Seminar

BIOLOGICAL
TREATMENT
Outline

• Antipsychotics
• Antidepressants
• 75
Anxiolytics
%
• Mood stabilizers
• Neurocognitive
enhancers
• ECT
Antipsychotic Drug

Nurul Amira binti Nizar 2016411016

 Introduction

● Used mainly to treat psychotic symptoms

Antipsychotic drug

● Indication:
○ Schizophrenia and schizophrenia related disorders
 brief reactive psychosis, schizophreniform,
schizoaffective, delusional disorder
○ Bipolar disorder
Typical Atypical
○ Depressive disorders ( MDD with psychotic
antipsychotic antipsychotic
symptoms )
(1st generation) (2nd generation)
○ Adjunct to antidepressant in the case of
treatment-resistant depression
○ Major neurocognitive disorders i.e. dementia with
psychotic symptoms or behaviour disturbances
Typical Antipsychotic
● 1st generation (Dopamine Receptor Antagonist)
● Effective for positive symptoms
High potency FGA Low potency FGA

- Haloperidol (Haldol) - Chlorpromazine

- Fluphenazine (Prolixin) (Thorazine)
- Loxapine - Thioridazine (Mellaril)
- Trifluoperazine
- Perphenazine
- Pimozide
- Thiothixene

- Higher incidence of EPS Vice versa

and NMS
- Lower incidence of
anticholinergic and
antihistaminic side effects
Mechanism of Action
 Side effects Features Treatment
Acute Extrapyramidal Symptoms (EPS)
Acute dystonia - Oculogyric crisis - Reduse dose
- Torticollis - IM/IV benzatropine
- Opistotonus
- Laryngeal spasm
Akathisia - Inner motor restlessness
Pseudo- - Slow movement
parkinsonism - Essential tremor
- Shuffling gait
- Cog wheel rigidity
Chronic Extrapyraidal Symptoms
Tardive dyskinesia - Involuntary oral-buccal -discontinue
movement (sucking -substitution with other
and smacking drugs
movement of lips)
- Irregular jerky
movement
 Side effects Feature

Neuroleptic Malignant F – fever/hyperthermia

Syndrome (rare) E – enchephalopathy
V – vitals unstable
E – elevated CK
R – rigidity of muscles
Hyperprolactinemia - Galactorrhoea
- Amenorrhoea
- Gynaecomastia

Others:
- Anti-HAM effect (sedation, hypotension, dry
mouth)
- Cholestatic jaundice i.e. Chlorpromazine
- Opthalmology problem
- Dermatology problem: rashes and
photosensitivity
Atypical Antipsychotic
● 2nd generation ( SGA)
● Mechanism of Action: mainly block the serotonin receptor (5HT2A) and less effect on dopamine
receptor
● Effective in improving negative symptoms and cognitive function

Drugs of SGA

- Clozaril/clozapine
- Olanzapine
- Risperidone
- Quetiapine
1) Clozaril/Clozapine
 Effective for the treatment resistant schizophrenia, which is defined as failure to response to
at least 2 antipsychotic drugs after adequate dosage, duration (4-6 weeks) and compliance.
 Adverse effect:
a) Agranulocytosis
b) Seizure
c) Hypotension
d) Weight gain
e) Myocarditis
 Extensive monitoring is needed
 Every week for 6 months
 Every 2 weeks for the second 6 months
 Then, every month after 1 year
 Starting dose:12.5mg -25mg daily
 Therapeutic dose: 300 – 600mg/day
 Maximum dose 900mg/day
 Name of drugs Dose/mg Side effects
2) Olanzapine  Starting dose: 5 –  Marked weight
 positive effect 10 gain
on  Sedation
negative  Maximum dose:  Metabolic
symptoms and 20 syndrome
also has mood  Diabetis mellitus
stabilizing
effect
3) Risperidone  Starting dose: 1-2  causes more EPS
mg/day and
 Maximum dose: 8 hyperprolactinemia
 Therapeutic dose:
2-4mg/day

