Biomechanical evaluation of two innovative locking implants for comminuted olecranon fractures under high-cycle loading conditions.

INTRODUCTION: The relatively high complication rate after fixation of olecranon fractures has led to an increasing application of anatomically pre-contoured locking plate systems. The purpose of the present study was to conduct a biomechanical comparison of olecranon osteosyntheses by applying the Olecranon VA-LCP and the 3.5mm LCP Hook Plate (LCP, locking compression plate) to an unstable fracture model under high-cycle loading conditions. METHODS: After creating an unstable fracture (Schatzker type B), osteosynthesis was performed on eight pairs of fresh-frozen cadaveric ulnae by application of either the Olecranon VA-LCP (Synthes, Solothurn, Switzerland) or the 3.5mm LCP Hook Plate (Synthes, Solothurn, Switzerland). Loading (50,000 alternating loads, cyclic and sinusoidal 10-300 N) was conducted by application of tensile load with the elbow in 90° flexion to simulate the tensile strength of the triceps brachii. For statistical analysis, angular displacement in the region of the humeral trochlea was taken as a measure of olecranon dislocation. RESULTS: In Group 1 (Olecranon VA-LCP), a median angular displacement of 0.36° (minimum 0.10°; maximum 0.80°) was observed after 500 alternating loads. In Group 2 (3.5-mm LCP Hook Plate), the medial displacement was 0.80° (minimum 0.13°; maximum 2.72°). The difference was nonsignificant (p = 0.128). The mean value for angular displacement in Group 1 after 50,000 cycles was 0.80° (minimum 0.31°; maximum 1.99°), whereas in Group 2 a mean angular displacement of 2.02° (minimum 0.71°; maximum 6.40°) was recorded. The difference was statistically significant (p = 0.017). In Group 2, implant failure in the form of proximal plate pullout occurred in one construct after 756 cycles. CONCLUSION: A significantly higher biomechanical stability can be achieved in the fixation of unstable olecranon fractures by application of the Olecranon VA-LCP rather than the 3.5mm LCP Hook Plate.

Glioblastoma multiforme: treatment by large dose fraction irradiation and metronidazole.

In an attempt to overcome the possible radioresistance of glioblastoma multiforme related to the large shoulder on the in vitro survival curves and to sensitize hypoxic tumor cells, a treatment protocol was instituted at Yale University Medical Center and affiliated hospitals, using large dose fraction irradiation therapy in conjunction with the hypoxic cell sensitizer metronidazole. Nineteen patients with biopsy-confirmed, previously untreated, cerebral grade IV glioblastoma multiforme were, following surgery, irradiated once a week at 600 rad per fraction, 3.5 to 4 hours after ingestion of metronidazole, 6 gm/m2. A total of 7 treatments were employed, with all patients maintained on antiseizure medications and corticosteroids. Metronidazole levels were determined prior to each treatment and patients were followed closely clinically and with serial computerized tomography (CT) scans. The treatment was well tolerated, in general, with no untoward side effects related to the high dose fraction irradiation. The majority of the patients experienced varying degrees of gastrointestinal upset lasting up to several hours following metronidazole administration. Three patients died of pulmonary emboli. One patient experienced moderately severe ototoxicity. A median survival of 9.4 months was obtained for all 19 patients, suggestive of a prolongation of survival compared to historical controls treated with conventionally fractionated radiation or with unconventional radiation fractionation schemes and metronidazole or misonidazole.

The effect of nimodipine on high-energy phosphates and intracellular pH during cerebral ischemia.

