Binge eating disorder (off-label use):
Oral: Initial: 100 mg/day for 7 days; may increase dose based on response and tolerability in increments of 100 mg/day every week to a maximum dose of 600 mg/day in 1 or 2 divided doses (Ref). Alternatively, 25 mg/day for 7 days has been studied; may increase dose based on response and tolerability in increments of 50 mg/day every week to a maximum daily dose of 100 mg in patients with a BMI <35 kg/m2 or 150 mg for a BMI ≥35 kg/m2 (Ref).
Focal (partial) onset seizures:
Note: FDA approved for adjunctive treatment of focal (partial) onset seizures; may be used off label as monotherapy for focal (partial) onset seizures (Ref).
Oral: Initial: 100 mg/day in 1 to 2 divided doses. May increase in increments of 100 mg/day every 2 weeks based on response and tolerability up to 400 mg/day. Doses of up to 600 mg/day have been studied; however, there is no evidence of increased response with doses >400 mg/day, and doses ≥300 mg/day are associated with increased side effects.
Discontinuation of therapy: In chronic therapy, withdraw gradually to minimize the potential of increased seizure frequency and status epilepticus (in patients with epilepsy) and withdrawal symptoms (eg, dysphoria, hallucinations, headache, insomnia, tremor), unless safety concerns require more rapid withdrawal. For seizure disorders, some experts suggest withdrawing antiseizure drugs over a few to several (eg, 2 to 6) months (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.
Altered kidney function:
Note: The manufacturer recommends against use at eGFR <50 mL/minute, due to lack of experience with drug dosing and toxicity in patients with kidney impairment; however, a single dose study suggests that pharmacokinetic parameters are not substantially impacted in renal impairment (Ref). Patients with kidney impairment may be at increased risk for metabolic acidosis and nephrolithiasis (Ref); use with caution.
eGFR ≥30 mL/minute: Oral: No dosage adjustment necessary (Ref).
eGFR <30 mL/minute: Oral: Consider alternative agents or use with caution. No initial dosage adjustment necessary but utilize a slow titration and frequent monitoring of tolerability and response (Ref). Consider therapeutic drug monitoring (when available) to optimize dose and/or monitor for toxicity (Ref).
Augmented renal clearance (measured urinary CrCl ≥130 mL/minute/1.73 m2):
Note: Augmented renal clearance (ARC) is a condition that occurs in certain critically ill patients without organ dysfunction and with normal SCr concentrations. Younger patients (<55 years of age) admitted post trauma or major surgery are at highest risk for ARC, as well as those with sepsis, burns, or hematologic malignancies. An 8- to 24-hour measured urinary CrCl is necessary to identify these patients (Ref).
Oral: No initial dosage adjustment necessary; titrate based on tolerability and response. Consider therapeutic drug monitoring (when available) to guide dosing (Ref).
Hemodialysis, intermittent (thrice weekly): Dialyzable (50%) (Ref):
Oral: Limited data available; consider alternative agents or use with caution. No initial dosage adjustment necessary; administer as a once daily dose; when scheduled dose falls on a dialysis day, administer after dialysis. Utilize a slow titration and frequent monitoring of tolerability and response. Consider a supplemental dose if seizures occur following dialysis sessions (Ref). Consider therapeutic drug monitoring (when available) to optimize dose, to evaluate drug removal by dialysis in patients with post-hemodialysis seizures, and/or to monitor for toxicity (Ref).
Peritoneal dialysis: Oral: No data available; consider alternative agents or use with caution. No initial dosage adjustment necessary. Utilize a slow titration and frequent monitoring of tolerability and response. Consider therapeutic drug monitoring (when available) to optimize dose and/or monitor for toxicity (Ref).
CRRT: Oral: Limited data; in one case report, zonisamide was readily cleared from serum. No initial dose adjustment necessary. Utilize a slow titration and frequent monitoring of tolerability and response. Given clearance of the drug by CRRT, patients previously stable on zonisamide may require titration to higher doses based on tolerability and response. Therapeutic drug monitoring (when available) is recommended (Ref).
PIRRT (eg, sustained, low-efficiency diafiltration): Oral: Limited data, but some removal is expected. No initial dosage adjustment necessary; administer as a once daily dose; when scheduled dose falls on a PIRRT day, administer after PIRRT. Consider a supplemental dose if seizures occur following PIRRT sessions. Utilize a slow titration and frequent monitoring of tolerability and response. Therapeutic drug monitoring (when available) is recommended (Ref).
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.
Dermatologic reactions: Discontinue at the first sign of rash, unless the rash is clearly not drug-related. If Stevens-Johnson syndrome or toxic epidermal necrolysis is suspected, do not resume zonisamide and consider alternative therapy.
Drug reaction with eosinophilia and systemic symptoms: Discontinue therapy if another cause for signs/symptoms of DRESS cannot be established.
