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Electroconvulsive Therapy and other Neurostimulation Techniques Dr. Patrick Clarke

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Major Depression Australian figures: 1 in 4 females 1 in 6 males 1 in 7 General Practice presentations (MJA 2008) 4 th most frequent managed condition in General Practice in 2004-2005

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Major Depression By 2020 predicted to be 2 nd main cause of disability worldwide (WHO, 1998). Over 50% of patients are severely depressed (Kendler et al, JAMA June 2003) STAR*D study demonstrates that clinical benefit declines with increased previous treatment failure. Relapse rate increases with each level.

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Major Depression Failure to achieve initial remission leads to worse long term outcomes (Judd et al, J Affect Disord 1998) With repeated episodes there is less need for a precipitating stressor (Kendler et al, AJPsych 2000).

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Major Depression Few proven effective and tolerated treatments in pharmacoresistent patients Significant unmet need Reduced compliance with increased treatment resistance

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Stages of TRD STAR*D Stage I Failure of 1 AD Stage II Failure of 2 classes of AD. Stage III Failure of 2 classes of AD plus TCA. (Remission with next intervention 13%) Stage IV Failure of 2 classes of AD plus TCA, plus MAOI. (Remission with next intervention 14%) Stage V Above plus failure of BL ECT. (Remission with next intervention 13%).

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Suicide 1987: 2,240 people died by suicide in Australia Since 1990, more male deaths in Australia have been attributed to suicide than to non- intentional motor traffic fatalities. Overall rate is stable at 11 per 100,00 population per year

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Electroconvulsive Therapy History Hippocrates saw that insane patients showed reduced symptoms after suffering from convulsions brought on by malaria Physician used an electric eel to cure headaches of the Roman emperor Claudius in AD 47 In the 1800s there were reports of insanity being cured with electric shock Chemically induced seizures used as treatment for schizophrenia in 1934 by Hungarian physician, Laszlo Meduna First human treatment in 1938, by Cerletti and Bini. Performed unmodified until 1950s to 1960s.

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ECT Historical Early machines provided the current in sine wave distribution. Energy inefficient and correlates with increased cognitive ADR. Replaced by machines providing the current in a series of pulses. Initially these were fixed dose (high), e.g. Kabtronics. Nevertheless, charge could vary according to pulse width, frequency, and current. Sackeim 1990 introduced dose titration.

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Electroconvulsive Therapy in Adelaide 2010-2011 6393 ECT treatments were given: 59% in public hospitals 41% in private hospitals. People from their 20s to their 80s receive ECT, with the majority in their 60s and 70s. ECT treatments: 69% inpatient/acute 20% maintenance 11% outpatient

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ECT Mechanism of action Mechanism of action remains unclear. Seizure is necessary, and for RUL ECT therapeutic dose is several times seizure threshold (Sackeim 1990). Seizure threshold varies 80 fold within the general population, and is influenced by age, gender, etc. Seizure results in changes in Serotonin receptors (5HT2). More recent theories focus upon how the brain physiology is recruited to bring the seizure to a halt.

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Physiology During ECT an electrical stimulus is delivered through the scalp and skull to the brain, which depolarises a sufficient number of neurones to cause a generalised seizure. With BL ECT, the seizure is believed to occur by direct activation of diencephalic nuclei. With RUL ECT, underlying cortical structures are activated first with a secondary activity arising in large pyramidal cell fields and related dendritic fields.

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EEG Post stimulus there is a recruiting phase. During the tonic and early clonic phase there is high voltage polyspike activity which decreases in frequency. The clonic motor response is followed by high amplitude slow waves. This is replaced by post-ictal suppression. The ictal EEG lasts longer than the motor activity.

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Recruitment Tonic phase of seizure The following four slides show a typical two lead EEG during an ECT treatment Robert Ostroff

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Clonic phase of seizure Robert Ostroff

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End of Motor Seizure Robert Ostroff

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Postictal Suppression Robert Ostroff

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Indications Major Depression Psychotic Agitated Retarded Treatment Resistant With significant risk

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Bipolar Affective Disorder Depressive Episode Manic Episode

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Schizophrenia Acute With Affective symptoms Catatonic Chronic, unresponsive to other treatment.

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Puerperal Disorders Post Natal Depression Puerperal Psychosis

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Other Neuroleptic Malignant Syndrome Parkinsons Disease Status Epilepticus

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Contraindications There are few true contraindications, provided that the patient is deemed fit for General Anaesthetic. Raised Intracranial Pressure.

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Work Up History of ECT, medical, G.A., allergies. Physical examination (Fundoscopy). CBE, MBA20, TFTs. ECG. CXR. CT Head. Consent (inform patient and family). Fasting.

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Side Effects and Risks Risk of G.A. (Mortality 1/64,000). Headache. Muscle Ache. Cognitive: Delerium, STM, Autobiographical Memory Loss. There is no evidence of structural brain damage.

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Dental: use a bite block. Enzyme deficiency. Burns. Mania. Prolonged seizure.

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Efficacy In Psychotic and Melancholic Major Depression, without comorbidity, remission rates over 80%, often over 90% achieved. Most efficacious treatment available for endogenous depression. High relapse rate i.e. 43% in 6 months, 46% in 12 months, if no maintenance treatment provided.

