No abstract

Traumatic coma was produced in 45 monkeys by accelerating the head without impact in one of three directions. The duration of coma, degree of neurological impairment, and amount of diffuse axonal injury (DAI) in the brain were directly related to the amount of coronal head motion used. Coma of less than 15 minutes (concussion) occurred in 11 of 13 animals subjected to sagittal head motion, in 2 of 6 animals with oblique head motion, and in 2 of 26 animals with full lateral head motion. All 15 concussioned animals had good recovery, and none had DAI. Conversely, coma lasting more than 6 hours occurred in one of the sagittal or oblique injury groups but was present in 20 of the laterally injured animals, all of which were severely disabled afterward. All laterally injured animals had a degree of DAI similar to that found in severe human head injury. Coma lasting 16 minutes to 6 hours occurred in 2 of 13 of the sagittal group, 4 of 6 in the oblique group, and 4 of 26 in the lateral group, these animals had less neurological disability and less DAI than when coma lasted longer than 6 hours. These experimental findings duplicate the spectrum of traumatic coma seen in human beings and include axonal damage identical to that seen in sever head injury in humans. Since the amount of DAI was directly proportional to the severity of injury (duration of coma and quality of outcome), we conclude that axonal damage produced by coronal head acceleration is a major cause of prolonged traumatic coma and its sequelae.

No abstract

Cerebral blood flow (CBF) measurements were made in 75 adult patients with closed head injuries (mean Glasgow Coma Scale score 6.2) using the xenon-133 intravenous injection method with eight detectors over each hemisphere. All patients were studied acutely within 96 hours of trauma, and repeatedly observed until death or recovery (total of 361 examinations). Arteriojugular venous oxygen differences (AVDO2) were obtained in 55 of the patients, which permitted assessment of the balance between metabolism and blood flow, and provided estimates of cerebral metabolic rate for oxygen (CMRO2). Based on mean regional CBF, the patients were classified into two groups: those who exhibited hyperemia on one or more examinations, and those who had a consistently reduced flow during their acute illness. "Hyperemia" was defined as a normal or supernormal CBF in the presence of coma, a definition that was independently confirmed by narrow AVDO2's indicative of "luxury perfusion". During coma, all patients showed a significant depression in CMRO2. Forty-one patients (55%) developed an acute hyperemia with an average duration of 3 days, while 34 patients (45%) consistently had subnormal flows. Although more prevalent in younger patients, hyperemia was found at all age levels (15 to 85 years). There was a highly significant association between hyperemia and the occurrence of intracranial hypertension, defined as an intracranial pressure above 20 mm Hg. Patients with reduced flow showed little or no evidence of global cerebral ischemia, but instead revealed the expected coupling of CBF and metabolism. The CBF responses to hyperventilation were generally preserved, with the hyperemic patients being slightly more reactive. In 10 patients with reduced flow, hyperventilation resulted in wide AVDO2's suggestive of ischemia.

✓ Recent studies attempting to define the outcome from severe head injury have implied, directly or indirectly, that the severity of injury (as determined by the Glasgow Coma Scale (GSC)) is the sole determinant of outcome. Little attention has been focused on the type of lesion that causes the low GCS score, and there exists an unstated hypothesis that the lesion type is not an important determinant of outcome. No attempt has been made to determine whether patients who have the same GCS score caused by different lesions have the same or different outcomes. Since this is impossible to test without a large number of cases, data were obtained from seven head-injury centers on patients who fulfilled the Glasgow criteria for severe head injury (GCS ≤ 8 for at least 6 hours). Patients were categorized according to a simple classification system comprising seven lesion types, each of which was further subdivided into two GCS score ranges (3 to 5 and 6 to 8). Of 1107 patients, the overall mortality was 41%, but ranged from 9% to 74% among the different lesion categories. Conversely, 26% had good recovery (at 3 months), but among the different lesion groups the range was 6% to 68%. Acute subdural hematoma with GCS scores of 3 to 5 was uniformly the worst problem (74% mortality and 8% good recovery), whereas diffuse injury coma of 6 to 24 hours with GCS scores of 6 to 8 had 9% mortality and 68% incidence of good recovery. Results of this study demonstrate marked heterogeneity within this severe head-injury group and point out that patients with the same GCS score have markedly different outcomes, depending on the causative lesion. The type of lesion is thus as important a factor in determining outcome as is the GCS score, and both must be considered when describing severely head-injured patients.