The regional cerebral blood flow (rCBF) distribution was measured by 133xenon inhalation using a gamma camera in 18 right-handed volunteers, 6 subjects performing a graphic task (writing numbers in letters) with the right hand, 6 subjects imagining the same task, and 6 subjects were assessed during two rest periods to determine the reproducibility of the technique. The mean rCBF increased between 10% and 25% (P less than 0.01) during both motor performance and motor ideation. However, there were regional differences. While motor performance activated mainly the rolandic regions bilaterally, motor ideation gave prefrontal and premotor rCBF augmentations. In both situations there was significant bilateral increase in regions corresponding to the cerebellum.
We performed 99mTc-hexamethylpropyleneamineoxime-single-photon emission computed tomography (SPECT) and 18F-fluorodeoxyglucose-positron emission tomography (PET) in 20 epileptic patients with well-lateralized temporal electroencephalographic focus, normal computed tomographic scan, and brain magnetic resonance imaging (MRI) either normal (n = 10) or showing nonspecific changes in the epileptogenic temporal lobe (n = 10). In patients with a normal MRI, PET exhibited focal hypometabolism in 80%, whereas SPECT showed corresponding hypoperfusion in only 20%. In patients with an abnormal MRI, PET and SPECT yielded 100% and 90% sensitivity, respectively. The metabolic and regional cerebral blood flow disturbances were topographically concordant with electroencephalographic and MRI findings in all these patients. Only patients with a large and pronounced hypometabolism on PET images exhibited hypoperfusion on SPECT. Spatial resolution appeared to be the critical factor responsible for the higher sensitivity of PET. However, this superiority of PET did not prove clinically useful in patients whose SPECT was abnormal, particularly when brain MRI showed nonspecific changes in the epileptogenic temporal lobe.
A significant hemodynamic compromise in patients who had unilateral symptomatic carotid occlusion was observed according to CBF and MTT values. This approach might be promising in the understanding of cerebral hemodynamics in patients with vascular disorders.
Thromboembolic stroke is likely to occur in patients with a restricted cerebral blood flow reserve. Our aims were to determine (1) whether symptomatic patients had any significant hemodynamic restriction ipsilateral to carotid occlusive disease compared with patients whose carotid stenosis is asymptomatic and (2) whether patients with carotid occlusive disease have impaired cerebral perfusion reserve compared with control subjects.
We compared cerebral blood flow and collateral capacity using the 133Xe inhalation method and acetazolamide test in symptomatic (n = 10) and asymptomatic (n = 10) patients who had a high-grade internal carotid artery stenosis (range, 70% to 99%). Results were compared with those from 10 healthy control subjects.
Mean baseline cerebral blood flow was 40.29 +/- 1.38 mL/100 g per minute on the symptomatic side in symptomatic patients versus 45.20 +/- 2.53 mL/100 g per minute on the lesion side in asymptomatic patients (control subjects, 46.91 +/- 2.11 mL/100 g per minute in the right hemisphere versus 46.17 +/- 1.93 mL/100 g per minute in the left). There was no statistical difference between patients in symptomatic and asymptomatic groups versus control subjects (P > .10). Mean cerebral blood flow increase after acetazolamide was in the same range in symptomatic (52.89 +/- 2.54 mL/100 g per minute) and asymptomatic (56.22 +/- 3.35 mL/100 g per minute) patients (P > .10), and no difference was observed regarding control subjects (54.25 +/- 2.94 mL/100 g per minute; P > .10). Three asymptomatic and two symptomatic patients and three control subjects had no significant cerebral blood flow increase after acetazolamide.
An additional hemodynamic factor in thromboembolic ischemia related to severe unilateral carotid stenosis might be an unusual finding in patients without apparent hemodynamic induction of symptoms. The lack of significant variation in postacetazolamide cerebral blood flow in some patients and control subjects implies that this procedure may be inconsistent in assessing the cerebral perfusion reserve in the individual case.
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