Cerebral Hemispheric Blood Flow Research Articles

Historical Review and Current Progress of the Cranioplasty

Cranialplasty is one of the typical neurosurgical procedures.As a result of their aesthetics and biocompatibility, autologous grafts are chosen. Numerous patients with skull defects experience local scalp depression as a result of atmospheric pressure, which can cause an imbalance in intracranial pressure, displacement of brain tissue, reduction in cerebral hemispheric blood flow, and problems with cerebrospinal fluid circulation, all of which can result in a variety of clinical manifestations. Then cranioplasty can effectively restore normal cerebrospinal fluid dynamics and cerebral cortical blood perfusion, which is conducive to reducing intracranial complications and assisting in the restoration of neurological function. It can also repair skull defects, restore the patient's skull appearance and protective function. This paper's goal is to investigate a foundation for the viability and timeliness of cranioplasty, This paper discussed the history of cranioplasty, the pathophysiological effects of recovery, complications, and rehabilitation issues from both qualitative and quantitative viewpoints. According to the average cranioplasty score, having a procedure done within three months following a traumatic DC may help with neurological function recovery. In addition, effective communication between the surgical team and the rehabilitation staff is crucial for maximizing recovery and enhancing results.

Regional brain blood flow and cerebral hemispheric oxygen consumption during acute hypoxaemia in the llama fetus.

Unlike fetal animals of lowland species, the llama fetus does not increase its cerebral blood flow during an episode of acute hypoxaemia. This study tested the hypothesis that the fetal llama brain maintains cerebral hemispheric O2 consumption by increasing cerebral O2 extraction rather than decreasing cerebral oxygen utilisation during acute hypoxaemia. Six llama fetuses were surgically instrumented under general anaesthesia at 217 days of gestation (term ca 350 days) with vascular and amniotic catheters in order to carry out cardiorespiratory studies. Following a control period of 1 h, the llama fetuses underwent 3 x 20 min episodes of progressive hypoxaemia, induced by maternal inhalational hypoxia. During basal conditions and during each of the 20 min of hypoxaemia, fetal cerebral blood flow was measured with radioactive microspheres, cerebral oxygen extraction was calculated, and fetal cerebral hemispheric O2 consumption was determined by the modified Fick principle. During hypoxaemia, fetal arterial O2 tension and fetal pH decreased progressively from 24 +/- 1 to 20 +/- 1 Torr and from 7.36 +/- 0.01 to 7.33 +/- 0.01, respectively, during the first 20 min episode, to 16 +/- 1 Torr and 7.25 +/- 0.05 during the second 20 min episode and to 14 +/- 1 Torr and 7.21 +/- 0.04 during the final 20 min episode. Fetal arterial partial pressure of CO2 (P(a,CO2), 42 +/- 2 Torr) remained unaltered from baseline throughout the experiment. Fetal cerebral hemispheric blood flow and cerebral hemispheric oxygen extraction were unaltered from baseline during progressive hypoxaemia. In contrast, a progressive fall in fetal cerebral hemispheric oxygen consumption occurred during the hypoxaemic challenge. In conclusion, these data do not support the hypothesis that the fetal llama brain maintains cerebral hemispheric O2 consumption by increasing cerebral hemispheric O2 extraction. Rather, the data show that in the llama fetus, a reduction in cerebral hemispheric metabolism occurs during acute hypoxaemia.

Seasonal affective disorder: response to light as measured by electroencephalogram, melatonin suppression, and cerebral blood flow.

This study was designed to test the hypothesis that patients with SAD have significantly different physiological responses to light than healthy age- and sex-matched controls. We studied retinal contrast sensitivity, visual evoked EEG responses, and melatonin suppression by, and cerebral blood flow response to, full-spectrum artificial daylight. There was no significant difference between 10 patients and 11 controls in retinal contrast sensitivity, or amplitude or latency of N2, P2, P100 or P300 on EEG. We compared melatonin suppression in 12 SAD patients and 12 controls. During exposure to 500 lux and 1500 lux artificial daylight both the SAD patients and controls had a significant melatonin percentage suppression; however, the percentage suppression did not differ significantly between the SAD patients and the controls. In addition, we carried out a small pilot study into the effect of light on cerebral blood flow in four SAD patients and four controls. Before exposure to 1500 lux artificial daylight there was no significant difference between patients and controls in global, regional or cerebral hemispheric blood flow. After light exposure the SAD patients and controls had a significantly different percentage change in cerebral blood flow. We suggest that patients with SAD do not have significantly physiological responses to light than controls, except perhaps in cerebral blood flow. Furthermore, mechanisms other than supersensitivity of melatonin suppression must explain both the pathophysiology of the disorder and its response to treatment with light.

