(zoe NIS a mide)
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Zonegran: 25 mg, 100 mg
Zonegran: 100 mg [contains fd&c red #40, fd&c yellow #6 (sunset yellow)]
Generic: 25 mg, 50 mg, 100 mg
Brand Names: U.S.
- Anticonvulsant, Miscellaneous
Stabilizes neuronal membranes and suppresses neuronal hypersynchronization through action at sodium and calcium channels; does not affect GABA activity.
Oral: Rapid and complete
Vd: 1.45 L/kg
Hepatic via CYP3A4; undergoes acetylation to form N-acetyl zonisamide and reduction via cytochrome P450 isoenzyme CYP3A4 to 2-sulfamoylacetylphenol (SMAP); SMAP then undergoes conjugation with glucuronide
Urine (62%, 35% as unchanged drug, 65% as metabolites); feces (3%); Note: Of the dose recovered in Japanese patients, 28% is as unchanged drug, 52% is as N-acetyl zonisamide, and 19% is as SMAP glucuronide (Glauser 2002)
Time to Peak
2 to 6 hours
Plasma: ~63 hours (range: 50 to 68 hours)
Special Populations: Renal Function Impairment
Renal clearance decreases with decreased renal function. Marked renal impairment (CrCl less than 20 mL/minute) was associated with an increase in AUC of 35%.
Use: Labeled Indications
Partial seizures: Adjunct treatment of partial seizures in adolescents >16 years of age and adults with epilepsy
Bipolar disorder; mania
Hypersensitivity to zonisamide, sulfonamides, or any component of the formulation
Note: Although the FDA approved product labeling states this medication is contraindicated with other sulfonamide-containing drug classes, the scientific basis of this statement has been challenged. See “Warnings/Precautions” for more detail.
Adjunctive treatment of partial seizures: Oral: Initial: 100 mg/day. Dose may be increased to 200 mg/day after 2 weeks. Further dosage increases to 300 mg and 400 mg/day can then be made with a minimum of 2 weeks between adjustments, in order to reach steady state at each dosage level. Doses of up to 600 mg/day have been studied, however, there is no evidence of increased response with doses >400 mg/day. Note: Doses of 300 mg/day and higher are associated with increased side effects.
Data from clinical trials is insufficient for patients older than 65. Begin dosing at the low end of the dosing range.
Adolescents >16 years: Refer to adult dosing.
Dosing: Renal Impairment
GFR ≥50 mL/minute: There are no dosage adjustments provided in the manufacturer’s labeling. However, slower titration and frequent monitoring are indicated in patients with renal disease; use with caution.
GFR <50 mL/minute: Use is not recommended. Marked renal impairment (CrCl <20 mL/minute) was associated with a 35% increase in AUC.
Dosing: Hepatic Impairment
There are no dosage adjustments provided in the manufacturer’s labeling (has not been studied). However, slower titration and frequent monitoring are indicated in patients with hepatic impairment; use with caution.
Hazardous agent; use appropriate precautions during preparation and disposal (NIOSH 2014 [group 3]).
A 10 mg/mL suspension may be made using capsules and either simple syrup or methylcellulose 0.5%. Empty contents of ten 100 mg capsules into glass mortar. Reduce to a fine powder and add a small amount of Simple Syrup, NF and mix to a uniform paste; mix while adding the chosen vehicle in incremental proportions to almost 100 mL; transfer to an amber calibrated plastic bottle, rinse mortar with vehicle, and add quantity of vehicle sufficient to make 100 mL. Label "shake well" and "refrigerate". When using simple syrup vehicle, stable 28 days at room temperature or refrigerated (preferred). When using methylcellulose vehicle, stable 7 days at room temperature or 28 days refrigerated. Note: Although no visual evidence of microbial growth was observed, storage under refrigeration would be recommended to minimize microbial contamination.Abobo CV, Wei B, and Liang D, "Stability of Zonisamide in Extemporaneously Compounded Oral Suspensions," Am J Health Syst Pharm, 2009, 66(12):1105-9.19498126
Capsules should be swallowed whole. Administer once or twice daily with or without food. Hazardous agent; use appropriate precautions for handling and disposal (NIOSH 2014 [group 3]).
