Frontal Cerebral Blood Flow Research Articles

Effects on regional cerebral blood flow of transcendental meditation

Previous blood flow measurements in this laboratory have indicated increased nonrenal nonhepatic blood flow during behaviorally induced rest states, especially during the stylized mental technique of transcendental meditation (TM). We have hypothesized that increased cerebral blood flow (CBF) may account for most of the increased nonrenal nonhepatic blood flow during TM. In this report we describe increased frontal and occipital CBF in TM determined by the electrical impedance plethysmographic methodology known as rheoencephalography (REG), which allows noninvasive, nondisturbing, continuous CBF monitoring. We also report high correlation between increased CBF and decreased cerebrovascular resistance (CVR) during TM, suggesting that a contributing vascular mechanism to the increased CBF may be decreased CVR. Because only a small amount of stage 1 sleep was observed during TM and because stage 1 sleep has been reported to be accompanied by decreased CBF, we believe that sleep did not contribute to the CBF increase. The data of this study are consistent with the hypothesis that blood flow changes during TM comprise a patterned response subserving needs of increased cerebral activity.

Cerebral blood flow changes in normal aging: Spect measurements

AbstractGlobal and regional cerebral blood flow (CBF) were evaluated with single photon emission computerized tomography (SPECT) utilizing both 133Xenon (133Xe) (47 subjects, 47–82 years old) and 99Tc‐hexamethylpropyleneamine oxime (99Tc‐HMPAO) (27 subjects, 47–80 years old). The 133Xe results showed: among total subjects, no age‐related decline in global CBF, but a significant regional decline in the occipital lobe (p < 0.05); among men, significant age‐related declines in global, frontal, temporal, occipital and right hemisphere CBF (all p < 0.05); among women, no age‐related decline in global or regional CBF. The 99Tc‐HMPAO results showed no age‐related decline in either global or regional perfusion among total subjects, men or women. These results suggest that age‐related global and regional (including frontal lobe) CBF declines do not occur in healthy control subjects after the age of 45 years. However, gender differences in age‐related CBF changes warrant further study.

Decreases in frontal and parietal lobe regional cerebral blood flow related to habituation.

We previously reported decreased mean CBF between consecutive resting conditions, ascribed to habituation. Here we address the regional specificity of habituation over three consecutive flow studies. Regional CBF (rCBF) was measured in 55 adults (12 right-handed men, 12 right-handed women, 14 left-handed men, 17 left-handed women), with the 133Xe inhalation technique, during three conditions: resting, verbal tasks (analogies), and spatial tasks (line orientation). Changes in rCBF attributable to the cognitive tasks were eliminated by correcting these values to a resting equivalent. There was a progressive decrease in mean rCBF over time, reflecting habituation. This effect differed by region, with specificity at frontal (prefrontal, inferior frontal, midfrontal, superior frontal) and inferior parietal regions. In the inferior parietal region, habituation was more marked in the left than the right hemisphere. Right-handers showed greater habituation than did left-handers. There was no sex difference in global habituation, but males showed greater left whereas females showed greater right hemispheric habituation. The results suggest that habituation to the experimental setting has measurable effects on rCBF, which are differently lateralized for men and women. These effects are superimposed on task activation and are most pronounced in regions that have been implicated in attentional processes. Thus, regional decrement in brain activity related to habituation seems to complement attentional effects, suggesting a neural network for habituation reciprocating that for attention.

Stage-dependent reductions of regional cerebral blood flow measured by HMPAO-SPECT in dementia of Alzheimer type

In the present study, we used HMPAO-SPECT to examine the rCBF patterns in two subgroups (moderately and severely demented) of patients with DAT. Temporoparietal and frontal cerebral blood flow were compared between the two patient groups

Regional Cerebral Blood Flow and Response to Carbon Dioxide during Controlled Hypotension with Isoflurane Anesthesia in the Rat

