Reader response: Teaching NeuroImages: A rare case of giant perivascular spaces in the midbrain manifesting as atypical parkinsonism

In this Teaching NeuroImage, Ferrer et al.¹ described vertical gaze palsy and parkinsonism. Vertical gaze palsy, in this patient, is a consequence of compression of the mesencephalic rostral interstitial nucleus, the interstitial nucleus of Cajal, the posterior commissure, the periaqueductal gray matter, or interruption of the supranuclear inputs passing through the medial thalamus en route to the pretectal and prerubral areas.^2,3 Though I agree that the most likely explanation of the bradykinesia and rigidity in this patient is secondary to midbrain compression and subsequent dopaminergic pathway degeneration,¹ the authors did not demonstrate presynaptic dopaminergic pathway degeneration by SPECT imaging like dopamine transporters scan (DaT-SPECT scan) to support the hypothesis. More than 60%–70% of dopaminergic neurons degenerate before clinical signs of parkinsonism become evident. Though from the CT or MRI the extent of vascular lesions is not clear, significant frontal lobe atrophy is evident. Frontal lobe dysfunction or vascular parkinsonism can also lead to a clinically indistinguishable parkinsonism in this patient, so DaT scan would be helpful to identify the actual cause and management of his parkinsonism.⁴ Classically vascular or postsynaptic parkinsonism would give a normal DaT scan, but not nigrastriatal pathway degeneration secondary to compression by the giant perivascular or Virchow-Robin spaces.⁵