Store at 25°C (77°F) excursions are permitted between 15°C and 30°C (59°F and 86°F). Protect from moisture and light.
Alcohol (Ethyl): CNS Depressants may enhance the CNS depressant effect of Alcohol (Ethyl). Monitor therapy
Alpha-/Beta-Agonists (Indirect-Acting): Carbonic Anhydrase Inhibitors may increase the serum concentration of Alpha-/Beta-Agonists (Indirect-Acting). Monitor therapy
Amphetamines: Carbonic Anhydrase Inhibitors may decrease the excretion of Amphetamines. Monitor therapy
Azelastine (Nasal): CNS Depressants may enhance the CNS depressant effect of Azelastine (Nasal). Avoid combination
Blonanserin: CNS Depressants may enhance the CNS depressant effect of Blonanserin. Consider therapy modification
Bosentan: May decrease the serum concentration of CYP3A4 Substrates. Monitor therapy
Brimonidine (Topical): May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
Buprenorphine: CNS Depressants may enhance the CNS depressant effect of Buprenorphine. Management: Consider reduced doses of other CNS depressants, and avoiding such drugs in patients at high risk of buprenorphine overuse/self-injection. Initiate buprenorphine patches (Butrans brand) at 5 mcg/hr in adults when used with other CNS depressants. Consider therapy modification
Cannabis: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
Carbonic Anhydrase Inhibitors: May enhance the adverse/toxic effect of other Carbonic Anhydrase Inhibitors. The development of acid-base disorders with concurrent use of ophthalmic and oral carbonic anhydrase inhibitors has been reported. Management: Avoid concurrent use of different carbonic anhydrase inhibitors if possible. Monitor patients closely for the occurrence of kidney stones and with regards to severity of metabolic acidosis. Avoid combination
CNS Depressants: May enhance the adverse/toxic effect of other CNS Depressants. Exceptions: Levocabastine (Nasal). Monitor therapy
CYP3A4 Inducers (Moderate): May decrease the serum concentration of CYP3A4 Substrates. Monitor therapy
CYP3A4 Inducers (Strong): May increase the metabolism of CYP3A4 Substrates. Management: Consider an alternative for one of the interacting drugs. Some combinations may be specifically contraindicated. Consult appropriate manufacturer labeling. Consider therapy modification
Dabrafenib: May decrease the serum concentration of CYP3A4 Substrates. Management: Seek alternatives to the CYP3A4 substrate when possible. If concomitant therapy cannot be avoided, monitor clinical effects of the substrate closely (particularly therapeutic effects). Consider therapy modification
Deferasirox: May decrease the serum concentration of CYP3A4 Substrates. Monitor therapy
Doxylamine: May enhance the CNS depressant effect of CNS Depressants. Management: The manufacturer of Diclegis (doxylamine/pyridoxine), intended for use in pregnancy, specifically states that use with other CNS depressants is not recommended. Monitor therapy
Dronabinol: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
Droperidol: May enhance the CNS depressant effect of CNS Depressants. Management: Consider dose reductions of droperidol or of other CNS agents (e.g., opioids, barbiturates) with concomitant use. Consider therapy modification
Enzalutamide: May decrease the serum concentration of CYP3A4 Substrates. Management: Concurrent use of enzalutamide with CYP3A4 substrates that have a narrow therapeutic index should be avoided. Use of enzalutamide and any other CYP3A4 substrate should be performed with caution and close monitoring. Consider therapy modification
Flecainide: Carbonic Anhydrase Inhibitors may increase the serum concentration of Flecainide. Monitor therapy
Fosphenytoin: May decrease the serum concentration of Zonisamide. Monitor therapy
Hydrocodone: CNS Depressants may enhance the CNS depressant effect of Hydrocodone. Management: Consider starting with a 20% to 30% lower hydrocodone dose when using together with any other CNS depressant. Dose reductions in the other CNS depressant may also be warranted. Consider therapy modification
HydrOXYzine: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
Kava Kava: May enhance the adverse/toxic effect of CNS Depressants. Monitor therapy
Lithium: Carbonic Anhydrase Inhibitors may decrease the serum concentration of Lithium. Monitor therapy
Magnesium Sulfate: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
Mefloquine: May diminish the therapeutic effect of Anticonvulsants. Mefloquine may decrease the serum concentration of Anticonvulsants. Management: Mefloquine is contraindicated for malaria prophylaxis in persons with a history of convulsions. Monitor anticonvulsant concentrations and treatment response closely with concurrent use. Consider therapy modification
