Verbal learning deficits following severe head injury: heterogeneity in recovery over 1 year

1991 ◽  
Vol 75 (Supplement) ◽  
pp. S50-S58 ◽  
Author(s):  
Ronald M. Ruff ◽  
David Young ◽  
Theresa Gautille ◽  
Lawrence F. Marshall ◽  
Jeff Barth ◽  
...  

✓ A total of 40 severely head-injured patients were selected from the Traumatic Coma Data Bank, supported by the National Institute of Neurological Disorders and Stroke, to analyze the recovery of verbal learning across baseline and 6- and 12-month evaluations postinjury. During the initial 6 months, the group demonstrated marked recovery, followed by an absence of improvement over the latter part of the year. Analysis of this recovery curve on a case by case basis revealed three recovery subtypes: namely, a flat curve, a peak-drop curve, or an improvement curve. These three subtypes proved to have concurrent validity when compared with another memory test. Adding 19 new patients to the sample cross-validated the subtypes. However, the memory performance of the 59 patients was dissociated from other neuropsychological tests which showed recovery at more equivalent rates across the subtypes. Analysis of the demographic and neurological characteristics disclosed that the group with a peak-drop recovery curve was less well educated and the group with a flat curve demonstrated a trend toward higher levels of hypoxia. Moreover, the three subgroups were rated by their relatives to have equivalent levels of depression at baseline and at 6 months, but only the improved subgroup demonstrated reduced depression at 1 year. The clinical relevancy of these differential recovery curves is discussed.

1991 ◽  
Vol 75 (Supplement) ◽  
pp. S8-S13 ◽  
Author(s):  
Mary A. Foulkes ◽  
Howard M. Eisenberg ◽  
John A. Jane ◽  
Anthony Marmarou ◽  
Lawrence F. Marshall ◽  
...  

✓ The Traumatic Coma Data Bank is a collaborative project to prospectively collect data on the clinical course and outcome of severely head-injured patients. The objectives were to further define the natural history of traumatic head injury, to identify prognostic factors, and to provide planning data for future studies. A brief historical development and a description of the organizational structure and methods are given. The characteristics of the cohort at baseline for the 1030 patients enrolled between January, 1984, and September, 1987, are presented, including a summary of the patients' demographic profile, mechanisms of injury, and intracranial diagnoses. The utility and limitations of these data are discussed.


1996 ◽  
Vol 85 (3) ◽  
pp. 419-424 ◽  
Author(s):  
Kathryn L. Holloway ◽  
Tom Barnes ◽  
Sung Choi ◽  
Ross Bullock ◽  
Lawrence F. Marshall ◽  
...  

✓ The investigators undertook a retrospective analysis of ventriculostomy infections to evaluate their relationship to monitoring duration and prophylactic catheter exchange. In 1984, the results of an epidemiological study of ventriculostomy-related infection were published. One of the conclusions of the paper was that the incidence of ventriculostomy-related infections rose after 5 days of monitoring. This led to the recommendation that catheters be prophylactically changed at 5-day intervals if prolonged monitoring was required. A recent randomized prospective study on central venous catheters showed no reduction in infection with prophylactic catheter exchanges. This has led the authors to reexamine their experience with ventriculostomy infections. Data on 584 severely head injured patients with ventriculostomies were prospectively collected in two data banks, The Traumatic Coma Data Bank and The Medical College of Virginia Neurocore Data Bank. These data were retrospectively analyzed for factors associated with ventriculostomy related infections. It was found that there is a relationship of ventriculitis to monitoring duration but it is not simple or linear. There is a rising risk of infection over the first 10 days, but infection then becomes very unlikely despite a population that continues to be at risk. Patients in whom catheters were replaced prior to 5 days did not have a lower infection rate than those whose catheters were exchanged at more than 5-day intervals. Based on these data, it is recommended that ventriculostomy catheters for intracranial pressure monitoring be removed as quickly as possible, and in circumstances in which prolonged monitoring is required, there appears to be no benefit from catheter exchange.


1983 ◽  
Vol 59 (2) ◽  
pp. 285-288 ◽  
Author(s):  
Lawrence F. Marshall ◽  
Belinda M. Toole ◽  
Sharon A. Bowers

✓ The records of the first 325 patients entered into the pilot phase of the National Traumatic Coma Data Bank were reviewed. Thirty-four severely head-injured patients who talked prior to deteriorating to a Glasgow Coma Scale (GCS) score of 8 or less were identified. Of those 34 patients, 18 died or were left vegetative and 16 recovered. While there were certain common factors between those who talked and died and those who talked and recovered, there were also significant differences. The common factors between the two groups were the length of time to deterioration or operative intervention (16 versus 18 hours, respectively), and the initial GCS scores (12.6 versus 12.4, respectively). The primary differences between the groups included the mean age, the degree of midline shift seen on computerized tomography (CT), and the presence of subdural hematoma. Those who talked at some point postinjury, but who subsequently died, had a mean age of 50 years. Those who talked, deteriorated, and then recovered were found to have a mean age of 32 years. Seven of the 18 patients who talked and died had a shift of greater than 15 mm on CT, while this degree of shift was demonstrated in only one of 16 patients who talked, deteriorated, and recovered. Subdural hematomas were significantly more common in the “talk and die” group, as was the overall need for operation. Since the overwhelming majority of patients with marked shift on CT have surgical lesions, early operative intervention is strongly recommended in these patients, prior to their inevitable deterioration.