Hypersensitivity or other serious reactions: Discontinue immediately if signs of hypersensitivity or other serious reactions (eg, fulminant hepatic necrosis, agranulocytosis, aplastic anemia, other blood dyscrasias) occur.
Metabolic acidosis: If metabolic acidosis develops and persists, consider decreasing dose or tapering dose to discontinue. If continuing zonisamide despite persistent acidosis, consider alkali treatment.
Ophthalmic effects: Discontinue in patients with acute onset of decreased visual acuity and/or ocular pain.
Refer to adult dosing. Use with caution; initiate therapy at the low end of the dosing range.
(For additional information see "Zonisamide: Pediatric drug information")
Partial-onset seizures; adjunct therapy: Note: Zonisamide is approved as adjunct therapy, and trials have also shown efficacy as monotherapy; however, based on results of the SANAD II trial, zonisamide should not be used as first-line therapy in patients ≥5 years, as other agents have shown greater efficacy with a more positive adverse effect profile (Ref).
Children <5 years: Limited data available: Oral: Initial: 1 to 2 mg/kg/day in 2 divided doses; increase dose in increments of 0.5 to 1 mg/kg/day once or twice daily every 2 weeks; usual dose: 5 to 8 mg/kg/day (Ref).
Children ≥5 years and Adolescents <16 years: Limited data available: Oral: Initial: 0.5 to 1 mg/kg/day in 1 to 2 divided doses; increase dose in increments of 0.5 to 1 mg/kg/day in 2 divided doses every 2 weeks; if patients require more rapid titration, dose may be increased in 1.5 mg/kg/day increments; if concomitant CYP3A4 inducing agent, may increase at weekly intervals. Reported usual dose: 5 to 8 mg/kg/day in 1 or 2 divided doses, although some patients may require up to 12 mg/kg/day or a maximum daily dose of 500 mg/day once daily or in 2 divided doses, whichever is less (Ref).
Adolescents ≥16 years: Oral: Initial: 100 mg once daily; dose may be increased to 200 mg/day after 2 weeks; further increases in dose should be made in increments of 100 mg/day and only after a minimum of 2 weeks between adjustments; usual effective dose: 100 to 600 mg/day (Ref). Note: There is no evidence of increased benefit with doses >400 mg/day. Steady-state serum concentrations fluctuate 27% with once-daily dosing, and 14% with twice-daily dosing; patients may benefit from divided doses given twice daily (Ref).
Discontinuation of therapy: Limited data available: Children ≥6 years and Adolescents: There is currently no standard method for the withdrawal of antiseizure medications in pediatric patients. Successful discontinuation of an antiseizure medication is dependent on several factors, including but not limited to: Time of seizure freedom, underlying reason for the seizures, neuroimaging abnormalities, underlying neurodevelopmental status, and medication to be withdrawn (including dose, duration of therapy, and other pharmacokinetic/dynamic considerations) (Ref). To minimize the potential of increased seizure frequency, chronic zonisamide therapy should be withdrawn gradually. In pediatric patients, it has been suggested to decrease dose in ~2 mg/kg increments at weekly intervals (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Slower dosage titration and more frequent monitoring are recommended. Do not use if GFR <50 mL/minute. Marked renal impairment (CrCl <20 mL/minute) was associated with a 35% increase in AUC.
Slower titration and frequent monitoring are indicated.
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Frequency not always defined. Frequencies noted in patients receiving other antiseizure medications:
>10%:
Gastrointestinal: Anorexia (13%)
Nervous system: Dizziness (13%), drowsiness (17%)
1% to 10%:
Cardiovascular: Facial edema (≤1%)
Dermatologic: Ecchymoses (2%), hypohidrosis (children), pruritus (≥1%), skin rash (3%), Stevens-Johnson syndrome, toxic epidermal necrolysis
Endocrine & metabolic: Metabolic acidosis
Gastrointestinal: Abdominal pain (6%), constipation (2%), diarrhea (5%), dysgeusia (2%), dyspepsia (3%), nausea (9%), vomiting (≥1%), weight loss (3%), xerostomia (2%)
Hematologic & oncologic: Agranulocytosis, aplastic anemia
Nervous system: Agitation (≤9%), anxiety (3%), ataxia (≥1% to 6%), confusion (6%), decreased mental acuity (4%), depression (6%), dysphasia (2%), fatigue (8%), headache (10%), hyperesthesia (≥1%), hyperthermia, hypotonia (≤1%), insomnia (6%), irritability (≤9%), lack of concentration (6%), memory impairment (6%), nervousness (2%), schizophreniform disorder (2%), seizure (≥1%), speech disturbance (5%), status epilepticus (1%), tiredness (7%)
Neuromuscular & skeletal: Abnormal gait (≥1%), asthenia (≥1%), paresthesia (4%), tremor (≥1%)
Ophthalmic: Amblyopia (≥1%), diplopia (6%), nystagmus disorder (4%)
Otic: Tinnitus (≥1%)
Renal: Nephrolithiasis (4%; children: 3% to 8%)
Respiratory: Increased cough (≥1%), pharyngitis (≥1%), rhinitis (2%)
