Antiseizure medications (ASMs), originally developed for epilepsy, are increasingly used across
non-epileptic neurological disorders. They modulate excitatory -inhibitory balance, nociceptive
sensitization, neuroplasticity, trigeminal activation, and sleep- wake regulation through actions
on voltage-gated ion channels, GABAergic and glutamatergic transmission, and synaptic vesicle
proteins. These mechanisms underlie their broader therapeutic potential. In migraine, topiramate
and valproate reduce attack frequency and chronification risk, and remain first- or second-line
preventive options in current guidelines. In neuropathic pain, gabapentin and pregabalin alleviate
peripheral and central sensitization and are effective in diabetic neuropathy, postherpetic
neuralgia, and trigeminal neuralgia, improving pain and sleep though requiring cautious use in
older or opioid-treated patients. ASMs enhance slow-wave sleep and are now preferred first-line
therapy for restless legs syndrome, offering lower augmentation risk than dopamine agonists. In
movement disorders, primidone and topiramate reduce tremor severity in essential tremor, while
carbamazepine and oxcarbazepine effectively prevent attacks in paroxysmal kinesigenic dyskinesia.
Lamotrigine, valproate, and carbamazepine are established mood stabilizers in bipolar disorder,
while gabapentinoids may be cautiously used as adjuncts in anxiety disorders or post-traumatic
stress disorder. While ASMs provide valuable alternatives for refractory or intolerant patients,
safety concerns, including cognitive impairment, respiratory depression, and severe skin reactions,
necessitate individualized selection, monitoring, and informed consent. Future research should
clarify their long-term safety and enable biomarker-guided, personalized use beyond epilepsy.