4) Quetiapine  Starting dose:  hypotension

25mg BID
 Therapeutic dose:
250 -750 mg
Typical antipsychotics Atypical antipsychotics
Act on the dopaminergic system, blocking the dopamine type 2 Predominant antagonism of serotonin (5-HT2A) receptors with a
(D2) receptors lesser degree antagonism of dopamine (D2) receptors

Ameliorate positive psychotic symptoms, no effect on negative Treat both positive and negative symptoms
symptoms

Has no significant effects on patient’s cognitive functions Improve patient’s cognitive functions

Has high sedative effect Less sedative effects, except olanzapine

Strong adverse effects on CVS, i.e. ECG changes and Minimal effects on CVS except clozapine and quetiapine can cause
hypotension hypotension

Has strong EPS especially drugs with potent dopamine Minimal EPS effect except risperidone
blockade

Relatively less risk of metabolic syndrome, i.e. hyperglycaemia, High risk of metabolic syndrome, i.e. hyperglycaemia,
hyperlipidaemia and hypertension, central obesity hyperlipidaemia and hypertension, central obesity

High risk of tardive dyskinesia Low risk of tardive dyskinesia

Relatively less risk of weight gain High risk of weight gain
Not effective for treatment-resistant schizophrenia Effective for treatment-resistant schizophrenia especially clozapine

Relatively less risk of insulin resistant High risk of insulin resistant

Less risk of agranulocytosis High risk of agranulocytosis, i.e. clozapine
Intramuscular Formulations of Antipsychotics
●Short Acting preparations : used to control acute agitated or psychotic
symptoms of behaviour i.e. aggressive behaviour
●e.g. IM haloperidol , Clopixol acuphase, Olanzapine(Zyprexa IM), Ziprazidone
●Long acting or depot antipsychotics : maintenance treatment for patients
with poor compliance to drug as well as to eliminates bioavailability
problems
●administered IM every 2-4 weeks and slowly releases over time
●e.g.
○Fluphenazine decanoate ( modecate )
○Flupenthixol decanoate (Depixol)
○Zuclopenthixol decanoate ( cloxipol )
○Olanzapine embonate (ZypAdhera)
○Risperidone (Risperdal Const)
 Pretreatment evaluation

● Informed consent
● History: blood disorder, epilepsy, cvs problem, hepatic or renal problem)
● Supine and standing BP – orthostatic hypotension
● Baseline measurement: BMI, waist circumference, heart rate
● Laboratory investigation: FBS, RP baseline, LFT, ECG, RBS, Lipid profile
 ANTI- For depressive and anxiety disorders

DEPRESSANT
alter and increase levels of the neurochemicals implicated for
depression i.e. 5HT , NA, dopamine to normal levels

 Responses 50% reduction depressive symptoms

 Remission >50% reduced symptoms, no longer meets syndrome
criteria, no/minimal symptoms
 Recovery after6-12months remission
 Relapse depressive symptoms worsens before recovery phase
 Recurrent symptoms recur after recovery phase

Nur’Izzaty Binti Yusnazery

2016411446 Ainsah Omar, & Osman Che Bakar. (2015). Principles and practice of psychiatry.
 INDICATIONS MECHANISM OF
1
ACTION
Depressive symptoms

