Noninvasive 133XE inhalation measurements of regional cerebral blood flow in migraine and related headaches.
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Publications and source records attributed to H Naritomi.
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To assess the effect of supratentorial cerebral ischemia on infratentorial brain function, changes in regional cerebellar blood flow (rCeBF), after right carotid occlusion for 4 hours, were studied in 30 mongolian gerbils. The regional cerebral blood flow (rCBF) in the occluded cerebral hemisphere and rCeBF in both cerebellar hemispheres were measured simultaneously by hydrogen clearance methods. Before carotid occlusion, rCBF was 0.44 +/- 0.07 ml/g brain/min, and rCeBF in the left and right cerebellar hemispheres was 0.37 +/- 0.09 and 0.40 +/- 0.09 ml/g brain/min, respectively. After carotid occlusion, rCBF decreased in all animals showing levels of above 0.20 ml/g brain/min in 14 (group A), between 0.10 and 0.19 ml/g brain/min in 7 (group B) and below 0.10 ml/g brain/min in 9 (group C). rCeBF exhibited no changes in group A and a mild reduction in group B after carotid occlusion. In group C, rCeBF was significantly reduced 30 min after carotid occlusion in the left cerebellar hemisphere followed subsequently by bilateral reduction. In groups B and C, supratentorial brain edema was observed 4 hours after occlusion, but the degree of edema was moderate. The results of the present study suggest that depression of infratentorial brain function may occur after supratentorial local cerebral ischemia, presumably due to diaschisis.
In 36 patients with angiographically proven middle cerebral artery (MCA) stenosis, local cerebral hemodynamics were studied employing angiography, 133Xe inhalation regional cerebral blood flow (rCBF) measurements and CT scans. They had transient ischemic attacks in 8 and completed stroke in 28. The patients with less than 50% stenosis (n = 16) had no hemodynamic abnormality in angiographical and rCBF examinations. The infarction in this group was small and located in the basal ganglia area. The patients with 50 to 74% stenosis (n = 9) often revealed a delayed filling of MCA branches in the angiography, however, they showed no significant rCBF reduction. The infarction in this group was also small and located in the basal ganglia area. The patients with 75 to 99% stenosis (n = 11) exhibited a significant flow depression both in angiographical and rCBF examinations. Three of them had large cerebral infarction in the watershed zone or the cerebral cortex. The results of the present study suggest that the hemodynamic effect of MCA stenosis begins to manifest at 50% in grade and becomes apparent at 75%. The danger of hemodynamic crisis as well as the risk of large cerebral infarction may increase when MCA stenosis exceeds 75% in grade.
In children with Moyamoya disease, transient ischemic attacks often occur during hyperventilation, and the frequency of attacks usually decreases with advancing age. To elucidate the mechanism of the attacks, the regional cerebral blood flow was measured during rest and/or hyperventilation in children aged 3-16 with Moyamoya disease. Regional cerebral blood flow during rest was significantly higher in younger children with Moyamoya disease, and it progressively decreased with advancing age through childhood. During hyperventilation, regional cerebral blood flow decreased in all the children, although blood flow in younger children was still higher than that in the older children. Nevertheless, transient ischemic attacks were more readily precipitated by hyperventilation in the younger than in the older children. Cerebral metabolic demand is much higher in the first decade of life than in later decades. Therefore, it seems likely that even a moderate reduction in cerebral blood flow can cause metabolic impairment in young children. Such high cerebral metabolic demand may play an important role in the frequent occurrence of transient ischemic attacks in young children with Moyamoya disease.
Cerebral hemispheric blood flow (HBF) and metabolism were measured before and after withdrawal of 20 to 30 ml of cerebrospinal fluid (CSF) over a 10-minute interval in eight patients with recent cerebral infarction and in four patients with Alzheimer's disease (AD). Immediately after CSF removal HBF decreased significantly in the AD group (-14%) but showed no significant change in the stroke group (-5%). There was rapid reduction in cerebral venous O2 content and some increase in cerebral venous PCO2 appearing within 60 seconds of CSF withdrawal, interpreted as a rapid reduction of cerebral blood flow (CBF) as judged by cerebral A-VO2 differences. The reduction in CBF was confirmed by the hydrogen clearance method. Reduction of CBF in response to lowering CSF pressure is presumably of neurogenic origin since it was rapid and occurred without changes in PaCO2 or MABP. Furthermore, measurement of HBF demonstrated that cerebral metabolism constant after CSF removal. It is postulated that in AD, reduction of HBF following CSF withdrawal is mediated by a disordered neurogenic veno-arterial vasoconstriction reflex which is stimulated by rapid reduction in CSF pressure (CSFP). In patients with stroke, when cerebral perfusion pressure is increased by lowering CSFP, CBF is maintained constant most likely by a physiological cerebral veno-arterial vasoconstrictive reflex. Apparently, this vasocontrictive reflex becomes excessive in Alzheimer's disease, possibly due to cerebral neurogenic imbalance.
