Levetiracetam

170.21

170.105530

200-659-6

44YRR34555

760119

DTXSID9023207

C47581

Crystals from ethyl acetate|White to off-white crystalline powder

N03AX14|N - Nervous system

2933790090

63.4

-0.3

White crystalline powder

1.2±0.1 g/cm3

115-117 °C @ Solvent: Acetone

395.9ºC at 760 mmHg

9℃

1.519

H2O: >5mg/mL

Store at RT

3.5X10-6 mm Hg at 25 deg C

-89.7 º

Faint

Bitter

Henry's Law constant = 2.7X10-10 atm-cu m/mol at 25 °C (est)

Hydroxyl radical reaction rate constant = 3.4X10-11 cu cm/molec-sec at 25 °C (est)

UN1230 - class 3 - PG 2 - Methanol, solution

22-36-39/23/24/25-23/24/25-11

26-45-36/37-16-7

UX9656166

Xn,T,F

P305 + P351 + P338

H302-H319

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl levetiracetam, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

|Warning|H302 (89.66%): Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P280, P301+P312, P305+P351+P338, P330, P337+P313, and P501|Aggregated GHS information provided by 118 companies from 13 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

The oral TDLO of levetiracetam in humans is 10 mg/kg. Symptoms of levetiracetam overdose are consistent with its adverse effect profile and may include agitation, aggression, somnolence, decreased level of consciousness, respiratory depression, or coma. There is no antidote for levetiracetam overdose, therefore management should involve general supportive measures and symptomatic treatment. Hemodialysis results in significant clearance of plasma levetiracetam (approximately 50% within 4 hours) and should be considered in cases of overdose as indicated by the patient's status.

Prospective studies reported that chronic brivaracetam therapy was not accompanied by significant elevations in serum aminotransferase levels and clinically apparent liver injury was not observed. Brivaracetam has had limited general use, but has not been linked to instances of clinically apparent liver injury. Levetiracetam, an anticonvulsant with similar structure and mechanism of action, has been linked to rare instances of acute liver injury, generally arising within 1 to 20 weeks and presenting with a hepatocellular pattern of injury without immunoallergic or autoimmune features. Whether similar cases will be linked to brivaracetam is not known.|Prospective studies reported that chronic levetiracetam therapy was not accompanied by significant elevations in serum aminotransferase levels and clinically apparent liver injury was not observed. Since its approval for use and wide spread availability, however, levetiracetam has been linked to rare instances of serum enzyme elevations and occasional cases of clinically apparent liver injury. The time to onset of liver injury after starting levetiracetam has ranged from 1 week to 5 months and the usual pattern of injury has been hepatocellular. Immunoallergic features and autoantibodies were rare. At least one case of acute liver failure attributed to levetiracetam has been published, but the number of reported cases clinically apparent cases of liver injury has been few. In addition, levetiracetam is usually considered a reasonable alternative therapy in patients who develop anticonvulsant hypersensitivity (DRESS) syndrome after aromatic anticonvulsant use despite the fact that it has been implicated in rare instances of DRESS and Stevens Johnson syndrome.

No interaction between probenecid and levetiracetam was observed; however, probenecid decreased the renal clearance of ucb L057 (inactive metabolite of levetiracetam) by 60%.|/Levetiracetam/ had no effect on the pharmacokinetic disposition of phenytoin in patients with refractory epilepsy. Pharmacokinetics of levetiracetam were also not affected by phenytoin.|Levetiracetam did not alter the pharmacokinetics of valproate in healthy volunteers. Valproate 500 mg twice daily did not modify the rate or extent of levetiracetam absorption or its plasma clearance or urinary excretion. There also was no effect on exposure to and the excretion of the primary metabolite, ucb L057. Potential drug interactions between /levetiracetam/ and other Antiepileptic Drugs (AEDs) (carbamazepine, gabapentin, lamotrigine, phenobarbital, phenytoin, primidone and valproate) were also assessed by evaluating the serum concentrations of levetiracetam and these AEDs during placebo-controlled clinical studies. These data indicate that levetiracetam does not influence the plasma concentration of other AEDs and that these AEDs do not influence the pharmacokinetics of levetiracetam.|/Levetiracetam/ did not influence the pharmacokinetics and pharmacodynamics (ECG) of digoxin given as a 0.25 mg dose every day. Coadministration of digoxin did not influence the pharmacokinetics of levetiracetam.|For more Interactions (Complete) data for LEVETIRACETAM (7 total), please visit the HSDB record page.