1991 ◽  
Vol 75 (Supplement) ◽  
pp. S21-S27 ◽  
Author(s):  
Anthony Marmarou ◽  
Randy L. Anderson ◽  
John D. Ward ◽  
Sung C. Choi ◽  
Harold F. Young ◽  
...  

✓ This report describes the methods used by the Traumatic Coma Data Bank (TCDB) for acquisition and recording of intracranial pressure (ICP) data of severely head-injured patients. Direct computerization of physiological data from all four participating locations within the United States and transmission to a central data bank was found to be logistically complex and costly. A simple manual method for recording ICP, blood pressure, and concomitant ICP therapy at the bedside is described. The method documents the temporal course of these variables for the duration of monitoring. The importance of relating ICP to the therapy intensity level used for ICP management is emphasized. Concomitant analysis of the therapy intensity level is considered imperative in correlative patient studies. The methods described in this report have been in use among all four TCDB hospitals. Examples of ICP data retrieved from the TCDB are presented to illustrate the adequacy of the methods for assessing temporal trends. Of 1030 patients admitted to the TCDB, 654 severely head-injured patients had at least 4 hours of monitoring recorded; elevated ICP (> 20 mm Hg) was observed in 72% of these 654 patients.


1987 ◽  
Vol 66 (6) ◽  
pp. 883-890 ◽  
Author(s):  
Anthony Marmarou ◽  
Angelo L. Maset ◽  
John D. Ward ◽  
Sung Choi ◽  
Danny Brooks ◽  
...  

✓ The authors studied the relative contribution of cerebrospinal fluid (CSF) and vascular parameters to the level of intracranial pressure (ICP) in 34 severely head-injured patients with a Glasgow Coma Scale score of less than 8. This was accomplished by first characterizing the temporal course of CSF formation and outflow resistance during the 5-day period postinjury. The CSF formation and outflow resistance were obtained from pressure responses to bolus addition and removal of fluid from an indwelling ventricular catheter. The vascular contribution to the level of ICP was assessed by withdrawing fluid at its rate of formation and observing the resultant change in equilibrium ICP level. It was found that, with the exception of patients with subarachnoid hemorrhage, CSF parameters accounted for approximately one-third of the ICP rise after severe head injury, and that a vascular mechanism may be the predominant factor in elevation of ICP.


1988 ◽  
Vol 68 (3) ◽  
pp. 409-416 ◽  
Author(s):  
Thomas G. Luerssen ◽  
Melville R. Klauber ◽  
Lawrence F. Marshall

✓ A series of 8814 head-injured patients admitted to 41 hospitals in three separate metropolitan areas were prospectively studied. Of these, 1906 patients (21.6%) were 14 years of age or less. This “pediatric population” was compared to the remaining “adult population” for mechanism of injury, admission Glasgow Coma Scale score, motor score, blood pressure, pupillary reactivity, the presence of associated injuries, and the presence of subdural or epidural hematoma. The relationship of each of these factors was then correlated with posttraumatic mortality. Except for patients found to have subdural hematoma and those who were profoundly hypotensive, the pediatric patients exhibited a significantly lower mortality rate compared to the adults, thus confirming this generally held view. This study indicates that age itself, even within the pediatric age range, is a major independent factor affecting the mortality rate in head-injured patients.


1991 ◽  
Vol 75 (5) ◽  
pp. 731-739 ◽  
Author(s):  
J. Paul Muizelaar ◽  
Anthony Marmarou ◽  
John D. Ward ◽  
Hermes A. Kontos ◽  
Sung C. Choi ◽  
...  

✓ 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.


1991 ◽  
Vol 75 (5) ◽  
pp. 766-773 ◽  
Author(s):  
Keith B. Quattrocchi ◽  
Edmund H. Frank ◽  
Claramae H. Miller ◽  
Asim Amin ◽  
Bernardo W. Issel ◽  
...  

