Focal Hypoperfusion Research Articles

Effect of small deep hemispheric infarction on the ipsilateral cortical blood flow in man.

The effect of small, deep ischemic lesions on the ipsilateral cortical circulation was investigated in 10 patients with persistent mild or moderate neurological deficits due to infarcts in the internal capsule. rCBF studies by the 133Xe intracarotid injection method were performed 14-180 days after the onset of the infarction. The rCBF functional image was made up from the data of 133Xe dynamic images measured by an Anger-type gamma camera and the rCBF values were calculated by the initial slope method. The average value of mean rCBFs (mCBF) in 10 patients was 44.9 +/- 7.1 ml/100g/min (average PaCO2; 39.9 +/- 4.3 mm Hg). In the rCBF functional images, a focal hypoperfusion area was observed in all cases and localized around the central sulcus, especially in the precentral and central areas. Significant decreases of mCBF and the tendency to decrease of the rCBFs in the hypoperfusion focus were noted in the patients with the larger infarcts in comparison with those with the smaller ones. These results suggest that a small, deep ischemic lesion such as a capsular infarct may have remote effects on the ipsilateral cortical circulation, due probably to the damage of a number of fibers passing through the lesion.

Focal cerebral hypoperfusion in children with dysphasia and/or attention deficit disorder.

The neural mechanisms involved in learning disorders are largely unknown. We studied three-dimensional regional cerebral blood flow (rCBF) in 13 children with dysphasia and/or attention deficit disorder (ADD), using xenon 133 inhalation and emission computed tomography. The rCBF distribution was abnormal in both hemispheres in all patients, as compared with the mean CBF distribution of nine normal children. Regions of hypoperfusion and, by inference, low metabolic activity were predominantly seen in the periventricular white matter and in border zones between major arterial territories. In patients with dysphasia, parts of both perisylvian regions were hypoperfused, and object-naming tasks failed to produce an increased flow in relevant cortical regions. Patients with different dysphasic syndromes appeared to have different patterns of rCBF. All 11 patients with ADD had hypoperfusion in the white matter of the frontal lobes and seven also in the caudate nuclei region. Methylphenidate hydrochloride increased perfusion in the central region, including the mesencephalon and the basal ganglia, and decreased perfusion of motor and primary sensory cortical areas. The location of hypoperfused structures in cognitive disorders of childhood is consistent with a role for an early hypoxic-ischemic event in their origin.

Fluorescein angiography in chronic simple and low-tension glaucoma.

Fluorescein angiograms were performed on a group of low-tension glaucoma and chronic simple glaucoma patients with similar extent of visual field loss, under standardised conditions, to see whether differences attributable to chronic intraocular pressure elevation could be detected. There was no evidence for difference in circulation times between these two groups. There was no evidence that hypoperfusion of the peripapillary choroid contributed to optic nerve hypoperfusion. Low-tension glaucoma patients demonstrated focal sector hypoperfusion of the optic nerve in every case, while the chronic simple glaucoma patients demonstrated a wide range of optic nerve fluorescence, suggesting both focal and diffuse optic nerve head hypoperfusion. It was concluded that, while focal hypoperfusion of the optic nerve may reflect susceptible vasculature at the nerve head with or without intraocular pressure elevation, diffuse hypoperfusion suggested that prolonged intraocular pressure elevation may simultaneously affect the whole of the optic nerve head. This could be a direct effect on blood vessels or a mechanical effect with secondary vascular changes.