Levetiracetam and its metabolites are largely unbound to plasma proteins (<10%).

While data specific to levetiracetam were not located(SRC, 2007), the literature suggests that some pharmaceutically active compounds originating from human and veterinary therapy are not eliminated completely in municipal sewage treatment plants and are therefore discharged into receiving waters(1). Wastewater treatment processes often were not designed to remove them from the effluent(2). Selected organic waste compounds may be degrading to new and more persistent compounds that may be released instead of or in addition to the parent compound(2).

To study the pharmacokinetics of levetiracetam (LEV) at birth, during lactation, and in the nursed infant. Eight consecutive breast-feeding women with epilepsy treated with LEV twice daily and their infants were studied. The mean umbilical cord serum/maternal serum ratio was 1.14 (range, 0.97-1.45) (n = 4). The mean milk/maternal serum concentration ratio was 1.00 (range, 0.76-1.33) at 3 to 5 days after delivery (n = 7). At sampling 2 weeks to 10 months after delivery (n = 5), it was similar (range, 0.85-1.38). At 3 to 5 days after delivery, the infants had very low LEV serum concentrations (<10-15 microM), a finding that persisted during continued breast-feeding. ...|Levetiracetam is distributed into milk.

Levetiracetam is indicated as an adjunctive therapy in the treatment of partial onset seizures in epileptic patients who are one month of age and older. Additionally, it is indicated as an adjunct in the treatment of myoclonic seizures in patients with juvenile myoclonic epilepsy who are 12 years of age and older, and in primary generalized tonic-clonic seizures in patients with idiopathic generalized epilepsy who are 6 years of age and older. Levetiracetam is also available as an orally dissolvable tablet that is indicated as an adjunct in the treatment of partial onset seizures in patients with epilepsy who are 4 years of age and older and weigh more than 20kg.|Levetiracetam Actavis is indicated as monotherapy in the treatment of partial-onset seizures with or without secondary generalisation in patients from 16 years of age with newly diagnosed epilepsy.Levetiracetam Actavis is indicated as adjunctive therapy:in the treatment of partial-onset seizures with or without secondary generalisation in adults, children and infants from one month of age with epilepsy;in the treatment of myoclonic seizures in adults and adolescents from 12 years of age with juvenile myoclonic epilepsy;in the treatment of primary generalised tonic-clonic seizures in adults and adolescents from 12 years of age with idiopathic generalised epilepsy.|Levetiracetam Actavis Group is indicated as monotherapy in the treatment of partial-onset seizures with or without secondary generalisation in patients from 16 years of age with newly diagnosed epilepsy.Levetiracetam Actavis Group is indicated as adjunctive therapy:in the treatment of partial-onset seizures with or without secondary generalisation in adults, children and infants from 1 month of age with epilepsy;in the treatment of myoclonic seizures in adults and adolescents from 12 years of age with juvenile myoclonic epilepsy;in the treatment of primary generalised tonic-clonic seizures in adults and adolescents from 12 years of age with idiopathic generalised epilepsy.|Levetiracetam Hospira is indicated as monotherapy in the treatment of partial onset seizures with or without secondary generalisation in adults and adolescents from 16 years of age with newly diagnosed epilepsy.Levetiracetam Hospira is indicated as adjunctive therapyin the treatment of partial onset seizures with or without secondary generalisation in adults, adolescents and children from 4 years of age with epilepsy.in the treatment of myoclonic seizures in adults and adolescents from 12 years of age with Juvenile Myoclonic Epilepsy.in the treatment of primary generalised tonic-clonic seizures in adults and adolescents from 12 years of age with Idiopathic Generalised Epilepsy.Levetiracetam Hospira concentrate is an alternative for patients when oral administration is temporarily not feasible.