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Electroconvulsive therapy
- 2. WHAT IS ECT? Electroconvulsive therapy (ECT), also known as electroshock therapy, is a standard psychiatric treatment in which electricity is delivered through the scalp to induce a controlled tonic clonic seizure, usually at regular interval, to achieve an improvement in an abnormal mental state. It is estimated that about one million patients worldwide and 100,000 in the United States received ECT annually. Its safety and efficacy has been much improved with modification of various aspects of the technique such as optimization of the stimulus energy, electrode placement, the use and optimization of general anesthesia, as well as improvement in cardiopulmonary management.
- 3. History In 16th century, the Swiss physician Paracelsus gave camphor by mouth to induce convulsions and “cure lunacy.” In 18th & 19th century,several cases of convulsions induced by chemical means were documented.
- 4. History Manfred Sakel was the developer of insulin shock therapy. He noted that insulin induced coma and convulsions had a change in the mental state of drug addicts and psychotics. Complications were high.
- 5. History In 1934, Lazlo Meduna, a Hungarian psychiatrist,injected camphor in oil into a catatonic schizophrenia, causing grand mal seizure. After series of such treatments patients recovered. Later Camphor was replaced by pentylenetetrazol.
- 6. History Pentylenetetrazol caused lot of unpleasant sensations. The concept of applying electricity was developed. Swiss scientists induced seizures in dogs using direct electrical current.
- 7. Birth of Ect Italian scientists, Ugo Cerletti and Lucio Bini subsequently succeeded in applying electricity directly to the human scalp. In 1938, they treated an unidentified 39-year-old man who was found delusional in a train station. He recovered fully after 11 treatments without adverse Effects.
- 8. History 1940- Ect was introduced in the US with use of curare as a muscle relaxant. 1951- introduction of succinylcholine. 1970-most common electrode position for right unilateral ECT is developed.
- 9. ELECTROPHYSIOLOGY Neurons maintain a resting membrane potential across plasma membrane. Normal brain activity is desynchronized,neurons fire action potential asynchronously. A convulsion or seizure occurs when a large percentage of neurons fire in unison. The rhythmical change in extracellular potential entertain the neighbouring neurons and propagates the seizure activity across the cortex into deeper structures. Eventually the entire brain shows high voltage synchronous neuronal firing.
- 10. How does ECT work? Neurotransmitter theory Neuro-endocrine theory Anti-convulsant theory Brain damage theory Psychological theory
- 11. ECT AND NEUROTRANSMITTER It has been seen that there are subtle changes in the neurotransmitter receptor and second messenger system. Virtually all the neurotransmitter system are affected. A series of ECT session show a downregulation of postsynaptic β-adrenergic receptors. Reported changes in dopamine,muscarinic and cholinergic receptors have been found. However,effect of ECT on serotonergic neurons remain controversial. In second messenger system,ECT has been reported to effect G-protein coupling to receptors Activity of adenyl cyclase and phospholipase c Regulation of calcium entry into neurons
- 12. Neuroendocrine Theory • The seizure causes the hypothalamus to release chemicals that cause changes throughout the body.The seizure may release a neuropeptide that regulates mood. Brain damage theory • Shock damages the brain,causing memory loss and disorientation that creates an illusion that problems are gone,and euphoria,which is a frequently observed result of brain injury.
- 13. Psychological Theories • Depressed people often feel guilty,and ECT satisfies their need for punishment. Alternatively, the dramatic nature of ECT and the nursing care afterwards makes patients feel they are being taken seriously –the placebo effect.
- 14. ANTICONVULSANT ROLE OF ECT ECT itself act as an anticonvulsant because its administration is associated with an increase in seizure threshold as treatment progress. Recent data shows that 1-2 months following an ECT session,EEG records a large increase in the slow wave delta activity in pre frontal cortex. Decreased slow wave sleep has been found to be associated with increased negative symptoms. ECT have been found to regulate cellular mechanism of memory an mood regulation. It has been hypothesized that ECT increases blood brain permeability resulting in increased drug delivery.
