Supratentorial Blood Flow Research Articles

Crossed cerebellar diaschisis-related supratentorial hemodynamic and metabolic status measured by PET/MR in assessing postoperative prognosis in chronic ischemic cerebrovascular disease patients with bypass surgery

ObjectiveCerebral ischemic status is an indicator of bypass surgery. Both hemodynamics and glucose metabolism are significant factors for evaluating cerebral ischemic status. The occurrence of crossed cerebellar diaschisis (CCD) is influenced by the degree of supra-tentorial perfusion and glucose metabolism reduction. This study aimed to investigate the relationship between the CCD-related supra-tentorial blood flow and metabolic status before bypass surgery in patients with chronic and symptomatic ischemic cerebrovascular disease and the prognosis of surgery.MethodsTwenty-four participants with chronic ischemic cerebrovascular disease who underwent hybrid positron emission tomography (PET)/magnetic resonance (MR) before bypass surgery were included. Arterial spin labeling (ASL)-MR and FDG-PET were used to measure blood flow and metabolism, respectively. The PET images were able to distinguish CCD. The supratentorial asymmetry index (AI) and volume in the decreased blood flow region, decreased metabolism region and co-decreased region on the affected side, except for the infarct area, were respectively obtained before bypass surgery. The neurological status was determined using the National Institutes of Health Stroke Scale (NIHSS) and modified Rankin Scale (mRS) scores. Differences between CCD-positive (CCD +) and CCD-negative (CCD−) groups were investigated.ResultsFourteen (58%) of the 24 patients were diagnosed as CCD +. Before surgery, the NIHSS and mRS scores of the CCD + were significantly higher than those of the CCD− (1.0(1.0) vs. 0.0(1.0), P = 0.013; 1.0(1.5) vs. 0.0(1.5), P = 0.048). After the surgery, the NIHSS and mRS scores of the CCD + showed a significant decrease (0.0(1.0) to 0.0(0.0), P = 0.011; 0.0(0.5) to 0.0(0.0), P = 0.008). Significant differences were observed in the supra-tentorial decreased metabolism region (all Ps ≤ 0.05) between the CCD + and CCD− groups, but no differences were observed in the preprocedural decreased supratentorial blood flow region (P > 0.05). The preprocedural NIHSS score was strongly correlated with the metabolism AI value in the decreased metabolism region (r = 0.621, P = 0.001) and the co-decreased region (r = 0.571, P = 0.004).ConclusionsSupratentorial blood flow and metabolism are important indicators of CCD. This study showed that CCD + patients benefited more from bypass surgery than CCD− patients. Staging based on CCD-related supra-tentorial blood flow and metabolic status by hybrid PET/MR may help to personalize treatment.

Cerebral blood flow and metabolism in complete apallic syndromes, in states of severe dementia, and in akinetic mutism.

In complete apallic syndromes with (almost total) loss of the telencephalic grey matter, the supratentorial blood flow and oxygen uptake were found to be only about 20 per cent of the normal. Such cases show no signs of higher functions and they have an isoelectric EEG. Due to the retention of brain stem structures they may, however, show clear-cut signs of arousability with lively brain stem reflexes and primitive motor reactions. In a permanently comatose case—also without higher functions—due to a selective reticular brain stem infarction, but with retained telencephalic morphology on the whole, extremely low values (about 20 per cent of normal) for the supratentorial oxygen uptake and blood flow were also demonstrated. Other states with a severe reduction, but not a complete loss of higher functions, due to posttraumatic stupor and advanced Alzheimer's disease showed higher cerebral blood flow and metabolic values than those related above. Such cases also showed a retention of an often pathological EEG. Two patients with akinetic mutism showed relatively high flow values and by and large a normal relative weight of the cortical grey matter, as well as a normal EEG. Both cases showed slight but definite signs of remaining higher functions. It is concluded that measurements of the supratentorial cerebral oxygen uptake and blood flow may be used to quantitate the functional state of the brain in patients with a loss of, or with a severe reduction of higher functions (signs of conscious awareness, voluntary motor activity, speech, and memory). It is emphasized that a complete loss of such functions may be caused by a total loss of the cortical grey matter (the complete apallic state), or by a selective lesion of the reticular system of the brain stem.

Regional cerebral blood flow and CSF pressures during Cushing response induced by a supratentorial expanding mass.