Miscellaneous: Accidental injury (≥1%), flu-like syndrome (4%)
<1%, postmarketing, and/or case reports: Abnormal dreams, acne vulgaris, acute myopia, acute pancreatitis, albuminuria, alopecia, amenorrhea, anemia, angle-closure glaucoma, aphthous stomatitis, apnea, arthralgia, arthritis, atrial fibrillation, bladder calculus, bladder pain, bradycardia, cardiac failure, cerebrovascular accident, chest pain, cholangitis, cholecystitis, cholelithiasis, cholestatic jaundice, colitis, conjunctivitis, deafness, decreased libido, decreased serum albumin, decreased serum bicarbonate, decreased serum calcium, dehydration, diaphoresis, drug reaction with eosinophilia and systemic symptoms, duodenitis, dysarthria, dyskinesia, dysphagia, dyspnea, dystonia, dysuria, eczema, edema, encephalopathy, esophagitis, euphoria, facial nerve paralysis, fecal incontinence, flank pain, flatulence, gastritis, gastroenteritis, gastrointestinal ulcer, gingival hemorrhage, gingival hyperplasia, gingivitis, glaucoma, glossitis, gynecomastia, heavy menstrual bleeding, hematemesis, hematuria, hemoptysis, hirsutism, hyperammonemia, hyperchloremia, hyperkinetic muscle activity, hyperreflexia, hypersensitivity reaction, hypertension, hypertonia, hypoglycemia, hypokinesia, hyponatremia, hypophosphatemia, hypotension, immunodeficiency, impotence, increased blood urea nitrogen, increased creatine phosphokinase in blood specimen, increased lactic dehydrogenase, increased serum alanine aminotransferase, increased serum alkaline phosphatase, increased serum aspartate aminotransferase, increased serum creatinine, increased thirst, iritis, leukopenia, lower limb cramp, lupus erythematosus, lymphadenopathy, maculopapular rash, malaise, mastitis, melena, microcytic anemia, movement disorder, myalgia, myasthenia, myoclonus, neck stiffness, neuropathy, nocturia, oculogyric crisis, oral mucosa ulcer, palpitation, peripheral edema, peripheral neuritis, petechia, photophobia, polyuria, psychomotor disturbance, psychosis, pulmonary embolism, pustular rash, rectal hemorrhage, rhabdomyolysis, stomatitis, suicidal behavior, suicidal ideation, syncope, tachycardia, thrombocytopenia, thrombophlebitis, twitching, urinary frequency, urinary incontinence, urinary retention, urinary urgency, urticaria, vascular insufficiency, ventricular premature contractions, vertigo, vesiculobullous dermatitis, visual field defect, weight gain, xeroderma
Hypersensitivity to zonisamide, sulfonamides, or any component of the formulation
Note: Although the FDA-approved product labeling states this medication is contraindicated in patients with hypersensitivity to sulfonamide-containing drugs, the scientific basis of this cross-sensitivity has been challenged.
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).
• Dermatologic reactions: Severe reactions, including Stevens-Johnson syndrome and toxic epidermal necrolysis, have been reported with an onset typically early in therapy.
• Hyperammonemia/encephalopathy: Hyperammonemia, with or without encephalopathy, may occur with monotherapy or in combination with other medications (eg, valproic acid, topiramate); incidence and severity may be dose related. Risk may be increased in patients with inborn errors of metabolism or decreased hepatic mitochondrial activity. May be asymptomatic; monitor for lethargy, vomiting, or unexplained changes in mental status. Hyperammonemia should resolve with a decreased dose or discontinuation of therapy.
• Metabolic acidosis: Use may be associated with the development of metabolic acidosis in certain patients; predisposing conditions/therapies include renal disease, severe respiratory disease, diarrhea, status epilepticus, ketogenic diet, and other medications. Onset typically occurs early in treatment but may develop at any time. Metabolic acidosis is generally dose-dependent but can occur at doses as low as 25 mg daily. Monitor serum bicarbonate. If metabolic acidosis occurs and treatment is continued, 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.
• Ophthalmic effects: Has been associated with acute myopia and secondary angle-closure glaucoma in adults and children, typically within 1 month of initiation.
• Renal effects: Creatinine and BUN elevations have been reported; monitor renal function. Kidney stones have also been reported.
• Suicidal ideation: Pooled analysis of trials involving various antiseizure medications (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.
Disease-related concerns:
• Hepatic impairment: Use with caution in patients with hepatic impairment.
• Renal impairment: Consider alternative agents or use with caution (slow titration with close monitoring) in patients with GFR ≤30 mL/minute (Bansal 2015).
Other warnings/precautions:
• Withdrawal: Antiseizure medications 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.