- 15. Mechanism of action Biological theories- they are related to ect's anticonvulsant effects. These effects manifest during a course of ECT. They include – progressive increases in seizure threshold. – progressive decrease in seizure duration. – increases in inhibitory neurotransmitters. – decreases in excitatory neurotransmitters.
- 16. Mechanism of action Recent studies- – Transient induction of increased proinflammatory cytokines, – Increased expression of brain-derived neurotrophic factor (BDNF), – Gene polymorphism, – Enhanced activity in the GABAergic, glutaminergic and dopaminergic systems, – Enhance neurogenesis, synaptogenesis and remodelling of synapses in hippocampus
- 17. Effects of ECT During ECT, brain imaging shows- Hypermetabolic state – increases in cerebral blood flow (CBF). – increase cerebral metabolic rate (CMR). Post-ictal state- functional suppression – decreases in CBF. – decrease in CMR. Also during & after ECT, there are δ waves indicating reduction in neural activity.
- 18. TYPES OF ECT A) According to technique: Direct ECT Modified ECT B) According to placement of electrodes Bilateral Unilateral
- 19. Electrode placement Bilateral Introduced first Electrodes are placed apart over each hemisphere. More rapid therapeutic response. Mc- Bitemporal. Unilateral Both electrodes placed apart over non dominant hemisphere. Less marked cognitive adverse effects. Mc- Right unilateral.
- 20. Electrode placement Bilateral Electrode is placed 2.5 -4cm above the midpoint of line joining tragus& lateral canthus both the side. Most common- Bitemporal. Unilateral One electrode is placed over the non dominant frontotemporal area. Another electrode usually placed on the nondominant centro-parietal scalp,just lateral to midline vertex.
- 22. Electrical Principles Electrical stimulus is delivered via a variety of waveforms. Cycles of negative and positive current flow is referred as frequency of the stimulus. Two types of waveforms:- Sine wave waveforms Brief square waveforms
- 23. Sine wave Waveforms Sine wave currents are characterized by a continuous stream of electricity that flows in alternating directions. The number of alterations in direction, or cycles of negative and positive current flow, is referred to as the frequency of the stimulus and is measured in hertz (Hz), defined as the number of cycles per second.
- 24. Brief Pulse ECT The brief pulse consists of a series of instantaneously rising and falling rectangular pulses of current, with adjacent pulses separated by brief periods of no electrical activity. Brief pulses are characterized by pulse width Frequency Duration The duration of each pulse is referred to as the pulse width, which is measured in milliseconds.
- 25. Ultra-Brief Pulse ECT “Brief ” pulse has a pulse width of 0.5–2.0 ms,whereas the width of an “Ultra-brief ” pulse is less than 0.5 ms.
- 26. Seizure Threshold Amount of electricity necessary to induce a seizure. It is a parameter that is integral to stimulus dosing in clinical practice. The physiological efficiency of the brief pulse stimulus in activating brain neurons is more optimal than the sine wave because of its rapid rise and fall.
- 27. Seizure Characteristics An adequate seizure is defined as – Motor seizure > 25 sec. – EEG seizure of 30-120 sec. – Rise of HR by > 50% during seizure. – Post-ictal rise in prolactin.
- 28. Mode of Stimulus Delivery In addition to the type of waveform used, ECT devices differ in whether they administer the stimulus via a constant current or constant voltage.
- 29. Indications Major depressive disorder Failed medication trials Medication intolerance Severe or psychotic symptoms Acutely suicidal or homicidal Markedly agitated or stupourous Acute Manic episode Acute episodes in Schizophrenia. Catatonic Schizophrenia Parkinson’s disease.
