Regional Cerebral Blood Flow in Patients with Ischemic Cerebrovascular Disease

Transient Ischemic Attack and Reversible Ischemic Neurological Deficit

Abstract

Regional cerebral blood flow (rCBF) was measured in 25 patients with transient ischemic attacks (TIA) and 34 patients with reversible ischemic neurological deficits (RIND) or ischemic strokes with full recovery. The rCBF measurements were performed by means of the ¹³³Xe intracarotid injection method, using a scintillation camera and an on-line computer system. The rCBF data were analysed and compared with the computed tomography (CT) and angiographic findings on each patient.
There was no significant difference in the average of the mean hemispheric values of rCBF (mean CBF) between TIA and RIND. The averages of mean CBF of TIA or RIND were significantly lower than those of the normal controls, and higher than those of the completed strokes. There was no correlation between the elapsed time from the last attack and the mean CBF in TIA. There was also no correlation between the elapsed time from the onset, or between the presence or absence of hemiparesis and the mean CBF in RIND. CT showed lacunae in 24% of TIA and 32% of RIND, whereas a cortical low density area was shown in only one case in each group. Angiographic abnormalities were found predominantly in the intracranial major arteries, rather than the extracranial carotid artery in both groups. Six patients of TIA (24%) and 6 of RIND (18%) had involvement of their extracranial internal carotid artery. There was no correlation between the mean CBF and angiographic findings. Although the mean CBF did not correlate to CT findings in TIA, it was significantly lower in RIND patients with lacunae on CT scans. Hemispheric pattern of flow distribution (HPFD) was disturbed in 88% of TIA and 74% of RIND. Focal ischemia was shown in only one case with RIND, whereas diffuse ischemia was shown in 2 cases with TIA and 5 cases with RIND. Loss of the hyperfrontal pattern which was thought to represent a mild diffuse cerebral dysfunction, was shown in 44% of TIA and 29% of RIND.
Because diffuse involvement of HPFD was shown without reference for the elapsed time from the last attack of TIA or the onset of RIND, the authors support the ‘hemodynamic’ theory as opposed to ‘microembolic’ theory as the cause of TIA or RIND. It is concluded that TIA and RIND have the same causative factors, and the clinical difference of TIA and RIND is the only difference in recovery times between TIA and RIND.