Description of multimodal detection and treatment of refractory cerebral vasospasm in two cases of aneurysmal subarachnoid hemorrhage presenting as hyperactive delirium.

Cerebral vasospasm in aneurysmal subarachnoid hemorrhage (aSAH) is associated with significant morbidity and mortality. Symptomatic cerebral vasospasm is a key pathomechanism of delayed cerebral ischemia. Delayed cerebral ischemia can be asymptomatic (silent cerebral infarction), have subtle clinical signs and symptoms, or can manifest with focal neurologic deficits (FND). At times, symptomatic cerebral vasospasm and delayed cerebral ischemia can present with neuropsychiatric manifestations such as abulia, apathy, loss of concentration, inattention which if unnoticed can be consequential. The relationship between delirium in aneurysmal subarachnoid hemorrhage and symptomatic cerebral vasospasm has been understudied thus far. Delirium in the setting of aneurysmal subarachnoid hemorrhage can make detection and management of delayed cerebral ischemia challenging. In this case series, we aim to demonstrate a successful multimodal approach in monitoring and treating two cases of aneurysmal subarachnoid hemorrhage with symptomatic cerebral vasospasm manifesting clinically as hyperactive delirium.

We identified two female patients, aged 49 and 53 years, who developed refractory cerebral vasospasm after aSAH presenting with clinical manifestations consistent with hyperactive delirium. Case 1 had worsening agitation with impulsive behavior development, while case 2 had unusual behavioral changes with executive dysfunction manifested by deteriorating Montreal Cognitive Assessment (MoCA) score. Serial transcranial doppler (TCD) studies showed cerebral vasospasm. Both cases had significant improvement of vasospasm and resolution of the neuropsychiatric symptoms after vasospasm treatment.

The relationship between delirium and cerebral vasospasm needs further evaluation and there is unproven causality. Delirium can be an unrecognized early clinical manifestation of refractory cerebral vasospasm causing cerebral ischemia. Timely recognition and treatment of this early marker of cerebral vasospasm in patients with aSAH is essential to reduce morbidity and mortality in aSAH.