- 30. Suicidal patient including Depressed suicidal pregnant patient who cannot take medicatons Geriartic patients who cannot take antidepressants Depressed suicidal children or adolescent who are not responding to drugs Obsessive compulsive disorder Delirium Other medical condition: Neuroleptic malignant syndrome Hypopituatarism Intactable seizure disorder
- 31. Contra-indications ECT has no absolute contraindications. Patient with space occupying lesion in cns are at increased risk for edema and brain herniation after ECT. Small lesion-pretreatment with dexamethasone is given. Increased intracranial pressure-increased risk of cva Patient with Acute MI-increased risk,Risk decreases 2 weeks later Patients with hyprtension should be stabilized.
- 32. Contra-indications Relative-. – Vascular aneurysm. – Recent Intra cranial hemorrhage. – Retinal detachment. – Pheochromocytoma. – Anesthesia risk.
- 33. Clinical guidelines A proper explanation about the benefits and adverse effects of ECT should be given to patient and their attendants. An informed consent should be taken properly. Involuntary is only for those patients who urgenly need the treatment and whose legally appointed guardian has given a written informed consent. Clinician must be aware of the local,state and federal laws about ECT use.
- 34. Pretreatment evaluation Complete medical history General physical examination Sysemic examination, Neurological examination Pre-anaesthetic examination Routine examination: Chest x-ray,Fundus ECG,serum electrolytes Blood and urine routine examination X-ray spine(in case of seizure disorder or sol ct/mri has to be performed) Dental examination
- 35. Clinical guidelines Cognitive evaluation and monitoring Pre-ect evaluation of: Memory Orientation Comprehension Attention Concentration Use of standard scale such as MMSE is useful.
- 36. Clinical guidelines Concomitant medication has to be discontinued Bezodiazepines anticonvulsant action Lithium increased post ictal delirium and may prolong seizure activity Clozapine development of late appearing seizure Buropion development of late appearing seizure Lidocaine markedly increases the seizure threshold Theophylline increased duration of seizure Reserpine compromise respiratory and cardiovascular system
- 37. Clinical guidelines Concomitant medications • Usage of following drug is considered safe • Tricyclics • Monoamine oxidase • Antipsychotic
- 38. Clinical guidelines Patient should not be given anything orally for 6 hours before treatment Patient mouth should be checked for any denture or foreign objects. IV line should be secured. A bite block is inserted just prior to administering the treatment. 100% oxygen @5 litre per minute is administered prior to and after the treatment is administered until spontaneous respiration returns. Emergency equipments for establishing an airway should be available.
- 39. Clinical guidelines Muscarinic anticholinergic drugs • Minimize oral and respiratory secretions . • Block bradycardia and asystole. • Should be used unless heart rate is above 90 beats per minute. • Should be used in patients on β blockers and with ventricular ectopic beats. • Most commonly used drug is atropine. • Dose:0.3 to 0.6 mg i.m. • Alternative drug :glycopyrrolate
- 40. Clinical guidelines Anaesthesia • general anaesthesia • Depth of anaesthesia :light • Most commonly used anaesthetic: • Methohexital[dose: 0.75 to 1.0mg/kg iv bolus) • Advantage short duration of action • Lower post ictal arrhythmias • Other alternative anaesthetics used: Etomidate,ketamine alfentanil,propofol
- 41. Clinical guidelines Muscle Relaxant • Given within minutes of injection of anaesthetics to reduce the motor activities during seizure. • Prevent muscle and bony injury. • Goal is profound relaxation of muscle not paralysis. • Most used muscle relaxant: succinylcholine[dose:0.5 to 1 mg/kg]. • Disappearance of fasciculation which occurs in rostro-caudal direction after peripheral nerve stimulation indicate maximum muscle relaxation. • If the patient is known to have pseudocholinesterase deficiency, atracurium is used instead of succinylcholine.