|Levetiracetam ratiopharm is indicated as monotherapy in the treatment of partial onset seizures with or without secondary generalisation in patients from 16 years of age with newly diagnosed epilepsy.Levetiracetam ratiopharm is indicated as adjunctive therapy:in the treatment of partial onset seizures with or without secondary generalisation in adults, children and infants from 1 month of age with epilepsy;in the treatment of myoclonic seizures in adults and adolescents from 12 years of age with juvenile myoclonic epilepsy;in the treatment of primary generalised tonic-clonic seizures in adults and adolescents from 12 years of age with idiopathic generalised epilepsy.|Levetiracetam is indicated as monotherapy in the treatment of partial-onset seizures with or without secondary generalisation in patients from 16 years of age with newly diagnosed epilepsy.Levetiracetam is indicated as adjunctive therapy:in the treatment of partial-onset seizures with or without secondary generalisation in adults, children and infants from one month of age with epilepsy;in the treatment of myoclonic seizures in adults and adolescents from 12 years of age with juvenile myoclonic epilepsy;in the treatment of primary generalised tonic-clonic seizures in adults and adolescents from 12 years of age with idiopathic generalised epilepsy.|Levetiracetam Teva is indicated as monotherapy in the treatment of partial onset seizures with or without secondary generalisation in adults and adolescents from 16 years of age with newly diagnosed epilepsy.Levetiracetam Teva is indicated as adjunctive therapy:in the treatment of partial onset seizures with or without secondary generalisation in adults, adolescents, children and infants from 1 month of age with epilepsy;in the treatment of myoclonic seizures in adults and adolescents from 12 years of age with juvenile myoclonic epilepsy;in the treatment of primary generalised tonic-clonic seizures in adults and adolescents from 12 years of age with idiopathic generalised epilepsy.|Keppra is indicated as monotherapy in the treatment of partial-onset seizures with or without secondary generalisation in patients from 16 years of age with newly diagnosed epilepsy.Keppra is indicated as adjunctive therapy:in the treatment of partial-onset seizures with or without secondary generalisation in adults, children and infants from one month of age with epilepsy;in the treatment of myoclonic seizures in adults and adolescents from 12 years of age with juvenile myoclonic epilepsy;in the treatment of primary generalised tonic-clonic seizures in adults and adolescents from 12 years of age with idiopathic generalised epilepsy.|Matever is indicated as monotherapy in the treatment of partial-onset seizures with or without secondary generalisation in patients from 16 years of age with newly diagnosed epilepsy.Matever is indicated as adjunctive therapy:in the treatment of partial-onset seizures with or without secondary generalisation in adults, children and infants from one month of age with epilepsy;in the treatment of myoclonic seizures in adults and adolescents from 12 years of age with juvenile myoclonic epilepsy;in the treatment of primary generalised tonic-clonic seizures in adults and adolescents from 12 years of age with idiopathic generalised epilepsy.|Levetiracetam Sun is indicated as monotherapy in the treatment of partial-onset seizures with or without secondary generalisation in patients from 16 years of age with newly diagnosed epilepsy.Levetiracetam Sun is indicated as adjunctive therapy:in the treatment of partial-onset seizures with or without secondary generalisation in adults and children from four years of age with epilepsy;in the treatment of myoclonic seizures in adults and adolescents from 12 years of age with juvenile myoclonic epilepsy;in the treatment of primary generalised tonic-clonic seizures in adults and adolescents from 12 years of age with idiopathic generalised epilepsy.Levetiracetam Sun concentrate is an alternative for patients when oral administration is temporarily not feasible.

Brivaracetam is a relatively unique anticonvulsant that is typically used in combination with other antiepileptic medications for partial onset seizures. Brivaracetam has been linked to rare instances of serum aminotransferase and alkaline phosphatase elevations during treatment and is suspected of causing rare cases of clinically apparent drug induced liver disease.|Levetiracetam is a relatively unique anticonvulsant that is typically used in combination with other antiepileptic medications for partial onset seizures. Levetiracetam has been linked to rare instances of serum aminotransferase and alkaline phosphatase elevations during treatment and to rare cases of clinically apparent drug induced liver disease.

