Electro Convulsive Therapy (ECT)

Introduction
Recent resurgence in past decade Excellent safety profile Superior Efficacy

Economic benefits
Less stigmatization

History
Early Theories Theory of Biological Antagonism Insulin Shock Therapy

Electrically induced seizures

Improvements in Anesthesiology

Early Theories
Hippocrates: Documented the cure of insane patient

following malaria-induced seizures. Swiss physician Paracelsus in 1500s, induced seizures with oral camphor to treat mania and psychosis.

Biological Antagonism Theory

Hungarian physician Meduna in 1934 reported an

inherent biological antagonism between schizophrenia and epilepsy. He reported beneficial effects of seizures induced by camphor in catatonic patient.

Insulin Shock Therapy

Manfred Sakel, a Viennese physician in 1920s. He documented insulin therapy for schizophrenia. Insulin was administered in patients to induce a hypoglycemic state.

Electrically induced Seizures

In 1937, Italian physicians Cerletti & Bini applied

electricity to head to induce therapeutic seizures. First patient had catatonia and he improved. Safer than chemically induced seizures. Widespread acceptance through out Europe and USA.

Improvements in Anesthesiology
Early period complications like bone fractures and

patient discomfort. Use of Curare, as muscle relaxant, by Bennett in 1940 allowed complete paralysis of patient during seizure. Development of short acting IV barbiturates in 1950s allowed rapid induction of sedation and amnesia surrounding procedure.

Mechanism of Action
Psychodynamic theories Placebo effects Memory Eraser Seizure as curative agent Biochemical changes Therapeutic effects of rise in seizure threshold Hippocampal Neurogenesis

Psychodynamic Theories
The beneficial effect of ECT is to its fulfillment of the

need for punishment in the self loathing, depressed patient.

Placebo Effect
The beneficial effects are due to wishful thinking on

the part of the staff and the patient

Memory Eraser
Beneficial effects of ECT are related to its ability to

disturb recent memory, thereby erasing the recall of recent traumas, that led to depressive episode.

Seizure, as Curative event

ECT is ineffective when seizure is sub-threshold or

pharmacologically blocked. Having a generalized seizure, is crucial to antidepressant effect of ECT.

Biochemical Theory
Variety of biochemical changes in neurotransmitters,

that are also implicated in the therapeutic effect of antidepressant medications. Serotonin , Norepinephrine Alteration in concentration or up-regulation of their receptors.

Rise in seizure threshold

The chemical changes responsible for terminating

the generalized seizure may play larger role in ECT effect. These chemical changes lead to gradual rise in the seizure threshold over a course of ECT.

Hippocampal Neurogenesis
Some neuroimaging studies have shown reduced

hippocampal volumes in depressed patients. Increased brain derived neurotrophic factor (BDNF) levels in hippocampus. Increased mossy fiber sprouting and and neurogenesis in the hippocampus

Indications for ECT

Major depression, particularly with psychotic

features. Bipolar illness (depressed, manic and mixed states) Schizophrenia (acute exacerbations) Catatonia

Other indications
Parkinsonism Status epilepticus Neuroleptic Malignant syndrome

Indications in Depression
Medication failure Medically ill, where antidepressants are precluded

(arrhythmias) Delusionally depressed Previous ECT responders Requesting ECT

Contraindications
Absolute None Relative Cardiovascular (Coronary artery disease, HTN, aneurysms, arrhythmias) Cerebrovascular effects (Recent strokes, space occupying lesions, aneurysms) Other conditions like Pregnancy and high anesthesia risk

Pretreatment Evaluation
Complete medical and psychiatric history. Physical examination CBC

Electrolytes
EKG CXR

Informed Consent
Fully explain the risks and benefits of procedure and

answer questions from patients or their relatives. Videotapes Information sheets Reduce patients anxiety and help establish good patient-doctor relationship

Concurrent medications
Psychotropic medications are discontinued during a

course of ECT to avoid interactions. Early morning hours NPO for 6-8 hours prior to ECT

Antidepressants
TCAs and MAOIs are discontinued to minimize

possible CVS complications. Newer generation SSRIs may be safer during ECT. Lithium may cause delirium when co-administered with ECT.

Anticonvulsants
They are not contraindicated but raise the electrical

stimulus necessary to induce seizure. For patients with pre-existing seizure disorder, it is safe to continue anticonvulsants and simply use a higher intensity stimulus.

Benzodiazipines
Usually withheld because they raise the seizure

threshold and may increase the degree of post-ictal confusion particularly in the elderly patient. Pre-ECT anxiety or insomnia may be managed by Benadryl or low dose neuroleptic.

Use of Anesthesia
Rapid induction with Amnesia Methohexitol, 0.5-1 mg/kg, agent of choice, rapid onset and short duration of action, little impact on seizure threshold. Propofol, 0.5-2mg/kg, it raises the seizure threshold. Prevention of injury from seizure Succinylcholine, the most commonly used agent today. Attenuation of sympathetic response Beta blocker like labetolol 10-20 mg IV, prior to induction.

Seizure induction
Electrode placement Two standard electrode placements In unilateral, both electrodes are placed on the same hemisphere, typically on non dominant right hemisphere. In bilateral, electrodes are placed symmetrically over the frontotemporal areas. Stimulus intensity Newer devices deliver constant-current brief-pulse stimulus of electricity Seizure properties The induced seizure must generalize. The optimal duration is more than 25 seconds. EEG monitoring is used to determine the nature of the induced seizure.

Complications
Mortality 1-3/10,000 Majority of ECT related deaths are due to cardiovascular complications.

Cognitive complications Post-treatment confusion: A brief (15-30 minutes) period of confusion immediately following treatment is seen in 10%. Delirium: Seen in elderly, with pre-existing dementia, with neurological impairment and with bilaterally applied ECT Memory loss: Associated with anterograde (returns to baseline 2-6 months post-ECT) and retrograde amnesia