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Shawn R. Eagle, Anish Puligilla, Vanessa Fazio-Sumrok, Nathan Kegel, Michael W. Collins, and Anthony P. Kontos


No studies to date have investigated the role of early clinical care in time to recovery from concussion in a pediatric population. The purpose of this study was to investigate the role of clinic presentation timing (≤ 7 days [early] compared to 8–20 days [late] from injury) in concussion assessment performance and risk for prolonged recovery (> 30 days) in pediatric concussion.


This study is a retrospective cross-sectional study from a concussion clinic between April 2016 and January 2019, including 218 children and adolescents with diagnosed concussion, separated based on clinic presentation timing following injury: early (≤ 7 days) and late (8–20 days). Outcomes were recovery time, Postconcussion Symptom Scale (PCSS), Immediate Post-Concussion Assessment and Cognitive Testing (ImPACT), Vestibular/Ocular Motor Screen (VOMS), and demographics, medical history, and injury information. A general linear model and chi-square analyses were used to assess differences between early and late presentation, along with logistic regression, to predict prolonged recovery (> 30 days).


Those with early presentation reported higher symptoms on VOMS subtests (79%–85%) compared to those with late presentation (61%–78%), with the exception of near-point of convergence distance and visual motion sensitivity (VMS). The strongest predictor of prolonged recovery was number of days to first clinic visit (OR 9.8). Positive VMS (OR 5.18), history of headache/migraine (OR 4.02), and PCSS score (OR 1.04) were also predictive of prolonged recovery.


Despite patients in the early presentation group presenting with more positive VOMS scores, the early presentation group recovered sooner than patients in the late presentation group. Even after controlling for vestibular dysfunction, history of headache or migraine, and total symptom severity, days to first visit remained the most robust predictor of recovery > 30 days. These findings suggest that early, specialized medical care and intervention for children and adolescents with recent concussion is associated with normal recovery time. Clinicians should educate children and parents on the potential importance of early treatment to improve the odds of positive outcomes following concussion.

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J. Paul Muizelaar, Anthony Marmarou, John D. Ward, Hermes A. Kontos, Sung C. Choi, Donald P. Becker, Hans Gruemer, and Harold F. Young

✓ There is still controversy over whether or not patients should be hyperventilated after traumatic brain injury, and a randomized trial has never been conducted. The theoretical advantages of hyperventilation are cerebral vasoconstriction for intracranial pressure (ICP) control and reversal of brain and cerebrospinal fluid (CSF) acidosis. Possible disadvantages include cerebral vasoconstriction to such an extent that cerebral ischemia ensues, and only a short-lived effect on CSF pH with a loss of HCO3 buffer from CSF. The latter disadvantage might be overcome by the addition of the buffer tromethamine (THAM), which has shown some promise in experimental and clinical use. Accordingly, a trial was performed with patients randomly assigned to receive normal ventilation (PaCO2 35 ± 2 mm Hg (mean ± standard deviation): control group), hyperventilation (PaCO2 25 ± 2 mm Hg: HV group), or hyperventilation plus THAM (PaCO2 25 ± 2 mm Hg: HV + THAM group). Stratification into subgroups of patients with motor scores of 1–3 and 4–5 took place. Outcome was assessed according to the Glasgow Outcome Scale at 3, 6, and 12 months. There were 41 patients in the control group, 36 in the HV group, and 36 in the HV + THAM group. The mean Glasgow Coma Scale score for each group was 5.7 ± 1.7, 5.6 ± 1.7, and 5.9 ± 1.7, respectively; this score and other indicators of severity of injury were not significantly different. A 100% follow-up review was obtained. At 3 and 6 months after injury the number of patients with a favorable outcome (good or moderately disabled) was significantly (p < 0.05) lower in the hyperventilated patients than in the control and HV + THAM groups. This occurred only in patients with a motor score of 4–5. At 12 months posttrauma this difference was not significant (p = 0.13). Biochemical data indicated that hyperventilation could not sustain alkalinization in the CSF, although THAM could. Accordingly, cerebral blood flow (CBF) was lower in the HV + THAM group than in the control and HV groups, but neither CBF nor arteriovenous difference of oxygen data indicated the occurrence of cerebral ischemia in any of the three groups. Although mean ICP could be kept well below 25 mm Hg in all three groups, the course of ICP was most stable in the HV + THAM group. It is concluded that prophylactic hyperventilation is deleterious in head-injured patients with motor scores of 4–5. When sustained hyperventilation becomes necessary for ICP control, its deleterious effect may be overcome by the addition of THAM.