Pediatric patients may also be at an increased risk and may have more severe metabolic acidosis. Untreated metabolic acidosis may increase the risk of developing nephrolithiasis, nephrocalcinosis, osteomalacia (or rickets in children), or osteoporosis; pediatric patients may also have decreased growth rates. Oligohydrosis (decreased sweating) and hyperthermia have been reported in 40 pediatric patients; many cases occurred after exposure to elevated environmental temperatures; some cases resulted in heat stroke requiring hospitalization; pediatric patients may be at an increased risk; monitor patients, especially pediatric patients, for decreased sweating and hyperthermia, especially in warm or hot weather; use zonisamide with caution in patients receiving drugs that predispose to heat-related disorders (eg, anticholinergic agents, carbonic anhydrase inhibitors). In children, agitation, anxiety, ataxia, and behavior disorders have been reported (Kimura 1994).
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Capsule, Oral:
Zonegran: 25 mg
Zonegran: 100 mg [contains fd&c red #40 (allura red ac dye), fd&c yellow #6 (sunset yellow)]
Generic: 25 mg, 50 mg, 100 mg
Suspension, Oral:
Zonisade: 100 mg/5 mL (150 mL) [contains sodium benzoate; strawberry flavor]
May be product dependent
Capsules (Zonegran Oral)
25 mg (per each): $21.71
100 mg (per each): $28.11
Capsules (Zonisamide Oral)
25 mg (per each): $0.17 - $0.55
50 mg (per each): $0.19 - $1.10
100 mg (per each): $0.66 - $2.19
Suspension (Zonisade Oral)
100 mg/5 mL (per mL): $3.36
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Oral:
Capsules: Swallow whole; administer with or without food.
Oral suspension: Shake well before use. Measure dose using provided oral syringe. A household teaspoon or tablespoon is not an adequate measuring device and should not be used. Administer with or without food.
Oral: May be administered without regard to meals.
Capsule: Swallow capsule whole; do not crush, chew, or break capsule.
Oral suspension: Shake well before use. Measure dose using provided oral syringe. A household teaspoon or tablespoon is not an adequate measuring device and should not be used.
Hazardous agent (NIOSH 2024 [table 2]).
Use appropriate precautions for receiving, handling, storage, preparation, dispensing, transporting, administration, and disposal. Follow NIOSH and USP 800 recommendations and institution-specific policies/procedures for appropriate containment strategy (NIOSH 2023; NIOSH 2024; USP-NF 2020).
Note: Facilities may perform risk assessment of some hazardous drugs to determine if appropriate for alternative handling and containment strategies (USP-NF 2020). Refer to institution-specific handling policies/procedures.
An FDA-approved patient medication guide, which is available with the product information and at https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/020789s036lbl.pdf#page=25, must be dispensed with this medication.
Focal (partial) onset seizures: Adjunctive therapy in the treatment of focal (partial) onset seizures in adolescents >16 years of age and adults.
Binge eating disorder
Zonegran may be confused with SINEquan
Zonisamide may be confused with lacosamide
Substrate of CYP2C19 (Minor), CYP3A4 (Major with inducers), CYP3A4 (Minor with inhibitors); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential;
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.
Acrivastine: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Alcohol (Ethyl): CNS Depressants may increase CNS depressant effects of Alcohol (Ethyl). Risk C: Monitor
Alizapride: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Allopurinol: CNS Depressants may increase sedative effects of Allopurinol. Risk C: Monitor
Amantadine: Carbonic Anhydrase Inhibitors may increase serum concentration of Amantadine. Risk C: Monitor
Amisulpride (Oral): May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Amphetamines: Carbonic Anhydrase Inhibitors may decrease excretion of Amphetamines. Risk C: Monitor
Articaine: May increase CNS depressant effects of CNS Depressants. Management: Consider reducing the dose of articaine if possible when used in patients who are also receiving CNS depressants. Monitor for excessive CNS depressant effects with any combined use. Risk D: Consider Therapy Modification
Azelastine (Nasal): May increase CNS depressant effects of CNS Depressants. Risk X: Avoid
Benperidol: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Blonanserin: CNS Depressants may increase CNS depressant effects of Blonanserin. Management: Use caution if coadministering blonanserin and CNS depressants; dose reduction of the other CNS depressant may be required. Strong CNS depressants should not be coadministered with blonanserin. Risk D: Consider Therapy Modification
Brexanolone: CNS Depressants may increase CNS depressant effects of Brexanolone. Risk C: Monitor
Brimonidine (Topical): May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Bromopride: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Bromperidol: May increase CNS depressant effects of CNS Depressants. Risk X: Avoid
Buclizine: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Buprenorphine: CNS Depressants may increase CNS depressant effects 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 at lower doses in patients already receiving CNS depressants. Risk D: Consider Therapy Modification
BusPIRone: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Cannabinoid-Containing Products: CNS Depressants may increase CNS depressant effects of Cannabinoid-Containing Products. Risk C: Monitor
