Blunt cerebrovascular injury

C6 vertebral body and right articular pillar fractures. Right C6 and C7 transverse process fractures involving the transverse foramen. T2 vertebral body fracture. 

Marrow edema in C6-T2 vertebral bodies with loss of height at C6 anteriorly and of T2 vertebral bodies of approximately 40-50%.

At C5/6 there is increased T2 disc signal with a superiorly projecting disc extrusion. At C6/7 there is increased T2 disc signal with posterior central/left subarticular disc extrusion, contacting the cord but only moderately narrowing the central spinal canal. PLL is stretched over these disc extrusions with some elevated signal, but otherwise appears intact. Ligamentum flavum is intact. ALL is ruptured at the level of the C6 superior endplate.

Increased T2 cord signal at C5/6. No susceptibility artifact to suggest cord contusion or epidural hematoma.

Prevertebral edema extends from C2 to T4. High T2 signal throughout the cervical and upper thoracic facet joints. High T2 signal within the posterior paraspinal soft tissues from C1-C7 and T1-2.

Loss of normal T2 flow void in the right vertebral artery from shortly after its origin to proximal basilar artery. Normal flow T2 void signal in the left vertebral artery. 

Restricted diffusion affecting the right hemipons, medial right cerebellar hemisphere in the right PICA vascular territory. Further patchy areas of diffusion restriction throughout the remainder of the cerebellar hemispheres and vermis as well as both occipital lobes, mesial temporal lobes, right thalamus, and the splenium of the corpus callosum. These areas have corresponding T1 hypointensity, T2 hyperintensity and positive mass effect. Partial effacement of the fourth ventricle. No hydrocephalus. No cerebral parenchymal herniation.

TOF MRA demonstrates absent flow signal in the right vertebral artery with irregularity and T1/T2 hyperintensity in the proximal basilar artery but normal flow in the remainder of the basilar artery. Scanty flow signal in the right PICA compared to the left.

No abnormal susceptibility artifact with no evidence of intracranial hemorrhage or DAI. Supratentorial deep white matter T2 and regions of hyperintensity are non-specific, but most likely represent the sequelae of chronic small vessel ischemic change, but are of an amount more than expected for this group.

Large scalp fluid intensity subgaleal collection with only minor susceptibility artifact. More anteriorly is a small left frontal scalp hematoma with a fluid-fluid level present.