Female, 6 years old, with C2 fracture and concern for vertebral dissection. Evaluate for ischemia. MRI brain:The external contour of the brain conforms to the dysmorphic calvarium, similar to prior exams. No evidence of restricted diffusion is seen. No parenchymal edema or mass effect is detected.A small area of encephalomalacia in the right frontal lobe related to prior ischemia is unchanged. Likewise, scattered foci of T2 hyperintensity in the bilateral cerebral watershed zones, in the periventricular tissues, the right greater than left occipital lobes, and the cerebellum are unchanged compatible with chronic ischemic lesions. A curvilinear area of cystic encephalomalacia involving the superior right thalamus related to prior ischemia is unchanged.No definite evidence of any new intracranial lesion is seen. No acute intracranial hemorrhage or any abnormal extra axial fluid collection is observed. The lateral and third ventricles remain prominent, similar to prior. A cavum septum pellucidum et vergae is redemonstrated.MRA neck:Although MRA images are degraded by motion artifact, the cervical intervertebral arteries of the neck appear to show normal caliber throughout. In particular, no evidence of significant narrowing or dissection is seen at any point in the vertebral arteries.MRI C-spine:Known bilateral fractures through the dysmorphic pedicles of C2 are better visualized on prior CT. However, the fractures are vaguely identified with edema in the adjacent marrow.The anterior prevertebral tissues are significantly thickened showing heterogeneous T1 isointense and T2 hyperintense signal suggesting a combination of edema and blood product. No evidence of injury of the adjacent intervertebral discs is seen which reduces concern for an anterior longitudinal ligament injury.The anterior atlantooccipital and atlantoaxial ligaments are visualized and appear intact. The apical ligament and tectorial ligament are both visualized and appear intact. No injury to the posterior longitudinal ligament is suspected. The posterior atlantooccipital ligament does not appear to be injured. However, between the posterior arch of C1 and the fused posterior elements of C2-4, extensive soft tissue edema is seen. The posterior atlantoaxial ligament appears attenuated and may have been avulsed from its attachment at the spinous process and laminae at C2. The nuchal ligament appears to be intact, though there is likely some injury of the interspinous connective tissue.There is minimal if any effacement of the dorsal thecal sac by edema or fluid posterior to the injured atlantoaxial ligament. However, no large or significant epidural collections are seen. The spinal canal is not compromised at any level. No evidence of spinal cord edema or intramedullary hemorrhage is seen.Multiple cervical anomalies are redemonstrated likely related to Crouzon syndrome. Briefly these include a bulbous and dysmorphic odontoid process; hypoplasia of the C2, C3 and C4 vertebral bodies; fusion of the C2-C4 posterior elements; and partial anterior midline clefting of the cervical vertebrae from C3 down.
1.No acute intracranial abnormality is seen. Multiple chronic ischemic lesions are redemonstrated scattered through the cerebral hemispheres and cerebellum without significant interval change.2.Findings are seen compatible with bilateral fractures through the C2 pedicles. Prevertebral edema and/or hemorrhage is noted, but there is no evidence of any additional vertebral body or disc injury.3.Findings are seen concerning for strain or tear of the posterior atlantoaxial ligament. The remaining craniocervical ligamentous attachments appear to be intact. There is likely interspinous connective tissue injury between C1 and C2.4.Within the limitations of a motion degraded examination, no findings are seen to suggest vertebral artery dissection or occlusion.