Experimental and clinical studies suggest that the calcium channel blocker nimodipine may reduce cerebral ischemic injury. Using rapid acquisition phosphorus-31 nuclear magnetic resonance (31P NMR) spectroscopy, we examined the effect of nimodipine on cerebral energy metabolism during severe ischemia in gerbils. High-energy phosphates and intracellular pH were characterized at baseline and at 2-min intervals following bilateral common carotid artery (CCA) ligation. Serial forebrain spectroscopy was continued until phosphocreatine (PCr) and adenosine triphosphate (ATP) resonances disappeared. Controls (n = 10) were compared to gerbils receiving intraperitoneal nimodipine 30 min prior to carotid ligation, at the following doses: 0.5 mg/kg (n = 8), 1.0 mg/kg (n = 10), 2.0 mg/kg (n = 8), or 4.0 mg/kg (n = 4). In the control group, PCr and ATP peaks were undetectable after a mean of 5.4 +/- 0.47 min following CCA ligation. Compared with controls, the mean time for depletion of high-energy phosphates following carotid ligation was prolonged at nimodipine doses of 0.5 mg/kg and 1.0 mg/kg, but the differences did not reach statistical significance. In the 2.0 mg/kg group, however, ATP was preserved until 9.8 +/- 1.0 min following the onset of ischemia, significantly longer than the control group (p = 0.005, Mann-Whitney test). Nimodipine had no effect on the time course or severity of intracellular acidosis. In this model of severe ischemia, relatively high doses of nimodipine slowed the depletion of high-energy phosphates without altering intracellular acidosis. This suggests that nimodipine may provide cerebral protection by directly altering ischemic cellular metabolism.

Impairment of helper T-cell function following severe head injury.

Major infections, such as sepsis and pneumonia, occur in 50-75% of patients following isolated severe head injury. Previous studies have demonstrated that this high incidence of infection following severe head injury may be related to a decrease in helper T-cell activation and function. The present study was designed to investigate the effect of severe head injury on specific subgroups of helper T cells known to enhance or suppress cellular immune function. Specifically, peripheral blood lymphocytes (PBLs) from 10 head-injured patients and 10 matched controls were evaluated following in vitro stimulation with the T-cell mitogen, phytohemagglutinin (PHA). Subsets of helper T cells evaluated included activated helper (CD4+/CD25+) T cells; helper/inducer (CD4+/CDw29+) T cells, which enhance cellular immune activity; and suppressor/inducer (CD4+/CD45R+) T-cells, which induce suppressor (CD8+) T-cells. In addition, the effect of intraventricular fluid (IVF) on PHA-stimulated in vitro CD4 and CD25 expression was investigated to determine whether severe head injury results in the production of mediators within the central nervous system capable of affecting T-cell activation. The results of this study indicate that isolated severe head injury selectively reduces the ability of PHA-stimulated PBLs to express the helper/inducer (CD4+/CDw29+) T-cell (p = 0.023) and activated helper (CD4+/CD25+) T-cell (P = 0.041) phenotypes. There was no significant change in PHA-stimulated CD4 or CD25 expression following incubation of PBLs with intraventricular fluid (IVF) from head-injured patients. The relationship between these changes in specific helper T-cell subpopulations and the infectious complications of severe head injury are discussed.

Suppression of cellular immune activity following severe head injury.

Infection is a major cause of morbidity following multiple traumatic and head injury. Although immunosuppression has been demonstrated after multiple traumatic injury, the effects of head injury on immune function have not been thoroughly investigated. In a prospective study of 10 severely head-injured patients, in vitro and in vivo parameters of cellular immune activity were assessed. In vitro measurements of lymphocyte surface antigen expression following mitogen stimulation were made serially over a 3-week period in 10 patients with severe head injury. The control group consisted of 20 healthy subjects. Phenotyping of peripheral blood lymphocytes (PBLs) was performed following incubation with and without mitogens. Phenotypes were determined by flow cytometry using monoclonal antibodies (MABs) to T lymphocyte subsets and the alpha subunit of interleukin 2 (IL-2) receptors. In vivo cellular immune function was determined by measuring patient responses to delayed-type hypersensitivity (DTH) skin testing within 24 h of injury. When head-injured patients were compared to controls, PBLs incubated in the presence of phytohemagglutinin (PHA) demonstrated a decrease in cells marking as T cells (p = 0.005), helper-inducer T cells (p = 0.001), and in the number of IL-2 receptor-bearing cells (p = 0.001). The functional ability of these lymphocyte subpopulations to proliferate in the presence of PHA was significantly suppressed within 24 h of injury and normalized within 3 weeks of injury. DTH skin testing to Candida, mumps, trichophyton, and PPD antigens was performed within 24 h of injury and resulted in anergic responses in all 10 patients when measured at 24, 48, and 72 h following administration. The overall infection rate was 60%, with the majority of infections occurring within the first 4 days following injury. The results of this study indicate that severe head injury results in suppression of cellular immune function with a corresponding high rate of infection. The possible significance of the decrease in the percentage of helper-inducer T cells and in the number of cells bearing IL-2 receptors following mitogen stimulation is discussed.

