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As we believe that restoration of cerebral cortical function is the most important factor determining the degree of clinical recovery after this type of injury, we shall discuss the findings from that point of view.
CBF calculated by the initial slope method CBFinit chiefly reflects flow in the compartments with highest perfusion, namely, the gray matter in normal brain. The immediate effect of blunt head injury on CBF in man is not known. Within a few hours of injury normal regulatory mechanisms are impaired, and CBF varies widely, far exceeding the range of normal.
This critical limit for brain recovery agrees well with estimations for critical flow levels during carotid clamping, 2 and in that situation this degree of flow reduction can only be tolerated for a few minutes. Critically reduced CPP resulting from severe elevation of intracranial pressure is probably the explanation for ischemia in most cases.
The causes are hematoma formation or brain swelling due to brain edema, hypoxia, or CO2 retention. Our studies suggest that severe elevation of ICP and brain ischemia may develop within hours and possibly even minutes after injury. The critical period in which treatment may alter the clinical course in these patients is probably within the first minutes, at the site of the accident and during transport to hospital.
Another cause of severe acute ischemia is impaired reflow, which we have observed in two patients in this series. Another flow pattern, often associated with survival accompanied by severe neurological deficits, is the hyperemic perfusion pattern commonly observed between 1 and 14 days after injury.
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At this time autoregulation is impaired, CO2 reactivity reduced, and clinical state is unchanged. Clinical experience indicates that this lactic acidosis is of short duration even after head injury. A histological picture specific for the condition has not yet been presented.
A factor not often mentioned in clinical studies is the blood pressure, but experimental studies have demonstrated that elevation of blood pressure can increase transudation of fluids from the blood into the brain parenchyma. Our hyperemic patients generally had high levels of CPP and impaired autoregulation.
We have not observed a consistent relationship between the later development of brain swelling or intracranial hypertension and abnormalities of CBF.
One major cause of secondary injury, intracranial hematomas, was diagnosed and removed early. Patients that died generally showed early clinical evidence of severe brain injury and progressive deterioration. Thus it appears that, in this group of patients at least, most of the brain injury occurred within the first few hours after trauma.
Brodersen and Jorgensen 3 have measured CMRO2 in patients very similar to these, and found levels depressed to between 0.
It may be that only severe reduction of CBF to the range of 20 or less produces cerebral ischemia in these patients with depressed cerebral function and metabolism. Furthermore, the good recovery of some patients in the oligemic flow range suggests that the low CBF was linked to cerebral metabolic depression after injury.
No patients were hypothermic but all had had barbiturates, which are known to depress cerebral metabolism. The possibility also remains that transneuronal functional and metabolic depression can be induced by focal lesions, for example, hematomas, and that this state is completely reversible.
The most frequently observed abnormalities of hyperemia, focal changes, impairment of autoregulation, and impaired CO2 reactivity may be accepted as signs of cortical injury when flow is determined by the initial slope method.
There is no doubt, however, that secondary brain-stem injury commonly results from severe intracranial hypertension. Low CBF values late in the convalescent period were associated either with posttraumatic hydrocephalus or with severe permanent brain damage.
Cortical loss was assessed by pneumoencephalography, and 24 of 33 long-term survivors had cortical atrophy.
This confirms our impression that diffuse cortical contusion was the most frequent injury in these patients. Distinct focal abnormalities of flow were almost always associated with focal lesions such as hematoma or laceration, but the diagnostic value of rCBF studies is not very great.
Prognostic Implications The CBF measurement and functional tests during the acute phase have a limited prognostic value. The prognostic significance of ischemic and hyperemic acute phase flow patterns have already been discussed. The poor outlook in hyperemic patients was also commented on by Fieschi, et al.
When permanently brain-damaged patients eventually recovered autoregulation, there was no associated change in clinical status. Perhaps their use of vigorous artificial hyperventilation explains the difference, since Paulson, et al. We did not monitor MIVP continuously, and therefore less prognostic significance can be attributed to it.curta calculator registry.
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The end-tidal carbon dioxide partial pressure (PCO2) response curves for the flow velocity in the middle cerebral artery were studied in 31 normal subjects with transcranial Doppler techniques. An exponential curve with an exponent of mm Hg−1 was found to be a good fit to the recorded data.
By means of this relationship, recordings of flow velocity in cerebral arteries can be. This paper is dedicated in memory of Dr. Donald Wiesler who passed away on November 12, He was a long-time, dedicated co-worker at the Institute for Pheromone Research at Indiana University. We thank Joe Taft, Jean Herrberg, the staff and volunteers at the EFRC for allowing us to conduct our research at the facility and helping with.
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