- Brivaracetam initiation in an elderly woman with temporal lobe epilepsy produced persistent intrusive sexual urges and self-stimulatory behaviour, resolving after drug discontinuation.
- Mechanisms may involve shared levetiracetam action, dopaminergic vulnerability linked to DRD2/ANKK1 polymorphisms, and bilateral hippocampal atrophy mimicking incomplete Klüver-Bucy syndrome.
- Clinicians should actively monitor for changes in libido after Brivaracetam initiation, recognising patients may conceal symptoms due to embarrassment.
Neuropsychopharmacol Rep. 2026 Sep;46(3):e70160. doi: 10.1002/npr2.70160.
ABSTRACT
BACKGROUND: Sexual dysfunction is a common comorbidity in patients with epilepsy; it correlates with seizure frequency and right temporal lobe epilepsy and affects quality of life (QOL). Despite its clinical significance, sexual dysfunction is often underassessed in clinical practice. Brivaracetam (BRV), an anti-seizure medication (ASM) introduced in recent years, is considered to have few psychiatric side effects, and no association with sexual dysfunction has been reported to date. We report a case of temporal lobe epilepsy in which the patient exhibited increased libido following the initiation of BRV.
CASE PRESENTATION: A woman in her 70s with drug-resistant temporal lobe epilepsy, weekly focal seizures, and mild cognitive impairment was treated with brexpiprazole (BXP) for delusions of theft. BRV (50 mg/day) was initiated due to worsening epileptic seizures. Three weeks later, she developed persistent, intrusive sexual urges accompanied by self-stimulatory behavior (e.g., genital touching). She initially concealed these symptoms due to embarrassment but disclosed them at the follow-up 1 month later. Given the temporal association with BRV initiation, the drug was discontinued, resulting in marked improvement within 2 weeks and subsequent resolution. Throughout the course of treatment, no changes were observed in seizure frequency, cognitive function, or other ASMs.
DISCUSSION: Previous reports have described increased libido with levetiracetam, which shares the same mechanism of action with BRV. Genetic factors, such as reduced striatal dopamine receptor density associated with DRD2/ANKK1 polymorphisms may contribute to psychiatric side effects. In this case, BRV-associated modulation of neurotransmission may have interacted with a vulnerable dopaminergic system, as indicated by the need for BXP. Preexisting bilateral hippocampal atrophy may also have provided a structural substrate resembling a pharmacologically induced incomplete Klüver-Bucy syndrome. Clinicians should be aware that patients may hesitate to report such symptoms and should actively monitor for changes in libido after initiating BRV.
PMID:42675017 | DOI:10.1002/npr2.70160
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