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Antonio A. F. DeSalles, Hermes A. Kontos, Donald P. Becker, Mildred S. Yang, John D. Ward, Richard Moulton, Hanns D. Gruemer, Harry Lutz, Angelo L. Maset, Larry Jenkins, Anthony Marmarou, and Paul Muizelaar

✓ Brain-tissue acidosis inferred by cerebrospinal fluid (CSF) lactic acidosis is considered to play an important role in the clinical course of severe head injury. Ventricular CSF lactate concentration was studied in 19 patients during the first 5 days after severe head injury. All patients were intubated, paralyzed, and artificially ventilated so that PaCO2 was kept at 33.2 ± 5.0 mm Hg and PaO2 at 122 ± 18 mm Hg (mean ± standard deviation). The mean Glasgow Coma Scale score on admission was 5.73 ± 2.42. The first CSF sample was drawn within 18 hours after head injury. Over the first 4 days postinjury, patients with a poor outcome had significantly higher ventricular CSF lactate levels than did those with moderate disabilities or a good outcome. Patients showing favorable outcome had a significant decrease in ventricular CSF lactate levels 48 hours after injury. This decrease was not observed in patients with a poor outcome. Increased ventricular CSF lactate concentration was also reliably associated with increased intracranial pressure (ICP). Ventricular CSF lactate levels did not correlate with the magnitude of intraventricular bleeding. Arterial and jugular venous blood lactate levels, although high after head injury, were usually lower than the levels in the ventricular CSF and reached a normal range by the 3rd day following head trauma. At that time, the ventricular CSF lactate concentration was still above normal in patients with a poor outcome but had decreased to normal in patients with moderate disabilities or a good outcome. Ventricular CSF pH did not generally correlate with the ventricular CSF lactate concentration in patients under controlled ventilation; however, in a few patients close to death or with ventricular infection, a correlation was noted. Ventricular CSF lactate levels were not related to cerebral blood flow. In this study, profiles of ventricular CSF lactate concentration are defined in relation to the patients' clinical course and outcome. High ventricular CSF lactate concentration is present within 18 hours after severe head injury. Its decrease to normal in the following 48 hours is a reliable sign of clinical improvement; however, ventricular CSF lactate levels that are persistently high or that increase over time indicate the patient's deterioration. Serial assessment of ventricular CSF for acid-base status and metabolites in head-injured patients with a ventricular catheter already placed for ICP monitoring is useful in the evaluation of prognosis and clinical course.

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Lennart Rabow, Antonio A. F. DeSalles, Donald P. Becker, Mildred Yang, Hermes A. Kontos, John D. Ward, Richard J. Moulton, Guy Clifton, Hanns D. Gruemer, J. Paul Muizelaar, and Anthony Marmarou

✓ The posttraumatic creatine kinase-BB isoenzyme (CKBB) activity and lactate concentration in ventricular cerebrospinal fluid (CSF) have been studied in 29 patients with severe head injuries. The CKBB activity reaches its maximum a few hours after trauma, and has a monoexponential drop with a half-time of approximately 10 hours. Ventricular CSF lactate concentration continues to rise in patients with a poor outcome, and decreases only slowly and inconsistently in most of the other patients. Thus, increase of lactate in the ventricular CSF is not, like CKBB, a direct one-stage consequence of the trauma but is due to continuous production from a derangement of metabolism caused by the trauma. Since even higher ventricular CSF lactate levels can be survived when not caused by head injury, and since no significant pH changes were related to the ventricular CSF lactic acidosis in these artificially ventilated patients, it is concluded that ventricular CSF lactic acidosis is indicative of a severe, although not necessarily intractable, disturbance of brain function associated with intracellular lactate production and acidosis.