Cerebral blood flow and vasoresponsivity within and around cerebral contusions
- 1 November 1996
- journal article
- Published by Journal of Neurosurgery Publishing Group (JNSPG) in Journal of Neurosurgery
- Vol. 85 (5) , 871-876
- https://doi.org/10.3171/jns.1996.85.5.0871
Abstract
There is increasing evidence that regional ischemia plays a major role in secondary brain injury. Although the cortex underlying subdural hematomas seems particularly vulnerable to ischemia, little is known about the adequacy of cerebral blood flow (CBF) or the vasoresponsivity within the vascular bed of contusions. The authors used the xenon-enhanced computerized tomography (CT) CBF technique to define the CBF and vasoresponsivity of contusions, pericontusional parenchyma, and the remainder of the brain 24 to 48 hours after severe closed head injury in 10 patients: six patients with one contusion and four with two contusions, defined as mixed or high-density lesions on CT scanning. The CBF within the contusions (29.3 +/- 16.4 ml/100 g/minute, mean +/- standard deviation) was significantly lower than both that found in the adjacent 1-cm perimeter of normal-appearing tissue (42.5 +/- 15.8 ml/100 g/minute) and the mean global CBF (52.5 +/- 17.5 ml/100 g/minute) (p < 0.004, repeated-measures analysis of variance). A subset of seven patients (10 contusions) also underwent a second Xe-CT CBF study during mild hyperventilation (a PaCO2 of 24-32 mm Hg). In only two of these 10 contusions was vasoresponsivity less than 1% (range 0%-7.6%); in the rim of normal-appearing pericontusional tissue, it was 0.4% to 9.1%. The authors conclude that CBF within intracerebral contusions is highly variable and is often above 18 ml/100 g/minute, the reported threshold for irreversible ischemia. Intracontusional CBF is significantly reduced relative to surrounding brain parenchyma, and CO2 vasoresponsivity is usually present. In the contusion and the surrounding parenchyma, vasoresponsivity may be nearly three times normal, suggesting hypersensitivity to hyperventilation therapy. Given this possible hypersensitivity and relative hypoperfusion within and around cerebral contusions, these lesions are particularly vulnerable to secondary injury such as that which may be caused by hypotension or aggressive hyperventilation.Keywords
This publication has 35 references indexed in Scilit:
- An additional therapeutic effect of adequate hyperventilation in severe acute brain trauma: normalization of cerebral glucose uptakeJournal of Neurosurgery, 1995
- Ultra-early evaluation of regional cerebral blood flow in severely head-injured patients using xenon-enhanced computerized tomographyJournal of Neurosurgery, 1992
- Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemiaJournal of Neurosurgery, 1991
- Does acute hyperventilation provoke cerebral oligaemia in comatose patients after acute head injury?Acta Neurochirurgica, 1989
- Effect of Stable Xenon Inhalation on ICP in Head InjuryPublished by Springer Nature ,1989
- Local “Inverse Steal” Induced by Hyperventilation in Head InjuryNeurosurgery, 1988
- Cerebral blood flow decrements in chronic head injury syndromeBiological Psychiatry, 1985
- The outcome from severe head injury with early diagnosis and intensive managementJournal of Neurosurgery, 1977
- Dynamic changes in regional CBF, intraventricular pressure, CSF pH and lactate levels during the acute phase of head injuryJournal of Neurosurgery, 1976
- Regional cerebral blood flow and intraventricular pressure in acute head injuriesJournal of Neurology, Neurosurgery & Psychiatry, 1974