Abstract Number: LBA15 Transient Ischemic Attack Uncovering An Absent ICA

Abstract

Introduction Absence of the Internal Carotid Artery (ICA) is a rare cerebrovascular anomaly signified by agenesis, aplasia, or hypoplasia of the ICA and its’ bony canal. Agenesis refers to complete absence whereas aplasia refers to some partial remanent of the ICA or the carotid canal however, these terms are often used interchangeably. There are 6 types of ICA agenesis/aplasia of which type A consists of collateral flow supplied to the MCA via the P‐comm and ACA via the A‐comm. The prevalence of such a condition is reported at around .01% of the population. Patients are usually asymptomatic due to robust collaterals but, in some cases, can present with focal neurologic deficits. Here, we present a case of a patient who endured a transient ischemic attack and was subsequently found to have type A Right ICA aplasia on cerebrovascular imaging. Methods Case Report Results A 24‐year‐old Right‐handed Female with no past medical history except for tobacco use presented with transient left arm monoparesis. The patient had received chiropractic treatment involving hyperextension of her neck to the left just prior to symptom onset which transiently caused her left arm to become plegic and she resolved back to her neurologic baseline within 10 minutes. Neurologic exam was normal and non‐contrast head CT was negative however, demonstrated significant hypoplasia of the right carotid canal (Figure 1‐A). Contrast enhanced CT Angiogram of the head and neck demonstrated lack of contrast opacification of the Right Internal Carotid artery with absent Right carotid bulb and opacification of only the Right ECA (Figure 1‐B). MRI of the brain did not demonstrate any acute infarction. Gadolinium enhanced MRA of the Head and Neck confirmed absence of the Right internal carotid (Figure 2‐A) with prominent Right P‐comm and absent Right A1 segment (Figure 2‐B). Due to this variant anatomy, the postulated mechanism of patient’s TIA was thought to be related to transiently decreased cerebral perfusion caused by partial mechanical compression of her vertebral arteries asymmetrically affecting the Right MCA distribution due to sole supply from the Right posterior communicating artery. Conclusions This case illustrates a fascinating variation from normal embryologic angiogenesis and highlights the importance of collateral blood flow through the circle of Willis in patient’s with congenitally absent internal carotid arteries. Particularly, this patient’s presentation demonstrates the risk that vascular compromise of posterior circulation vessels may play in patients with Type A ICA agenesis/aplasia and their subsequent risk of incurring transient ischemic events.