Regional (frontal, parietal, occipital, cortical, and basal ganglia) cerebral blood flow (rCBF) was examined at 1.5 and 3.5 MAC inspired isoflurane/O2 anesthesia in the rat using the radioactive microsphere technique to determine the effects of controlled hypotension with deep isoflurane anesthesia on rCBF and the response of rCBF to changes in PaCO2 when mean blood pressure (BP) was decreased to levels below the lower limit of the autoregulatory threshold. Four groups of six rats were studied with rCBF 1 determined at 1.5 MAC (mean BP 80-90 mm Hg) followed by two rCBF determinations at 3.5 MAC (mean BP 46-48 mm Hg). For CBF 1 the regional CO2 response was a 3.1-3.9% increase in rCBF/mm Hg increase in CO2. Regional cerebral blood flow (ml/g/min) ranged from 0.64 +/- 0.05-0.83 +/- 0.15 at PaCO2 of 19 mm Hg to 1.34 +/- 0.11-1.80 +/- 0.33 at PaCO2 of 41 mm Hg to 2.61 +/- 0.26-3.72 +/- 0.37 at PaCO2 of 59 mm Hg (mean +/- SEM). With controlled hypotension (CBF 2) rCBF was unchanged during normocarbia, increased 100% during hypocarbia, P less than 0.01 vs CBF 1 and decreased 30% during hypercarbia, P less than 0.01 vs CBF 1. For rCBF 3 measurements, the BP and inspired concentration of isoflurane were kept constant, while PaCO2 was increased in two and decreased in two of the four groups. Within-group comparisons between rCBF 2 and rCBF 3 results demonstrated loss of CO2 responsiveness of the rat cerebrovasculature in every region during controlled hypotension to below the autoregulatory threshold at 3.5 MAC isoflurane/O2 anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Steele-Richardson-Olszewski syndrome. Brain energy metabolism, blood flow and fluorodopa uptake measured by positron emission tomography.

Brain function was measured in 5 patients with clinically diagnosed Steele-Richardson-Olszewski syndrome using positron emission tomography and tracers of dopamine metabolism, blood flow and oxygen metabolism. A global decrease in blood flow and oxygen utilization compared with normal values was found but the decrease was more marked in the frontal regions. The degree of impairment in oxygen utilization in the frontal region paralleled roughly the duration of the disease. Blood flow was impaired to a greater extent than oxygen utilization, resulting in raised oxygen extraction. This can partially be explained by a lower pCO2 in the patients. Alternatively it may imply involvement of brain vasculature in the pathophysiology of the disease in addition to neuronal degeneration. Striatal dopamine formation and storage, as indicated by L-(18F)fluorodopa uptake, was significantly decreased compared with control values. The severity of this decrease paralleled the degree of reduction in frontal cerebral blood flow. The results suggest that the impairment of cerebral function in Steele-Richardson-Olszewski syndrome is determined to a large extent by brainstem pathology.

Cerebral blood flow decrements in chronic head injury syndrome

Global and regional cerebral blood flow (CBF) has been reported to be decreased immediately after head injury. Since neuropsychological deficits in patients with chronic head injury syndrome persist long after the initial trauma, we studied CBF, which reflects cerebral metabolism and activity, and evaluated the results of neuropsychological tests in 12 alert, responsive patients aged 18–26, both 2–13 months after head injury and 1–12 months after they regained consciousness. Global CBF was significantly decreased in patients with head injury relative to age-matched normal controls. Four patients had well-localized injury; in three of these, CBF over the affected region was significantly decreased relative to the same region in the opposite hemisphere and relative to the same region in an age-matched normal control. In one patient with right frontal injury, cognitive improvement on repeat testing was associated with a relative increase in right frontal CBF. The remaining eight patients had diffuse bilateral injury. Asymmetry ratios (larger value of mean hemispheric CBF divided by the smaller) were significantly higher for the group with localized dysfunction (1.2 ± 0.08 vs. 1.0 ± 0.01, p < 0.01), suggesting homolateral decrease in CBF in this group. Three patients with diffuse injury underwent repeat studies 5–14 weeks later; all improved on psychological tests, and two had a significant increase in global CBF. These results suggest that the chronic sequelae of head injury include decreased CBF, presumably reflecting decreased cerebral metabolism, which correlates with the neuropsychological impairment.

