Epilepsy & Treatment

Lamotrigine (LTG) is a widely used antiepileptic drug (AED) for the treatment of partial and generalized seizures. LTG is

metabolized predominantly in the liver through glucuronidation and when administrating with hepatic enzyme-inhibiting

AED such as valproate (VPA), the serum level of LTG is increasing significantly. A 32-year-old woman with a 13-year history

of epileptic seizures admitted to the hospital for exacerbating seizures. The seizures developed secondarily generalized and

occurred several times a day. She had taken a single AED of LTG 450 mg a day. After intraveonously administration of VPA and

then maintaining dose of VPA 600 mg and lamotrigine 450 mg a day, the seizure activity was resolved. However, she developed

blurred vision, dizziness and nausea five days after medication of multiple AEDs. Neurologic examination was notable for

prominent bilateral horizontal gaze-evoked nystagmus and perverted downward saccades during head impulses for horizontal

canals. After suspicion of LTG toxicity, LTG was discontinued and replaced with levetiracetam. The dizziness and gaze evoked

nystagmus markedly improved after discontinuation of the LTG and the seizure did not occur during six months of follow-up.

Gaze-evoked nystagmus and perverted downward corrective saccades during horizontal head impulses indicate dysfunction of

the vestibulocerebellum, especially flocculus and the floccular function of gaze holding and inhibition of the AC pathway could

be disrupted by LTG toxicity. Even though LTG has been reported to be well tolerated, the risk of toxic effects could increase

when VPA is combined.