Levetiracetam 500mg/105ml in Sodium chloride 0.9% infusion bags

The exact mechanism through which levetiracetam exerts its anti-epileptic effects is unclear, but is thought to be unique amongst other anti-epileptic medications. Current knowledge suggests that levetiracetam’s binding to synaptic vesicle protein 2A (SV2A) is a key driver of its action. SV2A is a membrane-bound protein that is found on synaptic vesicles and is ubiquitous throughout the CNS[A12546] - it appears to play a role in vesicle exocytosis[L8606][L8615] and in the modulation of synaptic transmission by increasing the available amount of secretory vesicles available for neurotransmission.[A12552] Stimulation of pre-synaptic SV2A by levetiracetam may inhibit neurotransmitter release,[A12551] but this action does not appear to affect normal neurotransmission. This has led to the suggestion that levetiracetam exclusively modulates the function of SV2A only under pathophysiological conditions.[A12546] Levetiracetam and related analogues showed a correlation between affinity for SV2A and anti-epileptic potency, further suggesting that action at this site contributes to the anti-epileptic activity of the drug.[L8606][L8615]

Levetiracetam has also been shown to indirectly affect GABAergic neurotransmission (despite having no direct effect on GABAergic or glutamatergic receptors) and modulate ionic currents.[A12552] Similarly, levetiracetam has been shown in vitro to inhibit N-type calcium channels.[A16562] How, or even if, these actions are implicated in its anti-epileptic action have yet to be elucidated.