Cerebral Hemodynamic Reserve Research Articles

Evaluation of cerebral blood flow and hemodynamic reserve in symptomatic moyamoya disease using stable xenon-CT blood flow

Moyamoya disease is a vascular abnormality seen in children and adults characterized by progressive narrowing of the internal carotid, middle, anterior, and posterior cerebral arteries and the development of leptomeningeal and proximal internal carotid artery collaterals, which appear diaphanous on angiogram. Although adults tend to present with subarachnoid hemorrhage and children with ischemic events, the clinical sequelae in these two populations overlap. Expanding upon work done at this institution using stable xenon computer tomographic blood flow determinations with acetazolamide and carbon dioxide challenge to predict which population of patients with severe carotid disease and hemodynamic compromise would benefit from surgical intervention, we used similar rationale to determine which patients with moyamoya disease would likely benefit from revascularization. Data and outcome concerning four such patients make up the body of this report.

Percutaneous transluminal angioplasty for severe stenosis of the posterior cerebral artery: Case report

The Stealth dilation catheter was used for the intravascular treatment of a patient who had hemodynamically significant stenosis of the posterior cerebral artery and had a history of recurrent transient ischemic attacks associated with right hemiparesis and ipsilateral hemianopia dating from March 1993. Cerebral perfusion studies prior to and after the intravenous administration of acetazolamide demonstrated regions of moderately low perfusion and low hemodynamic reserve in the territories of the left middle and posterior cerebral arteries. Cerebral angiograms demonstrated severe stenosis of the left posterior cerebral artery and occlusions of both middle cerebral arteries, which had leptomeningeal anastomoses with the posterior cerebral arteries. Percutaneous transluminal angioplasty (PTA) was performed using the Stealth catheter on the stenotic segment of the left posterior cerebral artery after left superficial temporal artery-middle cerebral artery anastomosis. The patient manifested marked improvement in her neurologic condition just after PTA, in association with marked increase in cerebral perfusion and hemodynamic reserve in the territories of the left middle and posterior cerebral arteries. We have presented evidence that PTA can be used to treat patients with stenosis of the first segment of the posterior cerebral artery and hemodynamic compromise in the territory that artery supplies.

Cerebral oxygenation monitoring.

To discuss theoretical and practical aspects of cerebral oxygenation, from isolated observational measurements to continuous interventional monitoring. Relevant articles from the pertinent literature, as well as a multivariate physiologic diagram developed in this article. Theoretical, experimental, and clinical information that further clarifies the physiologic relevance of cerebral oxygenation. All basic concepts of cerebral hemometabolism were used, up to cerebral hemodynamic reserve, and were interrelated accordingly. Cerebral perfusion pressure alone does not allow global cerebral hemometabolic optimization. The same situation is true for cerebral blood flow. The reason for this limitation is because these variables lack metabolic information. Cerebral arteriovenous differences do allow global cerebral hemometabolic optimization, because they reflect the exchange between the capillary and the tissue. In addition, cerebral hemodynamic reserve allows quantification of the cerebral microcirculatory tolerance to increases in intracranial "tightness" (decreases in intracranial compliance). Multivariate optimization of global cerebral oxygenation, primarily based on global cerebral oxygen delivery and extraction, may strongly affect outcome in a variety of predominantly diffuse, acute intracranial disorders. Cerebral hemodynamic reserve may be further explored in experimental and clinical areas, involving not just acute brain trauma.

Cerebral hemometabolism: from isolated measurements to monitoring and therapy

An overview is presented on historical and multivariate aspects of cerebral hemometabolism. This involves a full multivariate approach, from blood pressure to cerebral metabolism. From isolated measurements, to monitoring and management, a comprehensive overview of cerebral hemometabolism is addressed, from its inception to current days, up to a new concept, the cerebral hemodynamic reserve. A multivariate functional diagram is proposed, to summarize the multivariate interrelationships of cerebral hemometabolism. A generic proposition is made for studies of truly normal cerebral hemometabolism in children, for subsequent clinical applications. Another proposition is made for multivariate cerebral hemometabolic monitoring, in a broad variety of circumstances of predominantly global changes in intracranial dynamics, both in animal and clinical research.

Effects of graded hypotension on cerebral blood flow, blood volume, and mean transit time in dogs.