Cerebral hemodynamics in normal-pressure hydrocephalus

Cerebral hemodynamics in 31 patients with suspected normal-pressure hydrocephalus were studied by means of the xenon-133 (133Xe) inhalation method and on dynamic computerized tomography (CT) scanning. Cerebral blood flow (CBF) is reduced in all patients with dementia. Hypoperfusion was noted in a frontal distribution in these patients compared with normal individuals. There was no difference in CBF patterns between patients with good and those with poor outcome. The CBF was increased following cerebrospinal fluid (CSF) shunting in patients who responded to that procedure: increase in flow correlated with clinical improvement, frontal and temporal lobe CBF was most markedly increased, and the CBF pattern became normal. In contrast, CBF was decreased after shunt placement in patients who were considered to have suffered from degenerative dementia, as evidenced by non-response to shunting. Dynamic computerized tomography studies demonstrated that patients with a good outcome showed a postoperative reduction in mean transit time of contrast material, most prominent in the frontal and temporal gray matter, and slight in the deep frontal structures, but not in the major cerebral vessels. Patients with poor outcome after shunting, however, had an increase in transit time in all regions. This corresponded well with the results as determined by the 133Xe inhalation method.

Effect of flunarizine on canine cerebral cortical blood flow and vascular resistance post cardiac arrest

Twelve dogs were anesthetized and instrumental for determination of CVP, arterial pressure, intracranial pressure, left atrial pressure, and frontal cerebral cortical blood flow (CCBF) by the thermal method. A catheter was introduced into the venous return of the cerebral confluence to allow determination of cerebral A-V oxygen saturation differences. The animals were placed on cardiac bypass using a circuit from the right atrium to the pulmonary artery and a second circuit from the left ventricular apex to the left femoral artery. A heat exchanger was used to maintain a constant blood temperature of 37 C in the output of the left side bypass circuit. All animals were heparinized during bypass. Ventricular fibrillation was induced after completion of the bypass surgery. Two dogs served as controls. Pre-arrest determinations of hemoglobin, glucose, CCBF, and cerebral A-V oxygen differences were taken. Full circulatory arrest was carried out for 20 minutes by shutting off the cardiac bypass. Resuscitation was achieved by resumption of bypass perfusion. Acid-base balance was corrected quickly, and pre-arrest perfusion pressure was achieved and maintained for 90 minutes. All pressure parameters were monitored continuously. All pre-arrest determinations were repeated at 20, 40, 60, and 90 minutes post resuscitation. Five dogs were treated with 6 microgram/kg flunarizine administered IV drip over 10 minutes immediately post reperfusion. Five dogs were not treated post arrest. Treated animals had a prompt return of CCBF rates equal to or greater than pre-arrest flow, which persisted throughout the period of post-arrest observation. Untreated animals had markedly reduced CCBF and increased resistance. CCBF uniformly proceeded to near zero flow by 90 minutes. The ICP was not significantly altered by treatment.

Canine cerebral cortical blood flow and vascular resistance post cardiac arrest

seven dogs were anesthetized and instrumented for determination of central venous pressure (CVP), arterial pressure, intracranial pressure (ICP), left atrial pressure (LAP), and frontal cerebral cortical blood flow by the thermal method. A catheter was introduced into the venous return of the cerebral confluence to allow determination of cerebral A-V oxygen saturation differences. The animals were placed on cardiac bypass using a circuit from the right atrium to the pulmonary artery, and a second circuit from the left ventricular apex to the left femoral artery. A heat exchanger was used to maintain a constant blood temperature of 37 C in the output of the left-side bypass circuit. All animals were heparinized during bypass. Ventricular fibrillation was induced after completion of the bypass surgery. Two dogs served as controls for stability of the measured parameters on prolonged bypass. Pre-arrest determinations of hemoglobin, cerebral cortical blood flow, and cerebral A-V oxygen saturation differences were taken. Full circulatory arrest was carried out for 20 minutes in 5 dogs by shutting off the cardiac bypass. Resuscitation was achieved by resumption of bypass perfusion. Acid-base balance was corrected and pre-arrest perfusion pressures were achieved and maintained for 90 minutes. All pressure parameters were monitored continuously. Pre-arrest determinations were repeated at 20, 40, 60, and 90 minutes post resuscitation. A 50% reduction in cerebral cortical blood flow 20 minutes post resuscitation progressed to near zero flow 90 minutes post resuscitation. The changes in net cerebral perfusion pressure produced by the slowly rising intracranial pressure do not account for this flow reduction. Calculation of cerebral vascular resistance reveals a ten-fold increase in resistance post-arrest and -resuscitation.