About: MOA Not Known, But Induction of Bilateral Generalised Seizures Required For Effects. An in
About: MOA Not Known, But Induction of Bilateral Generalised Seizures Required For Effects. An in
About: MOA Not Known, But Induction of Bilateral Generalised Seizures Required For Effects. An in
About: MOA not known, but induction of bilateral generalised seizures required for effects. An in
GABA transmission (depletes cortical GABA) and receptor antagonism observed – these changes raise
seizure threshold during ECT. ECT may also lead to of endogenous opioids which may have
anticonvulsant properties. Nearly every neurotransmitter system is affected by ECT.
Major depression
Indications Mania
SCZ/Schizoaffective d/o
For pts ina cute phase of major derpession with high degree of SX severity +
functional impairment or those w/ psychotic SXs or catatonia
Depression
Therapeutic response not sustained w/o continuation or maintenance TX, approx.
90% relapse within 6 months of cessation of acute course
ECT-EEG
Recruiting phase: low amp, fast activity
Tonic phase: bilateral synchronouse polyspikes
Clonic phase: high amp, polyspike, slow wave complexes that slow to 1-3Hz just before
seizure termination
Postictal suppression: EEG flattening, lasts approx. 90s
Postictal phase: high amp, irregular delta waves, rhythmic theta waves progressively merge
into pre-seizure rhythms (20-30mins after seizure termination), as number of TX, EEG
slowing persists for longer into postictal period (returns to norm by 30days)