Carbonic Anhydrase Inhibitors: May increase adverse/toxic effects of 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. Risk X: Avoid
Cetirizine (Systemic): May increase CNS depressant effects of CNS Depressants. Management: Consider avoiding this combination if possible. If required, monitor for excessive sedation or CNS depression, limit the dose and duration of combination therapy, and consider CNS depressant dose reductions. Risk D: Consider Therapy Modification
Chloral Hydrate/Chloral Betaine: CNS Depressants may increase CNS depressant effects of Chloral Hydrate/Chloral Betaine. Management: Consider alternatives to the use of chloral hydrate or chloral betaine and additional CNS depressants. If combined, consider a dose reduction of either agent and monitor closely for enhanced CNS depressive effects. Risk D: Consider Therapy Modification
Chlormethiazole: May increase CNS depressant effects of CNS Depressants. Management: Monitor closely for evidence of excessive CNS depression. The chlormethiazole labeling states that an appropriately reduced dose should be used if such a combination must be used. Risk D: Consider Therapy Modification
Chlorphenesin Carbamate: May increase adverse/toxic effects of CNS Depressants. Risk C: Monitor
Cinnarizine: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
CNS Depressants: May increase adverse/toxic effects of CNS Depressants. Risk C: Monitor
CYP3A4 Inducers (Strong): May decrease serum concentration of Zonisamide. Risk C: Monitor
Dantrolene: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Daridorexant: May increase CNS depressant effects of CNS Depressants. Management: Dose reduction of daridorexant and/or any other CNS depressant may be necessary. Use of daridorexant with alcohol is not recommended, and the use of daridorexant with any other drug to treat insomnia is not recommended. Risk D: Consider Therapy Modification
Desmopressin: Hyponatremia-Associated Agents may increase hyponatremic effects of Desmopressin. Risk C: Monitor
DexmedeTOMIDine: CNS Depressants may increase CNS depressant effects of DexmedeTOMIDine. Management: Monitor for increased CNS depression during coadministration of dexmedetomidine and CNS depressants, and consider dose reductions of either agent to avoid excessive CNS depression. Risk D: Consider Therapy Modification
Difelikefalin: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Difenoxin: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Dihydralazine: CNS Depressants may increase hypotensive effects of Dihydralazine. Risk C: Monitor
Dimethindene (Topical): May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Dothiepin: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Doxylamine: CNS Depressants may increase CNS depressant effects of Doxylamine. Risk C: Monitor
DroPERidol: May increase CNS depressant effects of CNS Depressants. Management: Consider dose reductions of droperidol or of other CNS agents (eg, opioids, barbiturates) with concomitant use. Risk D: Consider Therapy Modification
Emedastine (Systemic): May increase CNS depressant effects of CNS Depressants. Management: Consider avoiding this combination if possible. If required, monitor for excessive sedation or CNS depression, limit the dose and duration of combination therapy, and consider CNS depressant dose reductions. Risk C: Monitor
Entacapone: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Esketamine (Nasal): May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Flecainide: Carbonic Anhydrase Inhibitors may decrease excretion of Flecainide. Risk C: Monitor
Flunarizine: CNS Depressants may increase CNS depressant effects of Flunarizine. Risk X: Avoid
Flunitrazepam: CNS Depressants may increase CNS depressant effects of Flunitrazepam. Management: Reduce the dose of CNS depressants when combined with flunitrazepam and monitor patients for evidence of CNS depression (eg, sedation, respiratory depression). Use non-CNS depressant alternatives when available. Risk D: Consider Therapy Modification
HydrOXYzine: May increase CNS depressant effects of CNS Depressants. Management: Consider a decrease in the CNS depressant dose, as appropriate, when used together with hydroxyzine. Increase monitoring of signs/symptoms of CNS depression in any patient receiving hydroxyzine together with another CNS depressant. Risk D: Consider Therapy Modification
Ixabepilone: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Kava Kava: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Ketotifen (Systemic): May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Kratom: May increase CNS depressant effects of CNS Depressants. Risk X: Avoid
Lacosamide: Antiseizure Agents (Sodium Channel Blockers) may increase adverse/toxic effects of Lacosamide. Specifically the risk for bradycardia, ventricular tachyarrhythmias, or a prolonged PR interval may be increased. Risk C: Monitor
LamoTRIgine: Zonisamide may increase arrhythmogenic effects of LamoTRIgine. LamoTRIgine may increase CNS depressant effects of Zonisamide. Management: Consider the risk of serious arrhythmias or death versus any expected benefit of lamotrigine in patients receiving concomitant sodium channel blockers. Additionally, if combined, caution patients that CNS depressant effects may be increased. Risk D: Consider Therapy Modification
