The Epilepsy Spectrum– a Unique Case of Migralepsy
Abstract number :
3.319
Submission category :
4. Clinical Epilepsy / 4B. Clinical Diagnosis
Year :
2024
Submission ID :
35
Source :
www.aesnet.org
Presentation date :
12/9/2024 12:00:00 AM
Published date :
Authors :
Nikita Nanavaty, DO – University of Cincinnati
Presenting Author: Heather McKee, MD, FAES – University of Cincinnati
Rationale: Hemicrania epileptica (HE) or Migralepsy, as per the International Classification of Headache Disorders (ICHD-II), is a rare diagnosis characterized as an ipsilateral headache with ictal EEG paroxysms (3). The new ICHD-III removes this diagnosis leaving two remaining diagnoses, post-ictal headache and ictal epileptic headache, which encompass the migraine and epilepsy overlay (3, 6).
This unique case is an example of dual migraine and epilepsy that does not fall within current ICHD guidelines for post-ictal headache or ictal epileptic headache (4, 5), suggesting a need to expand the diagnostic criteria or revisit the diagnosis of migralepsy itself (1, 2).
Methods: Data were collected from medical records, including neuroimaging and EEG data, with written informed consent provided
Results: PJ, a 21-year-old right-handed male with anxiety, depression, marijuana and alcohol use, and allergic rhinitis. His prior medications include propranolol and cetirizine. He presented with a new migraine lasting 24 hours. Initially intermittent and accompanied by visual disturbances, the headache resolved with ibuprofen but recurred the next day with left temporal pain, spots in vision, and nausea. A CT head scan was negative at that time. The headache resolved on day 2 with IV acetaminophen, prochlorperazine, and saline.
Ten days later, he had a generalized tonic-clonic seizure with residual left hemiparesis, dysarthria, and a left visual field cut. He also experienced headache and nausea. Arriving as a code stroke, he was dosed with tissue plasminogen activator. An MRI at the time of admission showed enhancement in the right frontal lobe, and his EEG showed focal slowing in the corresponding region. He started levetiracetam 1 gram twice daily.
He continued to have hemiplegic migraines lasting 20-30 minutes with left hemiparesis and fatigue. Transitioning from propranolol to verapamil 120 mg daily for migraines, and from levetiracetam to lamotrigine due to side effects, he has had no further seizures or migraines. Repeat EEG and MRI showed resolution of prior abnormalities.
Conclusions: PJ’s history partially coincides with and differs from current diagnostic criteria for epilepsy and migraine. According to earlier ICHD-II criteria for migralepsy, a seizure occurring within 1 hour of a migraine aura applies to PJ’s case (1, 2). PJ also experiences a visual aura, a trait seen in migralepsy cases (3). However, ICHD-III criteria for headaches linked with epilepsy require the headache to resolve after the seizure, which PJ’s case contradicts as his headache persists post-seizure (6). Unlike documented migralepsy cases with occipital migraines and corresponding EEG changes, PJ has a unilateral temporal headache with contralateral EEG and MRI abnormalities (3). PJ’s case suggests a need for expanded classification of migraine and epilepsy disorders, highlighting the potential utility of EEG in migraine with aura to identify epilepsy. The overlap in antiseizure medications used for migraines suggests shared pathogenesis and could inform treatment. With new diagnostic criteria we hope to incorporate all aspects of migralepsy, improve patient screening with EEG and MRI, and guide treatment choice.
Funding: NA
Clinical Epilepsy