Electroconvulsive Therapy and other Neurostimulation Techniques
Dr. Patrick Clarke
Slide 2
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
Slide 3
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.
Slide 4
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).
Slide 5
Major Depression Few proven effective and tolerated treatments
in pharmacoresistent patients Significant unmet need Reduced
compliance with increased treatment resistance
Slide 6
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%).
Slide 7
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
Slide 8
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.
Slide 9
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.
Slide 10
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
Slide 11
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.
Slide 12
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.
Slide 13
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.
Slide 14
Recruitment Tonic phase of seizure The following four slides
show a typical two lead EEG during an ECT treatment Robert
Ostroff
Slide 15
Clonic phase of seizure Robert Ostroff
Slide 16
End of Motor Seizure Robert Ostroff
Slide 17
Postictal Suppression Robert Ostroff
Slide 18
Indications Major Depression Psychotic Agitated Retarded
Treatment Resistant With significant risk
Schizophrenia Acute With Affective symptoms Catatonic Chronic,
unresponsive to other treatment.
Slide 21
Puerperal Disorders Post Natal Depression Puerperal
Psychosis
Slide 22
Other Neuroleptic Malignant Syndrome Parkinsons Disease Status
Epilepticus
Slide 23
Contraindications There are few true contraindications,
provided that the patient is deemed fit for General Anaesthetic.
Raised Intracranial Pressure.
Slide 24
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.
Slide 25
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.
Slide 26
Dental: use a bite block. Enzyme deficiency. Burns. Mania.
Prolonged seizure.
Slide 27
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.
Slide 28
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
Slide 29
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.
Slide 30
Metabolic Dehydration: risk of DVT. Hyperkalaemia: increased
risk of cardiac arrhythmias. Hyponatraemia: Occurs with SIADH, seen
occasionally with antidepressants and antipsychotics. Lowers
seizure threshold.
Slide 31
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.
Slide 32
GOR Increased risk of aspiration, therefore, consider
Ranitidine, or cuffed endotrachael tube.
Slide 33
Ophthalmic ECT causes a brief increase in intraocular pressure,
problematic in open-angle glaucoma.
Slide 34
Pregnancy Not contraindicated. Fetal monitoring is not
routine.
Slide 35
Elderly ECT efficacious in elderly. Have higher seizure
threshold. May require longer courses. EEG may be less
impressive.
Slide 36
Respiratory Disorders Sleep Apnoea: CPAP Machine available in
Recovery.
Slide 37
Skull Defect Avoid area of the defect. Avoid area of metal
plates.
Slide 38
Urine retention Catheterise.
Slide 39
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.
Slide 40
Anaesthetics Monitoring: Pulse Oximetry and ECG. Induction:
Propofol. Shorter seizure than Thiopentone. Methohexitone not
available. Muscle Relaxant: Suxamethonium. Cuff Technique.
Slide 41
Electrode Placement
Slide 42
Electrical Stimulus
Slide 43
Seizure Threshold
Slide 44
Seizure Duration
Slide 45
Dose Titration
Slide 46
Continuation ECT
Slide 47
Maintenance ECT
Slide 48
Standard ECT Variations in Electrical Dose and Electrode
Placement Less EfficacyMore Efficacy Less Side Effects More Side
Effects Unilateral ECTBilateral ECT Low DoseHigh Dose
Slide 49
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.
Slide 50
Pulse and sine wave comparison. Energy = area under curve
Slide 51
Stimulus Parameters Standard Pulsewidth Amplitude Duration 1
cycle. Frequency = No. cycles/second Ultrabrief Pulsewidth 0.5-2ms
0.2-0.4 ms
Slide 52
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.
Slide 53
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.
Slide 54
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.
Slide 55
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.
Slide 56
Total Patients Receiving ECT
Slide 57
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.
Slide 58
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