2 Anxiety symptoms

3 Sleep disturbances

4 Agitation

5 Chronic pain

6 Chronic insomnia

7 Psychotic disorders with prominent

depression symptoms
 CLASSIFICATION
MONOAMINE REUPTAKE INHIBITORS MONOAMINE OXIDASE MONOAMINE RECEPTOR
INHIBITORS (MAOI) ANTAGONISTS
Non-selective monoamine reuptake Irreversible MAOI Drug acting on adrenoreceptor
inhibitors (MARI) @ Tricyclic • Interact with (alpha2)
Antidepressant (TCA) sympathomimetic, CNS • NASSA (noradrenergic and
• Inhibits both 5HT and NE reuptake depressants, some anti- specific serotonergic
• Imipramine, Tofranil, Amitriptyline, hypertensive drugs and antidepressant) –
Prothiaden, Chlormipramine (Anafranil) tyramine containing foods Mirtazapine
• High risk of fatal
Selective Serotonin Reuptake Inhibitors hypertensive crisis 5HT1 receptor agonist
(SSRI) • Phenelzine, • Buspirone
• Selectively inhibit 5HT reuptake Tranylcypromine
• Fluvoxamine(Luvox), Escitalopram,
Fluoxetine, Zoloft (Sertraline),
Paroxetine
Reversible MAOI
• No hypertensive crisis
Selective dual action antidepressant(SNRI) • Maclobomide (aurorix) 5HT2 receptor antagonist
• Inhibit reuptake of 5HT and NE at • Nefazedone (serzone)
different dosages
• Venlafaxin (efexor), Duloxetin/Cymbalta
 SELECTIVE
inhibit reuptake of 5HT and NE with
SEROTONIN anticholinergic effects & alpha 2
REUPTAKE adrenergic
INHIBITORS (SSRI)
 multiple side effects i.e. highly
sedative, cardiotoxic and lethal in
overdose
 inhibits reuptake of 5HT , highly
• Migraine Low dose amitriptyline
selective thus causes lesser side
(50-200mg/day)
effect
• Panic disorder with poor SSRIs
• +anxiolytic effects
response Imipramine
paroxetine(20-50mg/day),
• OCD with poor SSRI response
fluvoxamine(100-300mg/day)
Chlormipramine
• +stimulating effects
escitalopram(10-20mg/day), NON-SELECTIVE
sertraline(50-200mg/day), MONOAMINE
fluoxetine(20-60mg/day)
• GAD escitalopram
REUPTAKE
INHIBITORS (MARI)/
TCA
 TCA SSRI
Highly sedative Less sedative
Cardiotoxic -
Prominent anticholinergic effects Minimal
Lethal if overdose Relatively is safe in overdose
Nausea and vomiting are not common Marked nausea and vomiting
Cause minimal anxiety symptoms Some induce marked anxiety symptoms
Headache less Common to have headache
No insomnia Some cause insomnia
Less common to have sexual dysfunction Prominent sexual dysfunction
Compliance is poor due to side effects Better compliance
Need multiple doses Single dose
 MONOAMINE • Mirtazepine(15-45mg/day) blocks
OXIDASE INHIBITORS alpha 2 adrenergic presynaptic
(MAOI) autoreceptors and serotonin
receptors (5HT2, 5HT3)
 inhibits tyramine metabolism by
• increase NA release and
inhbiting MAO enzymes
transmission resulting facilitation of
Irreversible MAOI 5HT release.
•  high risk of fatal hypertensive • Stimulates 5HT1 rec
crisis antidepressants therapeutic effect
• X prescribed with SSRI--> • spare nausea and sexual side
‘Serotonin syndrome’ effects( direct blockade 5HT2,5HT3)
• washout period of 2 weeks
NORADRENERGIC &
Reversible MAOI aka RIMA
• indicated in atypical depression
SPECIFIC
and social phobia SEROTONERGIC
• not causing HPT crisis ANTIDEPRESSANT
(NaSSA)s
Serotonin syndrome high level serotonintoo much nerve cell activity causing fatal condition—
sweating,vomiting,tremor, headache, stiffness, hyperreflexia,myoclonus,hyperpyrexia.
Tx- withdrawal agent, supportive mx
SIDE EFFECTS OF ANTIDEPRESSANTS
• Anticholinergicblurring of vision, dryness of mouth,
urinary retention, constipation
• Alpha adrenergic hypotension, increase potency anti-
HPT
• Histamine receptor blockade sedative , weight gain
1 2 (TCA, Mirtazapine)
• CVS (TCA)-cardiotoxic , hypotension , tachycardia,
decrease myocardial contractibility, ventricular arrhythmia,
quinidine like effects on ECG
• GIT (usually by SSRIs) nausea and vomitting
• Stimulation of 5HT2 receptor (usually in SSRI)Anxiety
symptoms, sexual problems
• Neuro fine tremor, headache, epileptic seizure,
peripheral neuropathy
• Others agranulocytosis, skin rashes, cholestatic jaundice
 ● Treats anxiety symptoms
● Ex : Benzodiazepines,
ANXIOLYTICS Buspirone, Beta-blocker,
Barbiturate, Gabapentin,
Pregbalin
 BENZODIAZEPINES
commonest and most effective
anxiolytic

