💹EEG IN ACUTE INTOXICATIONS

💠Barbiturates 

Usually they produce fast activity (15-35/sec ) In the acute overdose, these type of fast activity may still be present, with some deceleration (10-16/sec). The inability of the cortex to produce, barbiturate induced fast activity has been described as a sign of cerebral impairment 

💠Benzodiazepines 

〰Fast activity (15-25/sec) range

💠Tricyclic Antidepressants

〰Widespread and poorly reactive 8-10/sec activity with paroxysmal discharges

💠Lithium Carbonate

〰Marked slowing, paroxysmal bursts, and triphasic waves

💠Neuroleptic drugs ( phenothiazines, butyrophenones)

〰Diffuse slow activity; often with burst like appearance or intermingled with paroxysmal discharges. Fast frequencies are absent

💠Opioids:

〰Relatively little repercussion in EEG; if produces profound coma → diffuse slowing

💠Carbon monoxide

〰Massive slowing (1-4/sec)

💠Ethyl alcohol

〰Effect on EEG is mild

💠Methyl alcohol

〰EEG slowing is correlated with acidosis rather than blood and CSF methanol levels

💠Organophosphorous compounds

〰Initially, fast EEG activity may be supplanted by slow activity 

Ref: EEG and intensive care medicine : RB Hansen, E Niedermeyer; Prog neurol Surg, vol 12, pp 105-145 ( Karger, Basel 1987)