He noted during the course of a generalized tonic-clonic seizure brief episodes of bilateral pupillary miosis during the tonic phase and bilateral pupil mydriasis during the clonic phase. Pupil alterations during seizures were described as early as 1881 by Sir William Richard Gowers. She underwent tracheostomy and was discharged with close support from her family and therapy teams. Her mental status improved moderately following simple instructions by family members. As anticonvulsants were adjusted and a ketogenic diet was initiated, the associated LPDs decreased over the following days with resolution of pupil abnormalities throughout the subsequent 10-week hospital course. More often, she exhibited bilateral pupil dilation (9/12, 75%) with a single event of brisk left pupil and fixed right pupil (approximately 2.3-mm size bilateral) and single event of fixed, dilated left pupil and sluggish right pupil (left pupil dilated approximately 6 mm and right approximately 3 mm). 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.
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