Electroconvulsive Therapy (ECT)

Today, ECT is used effectively to treat various psychiatric disorders, including severe mood disorders (i.e. - severe depression with melancholic features, psychotic depression, and severe, acute mania). Techniques and safety protocols for administering ECT have also changed dramatically. ECT is now an anesthetic procedure, and requires the use of general anesthesia and muscle relaxants. The patient is therefore fully anesthetized and asleep during the procedure. Serious or persistent side effects now extremely rare. Although, ECT is often considered a treatment of last resort, in most jurisdictions, it remains under-utilized due to stigma. ECT can be extremely effective and, at times, a life-saving procedure. ECT remains a first-line treatment for many psychiatric disorders.^[2]

Indications for ECT include:

• Treatment-refractory mania
• Major depressive disorder (unipolar or bipolar depression)
  • ECT is generally recommended as a second-line treatment for major depressive disorder because of the increased risk for adverse events.
  • However, ECT can also be used as a first-line treatment in certain clinical situations including: acute suicidal ideation, psychotic features, treatment-resistant depression, repeated medication intolerance, catatonic features, prior favourable response to ECT, rapidly deteriorating physical status, during pregnancy (for any of the above indications), and patient preference.^[3]
• Refractory obsessive-compulsive disorder (OCD)
• Catatonia
• Refractory psychosis, from schizophrenia or schizoaffective disorder
• Parkinson's Disease^[4]
• Refractory status epilepticus^[5]
• Severe suicidality
• Neuroleptic malignant syndrome

• There are no absolute contraindications to ECT, only relative contraindications.^[6][7]
• Relative contraindications include:
  • Space-occupying cerebral lesion with increased intracranial pressure or mass effect
  • Recent myocardial infarction (if <1 month ago)
  • Recent stroke or cerebral hemorrhage (if <1 month ago)
  • Unstable vascular aneurysms or malformations
  • Pheochromocytoma
  • Class 4 or 5 anaesthesia risk (ASA IV, ASA V)
  • Recent orthopedic injury with unstable fracture/dislocation (if <1 month ago)

• ECT delivers an electrical stimulus, which induces an action potential in the neurons in the brain.
• The exact mechanism of action of ECT's antidepressant effects remains unknown, but it is hypothesized that the induced seizure leads to changes in neurotransmitters, neuroplasticity, functional connectivity, increased levels of brain-derived neurotrophic factor (BDNF), hormones, and/or neuropeptides.^[8]

• ECT affects autonomic nervous system activity, which causes rapid hemodynamic changes. The heart rate goes down (as ECT causes a parasympathetic drive). The effects of ECT on the heart is similar to a brief period of “vigorous exercise.”^[9]

• During ECT, cortical blood flow increases by up to 300%, which increases intracranial pressure (ICP). Cerebral oxygen demand also increases up to 200% during seizure activity. ECT remains safe in patients with brain tumours and intracranial masses provided that there is not significant cerebral edema (Hence, increased ICP is a relative contraindication).^[10] Brain volumes increase with ECT treatment,^[11] and there is also an increase in Brain Derived Neurotrophic Factor (BDNF) levels.^[12][13] During ECT, the brain will try to achieve homeostasis in response to the electrical current, and will release GABA to suppress seizures.^[14] The release of GABA is thought to play a role in the antidepressant effect of ECT as well.

It is important to inform patients about the risks and benefits of ECT. Below is a template for informed consent:

• Ask patient what they understand about ECT
• Explain procedure (# of treatments, what treatments will consist of, what happens just before and after treatment, how they will feel, how long each session lasts)
• Explain efficacy (with depression, bitemporal is 65%, RUL is 58%)
• Cover serious/life threatening risks (1 per 10,000 treatment deaths, risks of general anesthesia)
• Cover common side effects (confusion, headache, muscle pains, HTN, cardiac changes, nausea, cognitive difficulties - specifically memory 1-2 months prior and after procedure may be “hazy”)
• Discuss alternate treatment medications (continue with medications, change medications, psychotherapy options)
• Discuss next steps (work-place adjustment, change to medications prior to treatment course beginning)
• Limitations with treatment (no driving for 24 hours, time off work/school)

Some medications should be stopped prior to starting ECT, while others should be continued.

