration
 Depolarizing agent succinylcholine
 Placement of electrodes – RUL, BF, BT
 Seizure 20 sec – 2 minutes

20. ECT what to expect
 Rapid post procedure recovery, side effects generally few and minor.
 Minutes, hours: mild temporary amnesia, post ictal confusion,
headache, muscle aches, c/o nausea (toradol, phenergan, time)
 Patients don’t like going without food or coffee, getting up early.
 Some Pts are anxious about anything they do that involves needles,
anesthesia (like dental or colonoscopy).
 patients cannot drive during treatment.
 Several treatments are required before improvement is noticed. Not
instant fix.

21. Treatment Course
 Acute course: 2 – 4 weeks
 Average 6 to 12 weeks treatments at least.
 RUL three Tx’s per week
 BF twice per week, sometimes 3.
 Inpatient or outpatient
 Maintenance ECT sometimes.
 Every patient is unique. Evaluate and re-evaluate.

22. Choosing Electrode Placement
 Unipolar depression, try RUL first, unless other factors
 BL for: Catatonia, Patient not eating, Hx past response to
BL or RUL failure, or actively suicidal, severe depression.
 BF/BT in Bipolar D/O (This is what Emory is doing as of
2016)…schizoaffective d/o, schizophrenia w catatonia
…LART, etc.
 Placement varies somewhat by center, fine tuning dose and
placement still being worked out… overall trend: lower
doses, search for least cognitive side effects with greatest
efficacy.

23. Choosing Electrode Placement

24. Work Up, preselection process
 Detailed medical Hx, physical exam, neuro,
 Baseline cognitive exam
 Medication Hx (“what haven’t you tried?”)
 EKG
 Brain CT scan
 CMP
 Anesthesia w/u (Airways, cardiac, allergies)
 Other: implants, family support, transportation,
compliance, consent, consult (who is the primary
psychiatrist before, after Tx?)

26. Major Depression
 ECT is an effective treatment in more than 80% of
patients with treatment resistant depression (TRD),
resistant unipolar or bipolar depression.
 ECT is more effective than antidepressant
pharmacotherapy (Comparison to findings in STAR-D trial, general
consensus within the psychiatry field, figures from Emory lecture, Dr Hermida)

27. ECT as first line therapy?
 When faced with a profoundly ill patient, one who is
actively suicidal or so neglectful of personal care that
they refuse to eat, drink, take medications, some
clinicians recommend ECT as first line Tx.

28. Mania
 ECT raises the Sz threshold acting like anticonvulsant
medication
 ECT is effective in the Tx of mania
 ECT has been given safely to children with intractable
mania and to dementia patients with comorbid mania.

29. Schizophrenia
 ECT is effective in schizophrenia, catatonic type.
 When there is a Hx of positive response to ECT
 Patients with affective
component
(schizoaffective d/o)
 Initial acute psychotic break.

30. ECT for Parkinsons Disease
 Effective treatment for motor and mood symptoms
 Improves global function even in the absence of
psychiatric disorders
 Favorable predictors: advanced age, severe disability,
painful dyskinesias
 Works for a couple of weeks, then needs another tx. Of
course not permanent.

31. Contraindications
 No absolute contraindications for ECT
 Recent myocardial infarction or unstable cardiac
conditions
 Any illness that increases intracranial pressure (mass
lesion vs Idiopathic Intracranial Pressure aka NPH)
 Recent cerebral infarction, particularly hemorrhagic
kind
 Aneurysm or vascular malformation

32. Contraindications….and
precautions
 American Society of Anesthesiology (ASA) physical status
classification of level 4 or 5
 Severe Pulmonary Dz….
 LMA’s for the high BMI,
smokers are secretors…
 Metal plate in someone's head? Really bad teeth? ….Left
handed person’s language center?...dental implant?
….metallic tattoos? ….piercings? Pacemaker?