Anticonvulsants

Levetiracetam is indicated as adjunctive therapy in the treatment of partial onset seizures in adults and children 4 years of age and older with epilepsy. /included in US product labe/

Adverse neuropsychiatric effects reported during levetiracetam treatment are classified into 3 categories: somnolence and fatigue, coordination difficulties, and behavioral changes. In controlled studies, 14.8% of patients who received levetiracetam experienced somnolence compared with 8.4% of placebo-treated patients, and about 3% of levetiracetam-treated patients discontinued treatment due to somnolence. About 14.7% of patients who received levetiracetam experienced asthenia compared with 9.1% of placebo-treated patients, and 0.8% of levetiracetam-treated patients discontinued treatment due to asthenia. Coordination difficulties were experienced by 3.4% of levetiracetam patients compared with 1.6% of placebo-treated patients. Somnolence, asthenia, and coordination difficulties occurred most frequently within the first 4 weeks of treatment. Psychotic manifestations and hallucinations were reported rarely in patients receiving levetiracetam in clinical studies. Other behavioral symptoms (e.g., agitation, hostility, anxiety, apathy, emotional lability, depersonalization, depression, aggression, anger, irritability) occurred in 13.3% of levetiracetam-treated patients in clinical studies compared with 6.2% of placebo patients, and 1.7% of levetiracetam-treated patients discontinued treatment because of these events.|Because of the possibility of increased seizure frequency, anticonvulsant drugs, including levetiracetam, should not be discontinued suddenly. Levetiracetam should be withdrawn gradually by reducing the dosage by 1g daily at 2-week intervals.|Adverse effects occurring in 1% or more of patients receiving levetiracetam and more frequently than placebo include somnolence, asthenia, headache, infection, dizziness, pain, pharyngitis, depression, nervousness, rhinitis, anorexia, ataxia, vertigo, amnesia, anxiety, emotional lability, hostility, paresthesia, increased cough, sinusitis, and diplopia and were reported in clinical studies in which levetiracetam was administered in conjunction with other anticonvulsants. Asthenia, somnolence, and dizziness occurred predominantly during the initial 4 weeks of treatment.|Minor decreases in total mean erythrocyte count, mean hemoglobin, and mean hematocrit have been reported. Leukopenia, neutropenia, pancytopenia (with myelosuppression in some cases), and thrombocytopenia also have been observed, although a causal relationship to the drug has not been established.|For more Drug Warnings (Complete) data for LEVETIRACETAM (12 total), please visit the HSDB record page.

Levetiracetam appears to prevent seizure activity via the selective inhibition of hypersynchronized epileptiform burst firing without affecting normal neuronal transmission, though the exact mechanism through which this occurs is unclear. The therapeutic index of levetiracetam is wide, making it relatively unique amongst other anti-epileptic medications. Anti-epileptic drugs, including levetiracetam, may increase the risk of suicidal ideation or behaviour - patients taking levetiracetam should be monitored for the emergence or worsening of depressive symptoms, suicidal ideation, and behavioural abnormalities.

Drugs used to prevent SEIZURES or reduce their severity. (See all compounds classified as Anticonvulsants.)|Drugs used to specifically facilitate learning or memory, particularly to prevent the cognitive deficits associated with dementias. These drugs act by a variety of mechanisms. (See all compounds classified as Nootropic Agents.)

Levetiracetam is rapidly and nearly completely absorbed following oral administration, with a reported absolute oral bioavailability of essentially 100%. T_max is approximately 1.3 hours after dosing, and C_max is 31 μg/mL following a single 1000mg dose and 43 μg/mL following repeated dosing. Co-administration of levetiracetam with food delays T_max by approximately 1.5 hours and decreases C_max by 20%.|Approximately 66% of the administered dose of levetiracetam is excreted in the urine as unchanged drug, while only 0.3% of the total dose is excreted via the feces. The primary inactive metabolite of levetiracetam, L057, is also found in the urine as approximately 24% of the administered dose.|The volume of distribution of levetiracetam is approximately 0.5 to 0.7 L/kg.|The total plasma clearance of levetiracetam is 0.96 mL/min/kg, with renal clearance comprising 0.6 mL/min/kg. The primary inactive metabolite of levetiracetam, L057, has a renal clearance of 4 mL/min/kg. Given the relatively high proportion of drug undergoing renal clearance, overall clearance of levetiracetam is reduced in patients with renal impairment.|Absorption of levetiracetam is rapid, with peak plasma concentrations occurring in about an hour following oral administration in fasted subjects. The oral bioavailability of levetiracetam tablets is 100% and the tablets and oral solution are bioequivalent in rate and extent of absorption. Food does not affect the extent of absorption of levetiracetam but it decreases C max by 20% and delays T max by 1.5 hours.|The pharmacokinetics of levetiracetam are linear over the dose range of 500-5000 mg. Steady state is achieved after 2 days of multiple twice-daily dosing.|Levetiracetam is not significantly protein-bound (<10% bound) and its volume of distribution is close to the volume of intracellular and extracellular water.|Levetiracetam C max and AUC were 20% higher in women (N=11) compared to men (N=12). However, clearances adjusted for body weight were comparable.|For more Absorption, Distribution and Excretion (Complete) data for LEVETIRACETAM (12 total), please visit the HSDB record page.

