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Focal onset seizures Clinical criteria: The condition must be stable for the prescriber to consider the listed maximum quantity of this medicine suitable for this patient, AND The condition must have failed to be controlled satisfactorily by at least one other antiseizure medication. Treatment criteria: Must be treated by a health practitioner who is any of: (i) a medical practitioner, (ii) an authorised PBS prescriber who is not a medical practitioner, but who is: (a) sharing care of the patient with at least one medical practitioner; (b) intending to share care of the patient with a medical practitioner.
“The mechanism of action of zonisamide has not been fully elucidated, but it appears to act on voltage sensitive sodium and calcium channels, thereby disrupting synchronised neuronal firing, reducing the spread of seizure discharges and disrupting subsequent epileptic activity.”
“Apparent clearance of zonisamide from plasma at steady-state after oral administration is about 0.70 l/h and the terminal elimination half-life is about 60 hours in the absence of concomitant therapy with CYP3A4 inducers. However, the apparent clearance is increased by up to 2-fold in patients also receiving the antiepileptic drugs phenobarbitone, phenytoin, carbamazepine and/or sodium valproate, and elimination half-life is reduced by up to 50%.”
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Curated subset. The full adverse-effect list is in the TGA Product Information; click any citation above to open it.
“Zonisamide is metabolised primarily through reductive cleavage of the benzisoxazole ring of the parent drug by CYP3A4 to form 2-sulphamoylacetylphenol (SMAP) and also by N-acetylation to form N-acetyl zonisamide.”