Hypoperfusion and ischemia in cerebral amyloid angiopathy documented by 99mTc-ECD brain perfusion SPECT.

UNLABELLED Cerebral amyloid angiopathy (CAA) is known to be an important cause of spontaneous cortical-subcortical intracranial hemorrhage in normotensive older persons. CAA can also manifest as leukoencephalopathy, brain atrophy, and ischemia secondary to hypoperfusion. Our goal was to verify cerebral hypoperfusion in patients with CAA using (99m)Tc-ethylcysteinate dimer ((99m)Tc-ECD) brain perfusion SPECT. METHODS A total of 11 patients (5 men and 6 women; age range, 58-78 y; mean age +/- SD, 70.0 +/- 7.0 y) with clinically and radiologically established probable CAA who underwent (99m)Tc-ECD SPECT were included. (99m)Tc-ECD SPECT scans were also obtained from 13 age-matched healthy control subjects (7 men and 6 women; age range, 60-79 y; mean age +/- SD, 66.7 +/- 6.4 y) for comparison. The relative regional cerebral blood flow values obtained for patients and controls were compared using software. RESULTS Compared with controls, patients with probable CAA showed hypoperfusion in the inferior parietal lobule of both parietal lobes (Brodmann area [BA] 40), middle temporal gyrus of the left temporal lobe (BA 39), postcentral gyrus of the right parietal lobe, superior temporal gyrus of the right temporal lobe (BA 22), superior temporal gyrus of the right frontal lobe (BA 10), inferior temporal gyrus of the left temporal lobe (BA 20), and both caudate bodies (P < 0.0001, t = 4.65). CONCLUSION Patients with probable CAA had significantly decreased cerebral perfusion and may be at risk for leukoencephalopathy, atrophy, and ischemia.