Presentation
Investigation for an atypical parkinsonism. Previous history of trauma with frontal brain contusions.
Patient Data
Marked improvement when compared to the previous study, a left frontal hemorrhagic contusion now inapparent and with no remnant right frontal sulcal blood present. The previously noted left cerebral convexity subdural hematoma is not convincingly identified. No hydrocephalus or midline shift. No evidence of acute ischemia. Incidental cavum vergae. No calvarial fracture or suspicious bony abnormality seen. No other changes.
Elsewhere, extensive periventricular and deep white matter hypoattenuation is consistent with chronic small vessel ischemic change.
Scattered throughout the deep white matter are areas of high T2/FLAIR signal, suggestive of chronic small vessel ischemia. Brainstem and basal ganglia are unremakable other than many small perivascular spaces (etat crible).
SWI demonstrates some foci of blooming artefact in the frontal lobes and in the right parietal lobe consistent with sequelae related to the previous history of trauma and brain contusion.
Normal grey white matter differentiation. Loss of cerebral volume does not have a lobar distribution, and is within the range commonly seen in this age group. The hippocampi, as demonstrated on whole brain MPRAGE are commensurate with the remainder of the brain in size, signal, and morphology.Ventricular system and cisternal spaces appear normal for the age group. Cavum septum pellucidum and associated cavum vergae are noted (anatomical variant).Partial opacification of mastoid air cells on the right.
Conclusion: Cerebral volume loss without lobar distribution, signs of extensive chronic small vessel ischemia and sequelae of previous brain contusions.
Case Discussion
No evident features on imaging to justify the parkinsonism. However, an extensive chronic small vessel ischemia and sequelae of previous brain contusions are noted.
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