Knocked Out: Concussion as a trigger for encephalopathic hemiplegic migraine. (P3.108)

Objective: N/A Background: We describe a young athlete who was diagnosed with FHM2 due to an ATP1A2 mutation after presenting with encephalopathy following a concussion. This case highlights the common pathophysiological pathway of hemiplegic migraine and concussion. Design/Methods: Case Description: A 19 year old semi-professional cyclist fell from his bike on a training spin. His helmet was slightly damaged by the fall. He was confused and agitated at the scene. He became increasingly encephalopathic on arrival at the hospital and required intubation for imaging. He remained obtunded for two weeks with intermittent agitation and disinhibited behavior. He had a background history of occasional migraine but no family history. Neuropsychological assessment two weeks after the initial event revealed deficits in executive functioning and reduced phonemic fluency. The patient fully recovered within six weeks. Results: Initial observations revealed a tachycardia of 110bpm and the patient was pyrexial at 39°. C-Reactive Protein was 295 mg/l. Laboratory investigations, including CSF and autoimmune antibodies were normal. MRI Brain was normal. EEG was excessively drowsy with moderate amounts of theta bi-posteriorly. PET Brain revealed diffuse hypometabolism, particularly in the occipital and parietal regions. Subsequent PET Brain normalized. Based on diffuse hypometabolism, encephalopathy and background history of migraine, gene testing was carried out. A pathogenic variant in exon 12 of ATP1A2 gene was identified confirming a diagnosis of familial hemiplegic migraine type 2. Conclusions: Discussion: Hemiplegic migraine is due to a channelopathy resulting in neuronal excitability and subsequent spreading cortical depression. Recent descriptions of the neurometabolic cascade of discussion1 suggest a common pathophysiological pathway. A previous case report has shown fatal cerebral oedema following mild head trauma in a patient with hemiplegic migraine2. This case supports the hypothesis that genetic vulnerability may underlie severe response to mild concussion. Disclosure: Dr. Gaughan has nothing to disclose. Dr. Clarke has nothing to disclose. Dr. Healy has nothing to disclose.