1 / 29

Electro Convulsive Therapy

Electro Convulsive Therapy. Mohammed Jafferany, MD Resident H-R Psychiatry Program. Introduction. Recent resurgence in past decade Excellent safety profile Superior Efficacy Economic benefits Less stigmatization. History. Early Theories Theory of Biological Antagonism

alexia
Download Presentation

Electro Convulsive Therapy

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Electro Convulsive Therapy Mohammed Jafferany, MD Resident H-R Psychiatry Program

  2. Introduction • Recent resurgence in past decade • Excellent safety profile • Superior Efficacy • Economic benefits • Less stigmatization

  3. History • Early Theories • Theory of Biological Antagonism • Insulin Shock Therapy • Electrically induced seizures • Improvements in Anesthesiology

  4. 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.

  5. 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.

  6. 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.

  7. 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.

  8. 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.

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

  10. Psychodynamic Theories • The beneficial effect of ECT is to its fulfillment of the need for punishment in the self loathing, depressed patient.

  11. Placebo Effect • The beneficial effects are due to wishful thinking on the part of the staff and the patient

  12. 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.

  13. 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.

  14. 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.

  15. 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.

  16. 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

  17. Indications for ECT • Major depression, particularly with psychotic features. • Bipolar illness (depressed, manic and mixed states) • Schizophrenia (acute exacerbations) • Catatonia

  18. Other indications • Parkinsonism • Status epilepticus • Neuroleptic Malignant syndrome

  19. Indications in Depression • Medication failure • Medically ill, where antidepressants are precluded (arrhythmias) • Delusionally depressed • Previous ECT responders • Requesting ECT

  20. 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

  21. Pretreatment Evaluation • Complete medical and psychiatric history. • Physical examination • CBC • Electrolytes • EKG • CXR

  22. Informed Consent • Fully explain the risks and benefits of procedure and answer questions from patients or their relatives. • Videotapes • Information sheets • Reduce patient’s anxiety and help establish good patient-doctor relationship

  23. 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

  24. 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.

  25. 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.

  26. 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.

  27. 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.

  28. 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.

  29. 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

More Related