Haemodynamic evaluation of paraparetic transient ischaemic attacks in childhood moyamoya disease

Abstract

The haemodynamic mechanisms responsible for the appearance of paraparetic transient ischaemic attacks in ten patients with childhood moyamoya disease who subsequently underwent bifrontal omental transplantation were investigated. Cerebral perfusion (CP) was measured with ^99mTc-hexamethylene-propyleneamine oxime single photon computed tomography prior to and after administration of acetazolamide. Cerebral perfusion was obtained by dividing radioisotope uptake per pixel in regions of interest by that in cerebellum. Haemodynamic reserve was defined as [CP after acetazolamide - CP before acetazolamide]/CP before acetazolamide × 100. Amounts of CP in the anterior portion of the frontal lobe and in the paracentral lobule were 0.70±0.04 and 0.74 ±0.03, respectively, before appearance of the transient ischaemic attacks. The latter was significantly higher than the former (p <0.0001). Haemodynamic reserves were -11.1 ±2.8 and - 9.6 ± 3.0, respectively, at that time. These two parameters were significantly decreased just after paraparetic transient ischaemic attacks and two parameters in the paracentral lobule were more decreased than those in the anterior portion of the frontal lobe. But these increased again after bifrontal omental transplantation in these two regions. In summary, the watershed region was located anterior to the paracentral lobule before appearance of the transient ischaemic attacks, and widened and moved backward to include the paracentral lobule just before their appearance. [Neurol Res 1995; 17: 162-168]