Memantine: Carbonic Anhydrase Inhibitors may increase the serum concentration of Memantine. Monitor therapy
MetFORMIN: Carbonic Anhydrase Inhibitors may enhance the adverse/toxic effect of MetFORMIN. Specifically, the risk of developing lactic acidosis may be increased. Monitor therapy
Methenamine: Carbonic Anhydrase Inhibitors may diminish the therapeutic effect of Methenamine. Management: Consider avoiding this combination. Monitor for decreased therapeutic effects of methenamine if used concomitant with a carbonic anhydrase inhibitor. Consider therapy modification
Methotrimeprazine: CNS Depressants may enhance the CNS depressant effect of Methotrimeprazine. Methotrimeprazine may enhance the CNS depressant effect of CNS Depressants. Management: Reduce adult dose of CNS depressant agents by 50% with initiation of concomitant methotrimeprazine therapy. Further CNS depressant dosage adjustments should be initiated only after clinically effective methotrimeprazine dose is established. Consider therapy modification
Metyrosine: CNS Depressants may enhance the sedative effect of Metyrosine. Monitor therapy
Mianserin: May diminish the therapeutic effect of Anticonvulsants. Monitor therapy
Minocycline: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
Mirtazapine: CNS Depressants may enhance the CNS depressant effect of Mirtazapine. Monitor therapy
Mitotane: May decrease the serum concentration of CYP3A4 Substrates. Management: Doses of CYP3A4 substrates may need to be adjusted substantially when used in patients being treated with mitotane. Consider therapy modification
Nabilone: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
Orlistat: May decrease the serum concentration of Anticonvulsants. Monitor therapy
Orphenadrine: CNS Depressants may enhance the CNS depressant effect of Orphenadrine. Avoid combination
Osimertinib: May increase the serum concentration of CYP3A4 Substrates. Osimertinib may decrease the serum concentration of CYP3A4 Substrates. Monitor therapy
OxyCODONE: CNS Depressants may enhance the CNS depressant effect of OxyCODONE. Management: When oxycodone is combined with another CNS depressant, a dose reduction of one or both agents should be considered. The extended release oxycodone starting dose should be reduced 50% to 67% when initiated in patients already receiving CNS depressants. Consider therapy modification
Paraldehyde: CNS Depressants may enhance the CNS depressant effect of Paraldehyde. Avoid combination
Perampanel: May enhance the CNS depressant effect of CNS Depressants. Management: Patients taking perampanel with any other drug that has CNS depressant activities should avoid complex and high-risk activities, particularly those such as driving that require alertness and coordination, until they have experience using the combination. Consider therapy modification
PHENobarbital: May decrease the serum concentration of Zonisamide. Monitor therapy
Phenytoin: May decrease the serum concentration of Zonisamide. Monitor therapy
Pramipexole: CNS Depressants may enhance the sedative effect of Pramipexole. Monitor therapy
QuiNIDine: Carbonic Anhydrase Inhibitors may decrease the excretion of QuiNIDine. Monitor therapy
ROPINIRole: CNS Depressants may enhance the sedative effect of ROPINIRole. Monitor therapy
Rotigotine: CNS Depressants may enhance the sedative effect of Rotigotine. Monitor therapy
Rufinamide: May enhance the adverse/toxic effect of CNS Depressants. Specifically, sleepiness and dizziness may be enhanced. Monitor therapy
Salicylates: May enhance the adverse/toxic effect of Carbonic Anhydrase Inhibitors. Salicylate toxicity might be enhanced by this same combination. Management: Avoid these combinations when possible.Dichlorphenamide use with high-dose aspirin as contraindicated. If another combination is used, monitor patients closely for adverse effects. Tachypnea, anorexia, lethargy, and coma have been reported. Consider therapy modification
Selective Serotonin Reuptake Inhibitors: CNS Depressants may enhance the adverse/toxic effect of Selective Serotonin Reuptake Inhibitors. Specifically, the risk of psychomotor impairment may be enhanced. Monitor therapy
Siltuximab: May decrease the serum concentration of CYP3A4 Substrates. Monitor therapy
Sodium Oxybate: May enhance the CNS depressant effect of CNS Depressants. Management: Consider alternatives to combined use. When combined use is needed, consider minimizing doses of one or more drugs. Use of sodium oxybate with alcohol or sedative hypnotics is contraindicated. Consider therapy modification