used for short period

 indicated in early stage of treatment
Classified based on half-life
before antidepressant therapeutic
effects take place
 abort panic attack Oxazepam

 control acute agitation Short Temazepam

Used to treat
acting
 Used in GAD, panic ds, social phobia insomnia
Aprazolam

Intermedi Lorazepam
ate

Used to treat
Long
Clonazerpam

anxiety
acting
Diazepam

• Anti-panic properties Aprazolam &

Lorazepam
• Severe anxiety Lorazepam (Ativan)– high
potent with sedatives, anxiolytic, muscle relaxant
•
SIDE EFFECTS
CNS depression drowsiness,
Withdrawal Effects
somnolence, reduced motor coordination,
and memory impairment.
• Impairment of motor coordination,
impaired driving skills
• Cognitive function & memory impairment,
anterograde amnesia , poor attention
• Teratogenic effects, risk cleft palate
• Paradoxical effects worsening
agitation
• Long term use psychological/physical
dependencies, rebound anxiety
symptoms (discontinuation syndrome), ● Rebound anxiety symptoms @ 'discontinuation
withdrawal syndrome’ = dose BDZ reduced/completely stop
● Withdrawal / rebound symptoms may be
High BDZ intake associated with perceptual disturbances
Slurred speech, nystagmus, ataxia, reduced (hallucination/delusion)
reflexes, respiratory depression, stupor/coma ● To avoid withdrawal symptoms  tapered off
 Reversed by Flumazenil (BDZ antagonist)
slowly over a few weeks
 BUSPIRONE @ AZAPIRONE

 stimulates 5-HT1A
receptor (agonist)
• Short half life- doses
TDS ranging 15-30mg

• Anxiolytics effect after

a week
• Improves
psychological SIDE EFFECTS
symptoms, minimal
sedation, no Headache, nervousness, light headedness,
dependency problems tiredness, dizziness, drowsiness
 B-ADRENERGIC ANTAGONIST
Immediate anxiolytic effects
(30mins-2h)
 block B receptors at adrenergic
& noradrenergic
• Dosage = T.Propanolol 10mg prn
• Need to monitor BP, PR
 Reduce physical symptoms • No CNS depression, no
(tremelousness, cardiac drowsiness, no addiction
symptoms)
 Indicated in
situational/performance CONTRAINDICATIONS
anxiety (stage fright) Asthma
Diabetes
CHF
MOOD
STABILIZERS
Introduction

 Drug to prevent recurrence of affective illness

 Mainly lithium and some of antiepileptic drugs include Sodium Valproate, Carbamazepine
and Lamotrigine
 Also can be used to treat acute mood episode
 Lithium and Sodium Valproate used to treat acute mania
 Lithium and Lamotrigine used in depressive disorder especially bipolar disorder
Lithium

 Is the first and most established mood 3 Main Mechanism of

stabilizer.
Action
 Has comparable efficacy with atypical
antipsychotics in reducing both manic
and psychotic symptoms I. Inhibits Dopamine
neurotransmitter
 First line and gold std mood
stabilizers. II. Downregulates NMDA
receptor

III. Promotes GABAergic

neurotransmitter
Mechanism of action
Lithium inhibits Dopamine
neurotransmitter
 Inhibits Dopamine neurotransmitter
by alters the functionality of GPCR
subunits
 Postsynaptic activation of dopamine
receptor is mediated by GPCR
Lithium downregulates NMDA N-methyl-D-
aspartate receptor
 NMDA receptor: glutamate receptor
 Glutamate: excitatory neurotransmitter
elevated during mania
 Chronic administration of lithium –
NMDA downregulation
 Reduces glutamate neurotransmission
 Lithium promotes GABAergic
neurotransmitter
 GABA:
 Inhibitory NT, modulates dopamine and
glutamate NT
 Patients with BD: GABAergic
neurotransmission is reduced