This study tested the hypothesis that cerebral blood flow (CBF) is maintained by vasodilation, which manifests itself as a progressive increase in mean transit time (MTT) and cerebral blood volume (CBV) when cerebral perfusion pressure is reduced. Cerebral perfusion pressure was decreased in 10 pentobarbital-anesthetized dogs by controlled hemorrhage. Microsphere-determined CBF was autoregulated in all tested cerebral regions over the 40- to 130-mmHg cerebral perfusion pressure range but decreased by 50% at approximately 30 mmHg. MTT and CBV progressively and proportionately increased in the right parietal cerebral cortex over the 40- to 130-mmHg cerebral perfusion pressure range. Total hemoglobin content (Hb1), measured in the same area by an optical method, increased in parallel with the increases in CBV computed as the (CBF.MTT) product. At 30 mmHg cerebral perfusion pressure, CBV and Hb were still increased and MTT was disproportionately lengthened (690% of control). We conclude that within the autoregulatory range, CBF constancy is maintained by both increased CBV and MTT. Outside the autoregulatory range, substantial prolongation of the MTT occurs. When CBV is maximal, further reductions in cerebral perfusion pressure produce disproportionate increases in MTT that signal the loss of cerebral vascular dilatory hemodynamic reserve.

Continuous monitoring of cerebral hemodynamic reserve in acute brain injury: relationship to changes in brain swelling.

A new concept of cerebral hemodynamic and metabolic physiology, cerebral hemodynamic reserve (CHR), was evaluated in 20 comatose adults with acute traumatic brain swelling who were undergoing continuous monitoring of the arteriojugular difference in oxyhemoglobin saturation, along with cerebral perfusion pressure and expired PCO2. The CHR was measured as the ratio of relative (percent) changes in cerebral oxygen extraction to relative changes in cerebral perfusion pressure during spontaneous increases in intracranial pressure. In patients with initially severe brain swelling, the CHR was more frequently abnormal (compromised) on the first day, and tended to improve on the second day. In patients with initially moderate brain swelling, the CHR was more frequently normal (preserved) on the first day, but tended to become compromised on the second day if the brain swelling exacerbated. It is concluded that cerebral hemodynamic reserve abnormalities very closely associate with signs of increased intracranial "tightness" on computed tomographic scans of the head. Cerebral hemodynamic reserve could therefore become an important guide in the functional evaluation and management of acute brain swelling (focusing on cerebral oxygenation and perfusion pressure) in a variety of predominantly diffuse acute intracranial disorders.

Continuous Monitoring of Cerebral Oxygenation in Acute Brain Injury: Assessment of Cerebral Hemodynamic Reserve

Abstract A new index of cerebral hemodynamics, cerebral hemodynamic reserve (CHR), was evaluated in 12 comatose adults with severe, acute, traumatic, diffuse swelling of the brain, who underwent continuous monitoring with a fiberoptic catheter of the saturation difference in arteriojugular oxyhemoglobin. CHR was assessed as the ratio of changes in global cerebral oxygen extraction to changes in cerebral perfusion pressure (CPP) as a result of spontaneous increases in intracranial pressure (ICP). During the course of hyperventilation (Pco2 in the range of 20 mm Hg) for ICP control below 20 mm Hg. 34 observations were made over the initial 48 hours postinjury. Despite normal CPP. in 25 of the observations (73.5%). ICP elevations to the range of 20 mm Hg were associated with compromised CHR. as evidenced by decreases in jugular oxygenation directly attributed to the ICP increases. In the remaining nine observations (26.5%). CHR was preserved, as evidenced by no changes or increases in jugular oxygenation when ICP increased. The CHR improved on the second day. suggesting an improved tolerance of the cerebral hemodynamics to ICP increases. Before the ICP elevations, in most of the observations, the global cerebral blood flow was estimated as being optimally decreased (by hypocapnia). in relation to cerebral oxygen consumption. This was reflected by the occurrence of baseline normalized cerebral oxygen extraction. It is concluded that in this group of patients, under circumstances of profound hyperventilation. ICP elevations within the normal CPP range may result in decreased cerebral oxygenation, even when the normal CPP would imply otherwise. It is suggested that CHR assessment may provide information regarding the status of intracranial “tightness.” insofar as cerebral circulation and oxygenation are concerned.