St John's Wort: May decrease the serum concentration of CYP3A4 Substrates. Management: Consider an alternative for one of the interacting drugs. Some combinations may be specifically contraindicated. Consult appropriate manufacturer labeling. Consider therapy modification
Suvorexant: CNS Depressants may enhance the CNS depressant effect of Suvorexant. Management: Dose reduction of suvorexant and/or any other CNS depressant may be necessary. Use of suvorexant with alcohol is not recommended, and the use of suvorexant with any other drug to treat insomnia is not recommended. Consider therapy modification
Tapentadol: May enhance the CNS depressant effect of CNS Depressants. Management: Start tapentadol at a dose of one-third to one-half of the normal dose if being initiated in a patient who is taking another drug with CNS depressant effects. Monitor closely for evidence of excessive CNS depression. Consider therapy modification
Tetrahydrocannabinol: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
Thalidomide: CNS Depressants may enhance the CNS depressant effect of Thalidomide. Avoid combination
Tocilizumab: May decrease the serum concentration of CYP3A4 Substrates. Monitor therapy
Trimeprazine: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy
Zolpidem: CNS Depressants may enhance the CNS depressant effect of Zolpidem. Management: Reduce the Intermezzo brand sublingual zolpidem adult dose to 1.75 mg for men who are also receiving other CNS depressants. No such dose change is recommended for women. Avoid use with other CNS depressants at bedtime; avoid use with alcohol. Consider therapy modification
Frequency not always defined. Frequencies noted in patients receiving other anticonvulsants:
Central nervous system: Drowsiness (17%), dizziness (13%)
Gastrointestinal: Anorexia (13%)
1% to 10%:
Cardiovascular: Facial edema (1%)
Central nervous system: Headache (10%), agitation (9%), irritability (9%), fatigue (7% to 8%), tiredness (7%), confusion (6%), depression (6%), insomnia (6%), lack of concentration (6%), memory impairment (6%), ataxia (≥1% to 6%), speech disturbance (5%), decreased mental acuity (4%), anxiety (3%), nervousness (2%), schizophreniform disorder (2%), speech disturbance (2%), convulsions (≥1%), hyperesthesia (≥1%), seizure (1%), status epilepticus (1%), hypotonia (≤1%), hyperthermia
Dermatologic: Skin rash (1% to 3%), bruising (2%), pruritus (≥1%), hypohidrosis (children), Stevens-Johnson syndrome, toxic epidermal necrolysis
Endrocrine & metabolic: Metabolic acidosis
Gastrointestinal: Nausea (9%), abdominal pain (6%), diarrhea (5%), dyspepsia (3%), weight loss (3%), constipation (2%), dysgeusia (2%), xerostomia (2%), vomiting (≥1%)
Hematologic & oncologic: Agranulocytosis, aplastic anemia
Neuromuscular & skeletal: Paresthesia (4%), abnormal gait (≥1%), tremor (≥1%), weakness (≥1%)
Ophthalmic: Diplopia (6%), nystagmus (4%), amblyopia (≥1%)
Otic: Tinnitus (≥1%)
Renal: Nephrolithiasis (4%, children 3% to 8%), increased blood urea nitrogen
Respiratory: Rhinitis (2%), increased cough (≥1%), pharyngitis (≥1%)
Miscellaneous: Flu-like syndrome (4%), accidental injury (≥1%)
<1% (Limited to important or life threatening): Alopecia, amenorrhea, apnea, arthritis, atrial fibrillation, bladder calculus, bradycardia, brain disease, cardiac failure, cerebrovascular accident, cholangitis, cholecystitis, cholestatic jaundice, colitis, deafness, DRESS syndrome, duodenitis, fecal incontinence, gastrointestinal ulcer, gingivitis, glaucoma, hematemesis, hematuria, hemoptysis, hirsutism, hypermenorrhea, hypersensitivity reaction, hypertension, hypoglycemia, hyponatremia, hypotension, immunodeficiency, impotence, iritis, leukopenia, lupus erythematosus, lymphadenopathy, mastitis, neuropathy, oculogyric crisis, pancreatitis, photophobia, psychomotor disturbance, pulmonary embolism, rectal hemorrhage, stroke, suicidal behavior, suicidal ideation, syncope, thrombocytopenia, thrombophlebitis, urinary incontinence, ventricular premature contractions
Concerns related to adverse effects:
• CNS effects: Significant CNS effects include psychiatric symptoms (eg, depression, psychosis), psychomotor slowing (eg, difficulty with concentration, speech or language problems), and fatigue or somnolence; may occur within the first month of treatment, most commonly at doses of ≥300 mg/day. May cause sedation, which may impair physical or mental abilities; patients must be cautioned about performing tasks which require mental alertness (eg, operating machinery or driving).