 Lithium:
 Presynaptic: facilitates GABA release
 Postsynaptic: upregulates GABAB
receptors
 Increases GABA levels
 Pharmacokinetics
 Lithium is rapidly absorbed from the gut

 It is removed from the plasma by renal excretion and by entering cells and other body
compartments

 Therefore there is rapid excretion of lithium from the plasma, and a slower phase
reflecting its removal from the whole- body pool.
 Like sodium, lithium is filtered and partly reabsorbed in the kidney.
 When the proximal tubule absorbs more water, lithium absorption increases. Therefore
dehydration causes the plasma lithium concentration to rise.
 Because lithium is transported in competition with sodium, more is reabsorbed by the
kidney when sodium concentrations fall
Prior to administration, check
for:
FBC, RP, ECG, TFT, Cardiac
status
Dosage and plasma concentration
 Has narrow therapeutic index
 Lithium usually is started at 300 mg twice daily in typical patients and is then
titrated until a therapeutic blood level is achieved.

 Measurement of plasma of lithium during treatment

 Should first be made after 7 days
 Then, every 2 weeks
 Then, once every 6 weeks – achieve satisfactory steady
 Hence, once every 3 months – very stable lithium levels
 Suggested plasma concentration of lithium:
 Acute mania : 0.8 - 1.2 mmol/L
 Maintenance BD: 0.6-0.75 mmol/L (in persistent manic may need higher doses)
 Toxic effect
 toxicity with >1.2mmol/l and if serious above 2.0mmol/L
INDICATIONS
CONTRAINDICATIONS

• Acute treatment of mania • Cardiovascular disease; high risk of

lithium toxicity
• Prophylaxis of unipolar and • Renal disease especially renal failure;
bipolar mood disorder high risk of lithium toxicity

• Concomitant use of diuretics

• Augmentation therapy in
resistant depression • Severe dehydration; high risk of lithium
toxicity
• Prevention of aggressive
behaviour in patients with • Pregnant (female patient must be
learning disabilities warned not to get pregnant during the
treatment)— major congenital heart
• Schizoaffective and abnormalities
cyclothymic disorder
 Side effects
Short term Long term
Sedation Reversible renal dysfunction
Polyuria, polydipsia Hypothyroidism / rarely
Fine tremor hyperthyroidism
Nausea, metallic taste Weight gain
ECG changes Hyperparathyroidism

Toxic symptoms
• Nystagmus
• Vomiting, abdominal pain Convulsion
• Coarse tremor Renal failure
• Ataxia, slurred speech Coma/fits/death
• Confusion
• Delirium, circulatory failure
Drug interaction

 Pharmacodynamic interactions may involve potentiation of 5-HT-promoting agents,

leading to a serotonin syndrome
 In addition, therapeutic serum levels of lithium can be associated with neurotoxicity in the
presence of certain other centrally acting agents; for example calcium channel blockers and
carbamazepine
 neurotoxicity in the form of ataxia, tremors, nausea, vomiting, diarrhoea and/or tinnitus
 Diuretics— induced sodium loss, thus may reduce the renal clearance of lithium and cause
lithium toxicity.
Sodium valproate
 It is more safe than lithium as it has wider therapeutic window and relatively has
fewer side effects.
 MOA-exact is uncertain
1. Blocks activated Na+ channels
2. Enhances GABA synthesis and reduces degradation
3. Suppress glutamate action
4. Blocks T-type calcium channels
 Dosage :
 Recommended: 20mg/kg/day
 Starting: usually 500mg-1000mg/day
 Women who begin taking medication during adolescence should be closely
monitored for an evidence of polycystic ovarian syndrome
 It is contraindicated to women in child-bearing age due its teratogenicity.
Pharmacokinetic
 rapidly absorbed, with the peak plasma concentrations occurring
about 2 hours after ingestion.
 widely and rapidly distributed and has a half-life of 8–18 hours.
 metabolized in the liver to produce a wide variety of metabolites,
some of which have anticonvulsant activity.
 valproate does not induce hepatic microsomal enzymes, unlike
carbamazepine
S/E
 GI disturbances, tremor, sedation, tiredness, weight gain,
transient hair loss, elevation of hepatic enzymes,
thrombocytopenia, acute pancreatitis, edema, amenorrhea, rashes
Lamotrigine