- 42. The Procedure Stimulus is given in cycles. Each cycle contains a positive and negative wave. Old machine used sine wave. Modern ECT machine used a brief pulse waveform. A common technique is to initiate treatment at a stimulus less than seizure threshold. Then gradually the intensity is increased by 100% for unilateral placement and for bilateral placement till seizure threshold is reached.
- 43. Induced Seizure A brief muscle contraction usually strongest in patient’s jaw and facial muscle is seen concurrently with the flow of stimulus current,regardless of weather a seizure occur or not The first behavioural sign of seizure is often a plantar extension which lasts for 10-20 seconds and mark the tonic phase The tonic phase is marked by a higher frequency,sharp eeg activity on which a high frequency muscle artifact may be superimposed. Rhythmic/clonic contraction that decrease in frequency and finally disappears During the clonic phase burst of polyspiky activity occur simultaneously with contraction.
- 44. If seizure could not be induced Upto 4 attempts to induce seizure can be tried during the course of treatment. Sometimes the onset of seizure activity is delayed by 20-40 second after induction of stimulus. If stimulus fails to induce seizure, the contact between the electrode and skin should be checked. Intensity of stimulus can be increased by 25-100%. Anesthetic agent can be changed to reduce the seizure threshold. Additional procedures: Hyperventilation Administration of 500-2000 mg iv caffine sodium benzoate 5-10 mins prior to stimulus.
- 45. Number and spacing of ECT ECT treatments are usually administered 2-3 times per week. Twice weekly treatments are associated with less memory impairment. MDD-6-12 treatment Manic episodes -8 to 20 treatments. Schizophrenia more than 15 treatments Catatonia- 1 to 4 treatments Delirium-1to 4 treatment
- 46. ECT Treatment Course Treatment should continue until patient achieves what is considered the maximal therapeutic response. Maximal therapeutic response-the point of maximal improvement is thought to occur when a patient fails to continue to improve after 2 consecutive treatments. Further treatment does not yield any further benefits. Patients not improving after 6 to 10 sessions –bilaterally placed,high density treatment should be attempted before ECT is abandoned.
- 47. Multiple Monitored ECT Giving multiple ECT stimulus during a single session. Most commonly 2 bilateral stimuli within two minutes. Indicated in severely ill patients MMect is associated with most frequent occurences of serious cognitive adverse effects.
- 48. Maintenance Treatment Short term course of ECT induces a remission in symptoms but does not ,of itself,prevent relapse. Post ECT maintenance treatment should always be considered. Indication: Rapid relapse after initial ECT Severe symptoms Psychotic symptoms
- 49. Failure of ECT trial Failed ECT patient should again be treated with pharmacological agents. Studies have shown that patient unresponsive to antidepressants priorly do respond after a course of ECT treatment with the same medications.
- 50. Mortality Mortality rate with ECT is about 0.002 percent per treatment. Ect death are mostly due to cardiovascular complications and most likely to occur in patients whose cardiac status is already compromised.
- 51. Adverse effects CNS: Headache Confusion Delirium Marked confusion in 10% patients within 30 minutes of seizure Delirium is usually more pronounced After the first few treatments In patients who receive bilateral ECT Coexisting neurological disorder Visuospatial functioning errors.
- 52. Adverse effects Memory:memory impairment is the worst adverse side effect. Data indicates that almost all patient are back to their cognitive baseline after 6 months. Some patient complain of persistent memory difficulties. Memory impairment and time to return to baseline cognitive functioning is directly proportional to intensity of electrical stimulus. Patient of dementia with depression are at risk for greater adverse cognitive effects,delirium and confusion.
- 53. Adverse effects Retrograde amnesia • It is most marked for events occurring in the weeks or months before treatment. • One study showing that some people lose memories from years prior to treatment. • Recovery of such memories is usually complete by seven months post treatment with the only enduring loss being memories in the weeks and months prior to the treatment.
- 54. Adverse effects Anterograde Amnesia • It is usually limited to the time of treatment itself or shortly afterwards. • In the weeks and months following ECT these memory problems gradually improve. • Some people have persistent losses with bilateral ECT.