✓ Infection is a major complication of severe head injury, occurring in 50% to 75% of patients who survive to hospitalization. Previous investigations of immune activity following head injury have demonstrated suppression of helper T-cell activation. In this study, the in vitro production of interferon-gamma (INF-γ), interleukin-1 (IL-1), and interleukin-2 (IL-2) was determined in 25 head-injured patients following incubation of peripheral blood lymphocytes (PBL's) with the lymphocyte mitogen phytohemagglutinin (PHA). In order to elucidate the functional status of cellular cytotoxicity, lymphokine-activated killer (LAK) cell cytotoxicity assays were performed both prior to and following incubation of PBL's with IL-2 in five patients with severe head injury. The production of INF-γ and IL-2 by PHA-stimulated PBL's was maximally depressed within 24 hours of injury (p < 0.001 for INF-γ, p = 0.035 for IL-2) and partially normalized within 21 days of injury. There was no change in the production of IL-1. When comparing the in vitro LAK cell cytotoxicity of PBL's from head-injured patients and normal subjects, there was a significant depression in LAK cell cytotoxicity both prior to (p = 0.010) and following (p < 0.001) incubation of PBL's with IL-2. The results of this study indicate that IL-2 and INF-γ production, normally required for inducing cell-mediated immunity, is suppressed following severe head injury. The failure of IL-2 to enhance LAK cell cytotoxicity suggests that factors other than decreased IL-2 production, such as inhibitory soluble mediators or suppressor lymphocytes, may be responsible for the reduction in cellular immune activity following severe head injury. These findings may have significant implications in designing clinical studies aimed at reducing the incidence of infection following severe head injury.


1984 ◽  
Vol 60 (4) ◽  
pp. 687-696 ◽  
Author(s):  
Guy L. Clifton ◽  
Claudia S. Robertson ◽  
Robert G. Grossman ◽  
Susan Hodge ◽  
Richard Foltz ◽  
...  

✓ Caloric expenditure and nitrogen balance were measured in 14 steroid-treated comatose head-injured patients acutely and up to 28 days after injury. During this period patients were fed with a continuous enteral infusion of a formula containing 2 Kcal/cc and 10 gm nitrogen/liter. Indirect calorimetry was carried out for 102 patient-days. The mean resting metabolic expenditure (RME) for nonsedated nonparalyzed patients was 138% ± 37% of that expected for an uninjured resting person of equivalent age, sex, and body surface area. Nitrogen excretion was measured for 135 patient-days. The mean excretion was 20.2 ± 6.4 gm/day. The mean protein caloric contribution was 23.9% ± 6.7% and was greater than 25% for six patients, compared to normal values of 10% to 15%. Despite hyperalimentation, positive nitrogen balance for any 3-day period was achieved in only seven patients, and required replacement of 161% to 240% of RME with enterally administered formula. Head-injured patients had a metabolic response similar to that reported for patients with burns of 20% to 40% of the body surface.


1988 ◽  
Vol 69 (3) ◽  
pp. 386-392 ◽  
Author(s):  
Craig J. McClain ◽  
Bernhard Hennig ◽  
Linda G. Ott ◽  
Simeon Goldblum ◽  
A. Byron Young

✓ Severely head-injured patients are hypermetabolic/hypercatabolic and exhibit many aspects of the postinjury acute-phase response. These patients have hypoalbuminemia, hypozincemia, hypoferremia, hypercupria, fever, and increased synthesis of acute-phase proteins such as ceruloplasmin and higher C-reactive protein levels. It has been suggested that increased interleukin-1 (IL-1) in the ventricular fluid may be responsible, at least in part, for these metabolic abnormalities. In the present study, serum albumin levels were evaluated throughout an 18-day study period in 62 head-injured patients receiving aggressive nutritional support. Hypoalbuminemia (mean ± standard error of the mean 3.10 ± 0.2 gm/dl; normal value 3.5 to 5 gm/dl) was observed upon hospital admission; these albumin levels continued to decrease until 2 weeks postinjury, despite aggressive nutritional support. This hypoalbuminemia may be mediated via altered endothelial permeability properties due to endothelial cell dysfunction caused by cytokines such as IL-1. Transendothelial movement of albumin was assayed using a pulmonary artery endothelial cell culture system. Both a crude macrophage supernatant derived from a murine P388D cell line having IL-1 activity (mIL-1) and human recombinant IL-1 (rIL-1) were tested. The amount of albumin transferred was time- and concentration-dependent, with maximal transfer at 24 hours and 20 U of mIL-1 per 0.5 ml of culture medium. Endothelial permeability changes observed after incubation with mIL-1 were confirmed using rIL-1. Compared to control cultures, 20 U of rIL-1 and 20 U of mIL-1 increased albumin transfer across endothelial monolayers 205% and 459%, respectively. These findings suggest that the mechanism of hypoalbuminemia seen after severe head trauma can be explained in part by IL-1-induced endothelial cell injury, resulting in enhanced endothelial permeability to albumin.


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