💠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)