- 55. Respiratory System: Along with cardiac disease it is leading cause of mortality and morbidity. Its effects are mostly associated with anaesthesia procedure. Muscle relaxant can cause cessation of breathing. There may be exaggeration of asthma or chronic obstructive pulmonary disease. Increased secretion,aspiration and pulmonary edema. Pseudocholinestrase deficiency leads to decreased metabolism of succinylcholine.
- 56. • Due to direct stimulation of jaw muscle,patient bite down;unstable teeth may be broken and dislodged. Dental • Fracture of long bone and spine are common but in modified ECT they are less common. • Precautions should be taken in elderly patient, osteoporotic patient and temporomandibular joint problem. • Myalgia is common in first session. Musculoskeletal
- 58. Reference 1. Kho KH, van Vreeswijk MF, Simpson S, Zwinderman AH. A meta-analysis of electroconvulsive therapy efficacy in depression. J ECT 2003;19:139-47. 2. Medda P, Toni C, Perugi G. The mood-stabilizing effects of electroconvulsive therapy. J ECT 2014;30:275-82. 3. Versiani M, Cheniaux E, Landeira-Fernandez J. Efficacy and safety of electroconvulsive therapy in the treatment of bipolar disorder: A systematic review. J ECT 2011;27:153-64. 4. Mukherjee S, Debsikdar V. Unmodified electroconvulsive therapy of acute mania: A retrospective naturalistic study. Convuls Ther 1992;8:5-11. 5. Mukherjee S, Sackeim HA, Lee C. Unilateral ECT in the treatment of manic episodes. Convuls Ther 1988;4:74-80. 6. Bharadwaj V, Grover S, Chakrabarti S, Avasthi A, Kate N. Clinical profile and outcome of bipolar disorder patients receiving electroconvulsive therapy: A study from North India. Indian J Psychiatry 2012;54:41-7. 7. Fraser LM, O’Carroll RE, Ebmeier KP. The effect of electroconvulsive therapy on autobiographical memory: A systematic review. J ECT 2008;24:10-7. 8. Schat A, van den Broek WW, Mulder PG, Birkenhäger TK, van Tuijl R, Murre JM. Changes in everyday and semantic memory function after electroconvulsive therapy for unipolar depression.
- 59. Refrence 9. Vamos M. The cognitive side effects of modern ECT: Patient experience or objective measurement? J ECT 2008;24:18-24. 10. Porter RJ, Douglas K, Knight RG. Monitoring of cognitive effects during a course of electroconvulsive therapy: Recommendations for clinical practice. J ECT 2008;24:25-34. 11. Mayur P, Byth K, Harris A. Autobiographical and subjective memory with right unilateral high-dose 0.3-millisecond ultrabrief-pulse and 1-millisecond brief-pulse electroconvulsive therapy: A double-blind, randomized controlled trial. J ECT 2013;29:277-82. 12. Rami-Gonzalez L, Bernardo M, Boget T, Salamero M, Gil-Verona JA, Junque C. Subtypes of memory dysfunction associated with ECT:Characteristics and neurobiological bases. J ECT 2001;17:129-35. 13. Semkovska M, McLoughlin DM. Measuring retrograde autobiographical amnesia following electroconvulsive therapy: Historical perspective and current issues. J ECT 2013;29:127-33. 14. Ingram A, Saling MM, Schweitzer I. Cognitive side effects of brief pulse electroconvulsive therapy: A review. J ECT 2008;24:3-9. 15. Prudic J, Peyser S, Sackeim HA. Subjective memory complaints: A review of patient self-assessment of memory after electroconvulsive therapy. J ECT 2000;16:121-32. 16. Brakemeier EL, Berman R, Prudic J, Zwillenberg K, Sackeim HA. Self-evaluation of the cognitive effects of electroconvulsive therapy. J ECT 2011;27:59-66.