dr.faisal electro convulsive therapy
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Electro Convulsive Therapy
(ECT)
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Introduction
Recent resurgence in past decade
Excellent safety profile
Superior Efficacy
Economic benefits Less stigmatization
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History
Early Theories
Theory of Biological Antagonism
Insulin Shock Therapy
Electrically induced seizures Improvements in Anesthesiology
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Early Theories
Hippocrates: Documented the cure of insane patientfollowing malaria-induced seizures.
Swiss physician Paracelsus in 1500s,induced
seizures with oral camphor to treat mania andpsychosis.
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Biological Antagonism Theory
Hungarian physician Meduna in 1934reported aninherent biological antagonism betweenschizophrenia and epilepsy.
He reported beneficial effects of seizures induced bycamphor in catatonic patient.
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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.
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Electrically induced Seizures
In 1937, Italian physicians Cerletti & Bini appliedelectricity to head to induce therapeutic seizures.
First patient had catatonia and he improved.
Safer than chemically induced seizures.
Widespread acceptance through out Europe andUSA.
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Improvements in Anesthesiology
Early period complications like bone fractures andpatient discomfort.
Use of Curare, as muscle relaxant, by Bennett in
1940allowed complete paralysis of patient duringseizure.
Development of short acting IVbarbituratesin1950sallowed rapid induction of sedation and
amnesia surrounding procedure.
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Mechanism of Action
Psychodynamic theories
Placebo effects
Memory Eraser
Seizure as curative agent
Biochemical changes
Therapeutic effects of rise in seizure threshold
Hippocampal Neurogenesis
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Psychodynamic Theories
The beneficial effect of ECT is to its fulfillment of theneed for punishmentin the self loathing, depressedpatient.
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Placebo Effect
The beneficial effects are due to wishful thinking onthe part of the staff and the patient
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Memory Eraser
Beneficial effects of ECT are related to its ability todisturb recent memory, thereby erasing the recall ofrecent traumas, that led to depressive episode.
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Seizure, as Curative event
ECT is ineffective when seizure is sub-threshold orpharmacologically blocked.
Having a generalized seizure, is crucial to
antidepressant effect of ECT.
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Biochemical Theory
Variety of biochemical changes in neurotransmitters,that are also implicated in the therapeutic effect ofantidepressant medications.
Serotonin, Norepinephrine Alteration in concentration or up-regulation of their
receptors.
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Rise in seizure threshold
The chemical changes responsible for terminatingthe generalized seizure may play larger role in ECTeffect.
These chemical changes lead to gradual rise in theseizure threshold over a course of ECT.
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Hippocampal Neurogenesis
Some neuroimaging studies have shown reducedhippocampal volumesin depressed patients.
Increased brain derived neurotrophic factor (BDNF)levels in hippocampus.
Increased mossy fiber sprouting and andneurogenesis in the hippocampus
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Indications for ECT
Major depression, particularly with psychoticfeatures.
Bipolar illness (depressed, manic and mixed states)
Schizophrenia (acute exacerbations) Catatonia
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Other indications
Parkinsonism
Status epilepticus
Neuroleptic Malignant syndrome
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Indications in Depression
Medication failure
Medically ill, where antidepressants are precluded(arrhythmias)
Delusionally depressed Previous ECT responders
Requesting ECT
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Contraindications
Absolute None
Relative Cardiovascular(Coronary artery disease, HTN, aneurysms,
arrhythmias) Cerebrovascular effects(Recent strokes, space occupying
lesions, aneurysms)
Other conditions like Pregnancyand high anesthesia risk
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Pretreatment Evaluation
Complete medical and psychiatric history.
Physical examination
CBC
Electrolytes EKG
CXR
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Informed Consent
Fully explain the risks and benefits of procedure andanswer questions from patients or their relatives.
Videotapes
Information sheets Reduce patients anxiety and help establish good
patient-doctor relationship
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Concurrent medications
Psychotropic medications are discontinued during acourse of ECT to avoid interactions.
Early morning hours
NPO for 6-8 hours prior to ECT
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Antidepressants
TCAs and MAOIsare discontinued to minimizepossible CVS complications.
Newer generation SSRIs may be safer during ECT.
Lithiummay cause delirium when co-administeredwith ECT.
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Anticonvulsants
They are not contraindicated but raise the electricalstimulus necessary to induce seizure.
For patients with pre-existing seizure disorder, it is
safe to continue anticonvulsants and simply use ahigher intensity stimulus.
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Benzodiazipines
Usually withheld because they raise the seizurethreshold and may increase the degree of post-ictalconfusion particularly in the elderly patient.
Pre-ECT anxiety or insomnia may be managed byBenadryl or low dose neuroleptic.
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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 seizurethreshold.
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.
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Complications
Mortality 1-3/10,000
Majority of ECT related deaths are due to cardiovascularcomplications.
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, withneurological impairment and with bilaterally applied ECT
Memory loss:Associated with anterograde (returns to baseline 2-6
months post-ECT) and retrograde amnesia