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A Stone at the Siege of Cyropolis: Why it is Unlikely that Alexander had a Carotid Dissection Causing his Death 6 Years Later

Extracranial internal carotid artery dissection (ICAD) is now recognised as one of the most frequent causes of ischemic stroke in subjects under 50 years of age (Biousse et al., 1995; Baumgartner et al., 2001; Schievink, 2001). Patients with dissection are thought to have an underlying arteriopathy involving a defect in the extracellular matrix and an acute triggering factor such as head or neck trauma or infection (Baumgartner et al., 2001; Guillon et al., 1998). There is thus a continuum between the obviously traumatic ICAD occurring, for instance, after a motor vehicle accident (Opeskin, 1997; Guillon and Bousser, 2002), and the so called spontaneous ICAD, in which a history of minor or trivial trauma is frequently elicited, such as turning the head, coughing, vomiting or painting a ceiling. As regards Alexander at Cyropolis, the main argument for ICAD is that he received a stone on his head and neck after which he had blurred vision and speech disturbances. A stone on the neck could indeed precipitate carotid dissection (Opeskin, 1997) with subsequent ischemic symptoms in the middle cerebral artery territory explaining the occurrence of dysphasia. There are, however, two clinical points that warrant discussion. The first one is that there is no mention of unilateral head or neck pain which is the most frequent symptom of ICAD (Biousse et al., 1995; Baumgartner et al., 2001; Schievink, 2001). Most frequently there is a delay of several hours or days between the trauma and the occurrence of unilateral head or neck pain and a second delay between the pain and the ischemic signs. There are, however, some cases with an immediate onset of ischemic signs without pain or other local signs, such as Horner Syndrome. The other point that needs discussion is the ‘‘blurred vision’’ that is thought to be due to cortical blindness. Obviously a unilateral ICAD could explain monocular blindness on the basis of retinal ischemia or ischemic optic neuropathy, but cannot account for bilateral blurring of vision (Biousse et al., 1998; Schievink et al., 1998). Cortical blindness points to ischemia in the basilar territory, which would suggest an associated vertebral artery dissection (VAD). Again this is unlikely because most ischemic events in VAD are related to brain stem ischemia and not to bilateral occipital ischemia (Schievink, 2001). Another hypothesis that might explain blurred vision and dysphasia after head trauma is migraine with aura, in which trauma is one of the well established trigger factors. However, here again one would expect the occurrence of headache after the visual or dysphasic aura, although isolated auras have been reported after head trauma, particularly in children. Thus, although possible, ICAD seems unlikely as immediate complication of the stone received by Alexander at Cyropolis. The recurrence of dysphasia 6 years after a traumatic ICAD would be even more unlikely given