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Thomas W. Langfitt and Thomas A. Gennarelli

✓ In the past few years, considerable progress has been made in describing patients with head injuries in such a manner that comparisons in morbidity and mortality can be made among neurosurgical centers according to the seriousness of the injury. Less progress has been made in classifying the type of pathology, especially by computerized tomography. The authors have introduced a classification that includes both the type and the seriousness of the injury. There appear to be two principal causes of the brain damage produced by head injury: 1) mechanical damage to neurons and their processes, especially axons, and 2) ischemia. Mechanical damage produces axonal degeneration. Although central regeneration generally is quite limited, perhaps many of the axons damaged by head injury degenerate in continuity, a circumstance in which functional regeneration by axoplasmic outgrowth is much more likely to occur than in most experimental situations where the axons are physically divided. The ischemic brain damage that is so common in head injury appears to be due to mass lesions and brain swelling that both cause intracranial hypertension. The more the brain swells, and the higher the intracranial pressure, the more difficult it is to control the swelling and the pressure. In patients with acute subdural hematoma in particular, the brain swelling and the high mortality appear to be due to ischemic brain damage. There is recent evidence that the mortality rate in patients with acute subdural hematoma is a function of the time from injury to evacuation of the hematoma. Therefore, outcome from head injury can be improved by the earliest possible removal of space-occupying hematomas and by early, vigorous management of intracranial hypertension.

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Jurg L. Jaggi, Walter D. Obrist, Thomas A. Gennarelli, and Thomas W. Langfitt

✓ Cerebral blood flow (CBF) measurements were obtained acutely in 96 comatose patients with closed head injury, using the intravenous 133Xe technique. Arteriojugular venous oxygen differences and cerebral metabolic rate for oxygen (CMRO2) were determined in a subgroup of 66 patients. The relationship between each of these variables and outcome at 6 months was analyzed, using the Glasgow Outcome Scale.

The CMRO2 was significantly depressed in patients who subsequently died or remained in a vegetative state, whereas higher values were obtained in patients who later regained consciousness. Although CBF was not predictive of outcome in the total sample, omission of patients with acute hyperemia resulted in a significant relationship that paralleled the metabolic findings. Follow-up studies in the survivors revealed a correlation between CBF and degree of functional recovery, the lowest blood flows being obtained among patients with severe disability.

Age, initial Glasgow Coma Scale score, and occurrence of intracranial hypertension were each found to be predictive of outcome, thus confirming previous reports. When these variables were combined with CMRO2 in a logistic regression analysis, the probability of recovery was correctly predicted in 82% of the cases. The CMRO2 was relatively independent of the other prognostic indicators and, next to age, contributed most to the prediction.

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Cheryl A. Muszynski, Narayan Yoganandan, Frank A. Pintar, and Thomas A. Gennarelli

Object. Injury to the brain as a result of motor vehicle accidents (MVAs) represents a frequent cause of pediatric disability. The authors analyze the correlation between the relative risk of pediatric brain injury and the use of child safety seats (CSSs).

Methods. A national database of MVAs was examined to provide data for the analysis of four age categories (infant, toddler, young child, and adolescent) and four restraint categories (unrestrained, properly restrained, improperly restrained, and other). The Abbreviated Injury Scale (AIS) was used to assess the severity of head injury; children with no injuries and children with moderate-to-maximum head injuries were evaluated.

The data confirm that proper use of a CSS substantially increases the likelihood of not sustaining head injury in an MVA. The data are most dramatic for infants (the likelihood of sustaining no head injury was 15.2% for unrestrained infants compared with 92.8% for properly restrained infants) but the protective effect is seen in all age categories, with the least difference observed in the adolescent category. For children who sustain a moderate-to-maximum head injury, proper use of a CSS reduces the incidence of injury, again most dramatically for the infant category (unrestrained infants had a 7% risk of moderate-to-maximum head injury compared with only 0.5% for properly restrained infants).

Conclusions. Improvements in CSSs have reduced the risk of moderate-to-maximum head injuries in children of all age categories. Overall, a CSS is most protective for the infant and toddler categories. The improperly restrained child still has substantial protection, although the properly restrained child has more. Detailed parental education regarding appropriate restraint system installation and use should be required.