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Special Circumstances Cardiovascular Bradycardia occurs due to vagal stimulation. Catecholamine release associated with the seizure corrects this. May require Atropine. Cardiac Pacemakers and Defibrillators. HT. MI. Greatest risk in the first 10 days

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Endocrine Addisons Disease: ECT causes a transient adrenocortical stimulation, and increased corticosteroids may be required prior to ECT. Diabetes: exclude hypoglycaemia prior to ECT Thyroid: Treat hyperthyroidism as ECT can induce thyroid storm. Phaeochromocytoma.

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Metabolic Dehydration: risk of DVT. Hyperkalaemia: increased risk of cardiac arrhythmias. Hyponatraemia: Occurs with SIADH, seen occasionally with antidepressants and antipsychotics. Lowers seizure threshold.

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Neurological Dementia: increased risk of cognitive ADR. May need to space treatments. Epilepsy: Anticonvulsants raise seizure threshold. Raised intracranial pressure and intracranial masses: small, slow growing masses unlikely to cause problems. MS: Generally tolerate ECT well. Parkinsons Disease: ECT increases the permeability of the BBB, and therefore concomitant LDopa can increase to toxic levels. CVA: Wait 1 month or more.

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GOR Increased risk of aspiration, therefore, consider Ranitidine, or cuffed endotrachael tube.

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Ophthalmic ECT causes a brief increase in intraocular pressure, problematic in open-angle glaucoma.

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Pregnancy Not contraindicated. Fetal monitoring is not routine.

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Elderly ECT efficacious in elderly. Have higher seizure threshold. May require longer courses. EEG may be less impressive.

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Respiratory Disorders Sleep Apnoea: CPAP Machine available in Recovery.

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Skull Defect Avoid area of the defect. Avoid area of metal plates.

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Urine retention Catheterise.

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Concomitant Medication Antidepressants: MAOI may be associated with hyper-reflexia, seizures, and hypertension or hypotension. Anticonvulsants: increase seizure and should be avoided. If prescribed for epilepsy, continue. Antipsychotics: Clozapine can result in increased confusion with ECT. Lithium: Delerium, associated with increased permeability of BBB.

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Anaesthetics Monitoring: Pulse Oximetry and ECG. Induction: Propofol. Shorter seizure than Thiopentone. Methohexitone not available. Muscle Relaxant: Suxamethonium. Cuff Technique.

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Electrode Placement

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Electrical Stimulus

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Seizure Threshold

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Seizure Duration

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Dose Titration

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Continuation ECT

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Maintenance ECT

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Standard ECT Variations in Electrical Dose and Electrode Placement Less EfficacyMore Efficacy Less Side Effects More Side Effects Unilateral ECTBilateral ECT Low DoseHigh Dose

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Ultrabrief ECT A relatively recent advance in ECT has been the development of ultrabrief ECT. This uses a pulse width of 0.3 ms, compared with 1.0 ms used in standard pulse ECT. This results in the use of a far smaller stimulus dose in order to induce a seizure, and consequently a reduction in cognitive side effects, comparable to placebo (Sienaert 2010, Loo 2008, Sackheim 2008). Ultrabrief ECT has been associated with a slightly longer course of ECT (30 to 50% longer), and the need to switch to standard pulse ECT in 20 to 50% of patients who show inadequate response.

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Pulse and sine wave comparison. Energy = area under curve

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Stimulus Parameters Standard Pulsewidth Amplitude Duration 1 cycle. Frequency = No. cycles/second Ultrabrief Pulsewidth 0.5-2ms 0.2-0.4 ms

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ECT Study Ultrabrief ECT was introduced to 2 private psychiatric hospitals in Adelaide, The Adelaide Clinic and Fullarton Private Hospital, in August 2010. Data was gathered between August 2010 and April 2012 on patients receiving an acute course of ultrabrief ECT or standard pulse ECT. The treating Psychiatrist, together with the patient, decided whether patients would receive ultrabrief or standard pulse ECT.

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ECT was administered using a Thymatron Series IV ECT machine. The right unilateral electrode placement was used for all ultrabrief patients and was also most commonly used for patients receiving standard pulse width ECT. UB ECT was given at 5 to 6 times the seizure threshold, with a 0.3 ms pulse width, and standard pulse ECT was given at 3 to 5 times seizure threshold, with a 1.0 ms pulse width.

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Rating Scales included Montgomery-Asberg Rating Scale (MADRS), Mini-Mental State Examination (MMSE), and Zung Self-Rated Depression Scale (Zung). Data was gathered by trained nursing staff prior to treatment commencing, weekly during treatment, and after completion of the course.

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Results Total of 252 patients. 190 commenced UB ECT, and 35 (18.4%) changed to standard ECT during their course. 62 commenced standard ECT, and 3 (4.8%) changed to UB during their course. Loo 2008, reported that 41 of 74 (55.4%) patients switched from UB ECT.

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Total Patients Receiving ECT

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Number of ECT The Mean number of treatments for UB ECT was 10.1, versus 8.0 for Standard Pulse. This compares with the findings of Loo 2008 of 10.3 for UB ECT, and 7.6 for Standard Pulse. The longer course translates into an average 27% longer LOS for patients receiving UB cf patients receiving SPW. Patients who switch have the longest LOS, reflecting their relatively treatment resistant status.

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Number of treatments Number of Treatments MeanStandard Deviation MinimumMaximum Ultrabrief10.14.0125 Standard Pulse8.03.1118 UB change to Standard 8.63.4319 Patients receiving a full course of ultra-brief ECT had significantly more treatments than patients receiving a full course of standard pulse width ECT (t(212)=3.76, p