Name Levetiracetam Class Antiepileptic Chemistry Racetam Routes of administration Oral and IV Absorption Almost 100% oral bioavailability; rapidly and completely absorbed when given orally (96%) Solubility pKa -2.0; highly acid drug, and very water soluble. Distribution VOD=0.5-0.7 L/kg; mainly distriubuted into total body water. Minimally protein bound (less than 10%) Target receptor Multiple potential targets (calcium channels, potasium channels, AMPA and GABA receptors), with what appears to be some selectivity for epileptogenic foci Metabolism Minimally metabolised; about 30% of the drug is excreted in the urine as an inactive metabolite, the origins of which are unclear and almost certainly non-hepatic Elimination 70% of the drug is excreted unchanged in the urine Time course of action Half life is about 7-8 hours in healthy volunteers Mechanism of action Multiple effects on multiple excitatory and inhibitory neurotransmitters and ion channels. Appears to have some selectivity for abnormally firing tissue, i.e. this drug is selective for epileptic brain tissue. The precise mechanism of its effect remains unknown Clinical effects Main side-effects are neurocognitive and behavioural. These may include a change in mood, eg. depression, anixety, restlessness or fatugue, personality changes, cognitive decline, and an increased risk of suicide. Single best reference for further information Wright et al (2013)
For the rare reader who has plenty of time for a deep dive into levetiracetam pharmacology, one can recommend Wright et al (2013) for a birds' eye overview, Patsalos (2000) for pharmacokinetics, Stockis (2009) for something a bit more clinical and Surges et al (2008) for the cellular mechanisms of action, all free articles.
Levetiracetam is the S-enantiomer of etiracetam, a racetam drug like piracetam and aniracetam with which it shares a common pyrrolidone nucleus. It is in fact the α-ethyl analogue of piracetam. The other racetams are seldom seen in clinical pharmacology and are basically unknown in critical care, but in the community, this group is used as "nootropes", consumed by productivity bros to accelerate their rate of burnout. There's a few related molecules (brivaracetam, seletracetam), but apart from these the other racetam drugs do not tend to demonstrate any antiepileptic activity. Their structures will not be reproduced here because there is an entire column of chemical structures in Wikipedia dedicated to this, and in any case that would be pointless because nobody will ever be asked to draw their chemical structure in any exam.
Levetiracetam has pharmacokinetic characteristics which are highly attractive from the viewpoint of clinical use, but also extremely boring from the viewpoint of teaching people about basic pharmacology. Unless otherwise stated, all these numbers are coming from Wright et al (2013).To summarise:
It is difficult to overintellectualise this section because so little can be said about the mechanism of action of levitiracetam, or almost any antiepileptic, for that matter. What follows is really a series of speculations. Reading the academic output of professional researchers on the subject can be likened to listening to an epilepsy expert thinking out loud about potential mechanisms of depressing neurotransmission and neuronal activation, and musing "maybe it does this, as well?" The linked article contains excellent tables on page 17 and 18, a part of which is reproduced here as an unordered list of channel and receptor effects:
So, what does any of this mean? In summary, it appears that the mechanism of action of levetiracetam lays in its ability to restore the normal inhibitory influences on the neurons which are apparently impaired or absent in epilepsy. It does not so much act as a GABA-agonst, but it reverses seizure-induced GABA dysfunction, and does not seem to affect GABA sites which are working normally (i.e. it is selective for epileptic brain tissue). What exactly all those calcium and potassium effects do, remains to be established, and authors simply shrug about it, mouthing noncommittal nothings like "may preferentially modulate neuronal activity".
Putting this molecular nonsense aside, the breadth of effects listed above makes levetiracetam a "broad-spectrum anticonvulsant". Stockis et al (2009) notes that it is indicated for partial-onset seizures, myoclonic seizures, primary generalized tonic-clonic seizures, and there are many other possible indications, including status myoclonus following hypoxic brain injury (Venot et al, 2011). It is particularly attractive for the latter, as it has minimal sedating effects and therefore should not cloud serial neurological reassessment as benzodiazepines might.
Unlike the exciting side-effects of phenytoin (toxic epidermal necrolysis, etc), levetiracetam is not likely to produce some sort of nightmarish whole-body reaction. Its side effects are more subtle, which is not to trivialise them. The side-effects are mainly neurobehavioral, and range from fatigue or restlessness all the way to major personality changes, cognitive decline, and an increased risk of suicide.