Dual-energy x-ray projection imaging: two sampling schemes for the correction of scattered radiation.

In addition to the familiar problems of reduced contrast and signal-to-noise ratio (SNR) in the single energy case, dual-energy subtractions in the presence of scattered radiation suffer further degradations from: (1) artifacts due to nonuniform subtraction of scatter, and (2) a serious deterioration of the signal of interest. To determine the expected performance of scatter correcting schemes, we simulated energy subtractions performed in the presence of scatter. We discuss scatter's detrimental effects on contrast and SNR in these simulations and the expected improvements from scatter corrections to within 5% to 10%. We introduce two sampling schemes for the correction of scatter. Each scheme requires two measurements, and each involves placing an x-ray opaque sampling grid between the source and the object. In the first method, the grid is an array of lead disks present only during one measurement. Using these samples we generate an estimate of the scatter field and then subtract it from the second measurement yielding a scatter corrected image. In the second method, the grid is an array of lead strips present during both measurements but displaced between measurements by one-half of a strip spacing to completely sample the image. From the two measurements we generate an image to be corrected, an estimate of the scatter field, and a scatter corrected image. In phantom studies implemented on a digital fluoroscopy system, we observed for single energy images of blood vessel phantoms improved contrast and field uniformity. For scatter corrected selective material cancellations in human phantoms we observed improved contrast and significant reduction in artifacts. In both cases we observed no significant loss in SNR. These results facilitate the implementation of efficient large area detectors for dual-energy imaging.

Two interpolating filters for scatter estimation.

We have previously reported on a dual-measurement sample-and-estimate technique for scatter correction. In this paper, we present a scatter-correction technique that uses the previous sampling scheme but a different method of estimation. To provide samples of the scatter directly, an array of small, uniformly spaced lead disks is placed immediately before the object during only the first measurement. Interpolating from these samples we form an estimate of the scatter. We subtract this estimate from the second measurement to form a scatter-corrected image. Previously, we used least-squares interpolation to estimate the scatter. Because the samples are uniformly spaced, classical sampling theory motivated the investigation of interpolating filters for scatter estimation. To form the scatter image, we convolved the sample set with two different interpolating filters--a sinc function from classical sampling theory and a jinc function because the scatter function is radially symmetric. Using phantoms as objects, we applied both filters for scatter correction in vessel imaging and energy-subtraction imaging. Initial corrected images contained an artifact attributed to aliasing. We modified the filter widths to reduce the aliasing. Although improvements in image quality were measured and the artifact was less pronounced, the artifact was still present. We present the phantom results obtained with this class of filters and discuss methods for its improved performance.

Traumatic aneurysm of the superior cerebellar artery: case report and review of the literature.

Less than 10% of the 250 reported cases of traumatic intracranial aneurysms have involved the posterior circulation. Traumatic aneurysms of the superior cerebellar artery are extremely rare, with only three cases previously reported. This is the first report of a traumatic superior cerebellar artery aneurysm in which the diagnosis was suggested by computed tomographic scan. The potential for a good outcome suggests the value of early angiography when the history and diagnostic imaging studies suggest the possibility of a traumatic aneurysm.

Management of thoracolumbar fractures with accompanying neurological injury.