33. Clinical predictors of good
response
 Increasing age
 Presence of psychosis
 Catatonic symptoms
 Response by session 3 of ECT may predict long term
efficacy

34. Biological marker of response
 Post Ictal suppression is the most consistent biological
marker for ECT response. Increased frontal delta
activity on EEG post-ictal (Dr Adriana Hermida, Emory).

35. Negative predictors
 Failure after several antidepressant trials
 Personality disorders
 Longer current episode of depression
 Periventricular hyperintensities on MRI
 Substance Use

36. Medications and ECT
 Before ECT:
 NPO from midnight
 Limit number of medications to cardiac (take cardiac
pills as usual on day of Tx)
 Except:
 Lidocaine (shortens Sz length)
 Theophyline (associated with status epilepticus)
 Avoid Glaucoma medications (cholinesterase
inhibitors could interact with succynilcholine…
prolong apneic period.)

37. Medications…
 Pre-ECT…..
 Diabetics…. Hold hypoglycemic agents on the morning of Tx…(Pt NPO
after midnight).
 Antipsychotics and antidepressants…continue during ECT
 Lithium… hold or off.
 Anticonvulsants…usually tapered down or off before treatment in some
cases, or continued if believed really important for that patient, might
be held the night before, try Tx and see if difficulty eliciting a sz, then
re-evaluate.
 Benzos… hold or use flumazanil just before Tx.

38. Anesthesia agents
 Methohexital “brevital”: Short acting barbiturate with
minimal anticonvulsant effects. Dose: 0.75 to 1mg/Kg
 Propoful: Shortens Sz length. Dose: 0.75 – 1.5 mg/Kg
 Etomidate: increases sz duration. 0.15 – 0.3 mg/Kg

39. ECT Medications
 Succinylcholine / “anectine” : Muscle relaxant widely
used depolarizing agent (0.75 – 1.5 mg/Kg)
 Patients with musculoskeletal Dz/
pseudocholinesterase deficiency, a non-depolarizing
agent should be used.
 All of the anesthesia, muscle relaxants, adjunctive
meds are administered always by anesthesiologists. No
ECT happens without them.

40. Medications
 Anticholinergic agents such as atropine 04-1mg,
glycopyrrolate (Robinul) are used to prevent ECT – induced
bradycardia and minimize airway secretions.
 Anticholinergic agents should always be given with a B-
blocker to avoid ECT induced hypertension, increased HR.

41. What happens after the 6- 12
treatments?
 Patients should continue pharmacotherapy?
 DC?
 Taper?
 Continuation/maintenance ECT
 Currently most docs recommend slowish taper off ECT
with re-evaluate for need for M-ECT, most recommend
continue some meds, perhaps different ones (Li+ plus
elavil if not tried before… popular at Emory, for Pt’s after ECT course.)

42. Complications, Side effects
 Post Ictal Agitation (PIA) and delirium
 Cardiovascular side effects (associated with pre-
existing CV conditions, arrhythmias)
 Cognitive Side Effects
 Headaches
 Muscle Aches
 Nausea

43. CV, Respiratory Issues and ECT
 Know the medical history, screen patients carefully.
Arrhythmias, COPD, OSA, etc.
 Identify pre-existing conditions, modify Tx to manage these.
BP, HR and O2 Sat are monitored constantly, labetolol is
available, other agents if needed.
 Transient ischemic hypertension is predictable and manageable.
Anticholinergic medications (atropine, glycopyrrolate) are used
to prevent bradycardia whenever B-blockers are used.
 O2 by mask and bag valve always used pre-and post procedure,
on everyone. Some people with difficult airways get LMA’s every
time.

44. Dental and cranial issues with ECT
 Protect gums and teeth by prescreening for dental issues, bite block
for everyone.
 People with fragile teeth, recommend see a dentist, get extraction
before ECT.
 Dentures always out first. Dental implant, crown? ECT is done closer to
the top of your head, so not an issue.
 Metal plate in someone’s head? Treat the other side, or select electrode
placements that will spare the area.
 Metal eyebrow piercings? Patient to remove them first.