1442 REGIONAL CEREBRAL BLOOD FLOW (rCBF) IN THE IMMATURE RAT

7-day old rats (15 g body weight) were injected subcutaneously with iodo-[1C] antipyrine (5 μ Ci). After a variable period, each pup was decapitated and arterial blood collected for scintillation counting. Brains were immediately removed and either prepared for isotopic counting or frozen for autoradiography. The brain: blood partition coefficient was determined (0.944 ± .066 ml/g (mean ± S.E.)). Both cerebral hemispheric blood flow (CHBF) and rCBF were calculated according to a formula derived from the Fick equation. CHBF equaled 66 ± 4 ml/100 g/min (mean ± S.E.), a value midway between reported 1-day old rat CBF and adult rat CBF. Auto-radiograms were of sufficient quality to permit microdensitometric readings of a minimum of 11 structures. rCBF ranged from 20 ml/100 g/min in subcortial white matter to 71 ml/100 g/min in the brain stem. Immature rat rCBF, as a proportion of adult rat rCBF, was greatest in brain stem. Other 7 day old rats underwent right common carotid artery ligation and subsequent exposure to an 8% O2 environment. Right hemispheric flow was reduced to less than 5% of left hemispheric flow. This reduction was greatest in the distribution of the right middle cerebral artery. Vascular columns perpendicular to the pial surface, corresponding to columns seen metabolically and histopathologically, were not found. Thus, we have developed a relatively simple means of measuring rCBF in the immature rat and we have used it to study a model of cerebral hypoxia-ischemia.

Ophthalmoplethysmography in head and neck surgery.

Ophthalmoplethysmography (OPG) is a simple, noninvasive diagnostic test in which the cerebral hemispheric blood flow can be indirectly measured. Its use in head and neck surgery is invaluable because it enables the surgeon to predict preoperatively whether a patient will survive carotid artery resection. In a three-year period, nine patients have survived carotid resection on the basis of favorable OPGs, without a death or permanent neurologic complication. A comparison of the results of OPG testing with intraoperative measurement of internal carotid artery pressure showed close correlation in 14 of 20 patients who were tested. Lack of correlation in four patients can be explained by the circumstances of the intraoperative test. This study's findings demonstrate that this test has high clinical reliability.

Effect of cerebrospinal fluid removal on cerebral blood flow and metabolism in patients with Alzheimer's disease versus recent stroke.

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.

Influence of adrenergic receptor blockade on circulatory and metabolic effects of disordered neurotransmitter function in stroke patients.

Cerebral hemispheric blood flow and metabolism were measured before and after therapy with intracarotid infusion of combined PBZ and PPL in 15 patients with recent cerebral infarction. HBF was unaltered despite decrease in cerebral perfusion pressure. Cerebral hemispheric oxygen comsumption and carbon dioxide production decreased while cerebral hemispheric lactate production increased. Biphasic cerebral uptake of tyrosine was observed during and immediately after PBZ and PPL infusion. CSF HVA increased, indicating altered DA turnover. CSF 5HIAA levels also increased, suggesting altered 5HT turnover after PBZ and PPL. Release of cyclic AMP from ischemic brain into cerebral venous blood seen in the steady state was abolished after therapy. Cerebral hemodynamic studies suggest a functional balance between monaminergic neurogenic influences in the control of cerebral circulation. Imbalance of such controlling factors in ischemic brain may lead to paradoxical vascular responses to induced hypertension and hypotension. PBZ and PPL enhance such responses perhaps by increasing central neurotransmitter turnover and release. Further shift toward cerebral anaerobic metabolism may occur in ischemic brain following the use of phenoxybenzamine and propranolol. Worsening of neurological deficit occurred in four cases. Combined therapy with PBZ and PPL does not appear beneficial in the therapy of patients with recent stroke.

Cerebral metabolic changes during treatment of subacute cerebral infarction by alpha and beta adrenergic blockade with phenoxybenzamine and propranolol.

