ECT (PART I)

MIRA HEZRINA BINTI MARZAKI

GROUP 5
 CONTENT
• History
• Mechanism of Action
• Pre-treatment Evaluation
• Premedication
 1500s PARACELCUS
“… the remedy against a
spiritual disease is, and
must be, spiritual”

Paracelsus induces artificial

seizures by administering
camphor (by mouth) to treat
psychiatric illness

Camphor, spodii, unicorni, etc., powedered mixed in soft

boiled egg
 MANFRED SAKEL
(1933)
a) The injection

• Insulin shock therapy

• He noticed that insulin-induced coma & convulsions
had a change in the mental state of drug addicts &
psychotic patients
• Complications were high

b) Ending coma with NG administration of glucose

1934 Ladislas Von Medusa (Hungarian)
• Brain of epileptics had greater
than normal numbers of glial
cells, whereas those of
schizophrenics had fewer

• Try to find biological

antagonism

• Used 25% camphor in oil to

produce therapeutics seizures
in a catatonic psychotic patient

• Change to pentylenetetrazol
(metrazol) (cardiazol)
 1938 Ugo Cerletti & Lucio Bini

• Apply current across the head of animals

• 1938, administered electroshock therapy (EST) to a

delusional & incoherent patient

• Improved with 1 treatment and remitted after 11

treatments

• More reliable & shorter acting than chemical induced

convulsive therapy
 1940 (USA)
• 1st used in USA in 1940
• muscle relaxant used is the curare

CURARES

• Alkaloid arrow poisons originating from

Central and South America

• Competitively & reversibly inhibiting the

nicotinic acetylcholine receptor (nAChR)
at the neuromuscular junction

• Causes weakness of the skeletal muscles

• When administered in a sufficient dose,

eventually lead to death due to paralysis
of the diaphragm
YEAR EVENT
1958 First controlled study of unilateral ECT

1960s Artificial seizure with anticonvulsant (lidocaine) reduces the efficacy of

ECT. Subconvulsive treatment only produce weak response: seizure is
needed

1960s Randomized clinical trials of ECT vs medical treatment of depression- ECT is

higher good response.
Neuroleptics is better during acute treatment, ECT good in long term

1970s Development of most common electrodes positioning for right unilateral

ECT
 YEAR EVENT

1976 Constant current brief pulse ECT device, the prototype for modern device is developed

Late 1970s-early 1980 Randomized controlled trials reveals ECT is more effective than sham treatment for major
depression

The beliefs of seizure is sufficient for clinical response is challenged by H.A Sackheim and
1987 his collaborators, who reported that the combination of dosage just above seizure
threshold and right unilateral electrode placement while producing a seizure of
sufficient duration, is ineffective
YEAR EVENT
1998 Randomized controlled clinical trials of ECT vs Lithium: equally effective in mania

2000
Controlled trials of the dose response relationship for the right unilateral ECT is validated.
High dose right unilateral and bilateral ECT show equal response rate in MDD but right
unilateral electrode placement is associated with fewer adverse cognitive effect.
Convulsive treatment is induced with magnetic stimulation by S.H Lisanby and her colleagues

2001 Largest model controlled trials of relapse prevention post-ECT with continuation
pharmacotherapy has significant better outcome with TCA (nortryptyline) plus Lithium
compared with nortryptyline alone or placebo during 6 months post-ECT
 MECHANISM OF ACTION:
- Generally, linked with production of GTCS

- Duration of 25-30 seconds

- A hypothesis stated that ECT affect the pathway of catecholamine between

diencephalon (when seizure generalization occur) and limbic system (responsible
for mood disorder) and hypothalamus

- As ECT threshold increases for further seizure, it may paradoxically acts as

anticonvulsant

- ECT also causes down regulation of B1-receptor in cortex and hyppocampus

 PRE-TREATMENT EVALUATION:
• Inform consent

• Details medical and psychiatric history taking

CBC
• General + dentition and systemic examination + neurological ESR
• Routine lab investigation
Urinalysis
ECG
• NOT DONE ROUTINELY: (EEG + estimation of plasma CXR
pseudocholinesterase activity (GA))
• X ray spine – any spine disorder
• CT/MRI – seizure disorder/ space occupying lesion.

• Examination of fundus occuli to rule out papilloedema + SOL

 PREMEDICATION , ANESTHETIC, MUSCLE RELAXANT

MUSCARINIC ANTICHOLINERGIC DRUG

• Administered before ECT to minimize oral and respiratory secretions and
to block bradycardia and asystoles

ANAESTHESIA
• General anaesthesia and oxygenation. Depth of anaesthesia should be
as light as possible.

MUSCLE RELAXANT
• To minimize the risk of bone fractures and other injuries resulting from
motor activity during the seizures
• The goal is to produced profound relaxation of the muscles.