45. Delirium
 Risk of delirium in general,
and ECT associated delirium
increases with age of patient.
 Risk factors: low reserve capacity brain as pre-existing condition
to be aware of…Parkinson’s, Alzheimer’s, one or more CV risk
factors, structural changes in Caudate Nucleus.
 Why medical Hx and CT Head without contrast is needed prior.
 Medical co-morbidities…. Why recent labs are needed before
procedure. Tx reversible issues first if possible. Modify Tx to
suit the individual patient always.

46. Post Ictal Agitation
 It is normal for Pt to feel confused upon termination of a seizure.
Educate patient and family beforehand, offer reassurance during and
after. No Driving home!!!!
 PIA is not the same as post ictal confusion. It is similar to transitory
delirium, requires careful management. Important to differentiate
PIA from a seizure or status epilepticus. Track cessation of seizure on
EEG during procedure.
 Post Ictal Agitation (PIA) Difficult to predict, likely to recur in same
patient. Know each patient, prevent the next episode.

47. Post Ictal Agitation
 Consider increasing succinylcholine next time to
decrease muscle activity and decrease serum lactate.
Consider a small dose of brevital post Sz next time, to
ease post-ictal transition. If IV gone, consider IM
ativan if needed.
 Have trained staff available to physically hold patient
for safety . Offer patient constant calm reassurance.
“Baby-like state” for few minutes post. Always be
gentle, gentle, quiet and kind. Even if 5 staff needed
to hold them until IM gets here.

49. Cognitive side effects and ECT
 Electrode placement, electrical wave form, intensity of the stimulus and
frequency of the sessions determine the type of cognitive side effects.
 Memory loss is anterograde and retrograde. More profound right after the Tx,
during the treatment series.
 Usually anterograde memory clears more quickly. Some retrograde memory
impairment (particularly events immediately prior to Tx) can be permanent.

50. Weigh risks and benefits.
 Worse side effects are noted with BL ECT compared to
Right sided (RUL). SE’s tend to increase with increased
number of treatments.
 Ultra brief and brief therapy (shorter wave form,
lower more “targeted” dose, less electricity exposure,
using only the amount needed and no more) shows
generally better overall side effect profile compared to
the more old fashioned sine wave ECT.
 Assess and reassess before, during, after treatment. A
known risk of MDD is suicide.

51. complications with ECT and what
to do….
 Headache: 45% develop headache. Cause unclear, possibly a vascular
process. Acetaminophen, NSAIDS, Sumatriptan pre-ECT. IV toradol
pretreat.
 Nausea approx. 25% get this. Various things can be used. Phenergan
pretreat can help.
 Muscle aches, stiffness- counsel patient these typically go away
automatically, after a couple of treatments, likely are the result of using
muscles that haven’t been used much, like working out.
 Fatigue, mild confusion: like any other time a person has anesthesia +/-
a seizure, they can feel tired. Let them rest. No driving, no big
decisions today or tomorrow. Family member or friend to drive.

53. Learning Objectives
 Now that you have heard this, you can:
 Compare effectiveness of ECT vs pharmacotherapy for
Treatment Resistant Depression, and outline current
indications for ECT use
 Understand the historical context of ECT
 Describe side effects that can accompany ECT use and how
these are mitigated.
 Describe factors in patient selection which make some
patients ideal candidates for ECT.

54. Summary
 Increasing evidence supports ECT as superior in efficacy to standard medical Tx’s , as
measured by rates of remission compared to known rates of such from STAR*D trial.
 ECT as practiced by prevailing standards in United States is safe, well tolerated and
effective.
 Side effects of ECT, as in decisions regarding medications must be weigh known risks to
known benefits.
 Currently major indications for ECT include Tx resistant affective disorders, mainly
MDD, also catatonia, NMS, and others.
 Predictable and manageable side effects can occur, are mitigated by individualizing
treatment course, and adjusting parameters of electrical stimulus, placement, frequency.
 Misinformation exists, but important to counter this with scientific evidence, and patient
reports of their experience of ECT as lifesaving for treatment resistant depression.

