Cerebral blood flow distribution and reactivity during the symptom-free stages of transient ischemic attacks

Even during the symptom-free stages, patients with transient ischemic attacks (TIA) often show cerebral blood flow (CBF) disturbances. For evaluating the factors which cause these abnormalities, we studied CBF and CBF reactivity to acetazolamide (diamox) using a 99mTc-hexamethylpropyleneamine oxime (HMPAO) SPECT. The results from CBF-SPECT were compared with X-ray computed tomography (CT), cerebral arteriogram, clinical characteristics of TIA and cerebrovascular risk factors. The overall sensitivity rates in detecting the lesion were 68% in CBF-SPECT and 9% in CT. The size of the hypoperfused area tended to be wide in patients who had intracranial, severe stenotic or multiple arterial lesions on the ipsilateral side. No such relations were found between CBF and other examinations. Brain hypoperfusion was located in the subcortical region in eight patients; two patients showed a small hypodense lesion on CT which corresponded to the hypoperfusion on SPECT, and three patients showed no arteriographic abnormality. Hypoperfusion in the cortex was seen in seven patients; all patients showed arteriographic abnormality, but no CT abnormality. The severity rating of the vascular stenosis and hypoperfusion, and the incidence of the intracranial lesions were higher in this group than the group with subcortical hypoperfusion. Seven patients showed fixed normoperfusion before and after diamox injection. Two patients with a subcortical small infarction showed fixed hypoperfusion even after diamox injection. Twelve patients showed focal hypoperfusion before diamox with a new filling-in after diamox. Only one patient showed resting hypoperfusion and decreased CBF reactivity to diamox. The results suggest that most of the patients with a brain hypoperfusion in the symptom-free stages of TIAs have preserved cerebrovascular reactivity although a few patients show hypoperfusion having cerebral infarction or hemodynamically compromised tissue. (author)