A 44-year-old, right-handed, white male presents for an evaluation and opinion regarding the underlying etiology of his seizures. The patient had his first seizure in the summer of 2009. This occurred out of sleep. He noted significant work-related stress and alcohol usage the night before. His girlfriend awoke in the early morning hours when the patient experienced a generalized tonic-clonic seizure. He bit the left side of his tongue and had post-event confusion. He returned to sleep but had a second generalized tonic-clonic seizure 30 min later. EEG was normal awake and asleep. He was prescribed levetiracetam but did not take it for a long term. He did well until October 2010, when he had a third nocturnal generalized tonic-clonic seizure. This event was preceded by sleep deprivation for over 24 h, significant alcohol use, and the use of cocaine. His girlfriend awoke to vocalizations associated with a convulsion. He was replaced on levetiracetam 500 mg twice daily. Review of risk factors for epilepsy disclosed that he had been involved in a motor vehicle accident in 1985 where he sustained a skull fracture that was associated with a loss of consciousness for approximately 5 days. He did not require neurosurgical intervention and recovered. He was later involved in an altercation in 1996 and was stabbed near his right eye, from which he also recovered. No family history of seizures, meningitis or encephalitis, stroke, brain tumor, brain surgery, migraines, collagen vascular disease, or febrile convulsions was evident. A brain MRI was obtained (Fig. 13.1).
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