Levetiracetam is minimally metabolized within the body - the major metabolic pathway appears to be the enzymatic hydrolysis of its acetamide group which produces an inactive carboxylic acid metabolite, L057, which accounts for approximately 24% of the total administered dose. The specific enzyme(s) responsible for this reaction are unclear, but this pathway is known to be independent of hepatic CYP enzymes and has been proposed to be driven primarily by type B esterases in the blood and other tissues. Two minor metabolites involving modifications to the pyrrolidone ring have been identified, one involving hydroxylation of the ring (constituting 1.6% of the total dose) and the other involving opening of the ring structure (constituting 0.9% of the total dose).|Levetiracetam is not extensively metabolized in humans. The major metabolic pathway is the enzymatic hydrolysis of the acetamide group, which produces the carboxylic acid metabolite, ucb L057 (24% of dose) and is not dependent on any liver cytochrome P450 isoenzymes. The major metabolite is inactive in animal seizure models. Two minor metabolites were identified as the product of hydroxylation of the 2-oxo-pyrrolidine ring (2% of dose) and opening of the 2-oxo-pyrrolidine ring in position 5 (1% of dose). There is no enantiomeric interconversion of levetiracetam or its major metabolite.

The plasma half-life of levetiracetam is 6-8 hours and is not affected by dose or repeat administration. Half-life is increased in the elderly (by about 40%) and those with renal impairment.|... The plasma elimination half-life of the unchanged drug varied between 7.4 hr and 7.9 hr. ...|Levetiracetam plasma half-life in adults is 7 +/-1 hour and is unaffected by either dose or repeated administration.

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 - it appears to play a role in vesicle exocytosis and in the modulation of synaptic transmission by increasing the available amount of secretory vesicles available for neurotransmission. Stimulation of pre-synaptic SV2A by levetiracetam may inhibit neurotransmitter release, 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. 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. Levetiracetam has also been shown to indirectly affect GABAergic neurotransmission (despite having no direct effect on GABAergic or glutamatergic receptors) and modulate ionic currents. Similarly, levetiracetam has been shown in vitro to inhibit N-type calcium channels. How, or even if, these actions are implicated in its anti-epileptic action have yet to be elucidated.|The precise mechanism by which levetiracetam exerts its antiepileptic effect is unknown. The antiepileptic activity of levetiracetam was assessed in a number of animal models of epileptic seizures. Levetiracetam did not inhibit single seizures induced by maximal stimulation with electrical current or different chemoconvulsants and showed only minimal activity in submaximal stimulation and in threshold tests. Protection was observed, however, against secondarily generalized activity from focal seizures induced by pilocarpine and kainic acid, two chemoconvulsants that induce seizures that mimic some features of human complex partial seizures with secondary generalization. Levetiracetam also displayed inhibitory properties in the kindling model in rats, another model of human complex partial seizures, both during kindling development and in the fully kindled state. The predictive value of these animal models for specific types of human epilepsy is uncertain.|In vitro and in vivo recordings of epileptiform activity from the hippocampus have shown that levetiracetam inhibits burst firing without affecting normal neuronal excitability, suggesting that levetiracetam may selectively prevent hypersynchronization of epileptiform burst firing and propagation of seizure activity.|Levetiracetam at concentrations of up to 10 muM did not demonstrate binding affinity for a variety of known receptors, such as those associated with benzodiazepines, GABA (gammaaminobutyric acid), glycine, NMDA (N-methyl-D-aspartate), re-uptake sites, and second messenger systems. Furthermore, in vitro studies have failed to find an effect of levetiracetam on neuronal voltage-gated sodium or T-type calcium currents and levetiracetam does not appear to directly facilitate GABAergic neurotransmission. However, in vitro studies have demonstrated that levetiractem opposes the activity of negative modulators of GABA- and glycine-gated currents and partially inhibits N-type calcium currents in neuronal cells.|A saturable and stereoselective neuronal binding site in rat brain tissue has been described for levetiracetam. Experimental data indicate that this binding site is the synaptic vesicle protein SV2A, thought to be involved in the regulation of vesicle exocytosis. Although the molecular significance of levetiracetam binding to synaptic vesicle protein SV2A is not understood, levetiracetam and related analogs showed a rank order of affinity for SV2A which correlated with the potency of their antiseizure activity in audiogenic seizure-prone mice. These findings suggest that the interaction of levetiracetam with the SV2A protein may contribute to the antiepileptic mechanism of action of the drug.|For more Mechanism of Action (Complete) data for LEVETIRACETAM (6 total), please visit the HSDB record page.

