The temporal bone anatomy is complex, with many critical structures in close association with one another. The temporal bone region comprises cranial nerves V, VI, VII, and VIII; vascular structures such as the internal carotid and middle meningeal arteries; sigmoid sinus; jugular bulb; and sensorineural and membranous structures of the inner ear. Most temporal bone fractures are a result of high-energy blunt head trauma. Multidetector computed tomography (CT) plays a fundamental role in the initial evaluation of patients with polytrauma in the emergency department. Multidetector CT may help identify important structural injuries that may have devastating complications such as sensorineural hearing loss, conductive hearing loss, dizziness and balance dysfunction, perilymphatic fistulas, cerebrospinal fluid leaks, facial nerve paralysis, and vascular injury. Although classifying temporal bone fractures helps physicians understand and predict trauma-associated complications and guide treatment, identifying injury to critical structures is more important for guiding management and determining prognosis than is simply classifying temporal bone fractures into a general category. Many temporal bone fractures and complications may be readily identified and characterized at routine cervical, maxillofacial, and head multidetector CT performed in patients with polytrauma, without the need for dedicated temporal bone multidetector CT. Dedicated temporal bone multidetector CT should be considered when there is a high degree of suspicion for temporal bone fractures and no fractures are identified at head, cervical, or maxillofacial CT.

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A young male, with a known history of hepatitis C and heroin abuse, was admitted to the emergency department with altered sensorium, left-sided weakness, and no meningeal signs. Initial computed tomography imaging showed hypodensity involving right basal ganglia with mass effect but no hemorrhage. Magnetic resonance imaging revealed multiple nonenhancing small foci of restricted diffusion involving the right basal ganglia, T2 and FLAIR hyperintensity within the right basal ganglia, and internal capsule with mild surrounding edema. The patient was treated for encephalitis and atypical stroke given the history of intravenous drug abuse. Follow-up imaging showed worsening of the brain lesions, with involvement of the contralateral basal ganglia with necrosis and peripheral enhancement. Brain biopsy was ultimately performed and suggested infection with Aspergillus species and associated parenchymal infarction. The patient was treated with voriconazole with subsequent significant clinical improvement.

A non-bifurcating carotid artery is a rare variation in the carotid circulation. Here we present a rare case of a non-bifurcating carotid artery with an aberrant course of the internal carotid artery incidentally discovered in a patient who presented to the trauma center after a fall. To our knowledge, this is the first reported case of a non-bifurcating carotid artery with an aberrant course of the internal carotid artery. The embryonic mechanisms of this variation and the available literature regarding this condition are also reviewed. Knowing this variation is necessary before considering vascular intervention of the neck and ear surgery to avoid vascular injury and complications.