Cerebral hemispheric blood flow (HBF) and metabolism were measured in 30 patients with acute and subacute cerebral infarction before and after intracarotid infusion of the alpha adrenergic blocking agent phenoxybenzamine (PBZ) or the beta adrenergic blocker propranolol (PPL) dissolved in saline. Following intracarotid injection of 7 µg per kilogram per minute PBZ, HBF showed no change but cerebral hemispheric oxygen consumption (HMIO 2 ) and carbon dioxide production (HMICO 2 ) decreased. Glucose consumption (HMIGl) was unchanged but the glucose to oxygen utilization ratio (HG:O) increased. Intracarotid injection of 1.45 µg per kilogram per minute PPL caused reduction of HBF, HMIO 2 , HMICO 2 , HMIGl and HG:O. After PBZ infusion, mean systemic arterial blood pressure (MABP) decreased slightly, intracranial venous pressure (ICVP) and CSF pressure (CSFP) increased, and central venous pressure (CVP) remained unchanged. PPL infusion had no effect on intracranial dynamics. Possible mechanisms whereby PBZ and PPL influence cerebral metabolism and function were discussed. Inhibition of uncoupling of oxidative phosphorylation appeared to be the most likely explanation for the improvement in brain function and metabolic change associated with each of the drugs. These data support the concept that catecholamines released into brain tissue are a possible cause of uncoupled oxidative phosphorylation. Presently available evidence suggests that adrenergic blocking agents warrant clinical evaluation in the treatment of acute cerebral ischemia, infarction, hemorrhage, and anoxia.

A method for measuring cerebral hemispheric blood flow and metabolism.

A new method for measuring cerebral hemispheric blood flow together with metabolism using an injection of a 5 ml bolus of hydrogen-saturated saline into each internal carotid artery is described. This method was extensively evaluated in the monkey prior to being used in man. Under fluoroscopic control, a catheter was inserted into each cerebral transverse sinus via the basilic veins. Hemispheric blood flow was calculated from the clearance curves of hydrogen from the transverse sinus following injection using a formula based upon the Stewart-Hamilton principle. Hemispheric metabolic index for oxygen was estimated using a new formula by assuming that the distribution of hydrogen into each transverse sinus following injection of the bolus indicates the distribution of the blood from each hemisphere into each transverse sinus. This method has certain advantages over the conventional method for measuring cerebral blood flow, since the actual geometry of the brain in which the blood flow measured is known and simultaneous estimations of hemispheric metabolism are possible. Abnormalities of hemispheric blood flow and metabolism have been measured in 30 patients suffering from various neurological disorders including occlusion of one internal carotid artery. The new formula for estimating hemispheric metabolism is applicable to radioisotopic and other indicator injection methods in which blood is sampled from the cerebral transverse sinuses or internal jugular veins. It was also shown that the transverse sinus distribution of blood derived from each cerebral hemisphere varies from one individual to another.

Measurement of cerebral hemispheric blood flow by intracarotid injection of hydrogen gas. Validation of the method in the monkey.

To develop a reliable method for measuring hemispheric blood flow and metabolism in man, the clearance of hydrogen was measured in the cerebral lateral sinus blood of macaque monkeys after intracarotid injection. Hydrogen is an inert gas and its clearance from cerebral venous blood depends solely on arterial inflow, and since it is highly diffusible, rapid equilibrium is maintained between brain tissue and its capillary-venous blood. Cerebral venous clearance curves for hydrogen appeared to provide accurate and reproducible measures of cerebral blood flow. A bolus of 0.2 to 0.3 ml of saline saturated with hydrogen was injected rapidly into the internal carotid artery. Electrodes placed on the cortex showed that the bolus was almost exclusively distributed to the ipsilateral cerebral hemisphere. Blood flow of each hemisphere was calculated by Meier and Zierler's formula based on the Stewart-Hamilton principle, as well as by compartmental analysis. The values obtained for hemispheric blood flow were in good agreement with average cerebral blood flow measured by inhalation of hydrogen using the Fick principle. Values for hemispheric blood flow were the same whether the intracarotid injection of hydrogen was rapid or slow.

On the theory of the indicator-dilution method for measurement of blood flow and volume.

On the theory of the indicator-dilution method for measurement of blood flow and volume.