Maintain an open airway and assist ventilation if necessary. Administer supplemental oxygen. Treat stupor and coma if they occur. Protect the patient from self-injury caused by ataxia. Treat agitation and delirium if they occur. Monitor asymptomatic patients for a minimum of 4-6 hours. Admit symptomatic patients for at least 24 hours lamotrigine, felbamate, topiramate, or zonisamide ingestions. ... Administer activated charcoal orally if conditions are appropriate. Gastric lavage is not necessary after small to moderate ingestions if activated charcoal can be given promptly. ... /Anticonvulsants, Newer/|Standard hemodialysis procedures result in significant clearance of levetiracetam (approximately 50% in 4 hours) and should be considered in cases of overdose. Although hemodialysis has not been performed in the few known cases of overdose, it may be indicated by the patient's clinical state or in patients with significant renal impairment.|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/SIGNS AND SYMPTOMS/ Other than drowsiness, there were no adverse events in the few known cases of overdose in clinical trials. Cases of somnolence, agitation, aggression, depressed level of consciousness, respiratory depression and coma were observed with /levetiracetam/ overdoses in postmarketing use.|/CASE REPORTS/ A twelve year-old-girl with idiopathic partial epilepsy with secondary generalization, developed acute psychosis 10 days after the administration of levetiracetam. The patient was already on sodium valproate, and levetiracetam was given as add on therapy. A final dosage of 60 mg/kg was used. Complete seizure control was achieved but the patient developed hallucinations, agitation and self-harming behavior, as well as poor social contact. The psychotic behavior resolved completely soon after the discontinuation of levetiracetam.|/CASE REPORTS/ I In two patients Levetiracetam (LEV) was initiated to control refractory complex partial seizures (CPS). The first patient was treated with 1500 mg/day and complained of abdominal pain and weight loss 6 months later. Internal examination and colonoscopy revealed a punctate colitis. The second patient presented with bloody stool 1 month after LEV initiation. Colonoscopy showed punctate colitis. In both patients gastrointestinal symptoms disappeared following tapering of LEV. Three possible mechanisms of action are discussed. Colitis may be part of a hypersensitivity syndrome caused by LEV. Pharmacodynamic interactions with other anti-epileptic drugs, for example, carbamazepine may play a role. ...|/CASE REPORTS/ /Investigators/ report here the case of a 43-year-old woman who developed symptoms compatible with catatonia after being exposed to levetiracetam for the treatment of epilepsy. /Investigators/ review the difficulties that may be encountered in the differential diagnosis of medical catatonia.|For more Human Toxicity Excerpts (Complete) data for LEVETIRACETAM (8 total), please visit the HSDB record page.

alpha ethyl 2 oxo 1 Pyrrolidineacetamide

Human drugs -> Levetiracetam Actavis -> EMA Drug Category|Antiepileptics -> Human pharmacotherapeutic group|Human drugs -> Levetiracetam Actavis Group -> EMA Drug Category|Human drugs -> Levetiracetam Hospira -> EMA Drug Category|Human drugs -> Levetiracetam ratiopharm -> EMA Drug Category|Human drugs -> Levetiracetam Accord -> EMA Drug Category|Human drugs -> Levetiracetam Teva -> EMA Drug Category|Nervous sytem -> Human pharmacotherapeutic group|Human drugs -> Keppra -> EMA Drug Category|Human drugs -> Matever -> EMA Drug Category|Human drugs -> Levetiracetam Sun -> EMA Drug Category|Other antiepileptics -> Human pharmacotherapeutic group|Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients