Levetiracetam is a second-generation antiepileptic drug that is chemically unrelated to other antiepileptic drugs. Levetiracetam is a broad-spectrum antiseizure medication that is approved as an adjunctive therapy in the treatment of partial and generalized tonic-clonic seizures in children and adults with epilepsy. The mechanism by which Levetiracetam induces behavioral changes remains unknown. Its proposed mechanism of action involves binding to synaptic vesicle protein 2A (SV2A) and this leads to neuronal inhibition. Though, the drug has a convenient dosing regimen and is relatively well tolerated, neuropsychiatric side effects can emerge beyond the initial titration period and may be the most common reason for drug discontinuation. Levetiracetam has been reported to cause varying degrees of psychiatric adverse effects including behavioral disturbance such as agitation, hostility and psychosis, and mood symptoms and suicidality. It has been shown to induce psychiatric side effects in 13.3% of adults, with only 0.7% presenting with severe symptoms such as depression, agitation, or hostility. The prevalence rate of development of psychosis in these patients is estimated to be about 1.4%. A review of literature has demonstrated a relative correlation between Levetiracetam use and the development of neurobehavioral symptoms which is increased in predisposed individuals. This research describes the case of a 28-year-old woman with seizure disorder and a psychiatric history of schizoaffective disorder who developed aggressive behavior, paranoia, and severe hostility following administration of Levetiracetam 750 mg orally twice daily. She developed acute behavioral symptoms which were reversed with cessation of Levetiracetam. This report emphasizes the need for developing an appropriately high index of suspicion in promoting surveillance and prompt identification of behavioral adverse effects associated with Levetiracetam especially in high-risk patient population.

Tachycardia emergent from clozapine treatment is usually transient, often missed, unreported, and therefore frequently goes untreated resulting in possible premature discontinuation of an otherwise effective treatment. Clozapine-induced tachycardia results from direct effects on the sympathetic nervous system including the blockade of cardiac muscarinic M2 receptors, presynaptic α2 adrenoceptors, and indirect activation of the β adrenoceptors. Unfortunately, there are no clear guidelines for monitoring or treating tachycardia induced by clozapine. We present a case of a 55-year-old man with treatment-resistant schizophrenia initiated on clozapine who developed persistent tachycardia and right bundle branch block in the course of treatment. Tachycardia persisted despite treatment with metoprolol and necessitated a transfer to the intensive care unit. A reduction in clozapine dose with the addition of adjunctive antipsychotic(lurasidone) stabilized the patient’s heart rate. This case highlights the need for consistent physical examination and a multidisciplinary-based treatment approach for patients on clozapine. The case also suggests that clozapine dose reduction and combination antipsychotic treatments may preclude the need to discontinue clozapine in patients with persistent tachycardia.

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