Hypoxic ischemic injury, diffuse axonal injury and atlanto-occipital dislocation

Lateral x-ray demonstrates the patient to be intubated with apparent marked increase of the prevertebral soft tissues. There is widening and non-congruency of the atlanto-occipital articulation consistent with atlanto-occipital dissociation. 

There is atlanto-occipital dislocation with the cervical spine displaced posteriorly by approximately 13 mm as well as an associated rotatory component. There is gross widening of the basion-dens interval to 19 mm and widening of the basion-axial interval to 25 mm. Faint fracture fragments bilaterally lie within the interval between the dislocated occiput and atlas presumably representing avulsed fracture fragments. There is large volume prevertebral hematoma that extends from the clivus down to the upper thoracic spine. There is resultant high-grade central canal stenosis at the cervico-medullary junction which is severely compressed and kinked by the posteriorly displaced dens. Incidental accessory ossicle of the anterior arch of C1.

Atlanto-occipital dislocation with marked compression of the cervical medullary junction between the opisthion (posterior margin of the foramen magnum) and the dens and the overlying ascending band of the cruciform ligament. This is associated with extensive increased T2 signal (from C1/2 to the brainstem) and hemorrhage within the cord and in the surrounding subarachnoid space. There is disruption of the atlanto-occipital ligament and atlantoaxial membrane posteriorly at C0/1 and C1/2 respectively as well as disruption of the alar ligaments and apical ligaments of the dens. 

The theca is disrupted, with a high volume CSF leak seen within the epidural space with collapse of the theca surrounding the cervical cord. The cervical cord is unremarkable from the level of C2 down to upper thoracic cord. The discs, anterior and posterior longitudinal ligaments, ligamentum flavum, and interspinous ligaments are intact from C2/C3 down to the upper thoracic spine. Widespread muscular high T2 signal is demonstrated in the posterior and lateral muscles bilaterally, more so on the right. Normal flow voids are demonstrated within the vertebral arteries, and parts of the carotids that are visualized.

There are multiple bilateral punctate intra-axial hemorrhages throughout the cerebral hemispheres. There is acute subarachnoid blood within the posterior fossa cisterns. Increased attenuation relative to the parenchyma within the basal cisterns is however likely pseudosubarachnoid blood. The brain is diffusely swollen with early loss of grey-white matter differentiation bilaterally and crowding of the posterior fossa structures. 

Restricted diffusion is demonstrated within the occipital poles, perirolandic cortex, basal ganglia, and left hippocampus, in keeping with hypoxic-ischemic injury. In addition, very extensive punctate regions off signal loss on susceptibility weighted imaging are demonstrated throughout the brain, particularly at grey-white matter junction superiorly, within the corpus callosum, and within the brain stem, consistent with diffuse axonal injury (grade III). The ventricles are only slightly enlarged for an individual of 18 years of age, however, increased intracranial pressure is likely present as demonstrated by the prominence of the optic nerves sheaths and early papilledema. Increased flair signal within the sulci of the cerebral hemispheres likely represents subarachnoid blood, although high oxygen can have a similar appearance. Flow-induced signal voids are demonstrated within both carotid arteries, their branches, as well as the posterior circulation. Flow void within the dural venous sinuses is preserved.