• Metabolic acidosis: Use may be associated with the development of metabolic acidosis (generally dose-dependent) in certain patients; predisposing conditions/therapies include renal disease, severe respiratory disease, diarrhea, status epilepticus, ketogenic diet, and other medications. Metabolic acidosis can occur at doses as low as 25 mg daily. Serum bicarbonate should be monitored prior to initiation and during therapy; if metabolic acidosis occurs, consider decreasing the dose or tapering the dose to discontinue. If use continued despite acidosis, alkali treatment should be considered. Untreated metabolic acidosis may increase the risk of developing nephrolithiasis, nephrocalcinosis, osteomalacia, or osteoporosis.
• Multiorgan hypersensitivity reactions: Potentially serious, sometimes fatal drug reaction with eosinophilia and systemic symptoms (DRESS), also known as multiorgan hypersensitivity reactions, have been reported. Monitor for signs and symptoms (eg, fever, rash, lymphadenopathy, facial swelling, eosinophilia) in association with other organ system involvement (eg, hepatitis, nephritis, hematological abnormalities, myocarditis, myositis). Evaluate immediately if signs or symptoms are present. Discontinue therapy if alternative cause cannot be established.
• Renal effects: Creatinine and BUN elevations have been reported; monitor renal function and discontinue therapy if acute renal failure or significant sustained increase in creatinine/BUN concentration occurs. Kidney stones have also been reported.
• Suicidal ideation: Pooled analysis of trials involving various antiepileptics (regardless of indication) showed an increased risk of suicidal thoughts/behavior (incidence rate: 0.43% treated patients compared to 0.24% of patients receiving placebo); risk observed as early as 1 week after initiation and continued through duration of trials (most trials ≤24 weeks). Monitor all patients for notable changes in behavior that might indicate suicidal thoughts or depression; notify healthcare provider immediately if symptoms occur.
• Sulfonamide (“sulfa”) allergy: The FDA-approved product labeling for many medications containing a sulfonamide chemical group includes a broad contraindication in patients with a prior allergic reaction to sulfonamides. There is a potential for cross-reactivity between members of a specific class (eg, two antibiotic sulfonamides). However, concerns for cross-reactivity have previously extended to all compounds containing the sulfonamide structure (SO2NH2). An expanded understanding of allergic mechanisms indicates cross-reactivity between antibiotic sulfonamides and nonantibiotic sulfonamides may not occur or at the very least this potential is extremely low (Brackett 2004; Johnson 2005; Slatore 2004; Tornero 2004). In particular, mechanisms of cross-reaction due to antibody production (anaphylaxis) are unlikely to occur with nonantibiotic sulfonamides. T-cell-mediated (type IV) reactions (eg, maculopapular rash) are less well understood and it is not possible to completely exclude this potential based on current insights. In cases where prior reactions were severe (Stevens-Johnson syndrome/TEN), some clinicians choose to avoid exposure to these classes.
• Hepatic impairment: Use with caution in patients with hepatic impairment.
• Renal impairment: Do not use in patients with renal impairment (GFR <50 mL/minute).