In order to delineate the critical blood flow pattern during the Cushing response in intracranial hypertension, regional cerebral blood flow was measured with radioactive microspheres in 12 anesthetized dogs at respiratory arrest caused either by expansion of an epidural supratentorial balloon or by cisternal infusion. Regional cerebrospinal fluid pressures were recorded and the local cerebral perfusion pressure calculated in various cerebrospinal compartments. In the 8 dogs of the balloon expansion group, the systemic arterial pressure was unmanipulated in 4, while it was kept at a constant low level (48 and 70 mm Hg) in 2 dogs and, in another 2 dogs, at a constant high level (150 and 160 mm Hg) induced by infusion of Aramine. At respiratory arrest, regional cerebral blood flow had a stereotyped pattern and was largely independent of the blood pressure level. In contrast, concomitant pressure gradients between the various cerebrospinal compartments varied markedly in the 3 animal groups, increasing with higher arterial pressure. Flow decreased by 85-100% supratentorially and by 70-100% in the upper brain stem down to the level of the upper pons, while changes in the lower brain stem were minor, on the average 25%. When intracranial pressure was raised by cisternal infusion in 4 dogs, the supratentorial blood flow pattern at respiratory arrest was approximately similar to the flow pattern in the balloon inflation group. However, blood flow decreased markedly (74-85%) also in the lower brain stem. The results constitute another argument in favour of the Cushing response in supratentorial expansion being caused by ischemia in the brain stem. The critical ischemic region seems to be located rostrally to the oblongate medulla, probably in the pons.

Axilloaxillary Bypass for the Treatment of Subclavian Artery Stenosis Complicated by Bilateral Common Carotid Artery Occlusion: Technical Case Report

We successfully treated a patient with stenosis of the left subclavian artery, complicated by bilateral common carotid artery occlusion, via axilloaxillary bypass surgery. A 67-year-old patient with a history of hypertension and cerebral infarction underwent neck irradiation for treatment of a vocal cord tumor. Three months later, he began to experience transient tetraparesis several times per day. The blood pressure measurements for his right and left arms were different. Supratentorial blood flow was markedly low. The common carotid arteries were bilaterally occluded, and the right vertebral artery was hypoplastic. Therefore, only the left vertebral artery contributed to the patient's cerebral circulation; his left subclavian artery was severely stenotic. The patient underwent axilloaxillary bypass surgery because the procedure avoids thoracotomy or sternotomy, manipulation of the carotid artery, and interruption of the vertebral artery blood flow. The patient has been free of symptoms for more than 5 years. Neurosurgeons should be aware that extra-anatomic bypass surgery is an effective treatment option for selected patients with cerebral ischemia.

Effect of arrest time and cerebral perfusion pressure during cardiopulmonary resuscitation on cerebral blood flow, metabolism, adenosine triphosphate recovery, and pH in dogs.

To test the hypothesis that greater cerebral perfusion pressure (CPP) is required to restore cerebral blood flow (CBF), oxygen metabolism, adenosine triphosphate (ATP), and intracellular pH (pHi) levels after variable periods of no-flow than to maintain them when cardiopulmonary resuscitation (CPR) is started immediately. Prospective, randomized, comparison of three arrest times and two perfusion pressures during CPR in 24 anesthetized dogs. University cerebral resuscitation laboratory. We used radiolabeled microspheres to determine CBF and magnetic resonance spectroscopy to derive ATP and pHi levels before and during CPR. Ventricular fibrillation was induced, epinephrine administered, and thoracic vest CPR adjusted to provide a CPP of 25 or 35 mm Hg after arrest times of O, 6, or 12 mins. When CPR was started immediately after arrest with a CPP of 25 mm Hg, CBF and ATP were 57 +/- 10% and 64 +/- 14% of prearrest (at 10 mins of CPR). In contrast, CBF and ATP were minimally restored with a CPP at 25 mm Hg after a 6-min arrest time (23 +/- 5%, 16 +/- 5%, respectively). With a CPP of 35 mm Hg, extending the no-flow arrest time from 6 to 12 mins reduced reflow from 71 +/- 11% to 37 +/- 7% of pre-arrest and reduced ATP recovery from 60 +/- 11% to 2 +/- 1% of pre-arrest. After 6- or 12-min arrest times, brainstem blood flow was restored more than supratentorial blood flow, but cerebral pHi was never restored. A CPP of 25 mm Hg maintains supratentorial blood flow and ATP at 60% to 70% when CPR starts immediately on arrest, but not after a 6-min delay. A higher CPP of 35 mm Hg is required to restore CBF and ATP when CPR is delayed for 6 mins. After a 12-min delay, even the CPP of 35 mm Hg is unable to restore CBF and ATP. Therefore, increasing the arrest time at these perfusion pressures increases the resistance to reflow sufficient to impair restoration of cerebral ATP.

