62-year-old male with cervical myelopathy, vertebrobasilar vascular occlusive disease MRI of the brainNo diffusion weighted abnormalities are appreciated. The CSF spaces are appropriate for the patient's stated age with no midline shift. Redemonstrated is T2 hyperintensity involving the right anterior aspect of the medulla, best identified on T2 imaging. This was also present on the previous exam. As before, there are scattered foci of T2 hyperintensity within the periventricular and subcortical white matter without restricted diffusion or susceptibility abnormality consistent with stable chronic small vessel ischemic disease. No intracranial hemorrhage is identified. No edema is identified within the brain parenchyma. Normal vascular flow voids are present in the distal carotid arteries, the basilar artery and the proximal anterior, middle and posterior cerebral arteries as well as the internal cerebral veins and superior sagittal sinus. The left vertebral artery flow-void is present. The right vertebral artery is slightly smaller than the left vertebral artery but there is no flow void appreciated, as demonstrated previously. The visualized portions of the paranasal sinuses redemonstrate mucosal thickening. The visualized portions of the mastoid air cells are clear. The visualized portions of the orbits are intact.MRA brain:The anterior communicating artery is identified and is medium size. There is fetal origin of the right posterior cerebral artery. The right P1 segment is medium-sized. The left posterior communicating artery is very small..No intracranial flow is identified in the right vertebral artery. There are tandem stenoses present along the basilar artery. One is located between the level of the anterior inferior cerebellar arteries and the superior cerebellar arteries and has approximately 80% stenosis which has not changed since the prior exam; it is located closer to the anterior inferior cerebellar arteries than the superior cerebellar arteries. Another stenosis is present between the vertebrobasilar junction and the anterior inferior cerebellar arteries which has 70% stenosis which has not changed significantly since the prior exam.MRA neck:There is opacification of the aortic arch, great vessels from the aortic arch and carotid arteries and left vertebral artery. There is no stenosis identified of the great vessels from the aortic arch. On the basis of NASCET criteria there is no significant stenosis at the carotid bifurcations. There is no significant stenosis along the course of the left vertebral artery. The right vertebral artery is occluded at its origin with only minimal reconstitution of flow from muscular branches, as demonstrated previously.Cervical spine:The cervical vertebral bodies are appropriate in overall alignment and height. There is ossification of the posterior longitudinal ligament present extending from the C2-3 level to the C4-5 level associated with spinal stenosis. At C2-3 there has been interval progression of both ossification of the posterior longitudinal ligament and ligamentum flavum thickening, now causing slight deformation of the cord (without intrinsic cord signal abnormality) and new mild central stenosis. Mild right neural foraminal narrowing is stable.At C3-4 there has been minimal increase in ossification of the posterior longitudinal ligament, now narrowing the central canal to 4 mm (previously 5 mm), demonstrating a moderate to severe degree of central stenosis. There is resultant cord flattening without definite intrinsic cord signal abnormality. Redemonstrated is effacement of the spinal fluid anteriorly and posterior to the spinal cord, with ligamentum flavum thickening. There is encroachment of the exiting nerve bilaterally within the neural foramina at this level, unchanged.At C4-5 there is ossification of the posterior longitudinal ligament associated with a disc bulge and ligamentum flavum hypertrophy associated with effacement of spinal fluid ventral and posterior to the spinal cord. There is mild flattening of the spinal cord without intrinsic cord signal abnormality. Overall there is moderate spinal stenosis at this level. There is encroachment of the exiting nerve roots within the neural foramina. These findings are stable compared to the prior exam.At C5-6 there is no significant compromise to the spinal canal. There are some uncovertebral osteophytes present on the right-sided this level associated with disc material and mild narrowing of the right neural foramen. These findings are stable compared to the prior exam.At C6-7 there is no significant compromise to the spinal canal. There is narrowing of the neural foramina bilaterally at this level due to uncovertebral osteophytes and osteophyte disc complex asymmetric to the left. These findings are stable compared to the prior exam.At C7-T1 there is no significant compromise to the spinal canal or neural foramina, unchanged.
1.Tandem high-grade stenoses along the basilar artery. These are stable compared to the prior exam2.Occlusion of the right vertebral artery at its origin. No flow is appreciated in the right vertebral artery intracranially. These findings are unchanged.3.Stable chronic small vessel ischemic disease.4.There is no evidence for acute cerebral infarction.5.Old lacunar infarction along the anterolateral aspect of the right medulla.6.At C2-3 there has been interval progression of both ossification of the posterior longitudinal ligament and ligamentum flavum thickening, now causing slight deformation of the cord (without intrinsic cord signal abnormality) and new mild central stenosis. 7.At C3-4 there has been minimal increase in ossification of the posterior longitudinal ligament, now narrowing the central canal to 4 mm (previously 5 mm), demonstrating a moderate to severe degree of central stenosis, demonstrating minimal interval progression. 8.At C4-5 there is ossification of the posterior longitudinal ligament associated with a disc bulge and ligamentum flavum hypertrophy resulting in moderate spinal stenosis at this level, unchanged.9.Cervical degenerative changes at other levels, as well as neural foraminal stenoses are stable.