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Abstract Details

Prolonged reversible focal neurologic deficits in the elderly with contralateral EEG slowing: a post-ictal, migrainous, or vascular phenomenon?
General Neurology
General Neurology Posters (7:00 AM-5:00 PM)
026
To describe clinical features in elderly patients with prolonged reversible focal neurologic deficits with contralateral slowing on EEG without witnessed seizures or structural cause.
Unilateral slowing on EEG is seen in many conditions with focal cerebral dysfunction.  We have encountered elderly patients with prolonged focal neurologic deficits with contralateral slowing on EEG without preceding seizures or structural cause.

Utilizing Advanced Cohort Explorer, patients >60 years of age admitted to the neurology services at Mayo Clinic, Rochester, MN from 6/1/2015-6/1/2020 who had undergone MRI and EEG were identified. Charts were reviewed to determine patients with reversible prolonged neurologic deficits (>6 hours) and exclude patients with a structural cause, witnessed seizures, or CNS infection.

Of 934 patients identified, 16 were included (10 men, median age 78). Aphasia was the most common presenting symptom (n=14, 87.5%) with a median NIH of 8. Deficits lasted for approximately 16-96 hours.  Other factors included headache (n=7, 43.8%), fever (n=5, 29.4%), and systolic blood pressure >200 (n=6, 37.5%). Previous spells occurred in 10 (62.5%). Neuroimaging was unrevealing of a cause in all patients.  Ipsilateral interictal epileptiform discharges (including TIRDA) were captured on the EEG with slowing in 4 (25%) and found subsequently in 2 (12.5%).  Presumptive diagnoses included seizure with post-ictal slowing, migraine, Lewy Body dementia, posterior reversible encephalopathy syndrome, and reversible cerebral vasoconstriction syndrome. Anti-seizure medications (ASMs) were started in the majority (81.3%). With a median follow-up of 10 months after discharge, 3 (18.8%) had further spells, including 2 on ASMs.
Elderly patients presenting with prolonged focal neurologic deficits and EEG slowing without a structural cause are most likely to present with aphasia. The EEG slowing is frequently interpreted as ictal or post-ictal phenomena. However, the etiology of this clinico-electrophysiological presentation remains indeterminate in a majority of cases and 1/5th of patients continue to have spells.
Authors/Disclosures
Kelsey M. Smith, MD (Mayo Clinic)
PRESENTER
The institution of Dr. Smith has received research support from CURE Epilepsy. The institution of Dr. Smith has received research support from UCB Pharmaceuticals.
David B. Burkholder, MD, FAAN (Mayo Clinic) The institution of Dr. Burkholder has received research support from Longboard pharmaceuticals.
Michel Toledano, MD (Mayo Clinic) Dr. Toledano has nothing to disclose.