Case Presentation: An 86 year old man with atrial fibrillation on anticoagulation presented with altered mental status, right-sided weakness, and aphasia five days after a fall. CT head imaging demonstrated an acute left subdural hematoma (SDH). He was evaluated by Neurosurgery and managed non-operatively with reversal of his anticoagulation. Neurology was consulted for evaluation of his aphasia and weakness. Brain MRI and spot EEG were unremarkable. Within 48 hours, his deficits had essentially resolved and were attributed to cortical irritation from his SDH. Following several days without appreciable speech or strength deficits, he again developed right hemiparesis and aphasia. Repeat head CT demonstrated stability of his SDH. His symptoms initially improved over the next day then became progressively more pronounced. MRI showed relatively symmetric perfusion and no infarcts. Continuous EEG revealed left sided asymmetric slowing but no focal epileptiform activity. His symptoms persisted, although waxed and waned in severity. Ultimately, cortical spreading depression was considered, and he was treated empirically with magnesium and topiramate. His deficits improved considerably with initiation of therapy.

Discussion: Cortical spreading depression (CSD) has been described in several neurologic conditions, including migraine, stroke, subarachnoid hemorrhage, and traumatic brain injury (TBI). It is characterized by slow velocity depolarization waves propagating in cortical grey matter and is associated with detrimental cellular effects, including decreased cerebral blood flow and breakdown of ion homeostasis. CSD is challenging to diagnose, as it can mimic deficits seen with stroke or seizure, and it is undetectable by conventional EEG. Clinically, patterns of CSD can vary considerably, from clustered events lasting minutes to hours, to discrete recurrence of symptoms after several days. Our patient’s aphasia and weakness after his initial recovery was clinically concerning for expansion of his hematoma or stroke, yet his work up for these conditions was non-diagnostic. The pattern of waxing and waning severity of his neurologic symptoms was suggestive of seizure but perplexing with his non-focal EEGs. Other cases have described CSD presenting as episodic, stereotyped neurologic deficits following traumatic SDH, recognized only after an extensive negative evaluation. Several studies suggest CSD contributes to progressive tissue damage and worse outcomes in severe brain trauma, necessitating early and accurate recognition. In an era where hospitalists increasingly care for patients suffering from acute trauma, our case illustrates a clinical phenomenon associated with TBI that is difficult to identify and potentially unfamiliar to internists.

Conclusions: CSD is a complication of brain injury that can present with focal neurologic deficits. The diagnosis is challenging to recognize based on clinical similarity to better-known neurologic conditions. Hospitalists should consider CSD in patients with neurologic symptoms in the context of traumatic brain injury, particularly when evaluation for alternative etiologies is unrevealing.