Abstracts

Rationale:
Cerebral lesions are typically deemed epileptogenic only when the cortex is affected. Thalamic lesions rarely manifest with seizures and such occurrences are infrequently reported. Increasing evidence suggests that seizures may arise from network dysfunction, with thalamocortical circuits playing a pivotal role in ictogenesis. While seizures in bilateral thalamic infarcts have been reported, occurrences in unilateral thalamic infarcts are exceptionally rare. We present an unusual case of focal left temporal non-convulsive status epilepticus (NCSE) in a comatose patient with acute left thalamic infarct with no prior history of seizures.




Methods:
^{_{A 66-year-old man with a past medical history of hypertension, type II diabetes mellitus, hyperlipidemia, and recent left thalamic and midbrain stroke presented to an outside hospital for an episode of unresponsiveness and suspected seizure-like activity. His initial assessment revealed blood glucose of 67 mg/dl, a GCS score of 3, a temperature of 98F, and blood pressure of 211/116 mmHg. Serum electrolytes were normal. He was intubated and received intravenous lorazepam and levetiracetam before being transferred to our facility for further care. CT brain showed no acute hemorrhage. MRI of the brain demonstrated prior subacute left thalamic and midbrain infarcts and chronic hemorrhagic left cerebellar infarcts. CTA head and neck demonstrated moderate to severe stenosis of bilateral vertebral and internal carotid arteries and near occlusive right posterior cerebral artery. The patient was admitted to the neurocritical care unit, and continuous EEG monitoring was initiated for a suspicion of seizure-like activity upon presentation.}}























Results:





Continuous EEG monitoring recorded multiple focal seizures originating from the left posterior temporal region, each lasting 10-24 seconds and occurring 1-2 times per hour. These seizures began with low to medium voltage fast alpha/theta activity (7-9 Hz) in the left posterior temporal region, spreading to the left centro-parietal region, and evolving into low voltage, bluntly contoured theta/delta activity (3-6 Hz) before subsiding. Findings indicated focal electrographic status epilepticus, which resolved with levetiracetam and lacosamide. A repeat brain MRI showed no new structural changes. Despite weaning propofol, the patient remained comatose with intact brainstem reflexes. The patient's family opted for comfort measures due to lack of improvement, and the patient unfortunately passed away.

















Conclusions: In the absence of any structural insult in the left temporal region, we speculate that thalamic lesions, with subsequent disruption of thalamocortical networks, could escalate the susceptibility to focal seizures. In patients with thalamic lesions and altered mental status, EEG should be considered for prompt seizure detection. A deeper understanding of thalamocortical circuits in NCSE is warranted to help devise focused, therapeutic strategies to regulate abnormal neuronal activity and enhance patient outcomes.


Funding: None