Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 1998
The relationship of pulsatile cerebrospinal fluid flow to cerebral blood flow and intracranial pressure: a new theoretical model.
An electrical-equivalent circuit model of the cerebrovascular system is proposed, components of which directly relate to cerebrospinal fluid (CSF) compartment compliance and the determination of intracranial pressure (ICP). The model is based on three premises: 1) Under normal, physiologic conditions, the conversion of pulsatile arterial to nonpulsatile venous flow occurs primarily as a result of arterial compliance. Nonpulsatile venous flow is advantageous because less energy is required to maintain constant flow through the venous system, which comprises 75-80% of total blood volume. 2) Dynamic CSF movement across the foramen magnum is the primary facilitator by which intracranial arterial expansion occurs. ⋯ An interference of transcranial CSF movement results in a decrease in cerebral blood flow (CBF) due to inertial effects impeding pulsatile venous flow. Feedback regulation in response to this decreased CBF leads to arteriolar vasodilatation (decreased resistance), thereby lowering the pressure difference between internal carotid and capillary pressures. Assuming no changes in the BBB potential, ICP increases linearly as capillary pressure increases.
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Acta Neurochir. Suppl. · Jan 1998
High cerebral perfusion pressure improves low values of local brain tissue O2 tension (PtiO2) in focal lesions.
Arterial hypertension is widely applied to improve regional cerebral blood flow (rCBF). We measured local brain tissue O2 pressure (PtiO2) in low density lesions at computerized tomography (CT) of the head before and after manipulation of mean arterial pressure (MAP) in order to increase cerebral perfusion pressure (CPP). Nine patients, 7 subarachnoid hemorrhage (SAH), 1 severe head injury, 1 meningeoma, were included in our study. ⋯ Our results show that in ischemic areas PtiO2 is dependent on CPP suggesting both a derangement of pressure autoregulation and high regional cerebrovascular resistences (CVRs). Low PtiO2 was associated with normal CPP, thus indicating that CPP could be an inadequate estimate of rCBF in focal ischemic areas. Arterial hypertension, capable of increasing CPP above normal values, appeared useful in normalizing tissue oxygenation in ischemic areas.
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Acta Neurochir. Suppl. · Jan 1998
Cerebral hemodynamic changes during sustained hypocapnia in severe head injury: can hyperventilation cause cerebral ischemia?
Hyperventilation (HV) is routinely used in the management of increased intracranial pressure (ICP) in severe head injury. However, this treatment continues to be controversial because it has been reported that long-lasting reduced cerebral blood flow (CBF) due to profound sustained hypocapnia may contribute to the development or deterioration of ischemic lesions. Our goal in this study was to analyze the effects of sustained hyperventilation on cerebral hemodynamics (CBF, ICP) and metabolism (arterio jugular differences of lactates = AVDL). ⋯ According to AVDO2 and AVDL, no adverse effects were found during four hours of HV in hyperemic patients. Nevertheless, AVDO2 and AVDL are global measurements and might not detect regional ischemia surrounding focal lesions such as contusions and haematomas. We suggest that monitoring of AVDO2 or other haemometabolic variables should be mandatory when sustained HV is used in the management of head injury patients.
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Acta Neurochir. Suppl. · Jan 1998
Monitoring brain oxygen tension in severe head injury: the Rotterdam experience.
Cerebral ischemia is considered the central mechanism leading to secondary brain damage in patients with severe head injury. We investigated the technique of continuous monitoring of local brain tissue oxygen tension as parameter for cerebral oxygenation. Eighty-two patients with non penetrating severe head injury were studied. ⋯ Early occurrence of values below 10 mm Hg indicated a poor prognosis. Comparative measurements between two catheters performed in six patients showed differences in absolute values measured, but a good correlation of relative changes was observed. We conclude that continuous monitoring of PbrO2 is reliable, clinically applicable and provides the clinician with a better insight in cerebral oxygenation and hopefully should help in targeting therapy towards improved cerebral oxygenation.
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Acta Neurochir. Suppl. · Jan 1998
Moderate hypothermia and brain temperature in patients with severe middle cerebral artery infarction.
Elevated temperature is known to facilitate neuronal injury after ischemia. After head injury a gradient between temperature and body temperature of up to 3 degrees C higher in the brain has been reported. Hypothermia may limit some of the deleterious metabolic consequences of such increased temperature. ⋯ After MCA stroke, human intracerebral temperature is higher than central body-core temperature. Mild hypothermia in the treatment of severe cerebral ischemia using cooling blankets is safe and does not lead to severe side effects. Mild hypothermia can help to control critically elevated ICP values in severe space-occupying stroke and may improve clinical outcome in these patients.