Lemborexant: May increase CNS depressant effects of CNS Depressants. Management: Dosage adjustments of lemborexant and of concomitant CNS depressants may be necessary when administered together because of potentially additive CNS depressant effects. Close monitoring for CNS depressant effects is necessary. Risk D: Consider Therapy Modification
Levocetirizine: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Lisuride: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Lithium: Carbonic Anhydrase Inhibitors may decrease serum concentration of Lithium. Risk C: Monitor
Lofepramine: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Lofexidine: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Loxapine: CNS Depressants may increase CNS depressant effects of Loxapine. Management: Consider reducing the dose of CNS depressants administered concomitantly with loxapine due to an increased risk of respiratory depression, sedation, hypotension, and syncope. Risk D: Consider Therapy Modification
Magnesium Sulfate: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Mefloquine: May decrease therapeutic effects of Antiseizure Agents. Mefloquine may decrease serum concentration of Antiseizure Agents. Management: Mefloquine is contraindicated for malaria prophylaxis in persons with a history of seizures. If antiseizure drugs are being used for another indication, monitor antiseizure drug concentrations and treatment response closely with concurrent use. Risk D: Consider Therapy Modification
Melitracen: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Memantine: Carbonic Anhydrase Inhibitors may increase serum concentration of Memantine. Risk C: Monitor
Mequitazine: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Metergoline: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
MetFORMIN: Carbonic Anhydrase Inhibitors may increase adverse/toxic effects of MetFORMIN. Specifically, the risk of developing lactic acidosis may be increased. Risk C: Monitor
Methenamine: Carbonic Anhydrase Inhibitors may decrease therapeutic effects of Methenamine. Management: Consider avoiding the concomitant use of medications that alkalinize the urine, such as carbonic anhydrase inhibitors, and methenamine. Monitor for decreased therapeutic effects of methenamine if used concomitant with a carbonic anhydrase inhibitor. Risk D: Consider Therapy Modification
Methotrimeprazine: CNS Depressants may increase CNS depressant effects of Methotrimeprazine. Methotrimeprazine may increase CNS depressant effects of CNS Depressants. Management: Reduce the usual dose of CNS depressants by 50% if starting methotrimeprazine until the dose of methotrimeprazine is stable. Monitor patient closely for evidence of CNS depression. Risk D: Consider Therapy Modification
Methoxyflurane: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Metoclopramide: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
MetyraPONE: Coadministration of Antiseizure Agents and MetyraPONE may alter diagnostic results. Management: Consider alternatives to the use of the metyrapone test in patients taking antiseizure agents. Risk D: Consider Therapy Modification
MetyroSINE: CNS Depressants may increase sedative effects of MetyroSINE. Risk C: Monitor
Mianserin: May decrease therapeutic effects of Antiseizure Agents. Risk C: Monitor
Minocycline (Systemic): May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Moxonidine: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Nabilone: May increase CNS depressant effects of CNS Depressants. Risk X: Avoid
Nalfurafine: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Noscapine: CNS Depressants may increase adverse/toxic effects of Noscapine. Risk X: Avoid
Olopatadine (Nasal): May increase CNS depressant effects of CNS Depressants. Risk X: Avoid
Opicapone: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Opioid Agonists: CNS Depressants may increase CNS depressant effects of Opioid Agonists. Management: Avoid concomitant use of opioid agonists and benzodiazepines or other CNS depressants when possible. These agents should only be combined if alternative treatment options are inadequate. If combined, limit the dosages and duration of each drug. Risk D: Consider Therapy Modification
Opipramol: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Orlistat: May decrease serum concentration of Antiseizure Agents. Risk C: Monitor
Orphenadrine: CNS Depressants may increase CNS depressant effects of Orphenadrine. Risk X: Avoid
Oxomemazine: May increase CNS depressant effects of CNS Depressants. Risk X: Avoid
Oxybate Salt Products: CNS Depressants may increase CNS depressant effects of Oxybate Salt Products. Management: Consider alternatives to this combination when possible. If combined, dose reduction or discontinuation of one or more CNS depressants (including the oxybate salt product) should be considered. Interrupt oxybate salt treatment during short-term opioid use Risk D: Consider Therapy Modification
OxyCODONE: CNS Depressants may increase CNS depressant effects of OxyCODONE. Management: Avoid concomitant use of oxycodone and benzodiazepines or other CNS depressants when possible. These agents should only be combined if alternative treatment options are inadequate. If combined, limit the dosages and duration of each drug. Risk D: Consider Therapy Modification
Paliperidone: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Paraldehyde: CNS Depressants may increase CNS depressant effects of Paraldehyde. Risk X: Avoid
Perampanel: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Periciazine: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
