Progressive ataxia. Per EPIC, patient with gait difficulty and falls which started a few years following a motor vehicle accident in 1979. At the time of the accident there was a severe head injury with impaired consciousness for a couple of weeks. He was hospitalized for one month at that time (details unclear) and did not need any surgical intervention. He was told there was damage to his cerebellum due to the injury. MRI brain: There is diffusely severe volume loss of the cerebellum. There is no evidence of associated susceptibility or focal encephalomalacia. There is no evidence of acute intracranial hemorrhage, mass, or acute infarct. There are scattered punctate foci of abnormal T2/FLAIR hyperintensity within the periventricular and subcortical white matter, consistent with mild chronic small vessel ischemic changes. There is mild asymmetric increased T2 signal of the left medial temporal lobe with mild hippocampal volume loss suggested.The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. The right internal carotid artery flow void is mildly asymmetrically smaller, which may relate to an absent A1 segment. There is mild asymmetric prominence of the right superior ophthalmic vein.MR cervical spine: There is anterior cervical discectomy and fusion at C6-C7. There is minimal retrolisthesis of C4 on C5. The vertebral body heights are preserved. There is moderate loss of disc height at C5-6 with increased T1 signal, which may represent mineralization. The vertebral bone marrow signal is mildly heterogeneous. The spinal canal is congenitally narrowed, without significant superimposed spinal canal stenosis. The spinal cord displays normal signal and morphology. The paravertebral soft tissues are unremarkable.C2-C3: Mild posterior disc osteophyte complex and bilateral uncinate hypertrophy, contributing to mild bilateral foraminal stenosis. No significant spinal canal stenosis.C3-C4: Mild posterior disc osteophyte complex and bilateral uncinate hypertrophy, contributing to mild bilateral foraminal stenosis. No significant spinal canal stenosis.C4-C5: Mild posterior disc osteophyte complex, left paracentral annular fissure and bilateral uncinate hypertrophy, contributing to mild bilateral foraminal stenosis with minimal flattening of the ventral cord. No significant spinal canal stenosis.C5-C6: There is partial fusion of the anterior C5-C6 vertebra, which is developmental. There is a small central convexity, which may represent a mineralized disc. No significant spinal canal or foraminal stenosis.C6-C7: Bilateral uncinate hypertrophy, contributing to moderate left foraminal stenosis. No significant spinal canal or right foraminal stenosis. C7-T1: Bilateral uncinate hypertrophy, contributing to mild to moderate left foraminal stenosis. No significant spinal canal or right foraminal stenosis.
1.Diffusely severe cerebellar atrophy, concerning for etiologies such as chronic alcoholism and neurodegenerative disease and much less likely trauma. 2.Subtle asymmetric FLAIR hyperintensity suggested associated with the mesial left temporal lobe hippocampal volume loss. Findings are nonspecific but can be seen in medial temporal sclerosis in the appropriate clinical setting. Please correlate clinically.3.Minimal chronic small vessel ischemic changes. No evidence of acute intracranial hemorrhage, mass, or acute infarct.4.Degenerative cervical spondylosis, contributing to mild multilevel foraminal stenosis. Congenitally narrowed spinal canal, but no significant superimposed spinal canal stenosis.