The optimal surgical approach for spinal canal reconstruction of thoracolumbar fractures is controversial, and the relationship between spinal canal reconstruction and neurological recovery remains unclear. To address these issues, 22 consecutive cases of thoracolumbar fracture with accompanying neurological deficit were reviewed. Neurological status was graded at the time of admission, postoperatively, and at a mean of 15 months postinjury. By using preoperative and postoperative radiographs and computed tomographic scans, the degree of spinal canal compromise was quantified in the sagittal, coronal, and axial planes. All fractures were stabilized by posterior instrumentation and fusion, and in 10 injuries, retropulsed vertebral body fragments were further reduced by posterolateral decompression. Spinal canal dimensions, neurological function, and operative approach were compared by using nonparametric statistical analysis. The greater the initial spinal canal compromise, the more severe the neurological deficit (P = 0.04). With injuries involving L1 and above, this relationship increased (P = 0.003). The extent of spinal canal reconstruction failed to correlate with neurological recovery. Compared with spinal instrumentation alone, transpedicular decompression showed no benefit in terms of postoperative canal dimensions or neurological outcome. On the basis of this experience, transpedicular decompression offers no advantage over spinal instrumentation alone. The relationship between initial spinal canal encroachment and neurological deficit demonstrates that the degrees of bony and neurological injury directly reflect the kinetic energy transferred at the time of impact. The lack of correlation between the extent of spinal canal reconstruction and neurological recovery suggests that ongoing neural compression/distortion contributes little to the overall neurological injury.

Effect of lidocaine treatment on acute spinal cord injury.

The effect of continuous infusion of lidocaine on acute spinal cord trauma in cats was studied. Intravenous and subarachnoid administration of lidocaine did not alter generation and conduction of the spinal evoked responses (SERs) in intact animals. The cortical somatosensory evoked responses and SERs were abolished after weight drop injuries of 120 and 400 g-cm. No return of the evoked responses occurred within 4 hours after trauma in either the lidocaine- or the saline-treated groups. Loss of SERs and appearance of an evoked injury potential were sensitive determinants of spinal cord injury. We concluded that lidocaine treatment did not facilitate the return of spinal cord function in this model of acute spinal cord injury.

Early decompression and neurological outcome in acute cervical spinal cord injuries.

To evaluate the effect on neurological outcome of spinal core compression persisting after a closed injury, the authors reviewed 44 of 62 consecutively managed cases of cervical spinal cord and spine injuries at C3-7, inclusive. Decompression within 48 hours of injury confirmed by myelography or open reduction. Neurological status, graded numerically on a spinal trauma scale at admission and at follow-up review (an average of 1 year +/- 2 months after admission), and precent recovery of neurological deficit were compared to canal narrowing (22 severe, greater than or equal to 30%, versus 22 moderate, 11% to 29%; or mild, less than or equal to 10%) and to delay before treatment (30 within 8 hours of injury versus 14 treated 9 to 48 hours after injury). Severe narrowing was equated with compression. Status at admission and at follow-up review was positively correlated. Patients with admission scores of less than 2 recovered a mean of 15% of their deficit, while those with scores more than 2 recovered a mean of 77%. Admission status correlated significantly with spinal canal narrowing but not with vertebral body displacement. Time of treatment had no significant effect upon admission status and percent recovery. No significant difference in the percent of recovery was noted, whether decompression was early (up to 8 hours) or late (9 to 48 hours) after injury. Surgery did not significantly alter the percent of recovery. The findings indicate that the initial injury to the cervical spinal cord and spine remains the primary determinant of neurological outcome. Severe canal narrowing with cord compression thereafter appears to have comparatively little effect. The conclusion that decompression is without effect is not possible without comparison with a group of patients whose spinal canals remained narrowed at follow-up review.

Effect of trauma dose on spinal cord edema.

The spinal cord of anesthetized cats was subjected to impact trauma of different intensities to determine how changes in trauma magnitude affect the formation and distribution of edema. All animals underwent a laminectomy to expose the cord segments corresponding to the T5--7 vertebrae. Fourteen cats were injected with fluorescein-labeled albumin, and then subjected to 260, 360, 500, or 700 gm-cm injury to the spinal cord. They were sacrificed at 8 hours after trauma. Twelve cats were injected with fluorescein-labeled dextrans of 20,000, 40,000, 70,000, or 150,000 molecular weight (MW) prior to 500 gm-cm injury, and sacrificed 8 hours after trauma. Serial cord sections from both groups were studied by fluorescence microscopy. In nine cats, sections of cord were removed 8 hours after trauma of 260, 360, or 500 gm-cm impact, and 1-cm sections were assayed for dry weight. Extravasated tracers were present in areas of hemorrhage at the site of impact in all animals. Extension of tracers and increases in tissue water rostrally and caudally from the site of impact were observed consistently with time only in animals receiving 500 or 700 gm-cm trauma. The distance of migration was similar for all tracers. The longitudinal distribution of increased tissue water was consistent with the distribution of fluorescein markers. The findings indicate that the longitudinal extension of posttraumatic edema is directly related to the amount of initial trauma.