PHENobarbital: Zonisamide may increase CNS depressant effects of PHENobarbital. PHENobarbital may decrease serum concentration of Zonisamide. Risk C: Monitor
Pipamperone: May increase adverse/toxic effects of CNS Depressants. Risk C: Monitor
Piribedil: CNS Depressants may increase CNS depressant effects of Piribedil. Risk C: Monitor
Pizotifen: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Pramipexole: CNS Depressants may increase sedative effects of Pramipexole. Risk C: Monitor
Primidone: Zonisamide may increase CNS depressant effects of Primidone. Primidone may decrease serum concentration of Zonisamide. Risk C: Monitor
Procarbazine: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Rilmenidine: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Ropeginterferon Alfa-2b: CNS Depressants may increase adverse/toxic effects of Ropeginterferon Alfa-2b. Specifically, the risk of neuropsychiatric adverse effects may be increased. Management: Avoid coadministration of ropeginterferon alfa-2b and other CNS depressants. If this combination cannot be avoided, monitor patients for neuropsychiatric adverse effects (eg, depression, suicidal ideation, aggression, mania). Risk D: Consider Therapy Modification
ROPINIRole: CNS Depressants may increase sedative effects of ROPINIRole. Risk C: Monitor
Rotigotine: CNS Depressants may increase sedative effects of Rotigotine. Risk C: Monitor
Salicylates: May increase adverse/toxic effects of Carbonic Anhydrase Inhibitors. Carbonic Anhydrase Inhibitors may increase adverse/toxic effects of Salicylates. Management: Avoid these combinations when possible. If these agents are coadministered, monitor patients closely for adverse effects. Tachypnea, anorexia, lethargy, and coma have been reported. Risk D: Consider Therapy Modification
Suvorexant: CNS Depressants may increase CNS depressant effects 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. Risk D: Consider Therapy Modification
Thalidomide: CNS Depressants may increase CNS depressant effects of Thalidomide. Risk X: Avoid
Trimeprazine: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Valerian: May increase CNS depressant effects of CNS Depressants. Risk C: Monitor
Zolpidem: CNS Depressants may increase CNS depressant effects 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. Risk D: Consider Therapy Modification
Zuranolone: May increase CNS depressant effects of CNS Depressants. Management: Consider alternatives to the use of zuranolone with other CNS depressants or alcohol. If combined, consider a zuranolone dose reduction and monitor patients closely for increased CNS depressant effects. Risk D: Consider Therapy Modification
Food delays time to maximum concentration, but does not affect bioavailability. Management: Administer without regard to meals.
Patients who can become pregnant should use effective contraception during therapy and for 1 month after the last dose of zonisamide.
Manage epilepsy in patients who could become pregnant based on a shared decision-making process that optimizes seizure control and considers the possibility of pregnancy during treatment (Pack 2024). Regularly discuss age-specific and developmental needs, including pregnancy planning and contraceptive options, during the patient's reproductive lifespan (ACOG 2020; NICE 2022).
Obtain total serum trough concentrations of zonisamide twice prior to pregnancy while patient has stable seizure control and is on a minimal dose (Arfman 2020).
Zonisamide crosses the placenta (Schmidt 2023).
Data are insufficient to evaluate the risk of specific major congenital malformations and the risk of neurodevelopmental outcomes (IQ scores or autism spectrum disorder) in children following in utero exposure to zonisamide. Screen for major congenital malformations and monitor fetal growth when antiseizure medications are used during pregnancy. Conduct age-appropriate developmental screening in children who had in utero exposure to antiseizure medications (Pack 2024).
Metabolic acidosis is an adverse effect of zonisamide therapy; monitor newborns exposed to zonisamide in utero for transient metabolic acidosis.
Due to pregnancy-induced physiologic changes, the clearance of zonisamide may increase and plasma concentrations may decrease as pregnancy progresses (Arfman 2020; Pennell 2022; Schoretsanitis 2024). Monitor total zonisamide serum trough concentrations as needed during pregnancy and adjust doses based on decreasing concentrations and seizure control (Arfman 2020; Pack 2024). Formulate a plan to return to prepregnancy doses after delivery (NICE 2022).
Epilepsy is associated with adverse maternal and fetal outcomes (Kuang 2024; Mazzone 2023). Convulsive seizures should be minimized to reduce risks to the fetus and pregnant patient. Use caution if removing or replacing an effective seizure medication in patients who become pregnant during therapy. Folic acid supplementation prior to and during pregnancy minimizes the risk of congenital malformations and poor neurodevelopment (Pack 2024).
Data collection to monitor pregnancy outcomes following exposure to antiepileptic drugs is ongoing. Encourage patients to enroll in the North American Antiepileptic Drug (NAAED) Pregnancy Registry (1-888- 233-2334 or www.aedpregnancyregistry.org.)
Zonisamide is present in breast milk.
Data related to the presence of zonisamide in breast milk are available from case reports (Ando 2014; Kacirova 2024; Kawada 2002; Schmidt 2023; Shimoyama 1999).
