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Many previous studies have constructed several predictive models for outcome after severe head injury, but these have often used expensive, time consuming, or highly specialized measurements. The goal of this study was to develop a simple, easy to use a model involving only variables that are rapidly and easily achievable in daily routine practice. To this end, a classification and regression tree (CART) technique was employed in the analysis of data from 345 patients with isolated severe brain injury who were admitted to Asclepeion General Hospital of Athens from January, 1993, to December, 2000. A total of 16 prognostic indicators were examined to predict neurological outcome at 6 months after head injury. Our results indicated that Glasgow Coma Scale was the best predictor of outcome. With regard to the other data, not only the most widely examined variables such as age, pupillary reactivity, or computed tomographic findings proved again to be strong predictors, but less commonly applied parameters, indirectly associated with brain damage, such as hyperglycemia and leukocytosis, were found to correlate significantly with prognosis too. The overall cross-validated predictive accuracy of CART model for these data was 86.84%, with a cross-validated relative error of 0.308. All variables included in this tree have been shown previously to be related to outcome. Methodologically, however, CART is quite different from the more commonly used statistical methods, with the primary benefit of illustrating the important prognostic variables as related to outcome. This technique may prove useful in developing new therapeutic strategies and approaches for patients with severe brain injury.

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BACKGROUND: Head injury is associated with increased blood levels of catecholamines and cortisol. Catecholamines release neutrophil stores, and corticosteroids cause a decrease in the egress of neutrophils from the circulation. The acute-phase response is also characterized by a leukocytosis upon admission. Therefore, it is possible that an increase in the white blood cell (WBC) count might serve as an additional diagnostic and prognostic indicator in head injury. METHODS: We prospectively studied 624 patients with severe, moderate, or minor head injury who were admitted to the neurosurgical department of Asclepeion Hospital in Athens between December 1997 and March 1999. In all cases, WBC count was obtained on admission to the emergency department. Factors that might influence WBC were excluded from this study. RESULTS: Patients with severe head injury had significantly higher white blood cell counts than did those with moderate or minor injury (p < 0.001). Among the patients with severe head injury, a significant relationship was found between WBC counts and Glasgow Coma Scale score, pupillary reaction, and presence of subarachnoid hemorrhage (p < 0.001). In the same group of patients, WBC counts were significantly higher in those with an unfavorable outcome (p < 0.001). Multivariate analysis also showed that WBC counts were an independent predictor of outcome. CONCLUSIONS: WBC counts on admission could serve as a significant parameter of severity of injury and as an additional predictor of neurological outcome in patients with severe head injury.

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OBJECTIVE: Traumatic brain injury is associated with a stress response that includes hyperglycemia, which has been shown to worsen neurological outcome during cerebral ischemia and hypoxia. To better examine the relationship between hyperglycemia and outcome after head injury, we studied the clinical course of 267 head-injured patients who were admitted for treatment in the neurosurgical department of Asclepeion Hospital of Athens between January 1993 and November 1997. METHODS: We prospectively studied 267 patients with moderate or severe craniocerebral injury (Glasgow Coma Scale scores, 3-12) who were treated surgically for evacuation of an intracranial hematoma and/or placement of a device for intracranial pressure monitoring under general anesthesia to determine the relationship between serum glucose levels, severity of injury, and neurological outcome. RESULTS: Patients with severe head injury had significantly higher serum glucose levels than did those with moderate injury. Patients who subsequently had an unfavorable outcome had significantly higher glucose levels than did those with a better prognosis. Among the patients with more severe head injury, a glucose level greater than 200 mg/dl was associated with a worse outcome. In the same group of patients, a significant relationship was found between postoperative glucose levels, pupillary reaction, and maximum intracranial pressure during the first 24 hours. Multivariate analysis showed that postoperative glucose levels were an independent predictor of outcome. CONCLUSION: Early hyperglycemia is a frequent component of the stress response to head injury, a significant indicator of its severity, and a reliable predictor of outcome.

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The main metabolites of the neurotransmitters noradrenaline, dopamine, and serotonin, methoxy-hydroxyphenylglycol (MHPG), homovanillic acid (HVA), and 5-hydroxyindoleacetic acid (5HIAA) respectively, were estimated by HPLC with electrochemical detection in CSF samples from 24 patients in coma after head injury, 1 to 12 (mean 3.0) days from accident, and from 24 age- and sex-matched subjects undergoing myelography for possible herniated disk. Analysis of variance with age as covariate, revealed significantly elevated levels of all three metabolites in the patients group. The concentrations of 5HIAA were negatively correlated to the score in the Glasgow Coma Scale. Fourteen patients who recovered with no or minor neurological deficits, had significantly lower CSF 5HIAA levels compared to the ten patients who had a bad outcome (death), while there were no differences regarding HVA or MHPG concentrations. The possibility of a connection of the high neurotransmitter turnover during coma to the development of post-traumatic depression is discussed.

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We report the case of a man with ankylosing hyperostosis of the spine who developed spastic quadriparesis due to ossification of the posterior longitudinal ligament. The related literature is discussed.

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