A 25-year-old female patient visited the neurology outpatient clinic with severe holocranial headache that had persisted for 2 months. The pain was intermittent and relieved by analgesics. Clinical examination was unremarkable.\nComputed tomography (CT) scan of the brain showed absent bony carotid canal on the left side [Figure and ]. Magnetic resonance angiography (MRA) [Figure and ] showed complete absence of the cervical and petrous part of the left ICA. An abnormal vessel was seen arising from the cavernous segment of the right ICA. This vessel was passing across the floor of sella, reconstituting the cavernous and supraclinoid segments of the left ICA, and continuing as the left MCA. Aplasia of A1 segment of left ACA was also observed.\nMagnetic resonance imaging (MRI) showed absent left ICA flow void with an abnormal flow void in the sella [Figure and ]. No evidence of any SAH or aneurysm was seen. The vertebrobasilar system was normal.\nDoppler imaging [Figure –] showed complete absence of the left ICA. The left common carotid artery (CCA) was seen continuous with the external carotid artery (ECA). The left CCA and ECA showed high resistance flow with narrow systolic peak and low diastole. Since the right CCA has to compensate for the absent left ICA, it showed low resistance flow with broad systolic peak and high diastolic flow.\nLateral radiograph of the skull [] and the corresponding sagittal reformatted CT scan [] showed a well-defined lytic area in the anteroinferior aspect of the sella due to the abnormal intercavernous vessel traversing across it.
A 42-year-old woman applied to the ophthalmology department with a complaint and history of a half-hour-long visual loss of her left eye one day ago. At clinical examination, both of her eyes were found to have full vision, and also microscopic fundus examinations revealed no pathological conditions. The patient gave a history of a prior application to an outer medical center with the same complaint, and there she had been diagnosed with a left ICA occlusion, following Doppler US and angiographic examinations. The patient applied to our department with the demand of an extracranial carotid Doppler US examination. At Doppler US, the right CCA diameter was found to be 8 mm, whereas the left one came out to be 4 mm (Figures and ). The right CCA bifurcation and the ICA and ECA were found to be normal. At the left side, spectral data for the ECA () and the particular branching which demonstrates that the vessel is ECA indeed were present, whereas there was no Doppler signal and gray-scale findings for the ICA (). Because the left CCA was hypoplastic and there were no findings of atherosclerotic plaques in other arterial segments; it was thought that the left ICA might not be suffering an occlusion at all, but instead it might well be agenetic. Based on the presumption of an ICA agenesis, a computed tomographic (CT) examination of the skull base was performed. CT images revealed a normally appearing right carotid canal but no clear image of the left one (). Then, the previous angiographic images of the patient were reevaluated, and it was then recognized that the left ECA and its branches were well visible, while the left ICA and its branches did not show any filling with contrast (). It was also noted that the filling of the left anterior and medial cerebral arteries was sustained by the patent anterior communicating artery following the injection of contrast into the right carotid artery () and also via the posterior communicating artery following the injection of the vertebrobasilary system (). In addition to the ICA agenesis, another surprising finding was that the right vertebral artery was not stemming from the right subclavian artery but instead was originating from the aortic arch, as its first branch (). It was finally understood that the patient did not have an occlusion of the left ICA, but instead her left ICA was agenetic. She also had an additional aortic arch anomaly. At the end, it was concluded that an ipsilateral CCA hypoplasia might be taken as a valuable clue in the differential diagnosis of ICA agenesis and occlusion.