Bilateral vocal cord paralysis. Assess for intracranial cause. History of T3N1M0 left tonsil squamous cell carcinoma that was treated with CRT completed in September 2007. Endoscopy showed immobile vocal cords in paramedian position, with marginal airway patency. Artifact significantly limits the 3-D T1 postcontrast acquisition. There is confluent and patchy T2/FLAIR hyperintensity involving the periventricular and deep cerebral white-matter which has increased slightly since the previous examination from 2011 and most probably reflect chronic microvascular ischemia. There is development of a 7 mm CSF intensity lesion involving the right para median central pons which is compatible with chronic infarct. Subtle T2-hyperintensity extends caudally from this presumed infarct into the medulla. Small foci of CSF intensity just lateral to the left frontal horn (including the head of the caudate nucleus) and the right atrium remain unchanged and likely represent chronic lacunar infarcts.There is no acute infarct, intracranial hemorrhage or mass. There is no abnormal intracranial enhancement. The ventricles and basal cisterns are mildly expanded reflecting underlying mild brain volume loss. There is no midline shift or herniation. The major cerebral flow voids are intact. The orbits, skull, paranasal sinuses, and scalp soft tissues are grossly unremarkable. Subtle asymmetry between the petrous apices probably reflects asymmetric pneumatization, and fluid/mucosal thickening on the left.
1.Post contrast images are limited by artifact as described above.2.No evidence of intracranial hemorrhage, mass, or acute infarct. 3.Moderate changes of cerebral white-matter chronic microvascular ischemia and small chronic lacunar infarcts, as described above. A dedicated skull base MRI without and with contrast may provide better assessment of the cranial nerves, if clinically warranted.