 Compared to other mood stabilisers, it has a

stronger antidepressant effect with lesser side
effects.
 MOA-
 Enhances release of GABA
neurotransmitters Indicated for patients with:
 Blocks voltage-gated sodium channels • Patients who have more
depressive than manic
preventing sodium influx which inhibits
episodes
glutamate excitation (reduce excitatory
• Bipolar type II
neurotransmitter release)
• Those who are not
Dosage
 Range: 25mg-200mg/day responding to other mood
 Initial dose: 25mg/day stabilisers
 Can be increased by 12.5mg to 25mg every one
to 2 weeks (slowly increase the dose because of
SE)
Pharmacokinetic
 Rapidly absorbed, with peak plasma levels occurring after about 1.5 hours followed
oral administration
 Extensively metabolized by the liver but does not induce cytochrome P450
enzymes.
 Half-life is about 30 hours
S/E
 Skin eruptions, maculopapular in nature (3% associated with fever) Other side
effects include nausea, headache, diplopia, blurred vision, dizziness, ataxia, and
tremor.
 Rarely, very serious adverse effects, such as angioedema, Stevens–Johnson
syndrome, and toxic epidermal necrolysis
Carbamazepine

 One of the useful mood stabilizer

 MOA: mainly blocks neuronal sodium channel,
but it is unclear for the mood stabilizing effect
 Dosage (200mg-1200mg/day)
o Initial dose (200mg) Indicated for patients with:
o Can be increased by 200mg every 2 or 4 days ( depend • Mixed state (mixed
on severity of the symptoms and patients’ response) manic-depressive
 Adverse effects episodes)
• Rapid cycling bipolar
 Drowsiness disorder
 Dizziness • Those who do not respond
 Nausea to lithium
• Could not tolerate lithium
 Double vision
 Skin rash (severe exfoliative dermatitis, but rare)
 Agranulocytosis rare but serious
Pharmacokinetics & Pharmacodynamics

 Slowly but completely absorbed and widely distributed

 It is extensively metabolized, and at least one metabolite, carbamazepine epoxide, is
therapeutically active
 Half-life during long-term treatment is about 20 hours
 a strong inducer of hepatic microsomal enzymes, and can lower the plasma concentrations
of numerous other drugs
 Accelerate the metabolism of some other drug (TCA, BZP, antipsychotic drugs, OCP, thyroxine,
warfarin, other anticonvulsants and some abx) and of the hormones in the contraceptive pill
reducing its effectiveness
 Risk of neurotoxicity- combine with lithium
NEUROCOGNITIVE
ENHANCERS
 Donepezil
Indications • used to treat mild-moderately severe symptoms of Alzheimer’s
dementia
• improves mental function ( memory, attention, ability to interact
with others, speak, think clearly, and perform regular daily
activities)
Mechanism of Action binds reversibly to acetylcholinesterase and inhibits the hydrolysis of
acetylcholine, thus increasing the availability of acetylcholine at the
synapses, enhancing cholinergic transmission.
Metabolized metabolized by cytochrome P450 enzyme in the liver
Excretion mostly throughout the urine
Half-Life 70 hours
Dosage 5-10mg/day
Side-Effects diarrhea, nausea, vomiting, insomnia, dizzyness, drowsiness,
weakness, LOW/LOA
 Rivastigmine
Indications used to treat mild to moderate Alzheimer’s dementia
Mechanism of Action binds reversibly with butyrylcholinesterase and
acetylcholinesterase, inhibits the hydrolysis of acetylcholine,
and thus leading to an increased concentration of
acetylcholine at cholinergic synapses.
Metabolized metabolized by cholinesterase-mediated hydrolysis
Excretion mostly throughout the urine
Half-Life 1.5 hours
Dosage 3-6 mg/day (max:6mg/day)
Side-Effects diarrhea, nausea, vomiting, anorexia, dizzyness
 Galantamine
Indications used to treat mild to moderate Alzheimer’s dementia

