A 40-year-old Asian man presented in the emergency department with acute right-arm weakness and dysarthria, that spontaneously resolved within 18 h. The patient was asymptomatic and hemodynamically stable upon admission. Past medical history included prior ischemic stroke in the distribution of the left middle cerebral artery, for which the etiologic investigation, follow-up and treatment were inadequately conducted at an outside Institution, untreated hyperlipidemia with low-density lipoprotein levels of 160 mg/dl and tobacco use.
During the initial patient’s evaluation, an emergent brain CT was performed that excluded any acute brain lesions. Cervical duplex ultrasound revealed normal blood flow in the common carotid arteries and internal carotid arteries (ICA) with no evidence of carotid stenosis or atherosclerotic plaques. However, the carotid bifurcation and the external carotid arteries (ECA) could not be detected bilaterally. Transcranial color-coded duplex sonography was also performed, revealing normal blood flow in the large intracerebral arteries. Pulsatility index measured at the middle cerebral arteries bilaterally was within normal limits, indicating normal cerebral hemodynamics. No microembolic signals were identified after administration of agitated saline on Transcranial Doppler bubble study excluding the presence of a right-to-left shunt.
Brain MRI demonstrated a chronic ischemic lesion in the distribution of the left middle cerebral artery, compatible with the patient’s past medical history, without revealing any new ischemic lesions (Fig. 1a, b). Brain MRA revealed an extensive network of anastomotic arteries, while the circle of Willis appeared normal (Fig. 1c–f). Neuroimaging was completed with neck MRA demonstrating non-bifurcating carotid arteries bilaterally (Fig. 2). The common carotid arteries ascended in the neck as single carotid vessels without undergoing bifurcation and continuing as ICA. A digital subtraction angiography was suggested to the patient in order to better characterize the carotid anomaly and identify the branches that would normally originate from the ECA, but the patient refused.
Patient’s clinical examination was normal, without any signs of other developmental anomalies that could be associated with vessel abnormalities, as in the case of osteogenesis imperfecta. No headache following the patient’s symptoms or prior history of migraine were reported by the patient. Focal seizures were also included in the differential diagnosis. However, the patient’s history was negative for Jacksonian march or any positive symptoms such as paresthesia. Additionally, repeat electroencephalograms were normal.
Transient ischemic attack was considered the most probable diagnosis and complete work-up in order to identify the underlying mechanism was performed, including transthoracic and transesophageal echocardiography (revealing normal cardiac chambers’ size and further excluding right-to-left shunts), 24-h Holter rhythm monitoring, a-galactosidase levels, blood testing for autoimmune and hypercoagulable disorders; all diagnostic work-up was negative. Prolonged cardiac monitoring with implantable loop recorder was further suggested to the patient and long-term antiplatelet therapy and statins were administered as secondary stroke prevention therapy.