Intracranial pressure in nontraumatic ischemic and hypoxic cerebral insults.

Intracranial pressure (ICP) and cerebral perfusion pressure were monitored in 12 patients who were comatose secondary to hypoxic (five cases) or hypotensive (seven cases) nontraumatic cerebral insults. Patients who were hypotensive but not hypoxic developed significant increased ICP. In patients who were comatose from hypoxic cerebral insults without hypotension, ICP was normal. When an increase in ICP was diagnosed, patients were managed aggressively so as to improve cerebral perfusion and lower ICP. Although a functional salvage rate of 25% was obtained, this may reflect the severity of the initial cerebral insult rather than the effect of treatment. In order to prevent the potential deleterious effects of raised ICP, it is concluded that monitoring ICP and maintaining adequate perfusion may be warranted in comatose patients who have suffered nontraumatic diffuse ischemic but not purely hypoxic cerebral insults.

Digital angiographic quantification of blood flow dynamics in embolic stroke treated with tissue-type plasminogen activator.

Computer analysis of digital subtraction angiography (DSA) was utilized to quantify the effectiveness of tissue-type plasminogen activator (TPA) in a rabbit cerebroembolic stroke model. Fourteen animals underwent cannulation of the facial artery and a preembolus angiogram. Autologous blood clots were then injected, and occlusion of the internal carotid artery at the circle of Willis was documented with repeat angiogram. The experimental group received a 1-mg/kg intravenous infusion of TPA via a femoral catheter for 90 minutes. A control group received an equivalent volume of saline. Follow-up angiograms were performed every 15 minutes. The TPA-treated animals showed progressive improvement in flow through previously occluded vessels. Time-density curves of the contrast material over the middle cerebral artery trunk and brain parenchyma were generated. The best integrated curves for the two groups were compared at 30 minutes after occlusion and 90 minutes after treatment. Animals were then observed for 24 hours and their neurological status was documented. Premortem infusion of either Evans blue dye or neutral red dye was performed and the integrity of the blood-brain barrier and tissue perfusion were assessed by video planometry. Significant improvements were noted by DSA, and Evans blue and neutral red dye studies in animals treated with TPA.

The microvasculature in transitory traumatic paraplegia. An electron microscopic study in the monkey.

Fine structural alterations in the microvasculature, primarily of the gray matter, occur as one aspect of experimental spinal cord contusion. A force of 300 gm-cm, shown by the authors to produce a transitory paraplegia, was applied to the T-10 level of exposed primate spinal cord. At 5 min post-contusion, the muscular venules of the central gray matter were distended with erythrocytes. Erythrocytes were seen within the perivascular spaces of the post-capillary venules and muscular venules at 15 and 30 min post-contusion, and there was hemorrhage into the gray matter at 1 hour post-contusion. The appearance of erythrocytes within the perivenular spaces was apparently due to small ruptures in the walls of the muscular venules, which were first demonstrated by electron microscopy 15 min after contusion. Alterations in capillary and post-capillary venule endothelium of both gray and white matter were present at 4 hours post-contusion and consisted of vacuolation and endothelial swelling. In conclusion, following experimental contusion of the spinal cord sufficient to cause a transitory paraplegia, the principal changes were early perivascular and parenchymal hemorrhages followed by later evidence of ischemic endothelial injury in the microvasculature.

Histopathology of transitory traumatic paraplegia in the monkey.