55. Articles on ECT
 Andrade, Chittaranjan et al. Adverse Effects of Electroconvulsive Therapy (09/04/2016) Psychiatric Clinics of North America, Volume 39 ,
Issue 3 , 513 – 530
 Antunes, Rosa, Belmonte-de- Abreu et al, Electroconvulsoterapia na depressão maior: aspectos actuales (2009) Revista Brasileira de
Psiquiatria, vol 31, suppl 1
 Fochtmann, L, Evidence for Continuing Benefits of Electroconvulsive Therapy (Nov 2016) Am J Psychiatry 173:11 ajp.psychiatryonline.org
 Higgins S, George M; Brain Stimulation Therapies for Clinicians (2009) American Psychiatric Publishing Inc , Washington DC, London.
 Lisanby, S, Electroconvulsive Therapy for Depression, (11/8/200) NEJM, 357;19
 Lennon, K., ECT seems to be effective treatment for major depression in elderly (01/28/2016) Journal of Affective Disorders, Clinical
Psychiatry News
 Kellner, C Towards the Modal ECT Treatment (03/2001) The Journal of ECT Volume 17(1)
 Kellner, Greenburg, Murrough, Bryson, Briggs, Pasculli; ECT in Treatment Resistant Depression (12/2012) Am J Psychiatry 169:12
ajp.psychiatryonline.org
 Malberg, J. Implications of adult hippocampal neurogenesis in antidepressant action (03/17/2004) J Psychiatry Neurosci 2004; 29(3):196-
205
 McDonald W, Meeks T, McCall WV, Zorumski C.; Book Chapter, Electroconvulsive Therapy, (02/01/2013) The American Psychiatric
Publishing Textbook of Psychopharmacology, Third Edition American Psychiatric Publishing, Incorporated
 O’Reardon J., Takieddine N., Datto C., Augoustides, J; Propofol for the Management of Emergence Agitation After Electroconvulsive
Therapy, Review of a Case Series (12/2006) J ECT 22;4
 Tess A, Smetana G, Medical Evaluation of Patients Undergoing Electroconvulsive Therapy (04/02/200) NEJM 360;14
 Questions and Answers about the NIMH Sequenced Treatment Alternatives to Relieve Depression (STAR*D)Study – All Medication Levels
(November 2016) The National Institutes of Health www.nimh.nih.gov

57.  More resources for Clinicians
 ISEN (International Society for ECT and Neurostimulation) https://www.isen-ect.org
 Emory University School of Medicine, Office of Continuing Medical Education, ECT Mini
Fellowships emedevents.com
 Resources for patients, families
 https://www.theatlantic.com/health/archive/2016/10/how-shock-therapy-is-saving-some-children-
with-autism/505448/
 https://www.amazon.com/Each-Day-Like-Better-Treatment/dp/0826519768/
 http://www.thevitalbeat.ca/news/treating-severe-depression-electroconvulsive-therapy-ect/
 http://www.thevitalbeat.ca/news/beating-severe-depression-electroconvulsive-therapy-ect/
 http://www.thevitalbeat.ca/news/shedding-light-on-electroconvulsive-therapy-ect/

58. Thank You for supporting my efforts
 Dr’s Boyd, White, Harris, Da Cunha, Dorroh, Devah Shaw
RN, Robert, James, Randy, Lakeside Behavioral Health
 Adriana Hermida, MD, assistant professor, Dept psychiatry,
Emory University, ECT Mini-Fellowship
 Dr Hill, Dr Bell, Leigh Ann Barnes, THSC psychiatry
residency training program
 Kevin Goeta-Kreisler MD, The Aleph Center, Tucson AZ