Concurrent drug therapy issues:
• Drug-drug interactions: Potentially significant interactions may exist, requiring dose or frequency adjustment, additional monitoring, and/or selection of alternative therapy. Consult drug interactions database for more detailed information.
• Pediatric: Decreased sweating (oligohydrosis) and hyperthermia requiring hospitalization have been reported in children; use with caution when used in combination with other drugs that may predispose patients to heat-related disorders (eg, anticholinergics). Pediatric patients may be at an increased risk for and have more severe metabolic acidosis when compared with adults. Untreated metabolic acidosis may increase the risk of developing nephrolithiasis and/or nephrocalcinosis, osteoporosis and/or osteomalacia (possibly resulting in rickets), and may decrease growth rates.
• Hazardous agent: Use appropriate precautions for handling and disposal (NIOSH 2014 [group 3]).
• Withdrawal: Anticonvulsants should not be discontinued abruptly because of the possibility of increasing seizure frequency; therapy should be withdrawn gradually to minimize the potential of increased seizure frequency, unless safety concerns require a more rapid withdrawal.
Metabolic profile, specifically BUN, serum creatinine; serum bicarbonate (prior to initiation and periodically during therapy); suicidality (eg, suicidal thoughts, depression, behavioral changes); decreased sweating, elevated body temperature especially in warm or hot weather (particularly in pediatric patients)
Pregnancy Risk Factor
Teratogenic effects were observed in animal reproduction studies. Zonisamide crosses the placenta and can be detected in the newborn following delivery (Kawada 2002; Shimoyama 1999). Information related to pregnancy outcomes following maternal use of zonisamide is limited (Hernández-Díaz 2014; Kanemoto 2007; Kondo 1996; Ohtahara 2007). Metabolic acidosis is an adverse effect of zonisamide therapy; newborns exposed to zonisamide in utero should be monitored for transient metabolic acidosis after birth and pregnant women taking zonisamide should be monitored and treated as nonpregnant patients. In general, maternal polytherapy with antiepileptic drugs may increase the risk of congenital malformations; monotherapy with the lowest effective dose is recommended. Newborns of women taking antiepileptic medications may be at an increased risk of adverse events (Harden and Meader 2009).
Zonisamide clearance may increase during pregnancy, requiring dosage adjustment (Oles 2008; Reisinger 2013). Women of childbearing potential are advised to use effective contraception during therapy. Until additional data is available, other agents may be preferred for the treatment of epilepsy in pregnant women (Ohtahara 2007).
Patients exposed to zonisamide during pregnancy are encouraged to enroll themselves into the NAAED Pregnancy Registry by calling 1-888-233-2334. Additional information is available at http://www.aedpregnancyregistry.org.
• Discuss specific use of drug and side effects with patient as it relates to treatment. (HCAHPS: During this hospital stay, were you given any medicine that you had not taken before? Before giving you any new medicine, how often did hospital staff tell you what the medicine was for? How often did hospital staff describe possible side effects in a way you could understand?)
• Patient may experience asthenia, headache, lack of appetite, diarrhea, or insomnia. Have patient report immediately to prescriber signs of metabolic acidosis, signs of renal impairment, severe dizziness, syncope, change in balance, illogical thinking, anhidrosis, back pain, dyspepsia, hematuria, difficulty focusing, difficulty speaking, paresthesia, involuntary eye movements, vision changes, memory impairment, osteodynia, considerable myalgia, significant fatigue, edema of extremities, tremors, difficulty moving, signs of severe sulfonamide reaction, signs of Stevens-Johnson syndrome/toxic epidermal necrolysis, suicidal ideation, depression, anxiety, akathisia, irritability, panic attacks, or mood changes (HCAHPS).
• Educate patient about signs of a significant reaction (eg, wheezing; chest tightness; fever; itching; bad cough; blue skin color; seizures; or swelling of face, lips, tongue, or throat). Note: This is not a comprehensive list of all side effects. Patient should consult prescriber for additional questions.
Intended Use and Disclaimer: Should not be printed and given to patients. This information is intended to serve as a concise initial reference for healthcare professionals to use when discussing medications with a patient. You must ultimately rely on your own discretion, experience and judgment in diagnosing, treating and advising patients.
More about zonisamide
- Other brands: Zonegran