This study presents ultrastructural confirmation of the embolic method of producing an ischemic lesion. The embolic method was shown to produce more advanced parenchymal changes than those reported for the same postocclusion period following vascular clipping. With this method there was less alteration in the morphological intergrity of occluded extraparenchymatous areas of the arterial bed, especially in the associated nerve bundles.
Cerebral blood flow (CBF) and metabolism were measured before and after withdrawal of 5 to 6 ml of cerebrospinal fluid (CSF) in 17 baboons. The measurements were made before and after infusion of tyrosine, the precursor amino acid of the putative neurotransmitters, dopamine and norepinephrine, in the brain. The same observations were made in another experimental group, i.e., before and after acute cerebral multiembolization induced by microfil emboli. In the steady state CBF was unaltered following reduction of intracranial pressure by removal of CSF. After infusion of tyrosine, CBF was decreased, and cerebrovascular resistance increased significantly on removal of CSF. Cerebral embolization did not influence changes in CBF at reduced intracranial pressure. It appears that the cerebral resistance vessels constrict following reduction of intracranial pressure by removal of CSF and that cerebrospinal fluid pressure-CBF autoregulatory mechanisms are resistant to cerebral ischemia induced by middle cerebral artery embolization.
A clinical method for noninvasive measurement of regional cerebral blood flow (rCBF) and blood volume (rCBV) is described, based on Obrist's 10 minute, desaturation method after 1 minute inhalation of 133Xe. Sixteen collimated probes are placed over both hemispheres and brain stem-cerebellar regions. End-tidal 133Xe curves are used for correction of recirculation. KEV discriminators are set to record gamma and x-ray activity separately. Values are printed out automatically by a computer on a brain map. Extracerebral contamination is reduced by 1) computing curves from gamma activity, 2) applying pressure on the scalp beneath the probes, 3) 1 minute inhalation of 133Xe and recording desaturation curves for 10 minutes, thereby minimizing slow clearance from extracranial tissues. Normal values for both fast and slow compartments are reproducible and are in good agreement with the carotid injection method. The speech dominant hemishpere has higher flow than the right under conditions described. Posterior portions of the cranium over the cerebellum and brain stem appear to have higher flow gray values than the cerebral cortex. Gray matter flow decreases with advancing age.
UNLABELLED: Blood components were reported to be aggravating factors of ischemic cerebral injury. We previously reported that a partial blood replacement with Fluosol DA reduced ischemic neuronal injury. The purpose of this study is to elucidate whether pyridoxalated hemoglobin polyoxyethylene conjugate solution (PHP) exerts neuro-projective effects against cerebral ischemia. METHODS: 38 adult male gerbils were divided into 4 groups, such as normal group without ischemia or treatment, PHP group undergoing an exchanging blood transfusion with 5.0 ml PHP, ischemia group undergoing 5-min forebrain ischemia, and PHP-ischemia group with 5.0 ml PHP partial blood replacement prior to 5-min forebrain ischemia. Cerebral injury was assessed 7 days after treatment. In another group, effects of PHP on blood nitric oxide (NO) and cerebral blood flow (CBF) were studied. RESULTS: CA1 cell density was 140-2/mm in normal group and 142-5/mm in PHP group. The cell density was markedly reduced to 38-13 in ischemia group. The cell density was further reduced 27-10/mm in PHP-ischemia group. PHP was found to have a potent NO scavenger action and reduce CBF. CONCLUSION: Partial blood replacement with PHP prior to ischemia may cause cerebral vasoconstriction due to NO scavenger action and may worsen ischemic injury.
BACKGROUND AND PURPOSE: The clinical significance of microembolic signals (MESs) detected by transcranial Doppler sonography (TCD) in acute ischemic stroke remains unclear. The purpose of the present study was to assess the findings of diffusion-weighted MR imaging (DWI) and other clinical characteristics in patients with acute ischemic stroke and MESs. METHODS: We performed TCD and DWI within 48 hours and 7 days, respectively, after stroke onset in 28 patients with acute brain infarction. The relationship between the number of MESs and DWI findings, risk factors for stroke, National Institutes of Health Stroke Scale (NIHSS) score on admission, and arterial disease was examined. RESULTS: Ten patients had MESs detected by TCD (MES group) and 18 had no MESs (control group). The frequency of hypertension, diabetes mellitus, hyperlipidemia, and smoking; NIHSS score; blood-coagulation parameters; and interval between stroke onset and DWI study did not differ between the two groups. However, arterial disease was more frequent in the MES group than in the control group. Small, multifocal ischemic lesions (<10 mm in diameter) on DWI were more frequent in the MES group than in the control group. Conventional CT and MR imaging often failed to show these lesions. CONCLUSION: Small, often asymptomatic DWI abnormalities were more frequent in patients with MESs detected by TCD and with large-vessel occlusive diseases than in stroke patients without MESs. TCD and DWI may provide early clues to the mechanism of stroke in the acute phase.