Mechanism of Action centrally-acting cholinesterase inhibitor (competitive and

reversible). It elevates acetylcholine in cerebral cortex by slowing
the degradation of acetylcholine. Modulates nicotinic acetylcholine
receptor to increase acetylcholine from surviving presynaptic nerve
terminals. May increase glutamate and serotonin levels.

Metabolized metabolized by cytochrome P450 enzyme in the liver

Excretion excreted unchanged in the urine
Half-Life 7 hours
Dosage 8-24 mg/day
Side-Effects nausea, vomiting, diarrhea
 Memantine
Indications used to treat moderate to severe Alzheimer’s dementia (cognition
and function)
Mechanism of Action an N-methyl-D-aspartate (NMDA)- type glutamate receptor
antagonist which blocks the effects of glutamate(a neurotransmitter
in the brain that leads to neuronal excitability and excessive
stimulation in Alzheimer's Disease) and inhibits calcium influx into
cells
Metabolized metabolized by cytochrome P450 enzyme in the liver
Excretion excreted through urine
Half-Life 60-100 hours (may increase in patient with moderate to severe renal
impairment)
Dosage 5-20 mg/day
Side-Effects hypersensitivity, somnolence, dizzyness
ELECTROCONVULSIVE
THERAPY
a procedure done under general anaesthesia in which a small
electric current are passed through the brain , and
intentionally triggering a brief generalised seizure
 Mechanism of ECT
• Improves dopaminergic, serotonergic and adrenergic
neurotransmission
• Increases in brain-derived neurotrophic factor (BDNF) – regulates
neuro cell growth and involved with noradrenaline and serotonin
• Anticonvulsant effect related to antidepressant effect
 Indications
• Severe major depression with • Schizophrenia patient with severely
melancholia which does not disturbed or aggression
respond to medications • Catatonic schizophrenia
(adequate dose and duration) • Puerperal psychosis
• To achieve rapid response (when • Bipolar disorder (both at
the patient does not respond to depressive/manic state)
medications) i.e. depressed • Past history of favourable response
patient with active or high to ECT
suicidal tendency.
• Patient with acute manic
excitement or highly disturbed
 Contraindications

Relative contraindications:
 Elevated intracranial pressure including SOL & cerebral hemorrhage
 Recent myocardial infarction
 Severe arterial hypertension
 Cardiac disease, aneurysm, thrombophlebitis, bleeding disorders with
increased risk of embolism
 Severe pulmonary disease such as pneumonia and TB
 Patient who is contraindicated for anaesthesia
 Recent CVA
 Pre-ECT preparation
 Informed consent
 Medical and psychiatric evaluation
 Drugs that have effect on the induction of seizure should be stopped or reduced
 Lithium should be suspended/ reduce the dose the day before ECT if patient is on
lithium (risk of toxicity)
 KNBM for at least 8 hours before ECT
 Remove dentures or hearing aids
 Premedication- atropine (to reduce parasympathetic effects)
 Post-ECT
 Record amount of voltage used, duration of current, type of wave,
duration of seizure, premedication given and vital signs.
 Closely monitored the vital signs until at least 30minutes after ECT.
 Complications
 Headache and body ache  Thoracic spine or long bones
 Memory disturbance fracture
 Postictal confusion  Dislocation of shoulder joint and
wrist
 Vomiting due to increased ICP
 Arrhythmia, cardiac arrest
 Memory lost from a day or a
month due to hypoxia of the brain  Status epilepticus
Aspiration pneumonia  Muscle pain