Hyperdense Middle Cerebral Artery Sign in the Setting of Acute Cerebral Ischemia: A Case Report

Background: Non-contrast computed tomography (CT) remains the initial diagnostic study of choice when ischemic stroke is suspected.⁴ This is due to the ability of non-contrast CT to differentiate between hemorrhagic and ischemic stroke.¹ In the setting of acute ischemia, one of the earliest markers on non-contrast CT is the hyperdense middle cerebral artery sign (HMCAS).^3,5 This hyperdensity is suggestive of thromboemboli within an artery, most commonly the middle cerebral artery (MCA), causing vascular occlusion. Identification of HMCAS is diagnostically advantageous, expediting the patient towards anticoagulation therapy or surgical intervention. Therefore, the recognition of early manifestations of cerebral ischemia on non-contrast CT is imperative for accurate diagnosis and therapeutic guidance.

Case Presentation: Our patient was a 40-year-old female with a past medical history of non-ST elevated myocardial infarction, peripheral artery disease, and deep vein thromboembolism who presented to the emergency room with respiratory distress, nausea, and vomiting. Upon arrival, the patient was unable to follow commands, obtunded, and hypoxic with a room oxygen saturation of 86%. Given the patient's altered mental status, non-contrast CT, CT angiogram, and CT perfusion studies of the head were ordered.

Imaging revealed high-attenuation of the right middle cerebral artery (MCA) signifying arterial occlusion without intracranial hemorrhage. Reevaluation of the patient showed new-onset left-sided facial drooping as well as left upper and lower extremity paralysis. Thrombolytics were not administered due to the patient’s symptomatic onset exceeding the therapeutic window. Thrombectomy was deemed a suitable treatment and the patient was transferred for urgent neuro-intervention evaluation.

Thrombectomy resulted in complete reperfusion of the right MCA with successful stabilization of the patient. Post-surgical CT demonstrated right basal ganglia parenchymal hemorrhage transformation and effacement of the right anterior horn. Days later, repeat CT revealed stabilization of the basal ganglia hemorrhage with expected evolution.

The following month, the patient revisited the emergency department with encephalopathic changes, intraparenchymal hemorrhage of the brain, and multiple clots occluding branches of the abdominal aorta. Unfortunately, the patient passed away at this time and successful interventions ceased.

Discussion: In this study, our patient presented to the emergency room with a history of chronic vascular disease and new-onset neurological symptoms. Subsequent imaging revealed HMCAS on non-contrast CT suggestive of acute ischemia. Additional imaging confirmed a thromboembolic occlusion within the first segment of the right MCA. Due to the significance of MCA involvement, neurosurgery was consulted and an endovascular thrombectomy was performed to initiate MCA reperfusion. Our findings coincide with poor clinical outcomes and neurologic deterioration in patients with ischemic stroke presenting with a HCMAS.

Conclusion: The presence of the HMCAS on non-contrast CT is specific for acute embolism and shows an increased likelihood of poor clinical outcomes with associated acute neurological deterioration. Moreover, additional studies can be useful in reducing disability by identifying salvageable tissue before initiating reperfusion therapy.¹ Due to the increased morbidity and mortality, it is crucial to be aware of early ischemic signs on non-contrast CT to guide therapeutic intervention in patients with HMCAS.