Effect of the no-flow interval and hypothermia on cerebral blood flow and metabolism during cardiopulmonary resuscitation in dogs.

We sought (1) to determine the effect of brief periods of no flow on the subsequent forebrain blood flow during cardiopulmonary resuscitation (CPR) and (2) to test the hypothesis that hypothermia prevents the impact of the no-flow duration on cerebral blood flow (CBF) during CPR. No-flow intervals of 1.5, 3, and 6 minutes before CPR at brain temperatures of 28 degreesC and 38 degreesC were compared in 6 groups of anesthetized dogs. Microsphere-determined CBF and metabolism were measured before and during vest CPR adjusted to maintain cerebral perfusion pressure at 25 mm Hg. Increasing the no-flow interval from 1.5 to 6 minutes at 38 degreesC decreased the CBF (18. 6+/-3.6 to 6.1+/-1.7 mL/100 g per minute) and the cerebral metabolic rate (2.1+/-0.3 to 0.7+/-0.2 mL/100 g per minute) during CPR. Cooling to 28 degreesC before and during the arrest eliminated the detrimental effects of increasing the no-flow interval on CBF (16. 8+/-1.0 to 14.8+/-1.9 mL/100 g per minute) and cerebral metabolic rate (1.1+/-0.1 to 1.3+/-0.1 mL/100 g per minute). Unlike the forebrain, 6 minutes of preceding cardiac arrest did not affect brain stem blood flow during CPR. Increasing the no-flow interval to 6 minutes in normothermic animals decreases the supratentorial blood flow and cerebral metabolic rate during CPR at a cerebral perfusion pressure of 25 mm Hg. Cooling to 28 degreesC eliminates the detrimental impact of the 6-minute no-flow interval on the reflow produced during CPR. The brain-protective effects of hypothermia include improving reflow during CPR after cardiac arrest. The effect of hypothermia and the impact of short durations of no flow on reperfusion indicate that increasing viscosity and reflex vasoconstriction are unlikely causes of the "no-reflow" phenomenon.

Infratentorial ischaemia following experimental cerebellar haemorrhage in the rat.

Early changes of cerebellar and cerebral blood flow, as well as subsequent infratentorial ischaemia, were evaluated in an experimental model of cerebellar haemorrhage. Eight anaesthetized male adult Sprague-Dawley rats received an injection of autologous arterial blood (50 microliters) into the right cerebellar hemisphere. Eight animals were sham-operated and served as controls. Cerebellar blood flow, measured at regular time intervals in the hemispheric cortex ipsilateral to the lesion by the hydrogen clearance method, was significantly depressed in the experimental group as compared with the control animals. This drop in cerebellar blood flow was evident 5, 30, 60, 90, and 120 min postoperatively, with a return to pre-injection values recorded 180 min after surgery. No significant difference in supratentorial blood flow was detected over the entire period examined between the two groups of animals. Enzyme histochemistry demonstrated areas of ischaemia around the clot and within the brain stem in animals with an intracerebellar haemorrhage at the end of the experiment. These results provided evidence of ischaemic damage within the infratentorial compartment after the induction of experimental cerebellar haemorrhage.

Effects of secondary polycythemia on cerebral blood flow in chronic obstructive pulmonary disease.

Cerebral blood flow was measured before and after venesection in 6 patients with chronic obstructive pulmonary disease and secondary polycythemia. The hematocrit was decreased from a mean of 59.6 to 43.9%, and whole blood viscosity was decreased by 35%. The supratentorial blood flow increased 78.2% (p < 0.005) after venesection; subtentorial flow also increased, but not significantly. The improvement in cerebral blood flow appeared to be related to a decrease in blood viscosity, because pulmonary function and arterial blood gases did not change significantly. There was subjective improvement in all patients, and this improvement might have been due to the increased supratentorial blood flow.