

She exhibited an abnormal pupillary light response 12 additional times over 4 days ( Supplementary Table 1). Anesthetics were escalated to achieve burst suppression EEG along with escalating anti-seizure medications.

The patient’s pupils were reactive following the administration of a midazolam bolus. Without imaging evidence of ICP increase or mass effect, management was focused on the treatment of focal status epilepticus rather than cerebral herniation. The electroclinical motor seizures were controlled with anti-seizure medications however, EEG continued to be highly epileptiform with near continuous right hemispheric lateralized periodic discharges (LPDs) with sharp wave morphology, occurring at approximately 0.7–1.0 Hz. Anti-seizure regimen was escalated to valproic acid, levetiracetam, lacosamide, briefly perampanel, and ultimately midazolam and ketamine infusion. On cEEG, these movements corresponded with right hemispheric lateralized rhythmic delta activity with sharp waves at 1.5–2 Hz with frequent evolution into well-formed seizures, meeting the criteria for electroclinical status epilepticus (occupying >20% of a 60-minute EEG period). Over the course of several days, the patient exhibited intermittent left forehead, cheek, and thumb twitching. cEEG was started and showed focal slowing over the right parietotemporal region, without clinical events.

Ultimately, the patient was intubated to protect the airway. She was initially treated with lorazepam and lacosamide with resolution of movements however, persistent tactile stimulation was required to maintain arousal. We describe a patient with focal status epilepticus with FDPs documented by Neurological Pupil index (NPi) and interpret a possible pathophysiologic correlate on continuous electroencephalogram (cEEG). Furthermore, reports of pupillary changes during seizures are often singular events without objective data. Alterations in pupillary light response have been described with seizures however, the loss of pupillary response and pathophysiologic mechanism remains unknown in this population. Fixed and dilated pupils (FDPs) are commonly associated with mass effect in several conditions (vascular, neoplastic, demyelinating, or inflammatory), leading to damage in the midbrain, oculomotor nuclei, or efferent fiber pathways. Abnormal pupillary response to light, based on reactivity or pupil size and asymmetry, can be seen in a variety of conditions, ranging from benign or congenital conditions to a life-threating intracranial process. Pupillary size and light response are valuable components of neurological examination, especially in the care of critically ill patients when pupillary size and reactivity to light may provide an objective finding of neurological changes.