Treatment parameters for ECT include:

1. Electrode placement and position
2. Electrical intensity/stimulus
3. Pulse width

• ECT has the best response rate in geriatric depression, patients with a greater severity of illness, psychotic depression, and when there is an absence of personality disorders.
• In individuals with borderline personality disorder, the rates of ECT response are significantly lower, and this is an important risk/benefit consideration that needs to be discussed with patients.^[20]
• The effects of ECT are also dose-dependent, with a better response at higher doses.^[21]
• Patients can expect improvement in symptoms by the third treatment, and achieve remission beginning by the seventh treatment.^[22] Suicidal ideation also similarly decreases greatly by around the fourth treatment.^[23] ECT also improves quality of life measures significantly for patients post-treatment.^[24]
• The best and strongest predictor of non-response to ECT is the degree of non-response to previous antidepressant medications. Response rates are about 50% in those who have treatment-resistant depression and up to 90% in treatment-naive patients.^[25]

• ECT treatment ranges between 6 to 18 treatments, and can be delivered 2 to 3 times per week.
  • Administering ECT only 2 times per week confers a better cognitive profile.
  • More than 3 treatments per week are not recommended, as they are associated with higher frequency of cognitive side effects.
• If after 12 sessions there is no response, no further ECT should be pursued.

• About 50% of patients will relapse with depressive symptoms at the 12-month mark, even after a successful course of ECT.^[26]
• Patients who receive ongoing antidepressant pharmacotherapy reduce their relapse rate by approximately half compared to patients who do not have any treatment post-ECT.^[27]
  • Thus it is recommended that patients receive pharmacotherapy (and psychotherapy) after their first ECT treatment.^[28][29]
• Post-ECT pharmacotherapy should be continued for at least 12 to 24 months. Antidepressant choice should be the one that the patient responded the best to in the past. In absence of an effective antidepressant, nortriptyline plus lithium, or venlafaxine plus lithium is recommended.^[30]

• Maintenance ECT (“prophylactic ECT”) should be added after an individual has gone through a second course of ECT. In addition to maintenance ECT, augmentation with an antidepressant, plus lithium should be considered.^[31]
• The most commonly used maintenance ECT schedule involves weekly treatments for 4 weeks, then biweekly for 8 weeks, and then monthly treatments. If signs of relapse occur, more frequent treatments should be given.^[32]
• Again, post-ECT, pharmacotherapy should be continued for at least 12-24 months.^[33] There is evidence to support maintenance ECT as an augmentation treatment to psychopharmacological treatment in mood disorders.^[34]

Possible side effects and adverse events during ECT and post-ECT include:

• Cognition is a broad term that encompasses several components, including: attention, anterograde memory (ability to remember new information), retrograde memory (ability to remember past memory), procedural memory, and reaction time.
• Memory loss (both retrograde and anterograde) is a known side effect from ECT, particularly around the time of ECT treatment:^[42]
  • Subjective memory worsening is reported by a minority of patients, and those at greatest risk are:
    • Young women^[43]
    • Individuals with prexisting cognitive impairment
    • Older adults
    • Those receiving bitemporal ECT
    • More frequent ECT administration (i.e. - 2 sessions per week vs. 3 sessions)
    • Use of lithium during ECT treatment
    • Higher anesthetic doses
  • The amnestic effects of ECT are greatest and most persistent for knowledge about the world (impersonal memory) compared with knowledge about the self (personal memory).
• Overall, ECT is associated with short-term cognitive effects, but cognition eventually returns or surpasses their pre-ECT baseline.^[44]
• The majority of evidence suggests that ECT given over a period of years will not cause cumulative cognitive deficits.
• There are also reduced rates of dementia in geriatric patients with mood disorders who receive ECT.
  • Importantly, this means ECT does not increase the risk of dementia in the elderly, making it a safe and appropriate option.^[45]
• It is important to note however, in rare cases, some individuals can experience significant and distressing memory loss, and this remains an under-researched area in ECT.
• If there are cognitive side effects from ECT, you can try to:
  • Reduce the frequency of treatments (i.e. - 3× per week to 2× per week)
  • Reduce the electrical stimulus intensity during treatment

• Overall, ECT is very safe and rapid acting. Out of all medical procedures involving anesthesia, it is the lowest risk procedure.^[46]
• The mortality rate from ECT has been estimated to be less than 1 death per 98,000 treatments, which is similar to the background rate associated with anesthetic induction for any surgical procedure.^[47]
• Several studies have shown overall lower all-cause mortality in those who receive ECT:
  • One study showed a lower overall mortality rate from natural causes in inpatients who have received ECT compared to those who did not.^[48]
  • In one study, older adults with geriatric depression, those who ECT treatment had overall lower mortality than those on antidepressants.^[49]

• No clinical studies have shown damage to the brain structures related to ECT.^[50]