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Brian D. Stemper, Narayan Yoganandan, Thomas A. Gennarelli, and Frank A. Pintar

Object. Although facet joints have been implicated in the whiplash injury mechanism, no investigators have determined the degree to which joint motions in whiplash are nonphysiological. The purpose of this investigation was to quantify the correlation between facet joint and segmental motions under physiological and whiplash loading.

Methods. Human cadaveric cervical spine specimens were exercise tested under physiological extension loading, and intact human head-neck complexes were exercise tested under whiplash loading to correlate the localized component motions of the C4–5 facet joint with segmental extension. Facet joint shear and distraction kinematics demonstrated a linear correlation with segmental extension under both loading modes. Facet joints responded differently to whiplash and physiological loading, with significantly increased kinematics for the same-segmental angulation. The limitations of this study include removal of superficial musculature and the limited sample size for physiological testing.

Conclusions. The presence of increased facet joint motions indicated that synovial joint soft-tissue components (that is, synovial membrane and capsular ligament) sustain increased distortion that may subject these tissues to a greater likelihood of injury. This finding is supported by clinical investigations in which lower cervical facet joint injury resulted in similar pain patterns due to the most commonly reported whiplash symptoms.

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John A. Jane, Osward Steward, and Thomas Gennarelli

✓ Minor head injury or concussion was produced in experimental animals by an acceleration-deceleration non-impact injury. The animals sustained a brief loss of consciousness and no sequelae were observed. The brains were examined at 7 days by means of the Nauta and Fink-Heimer techniques. Degenerating axons were noted in the inferior colliculus, pons, and dorsolateral medulla. Degeneration was not seen in the subcortical white matter, thus suggesting a primary brain-stem locus for concussion. These findings also suggest that, in some instances, minor head injury or concussion can be associated with organic damage to the central nervous system.

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Walter D. Obrist, Thomas A. Gennarelli, Hiromu Segawa, Carol A. Dolinskas, and Thomas W. Langfitt

✓ Noninvasive studies of regional cerebral blood flow (CBF) were performed on 36 head-injured patients in varying degrees of coma, using the intravenous xenon-133 method. Serial examinations, averaging four per patient, were begun during the acute phase of illness and continued until death or recovery of normal consciousness. Comparison of the initial and final studies revealed that CBF declined to very low levels in all nine patients who died, and remained subnormal in a patient with persistent vegetative state. In contrast, 25 of 26 patients who recovered consciousness showed increases in blood flow.

Because of the presence of both reduced and elevated blood flows on the initial study, CBF was not predictive of outcome. Absolute or relative hyperemia, observed in nine acute cases, was associated with either diffuse cerebral swelling (observed on computerized tomography) or recovery from systemic shock. Cerebral metabolic studies in hyperemic patients yielded a very low oxygen uptake and arteriovenous oxygen difference, indicating that the high blood flow was a true “luxury perfusion.” When instances of presumed luxury perfusion were excluded, CBF was positively correlated with level of consciousness, assessed on a four-point coma scale.

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Walter D. Obrist, Thomas W. Langfitt, Jurg L. Jaggi, Julio Cruz, and Thomas A. Gennarelli

✓ 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.

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Iwao Yamakami, Robert Vink, Alan I. Faden, Thomas A. Gennarelli, Robert Lenkinski, and Tracy K. McIntosh

