Antiseizure Medication-Induced Nystagmus During Eye Closure Identified by Electroencephalography.

Nystagmus is a well-known side effect of antiseizure medicines (ASMs), but it is often underestimated and overlooked. Here, we describe a case in which nystagmus during eye closure was identified early using routine electroencephalography (EEG). A 34-year-old man developed focal epilepsy after head trauma at the age of 25 years. The patient was treated with carbamazepine but liver dysfunction was observed; therefore, treatment was attempted with lacosamide (LCM) and lamotrigine. With an increase in the LCM dose, steep potential changes suggestive of horizontal nystagmus were observed in the electrooculogram, F7, and F8 on EEG, and the patient complained of eye shaking during eye closure. These symptoms and EEG findings improved with LCM dose reduction. If the presence of nystagmus is identified on EEG coincidentally and a patient's subjective symptoms with ASM are confirmed, it is advisable to taper and/or discontinue the causative agent.

Generalized Epilepsy With Repetitive Sinus Pauses Following Generalized Tonic-Clonic Seizures Due to Reduced Baroreflex Sensitivity.

Epilepsy and syncope are sometimes difficult to differentiate, and they often occur together. We report here a unique case of severe neuromodulatory syncope associated with generalized epilepsy. A 24-year-old right-handed female with no remarkable history had her first epileptic seizure when she was 15 years old and was diagnosed with epilepsy. However, she had epileptic seizures or fainting spells every few months and was referred to Nara Medical Center at the age of 23 years. No obvious neurological abnormality was present, and no organic abnormality was found on head magnetic resonance imaging. The seizures were symmetrical generalized tonic-clonic seizures (GTCS) without aura, and the patient was unable to stand up for several hours after the seizure. Long-term video electroencephalogram monitoring revealed two types of seizures: (1) GTCS starting with generalized polyspikes and waves and (2) fainting with sinus arrest for up to 10 seconds when the patient tried to stand up after GTCS. After the addition of valproic acid following the diagnosis of generalized epilepsy, her epileptic seizures improved, but syncope remained. We consulted the cardiology department of our hospital and diagnosed mixed neuromodulatory syncope after performing the tilt test. She underwent catheter ablation for cardioneuromodulation, and her syncope improved. Several reports have described reduced baroreflex sensitivity during the interictal period in epilepsy, and seizure-related autonomic dysfunction has been implicated in sudden unexpected death in epilepsy (SUDEP). In addition to suppression of epileptic seizures, when autonomic nervous system symptoms associated with epilepsy are severe, as in this case, a thorough cardiovascular examination should be performed, and the patient should be treated with the goal of preventing SUDEP.