The microscopic appearance of the primate spinal cord within a 4-hour interval following the delivery of a direct force sufficient to produce a transitory paraplegia was investigated by light microscopy. The resulting hemorrhagic lesion involved primarily the central gray matter and was attributed to the direct effect of the trauma on the vessels in the gray matter with a consequent impairment of blood supply to the injured area. Chromatolysis, vacuolation, and alterations in cytoplasmic density and stainability were observed within the neurons. The edematous changes in the white matter, which were more marked in the internal layers relative to the external layers, appeared minimal and explain in part why the paraplegia was transient.

A scale for evaluation of spinal cord injury.

A scale has been developed for assessment of the severity of spinal cord injury and the prognosis for recovery. Based on neurological examination, this scale employs numerical grading of selected functions below the level of the injury. The scale is adaptable to prospective as well as retrospective studies, and provides a reliable estimation of prognosis and, therefore, a means of comparing the effectiveness of differing treatment modalities. In relation to a group of 37 patients with cervical spinal cord injury treated under one protocol and assessed within 24 hours and again at 1 year from injury, a descriptive model of the patterns of recovery has been obtained. Relative recovery of the initial deficit measured as a "percentage recovery ratio" is presented as an analytical tool for comparison of effectiveness of different methods of therapy.

Pathological changes from acute to chronic in experimental spinal cord trauma.

The pathological changes occurring in the thoracic spinal cords of 41 cats were studied by light microscopy at 4 hours, 4 weeks, and 4 months after graded transdural trauma. Alterations characteristic of a vascular injury proportionate to the magnitude of the original trauma which results in tissue hypoxia, destruction, and reparation were identified at each interval studied. In more severely injured animals these changes consisted of an initial hemorrhagic infarction followed by the removal of necrotic parenchyma and the development of an adhesive arachnoiditis and intramedullary carvitation. A comparison of the findings in the present investigation with what has been described in postmortem studies of spinal cord injured patients indicates that the response of the spinal cord to non-disruptive trauma is similar in both cases.

Cell-mediated immunity in severely head-injured patients: the role of suppressor lymphocytes and serum factors.

Severe head injury results in suppression of cellular immunity associated with defective in vitro functioning of effector lymphocytes, such as helper T cells and cytotoxic T cells. It is not known whether this suppression in effector lymphocyte function is due to intrinsic lymphocyte dysfunction, to suppressor peripheral blood mononuclear cells (PBMC's) such as suppressor lymphocytes or suppressor monocytes, or to serum factors capable of inhibiting effector lymphocyte function. The purpose of this study was to determine whether a subpopulation of PBMC's and/or serum factor(s) are responsible for this observed suppression in cell-mediated immunity. Cell-mediated immune activity was determined measuring in vitro lymphokine-activated killer (LAK) cytotoxicity following incubation of PBMC's from 15 head-injured patients with those from 15 heterologous normal subjects. The PBMC's were separated into lymphocyte-enriched and monocyte-enriched subpopulations by plastic adherence techniques, and the effect of each population on LAK cytotoxicity was determined. Additionally, the effect on cytotoxicity of serum from the head-injured patients was determined in a dose-response fashion. There was significant depression in LAK cytotoxicity when: 1) PBMC's from normal subjects were incubated with PBMC's from head-injured patients (p < 0.001); 2) lymphocytes (PBMC's depleted of monocytes) from head-injured patients were incubated with PBMC's from normal subjects (p < 0.001); and 3) PBMC's from normal subjects were incubated with serum from head-injured patients (p < 0.001). No suppression in cellular immunity was noted when lymphocytes from normal subjects were incubated with monocytes from head-injured patients. The results indicate that lymphocytes rather than monocytes actively inhibit cellular immunity following severe head injury. The detection of immunosuppressive serum factors suggests a mechanism by which lymphocytes might be modulated by severe head injury.

Impairment of helper T-cell function and lymphokine-activated killer cytotoxicity following severe head injury.

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-gamma), 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 phytohemagglutin (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-gamma and IL-2 by PHA-stimulated PBL's was maximally depressed within 24 hours of injury (p less than 0.001 for INF-gamma, 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 less than 0.001) incubation of PBL's with IL-2. The results of this study indicate that IL-2 and INF-gamma production, normally required for inducing cell-mediated immunity, is suppressed following severe head injury. The failure of IL-2 to enhance LAK cell cytotoxicity suggest 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.