A 69-year-old Man with Sudden Loss of Consciousness, Non-reactive Pupils, and a Bilateral Positive Babinski Sign.

LEARNING POINTS: Pathologic findings In figure 1, the basilar artery appears homogenously hyperdense in comparison with the adjacent left middle cerebral artery (MCA), using brain parenchyma as a reference point; thus indicating a hyperdense basilar artery sign (HBAS) (Figure 2, white arrow). Also, the right superior cerebellar artery and left posterior cerebral artery appear to be hyperdense (Figure 2, the red and green arrows, respectively). This is called a hyperdense artery sign (HAS). The artery becomes hyperdense because the intra-arterial clotted blood has a higher Hounsfield unit (80 HU) than the non-clotted flowing blood (40 HU) and thus appears white on non-contrast computed tomography (CT) scan. Pathologically, high hematocrit levels and calcium deposits in the vessel wall (due to arteriosclerotic disease) can result in an incorrect diagnosis of HAS. Sometimes, infections or tumors can make the brain parenchyma surrounding the vessel hypodense, which can give the false impression of a hyperdense vessel (1). To avoid misdiagnosis, these considerations are useful:  Ensure the attenuation value (Hounsfield units) of all intracranial arteries and veins are nearly the same when there are high hematocrit levels.  Calcifications are usually located at the periphery of the vessels.  In contrast to atheromatous calcifications, a hyperdensity thought to be a HAS is reversible (2).  Koo et al. defined hyperdensity as an absolute density of > 43 HU and a MCA ratio (the ratio of the dense MCA to the contralateral MCA) of > 1.2. He showed that using a combination of these two parameters had 100% specificity for the HAS for acute ischemic stroke cases (3). Importance Acute basilar artery occlusion (BAO) is a rare catastrophic form of stroke, roughly causing around 1% of all strokes (4). BAO occurs usually due to an embolus with a cardiac or large vessel origin, or the formation of a local atherosclerotic thrombosis. In this patient, BAO occurred soon after myocardial infarction. Depending on the location and extent of occlusion and on the degree of collateral flow, BAO has quite variable clinical and imaging manifestations. The clinical presentation of BAO ranges from nonspecific symptoms such as headache, neck pain, or vertigo to severe disabilities such as decreased consciousness, hemiplegia or quadriplegia, extensor plantar sign, dysarthria, dysphagia, aphagia, ataxia, nuclear oculomotor nerve palsy, bilateral ptosis, anisocoria, non-reactive pupils, Figure 1: Axial non-enhanced computed tomography scan of the patient’s brain Mehran Sotoodehnia*, Mehrnoosh Aligholi-Zahraie