✓ Using the lateral fluid-percussion model of experimental brain injury in the rat, the authors investigated the effect of acute ethanol (EtOH) intoxication on cardiovascular changes, neurological motor deficits, brain bioenergetics, and mortality associated with traumatic brain injury. Two hours after gastric administration of EtOH (low dose in 20 animals, 1.5 g/kg; high dose in 28, 3.0 g/kg) or saline (equal volume), animals were subjected to a fluid-percussion brain injury centered over the left parietal cortex. These injuries were of either moderate (X = 2.2 atm; 10 animals/treatment) or high severity (X = 3.0 atm; 18 animals/saline, 10 animals/low-dose EtOH, and 18 animals/high-dose EtOH). Neurological motor function was evaluated daily over a 1-week period, while a subset of eight animals receiving high-dose EtOH and subjected to brain injury of high severity were monitored for 4 hours using phosphorus-31 nuclear magnetic resonance spectroscopy to determine intracellular pH, free magnesium, and brain cytosolic phosphorylation potential. A significant (p < 0.05) and prolonged (up to 1 hour) hypotension was observed in animals pretreated with either low- or high-dose EtOH. Neither low-dose (blood—EtOH concentration = 110 ± 40 mg/dl) nor high-dose (blood—EtOH = 340 ± 70 mg/dl) EtOH had any effect on survival or neurological motor function after moderate brain injury. Following severe brain injury, animals pretreated with high-dose (blood—EtOH concentration = 352 ± 65 mg/dl) EtOH showed a significantly increased mortality and markedly worsened neurological deficits at 24 hours postinjury. Following injury, free magnesium and cytosolic phosphorylation potential declined in both groups by approximately 50% to 60%, with no significant differences between groups with respect to these variables. In contrast, brain intracellular pH in the EtOH-treated animals was consistently higher than in the control group after injury. These data suggest that prior exposure to EtOH, particularly at high concentrations, may have detrimental effects on neurobehavioral function and survival in the acute period (up to 24 hours) after severe brain injury, and may be associated with posttraumatic cerebral alkalosis.

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Julio Cruz, Michael E. Miner, Steven J. Allen, Wayne M. Alves, and Thomas A. Gennarelli

✓ Global cerebral oxygenation, perfusion pressure, and expired pCO2 were continuously monitored in 10 adults with acute severe closed head trauma. Cerebral oxygenation was monitored by fiberoptic catheter oximetry, which allowed simultaneous measurements of arterial and jugular bulb oxyhemoglobin saturation. Intracranial pressure levels over 20 mm Hg were recorded several times in all patients, in spite of sedation, muscle paralysis, and profound hyperventilation. Intracranial hypertension was frequently associated with oligemic cerebral hypoxia, identified as abnormally low jugular oxygen saturation in the presence of normal arterial oxygenation. Intracranial hypertension was then managed with intravenous administration of mannitol boluses, which yielded simultaneous decreases in intracranial pressure and increases in cerebral oxygenation to highly statistically significant levels. Monitoring cerebral oxygenation was clinically useful because it allowed identification of impaired cerebral oxygenation even when cerebral perfusion pressure was normal. It is therefore proposed as a new monitoring technique, to supplement conventional monitoring of cerebral perfusion pressure.

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The shaken baby syndrome

A clinical, pathological, and biomechanical study

Ann-Christine Duhaime, Thomas A. Gennarelli, Lawrence E. Thibault, Derek A. Bruce, Susan S. Margulies, and Randall Wiser

✓ Because a history of shaking is often lacking in the so-called “shaken baby syndrome,” diagnosis is usually based on a constellation of clinical and radiographic findings. Forty-eight cases of infants and young children with this diagnosis seen between 1978 and 1985 at the Children's Hospital of Philadelphia were reviewed. All patients had a presenting history thought to be suspicious for child abuse, and either retinal hemorrhages with subdural or subarachnoid hemorrhages or a computerized tomography scan showing subdural or subarachnoid hemorrhages with interhemispheric blood. The physical examination and presence of associated trauma were analyzed; autopsy findings for the 13 fatalities were reviewed. All fatal cases had signs of blunt impact to the head, although in more than half of them these findings were noted only at autopsy. All deaths were associated with uncontrollably increased intracranial pressure.

Models of 1-month-old infants with various neck and skull parameters were instrumented with accelerometers and shaken and impacted against padded or unpadded surfaces. Angular accelerations for shakes were smaller than those for impacts by a factor of 50. All shakes fell below injury thresholds established for subhuman primates scaled for the same brain mass, while impacts spanned concussion, subdural hematoma, and diffuse axonal injury ranges. It was concluded that severe head injuries commonly diagnosed as shaking injuries require impact to occur and that shaking alone in an otherwise normal baby is unlikely to cause the shaken baby syndrome.