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Cerebral circulation after head injury

Part 4: Functional anatomy and boundary-zone flow deprivation in the first week of traumatic coma

Jørn Overgaard and William A. Tweed

✓ A considerable body of evidence suggests that posttraumatic disturbances of the cerebral circulation contribute to poor neurological outcome after blunt head injury, especially when regional cerebral blood flow (rCBF) falls to the ischemic range (below 17 ml/100 gm/min). Cerebral infarction concentrated in the arterial boundary regions has been described in patients who died. Since arterial boundary zones are the cortical areas most susceptible to cerebral ischemia, the authors have investigated the relationship between neurological outcome and the anatomic pattern of rCBF values in the acute phase. The bolus-injection xenon-133 washout technique was used to measure rCBF in 35 regions of the hemisphere during the 1st week after head injury. Eighty-eight hemispheres were studied in 80 patients whose Glasgow Coma Scale (GCS) score was less than 8 on admission to the neurosurgical department.

A characteristic pattern of rCBF was found in patients who later died of neurological complications, or who survived in a persistent vegetative state, with low flows in regions conforming to the arterial boundary zones. These patients also had lower average global cerebral blood flow (CBF), GCS scores, and cerebral perfusion pressure compared with those who recovered, with or without neurological deficits; the latter group had an rCBF pattern similar to that of normal individuals.

There was little change in the GCS score between the time of hospital admission and CBF measurement, suggesting that the major neurological injury had occurred prior to admission. It was not possible to determine whether boundary-zone ischemia preceded neurological deterioration, but the rCBF pattern of boundary-zone flow deprivation was clearly related to poor neurological outcome. These observations suggest that elevated intracranial pressure and arterial hypotension were important etiological factors. Measures to protect regional cerebral perfusion should be instituted as early as possible after injury, preferably before the patient reaches the hospital.

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Cerebral circulation after head injury

Part 1: Cerebral blood flow and its regulation after closed head injury with emphasis on clinical correlations

Jørn Overgaard and William A. Tweed

✓ Measurements of cerebral blood flow (CBF), mean intraventricular pressure (MIVP), CSF acid-base status, and tests of autoregulation and CO2 reactivity of 43 patients were made at varying times after severe closed head injury. There was a distinct hyperemia or “luxury perfusion” in the acute phase of 1 to 14 days, followed by recovery to normal or below normal values. Metabolic CSF acidosis was found with hyperemia and probably reflected severe, diffuse cortical injury. Distinct regional CBF abnormalities, either ischemic or hyperemic, were only observed in regions of focal pathology. Severe ischemia, hyperemia, persistent elevation of MIVP, or generalized “vasoparalysis” indicated an unfavorable prognosis. Autoregulation was impaired and CO2 reactivity was reduced after injury, but both had usually returned to normal by 14 days.

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Cerebral circulation after head injury

Part 2: The effects of traumatic brain edema

Jørn Overgaard and William A. Tweed

✓ The authors have assessed the effects of subacute traumatic brain edema (BE) on cerebral circulation and metabolism, and on clinical outcome. Fifty-five severely injured, comatose, young patients who survived for more than 24 hours were studied on 78 occasions within 30 days of injury. After hematomas had been surgically evacuated, BE was diagnosed by radiological evidence of brain swelling, demonstrated by cerebral angiograms and ventriculograms. At identical levels of carbon dioxide pressure, intracranial pressure was significantly elevated in the Edema Group to twice the value in the No Edema Group (27.1 vs 14.1 torr). There were, however, no significant differences in cerebral perfusion pressure, cerebral blood flow, resistance to blood flow, cerebral metabolic oxygen rate, ventricular cerebrospinal fluid acidbase, lactate, K+ or Na+ concentrations, or in clinical outcome. It is concluded that this type of subacute traumatic BE, which is significantly associated with surgical lesions, is not of major hemodynamic or clinical significance in intensively treated patients, and does not cause cerebral ischemia. Patient outcome is determined more by the severity of the initial diffuse cortical and subcortical injury than by the presence or absence of subacute BE.

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Cerebral circulation after head injury

Part 3: Does reduced regional cerebral blood flow determine recovery of brain function after blunt head injury?

Jørn Overgaard, Claus Mosdal and William A. Tweed

✓ A series of comatose young patients with head injuries is presented in whom early regional cerebral blood flow (rCBF) is correlated with neurological outcome, and the critical threshold of rCBF compatible with recovery of responsive communicative interaction with the environment is estimated. Within the 1st week following injury, 63 patients had rCBF studies performed with radioactive xenon by the intracarotid bolus-injection technique and 35-channel external counting. A comparison was made between 2724 rCBF values from this group of patients with 381 from nine controls. Surviving patients were followed for 2 years to determine their eventual neurological outcome.

When histograms of the frequency distribution of rCBF values were examined, it was evident that there was both a wider spread of rCBF and a shift to the left in all outcome groups. In awake controls, no rCBF values were less than 40 ml/100 gm/min, whereas in comatose patients the threshold for recovery of communicative brain function (with or without neurological deficits) was between 17 and 20 ml/100 gm/min. There was a clear difference, however, between patients who recovered communicative brain function (with or without neurological deficit) and those who did not (dying or surviving in a persistent vegetative state). In the latter two outcome groups, 14.5% of rCBF values were less than 20 ml/100 gm/min, with the highest incidence in those examined within the first few hours of injury. The distribution of ischemic rCBF was mainly in the frontal and parietal lobes.

These investigations confirm previous postmortem pathological studies in revealing that cerebral ischemia in the frontoparietal “watershed” areas antemortem is a major factor leading to telencephalic brain death in the early hours after head injury. The pathophysiological mechanisms of this localized ischemia in patients with head injury are not well understood, but probably hemodynamic alterations resulting from increased intracranial pressure are a major factor. The critical threshold for survival of cortical function seems to be similar to that of normal brain, about 17 to 20 ml/100 gm/min.