drug-induced seizures

NB. AVOID phenytoin in drug-induced seizures.

mechanisms of seizures

⇒ inhibits pyridoxyl phosphate ⇒ impairs glutamic acid decarboxylase ⇒ impaired production of GABA ⇒ seizures
Rx of OD: pyridoxine - see isoniazid overdose
NB. barbiturates/benzodiazepines no help as need GABA to work although GA dose of barbiturates open GABA-A without GABA

see ethanol (alcohol and alcohol withdrawal)
⇒ early seizures via GABA-A down-regulation & lack of ethanol as agonist
- ⇒ Rx with benzodiazepines
⇒ late seizures due to up regulation of NMDA receptor
- ⇒ less easily treated & thus higher mortality
- ? try Mg as:
  - alcoholics tend to be Mg deficient
  - Mg inhibits NMDA
  - Mg assists with thiamine metabolism

see methylxanthines
⇒ antagonist at adenosine A1 & A2 receptors
⇒ seizures with loss of post-ictal period ⇒ continuous seizures ⇒ increased CNS oxygen demand ⇒ vasoconstriction ⇒ unable to increase oxygen supply ⇒ poorer prognosis than with other seizures

eg. high dose cocaine or amphetamines
- all forms of cocaine use can cause seizures within seconds, minutes, or hours after it is taken
- seizures caused by cocaine are uniquely dangerous and may be associated with heart attacks, disrupting the heart's normal rhythm (cardiac arrhythmia), and death
- pharmacological studies have demonstrated that cocaine-induced seizures were efficiently inhibited by GABA-A receptor agonists and NMDA receptor antagonists, whereas sodium and calcium channel blockers were ineffective¹⁾
- the acetylcholinesterase (AChE) activity and reactive oxygen species (ROS) levels as two factors capable of mediating the effect of crack cocaine in epilepsy relationship - inhibition of AChE activity causes an accumulation of acetylcholine, triggering neurological damage that contributes to the development of seizures ²⁾

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²⁾