Continuous monitoring of cerebral oxygenation in acute brain injury

A new index of cerebral hemodynamics, cerebral hemodynamic reserve (CHR), was evaluated in 12 comatose adults with severe, acute, traumatic, diffuse swelling of the brain, who underwent continuous monitoring with a fiberoptic catheter of the saturation difference in arteriojugular oxyhemoglobin. CHR was assessed as the ratio of changes in global cerebral oxygen extraction to changes in cerebral perfusion pressure (CPP) as a result of spontaneous increases in intracranial pressure (ICP). During the course of hyperventilation (Pco2 in the range of 20 mm Hg) for ICP control below 20 mm Hg, 34 observations were made over the initial 48 hours postinjury. Despite normal CPP, in 25 of the observations (73.5%), ICP elevations to the range of 20 mm Hg were associated with compromised CHR, as evidenced by decreases in jugular oxygenation directly attributed to the ICP increases. In the remaining nine observations (26.5%), CHR was preserved, as evidenced by no changes or increases in jugular oxygenation when ICP increased. The CHR improved on the second day, suggesting an improved tolerance of the cerebral hemodynamics to ICP increases. Before the ICP elevations, in most of the observations, the global cerebral blood flow was estimated as being optimally decreased (by hypocapnia), in relation to cerebral oxygen consumption. This was reflected by the occurrence of baseline normalized cerebral oxygen extraction. It is concluded that in this group of patients, under circumstances of profound hyperventilation, ICP elevations within the normal CPP range may result in decreased cerebral oxygenation, even when the normal CPP would imply otherwise. It is suggested that CHR assessment may provide information regarding the status of intracranial "tightness," insofar as cerebral circulation and oxygenation are concerned.

Patterns of brain infarctions in internal carotid artery dissections

In 15 patients with internal carotid artery (ICA) dissections, patterns of brain infarctions visible on CT were categorized according to a pathogenetically oriented classification system. This differentiated ischemic brain damage due to low flow from thromboembolic infarctions. Simultaneously, cerebral hemodynamic reserve was evaluated by means of both CO2-dependent vasomotor reactivity and HMPAO- and 99mTc-RBC-SPECT. Six out of 11 patients with ischemic infarctions had the territorial type of brain lesion, suggesting distal embolism. Five patients revealed the pattern of hemodynamically induced low-flow infarctions. Cerebral hemodynamic reserve was significantly decreased only in these latter patients. In ICA dissections the frequencies of hemodynamically and thromboembolically induced brain infarctions is approximately equal. This finding suggests that only half of the patients with symptoms of symptomatic dissections had brain emboli, whereas in the other half the dissections lead to a low-flow effect in terminal supply areas which is so severe that non-embolic brain infarctions occur. This differentiation can help decide whether antithrombotic or hemodynamic treatment should be given.

Dissektionen der A. carotis interna - neue diagnostische und pathogenetische Aspekte

Initial and follow-up investigations were done systematically in 15 cases of internal carotid artery (ICA) dissections by means of angiography, computerized tomography, Magnetic Resonance Imaging, extracranial and transcranial Doppler sonography, as well as B-mode imaging. Cerebral hemodynamic reserve was evaluated by means of both SPECT and CO2-dependent vasomotor reactivity. The findings are focussed on two major issues: Do modern diagnostic tools permit to make the diagnosis of ICA dissection without angiographical proof? What is the pathogenesis of brain infarctions due to ICA dissections? Our findings demonstrate that the diagnosis of carotid artery dissection can reliably be done noninvasively by means of ultrasound techniques and MRI. These methods also allow for frequent follow-up investigations without any inconvenience for the patient. Embolic brain infarctions caused by carotid artery dissections are equally frequent as low flow induced lesions. Acute and follow-up findings suggest that surgical intervention is contraindicated in the acute phase, but may be considered for chronic pseudoaneurysms. Initial anticoagulation with high dose heparin is safe and seems to be efficacious. In certain cases, subsequent cumarine therapy may be indicated for a maximum of six months. Measures improving hemodynamics, e. g. induced hypertension, are reasonable, as long as the vasomotor reserve is exhausted.