The intoxicated EEG
نویسندگان
چکیده
A 38-year old male patient with pharmacoresistant bilateral temporal-lobe epilepsy was referred to our department for adjustment of antiepileptic-drug dosage with continuous VideoEEG monitoring. In 2013, bilateral deep brain electrodes were implanted for chronic stimulation in both anterior thalamic nuclei. After implantation, the patient remained seizure free of generalized tonic-clonic seizures, but continued to experience daily complex-partial seizures typically presenting with initial dizziness, shortness of breath and a short period of unresponsiveness. Before admission, he was treated with levetiracetam (1 g twice a day), lamotrigine (500 mg twice a day) and oxcarbazepine (600 mg twice a day). Due to insufficient seizure control and likely levetiracetam-associated aggressive behavior the following modifications were applied: At admission (day1) levetiracetam dosagewasreducedtothehalf (and completely stopped on day 3), while valproid acid was started at a low dose (300 mg twice a day). Accidentally, on day 2 the oxcarbazepine dosage was doubled in the evening (from 600 mg to 1200 mg). The next day (day 3) the patient again received the double oxcarbazepine dose in the morning and few hours later he presented with acute vertigo, nausea and vomiting. Continuous EEG-monitoring showed steep surface-negative excursions followed by shallow return to baseline (frequency = 2–3/s) that were most prominent in frontal derivations after eyes opening (Fig. 1A, arrows). This pattern was interpreted as rhythmic eye movements with slow upward phase and fast downward phase, i.e., downbeat-nystagmus (DBN). On clinical neurological examination DBN was confirmed, while no otherfocal neurologicaldeficits were found. Emergency brain CT was reportedly normal, excluding structural causes of acute DBN. Oxcarbazepine serum levels were supra-therapeutic (147.4 mmol/
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ورودعنوان ژورنال:
- Seizure
دوره 45 شماره
صفحات -
تاریخ انتشار 2017