• Data are available from 2 lactating patients who initiated zonisamide prior to or during pregnancy. The zonisamide dose in the first patient was 100 mg in the morning and 200 mg in the evening. On postpartum day 5, concentrations of zonisamide were 18 mcg/mL (breast milk) and 24.5 mcg/mL (maternal serum) when sampled 12.5 hours after the 200 mg dose. Authors of the study calculated the estimated infant dose of zonisamide via breast milk to be 2.7 mg/kg/day providing a relative infant dose (RID) of 44% compared to the weight-adjusted maternal dose (maternal weight 48.4 kg). The infant was fully breastfed until postpartum day 9, then partial breastfeeding was initiated. Thirty-four days after delivery, zonisamide concentrations in the infant serum were below the limit of quantification (<0.5 mcg/mL). Adverse events were not observed in the breastfed infant. Data is also available from a second patient taking zonisamide 100 mg/day. On postpartum day 5, concentrations of zonisamide were 5.1 mcg/mL (breast milk) and 5.9 mcg/mL (maternal serum), when sampled 5.1 hours after the dose. Authors of the study calculated the estimated infant dose of zonisamide via breast milk to be 0.77 mg/kg/day providing an RID of 36% compared to the weight adjusted maternal dose (maternal weight 47 kg). Adverse events were not observed in this infant who was partially breastfed for 2 weeks (Ando 2014). In general, breastfeeding is considered acceptable when the RID of a medication is <10%; when the RID is >25% breastfeeding should generally be avoided (Anderson 2016; Ito 2000).
• Breast milk was sampled in a patient over 30 days postpartum following a dose of zonisamide 100 mg 3 times/day. Zonisamide concentrations were 8.25 mcg/mL (breast milk) and 10.16 mcg/mL (maternal plasma) 2.5 hours after a maternal dose on postpartum day 3. The highest breast milk concentrations were obtained on postpartum day 30 when sampling occurred 1.5 hours after the dose (breast milk: 10.5 mcg/mL, maternal serum: 10.24 mcg/mL). The mother was taking other antipsychotic drugs in addition to zonisamide (not stated). Behavioral problems were not observed in the breastfed infant (Shimoyama 1999).
Zonisamide can be detected in the serum of breastfed infants (Birnbaum 2020; Kacirova 2024). Maternal and infant serum concentrations were evaluated in a study of patients taking zonisamide for epilepsy during pregnancy and postpartum. Maternal doses ranged from 200 to 500 mg/day (median 350 mg/day) and sampling occurred in 4 mothers and their breastfed infants between 6 and 19 weeks postpartum. The median infant zonisamide serum concentrations were 44.2% of the maternal serum concentration (range 35.2% to 125.3%). Breast milk was not sampled in this study (Birnbaum 2020).
According to the manufacturer, the decision to breastfeed during therapy should consider the risk of infant exposure, the benefits of breastfeeding to the infant, and the benefits of treatment to the mother. Monitor infants exposed to antiseizure medications via breast milk for sedation, signs of poor sucking, proper weight gain, abnormal platelet counts, abnormal liver function, and achievement of developmental milestones (Shawahna 2022; Tomson 2022). Measure antiseizure medication serum concentrations in the infant if symptoms of toxicity occur (Tomson 2022). Also monitor for decreased sweating and hyperthermia following zonisamide exposure.
Formulate a plan to return to pre-pregnancy doses if the dose of zonisamide was changed during pregnancy (Arfman 2020; NICE 2022); gradual dose adjustments over the first 21 days after delivery and maternal therapeutic drug monitoring are recommended if the dose of zonisamide was changed (Arfman 2020).
BUN, serum creatinine (periodically as clinically indicated); serum bicarbonate (prior to initiation and periodically during therapy); ammonia level (if signs/symptoms of encephalopathy occur); suicidality (eg, suicidal thoughts, depression, behavioral changes); decreased sweating, elevated body temperature especially in warm or hot weather (particularly in pediatric patients).
Timing of serum samples: Draw trough just before next dose.
Laboratory alert level: 40 mcg/mL (SI: 188.4 micromol/L).
Epilepsy: 10 to 40 mcg/mL (SI: 47.1 to 188.4 micromole/L) (AGNP [Hiemke 2018]).
Stabilizes neuronal membranes and suppresses neuronal hypersynchronization through action at sodium and calcium channels; does not affect GABA activity.
Absorption: Rapid (Patsalos 2018); food may delay time to peak.
Distribution: Vd: 1.45 L/kg; highly concentrated in erythrocytes.
Protein binding: 40%.
Metabolism: 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.
Bioavailability: Capsule: >90% (Patsalos 2018).
Half-life elimination: Plasma: ~63 hours (range: 50 to 68 hours).
Time to peak: Capsule: 2 to 6 hours; Oral suspension: 0.5 to 5 hours.
Excretion: Urine (62%, 35% as unchanged drug, 65% as metabolites); feces (3%).
Altered kidney function: 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%.
Pediatric: Renal clearance is significantly faster (1.7-fold) in children <5 years of age than children ≥5 years and adolescents. Clearance was more pronounced in pediatric patients receiving concurrent enzyme-inducing antiseizure medications (Wallander 2014).
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