Electroconvulsive Therapy and other Neurostimulation Techniques Dr. Patrick Clarke
Major Depression • Australian figures: • 1 in 4 females • 1 in 6 males • 1 in 7 General Practice presentations (MJA 2008) • 4th most frequent managed condition in General Practice in 2004-2005
Major Depression • By 2020 predicted to be 2nd 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.
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).
Major Depression • Few proven effective and tolerated treatments in pharmacoresistent patients • Significant unmet need • Reduced compliance with increased treatment resistance
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%).
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
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 1950’s to 1960’s.
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.
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
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.
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.
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.
The following four slides show a typical two lead EEG during an ECT treatment Recruitment Tonic phase of seizure Robert Ostroff
Clonic phase of seizure Robert Ostroff
End of Motor Seizure Robert Ostroff
Postictal Suppression Robert Ostroff
Indications • Major Depression • Psychotic • Agitated • Retarded • Treatment Resistant • With significant risk
Bipolar Affective Disorder • Depressive Episode • Manic Episode
Schizophrenia • Acute • With Affective symptoms • Catatonic • Chronic, unresponsive to other treatment.
Puerperal Disorders • Post Natal Depression • Puerperal Psychosis
Other • Neuroleptic Malignant Syndrome • Parkinson’s Disease • Status Epilepticus
Contraindications • There are few true contraindications, provided that the patient is deemed fit for General Anaesthetic. • Raised Intracranial Pressure.
Work Up • History of ECT, medical, G.A., allergies. • Physical examination (Fundoscopy). • CBE, MBA20, TFT’s. • ECG. • CXR. • CT Head. • Consent (inform patient and family). • Fasting.
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.
Dental: use a bite block. • Enzyme deficiency. • Burns. • Mania. • Prolonged seizure.
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.
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
Endocrine • Addison’s 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.
Metabolic • Dehydration: risk of DVT. • Hyperkalaemia: increased risk of cardiac arrhythmias. • Hyponatraemia: Occurs with SIADH, seen occasionally with antidepressants and antipsychotics. Lowers seizure threshold.
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. • Parkinson’s Disease: ECT increases the permeability of the BBB, and therefore concomitant LDopa can increase to toxic levels. • CVA: Wait 1 month or more.
GOR • Increased risk of aspiration, therefore, consider Ranitidine, or cuffed endotrachael tube.
Ophthalmic • ECT causes a brief increase in intraocular pressure, problematic in open-angle glaucoma.
Pregnancy • Not contraindicated. • Fetal monitoring is not routine.
Elderly • ECT efficacious in elderly. • Have higher seizure threshold. • May require longer courses. • EEG may be less impressive.
Respiratory Disorders • Sleep Apnoea: CPAP Machine available in Recovery.
Skull Defect • Avoid area of the defect. • Avoid area of metal plates.
Urine retention • Catheterise.
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.
Anaesthetics • Monitoring: Pulse Oximetry and ECG. • Induction: Propofol. Shorter seizure than Thiopentone. Methohexitone not available. • Muscle Relaxant: Suxamethonium. • Cuff Technique.
Standard ECT Unilateral ECT Bilateral ECT Low Dose High Dose Less Efficacy More Efficacy Less Side Effects More Side Effects Variations in Electrical Dose and Electrode Placement
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.