Journal of neurotrauma
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Journal of neurotrauma · Aug 2001
Intrathecal levels of complement-derived soluble membrane attack complex (sC5b-9) correlate with blood-brain barrier dysfunction in patients with traumatic brain injury.
It has become evident in recent years that intracranial inflammation after traumatic brain injury (TBI) is, at least in part, mediated by activation of the complement system. However, most conclusions have been drawn from experimental studies, and the intrathecal activation of the complement cascade after TBI has not yet been demonstrated in humans. In the present study, we analyzed the levels of the soluble terminal complement complex sC5b-9 by ELISA in ventricular cerebrospinal fluid (CSF) of patients with severe TBI (n = 11) for up to 10 days after trauma. ⋯ The analysis of the extent of posttraumatic blood-brain barrier (BBB) dysfunction, as determined by CSF/serum albumin quotient (Q(A)), revealed that patients with a moderate to severe BBB impairment (mean Q(A) > 0.01) had significantly higher intrathecal sC5b-9 levels as compared to patients with normal BBB function (mean Q(A) < 0.007; p < 0.0001). In addition, a significant correlation between the individual daily Q(A) values and the corresponding sC5b-9 CSF levels was detected in 8 of 11 patients (r = 0.72-0.998; p < 0.05). These data demonstrate for the first time that terminal pathway complement activation occurs after head injury and suggest a possible pathophysiological role of complement with regard to posttraumatic BBB dysfunction.
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Journal of neurotrauma · Jul 2001
Case ReportsDelayed hemispheric neuronal loss in severely head-injured patients.
Recent experimental studies have revealed that traumatic brain injury as well as ischemic brain injury can cause chronic progressive neuronal damage. In the present study, we demonstrate previously unreported delayed cerebral atrophy on computerized tomography (CT) scans in severely head-injured patients. Seventeen severely head-injured patients who required mild hypothermia to control intracranial hypertension after the failure of conventional therapies were retrospectively analyzed. ⋯ Six of these eight patients with DNL achieved functional recovery despite progressive atrophic changes demonstrated on CT scans. On CT scans, DNL was characterized by (1) the sudden appearance at several months postinjury of a low-density area in the hemisphere ipsilateral to the injury; (2) the preservation of essential cortical structure although related white matter structures showed severe atrophic changes; and (3) no spread of the low-density area to the contiguous territory of the other main cerebral artery. It is concluded that focal primary injury to underlying brain, if severe enough, can result in delayed hemispheric atrophy.
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Journal of neurotrauma · Jul 2001
Evaluation of the traumatic coma data bank computed tomography classification for severe head injury.
This study determines the interrater and intrarater reliability of the Traumatic Coma Data Bank (TCDB) computed tomography (CT) scan classification for severe head injury. This classification grades the severity of the injury as follows: I = normal, II = diffuse injury, III = diffuse injury with swelling, IV = diffuse injury with shift, V = mass lesion surgically evacuated, or VI = mass lesion not operated. Patients with severe closed head injury were included. ⋯ Glasgow outcome scores after 6 months were as follows: 19 dead (30%), one vegetative (2%), five severely disabled (8%), 17 moderately disabled (27%), and 21 good recovery (33%). Association measures (Sommers' D) between CT and GOS scores were statistically significant for all observers. This study shows a high intra- and interobserver agreement in the assessment of CT scan abnormalities and confirms the predictive power on outcome when the TCDB classification is used.
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Journal of neurotrauma · Jun 2001
Clinical TrialBedside monitoring of cerebral blood flow by transcranial thermo-dye-dilution technique in patients suffering from severe traumatic brain injury or subarachnoid hemorrhage.
Bedside measurement of cerebral blood flow (CBF) represents an important feature in monitoring of neurointensive care patients which is hard to establish. Therefore, we adopted a recently described thermo-dye-dilution-based approach for monitoring CBF in patients suffering from severe cerebral insults, that is, traumatic brain injury (TBI) or subarachnoid hemorrhage (SAH). Combined fiberoptic-thermistor catheters were placed in one jugular venous bulb and in the abdominal aorta of 16 patients. ⋯ The thermo-dye-dilution method proved a reasonably reproducible technique, enabling repeated long-term bedside measurements of CBF in neurointensive care patients with a minimum of time effort. However, a high failure rate was also noted, and consistent overestimation of perfusion was observed in comparison to sXe-CT measurements. Although the thermo-dye-dilution technique has been successfully validated in patients with normal neurovascular function, its applicability for bedside monitoring of CBF appears uncertain in patients suffering from severe TBI or SAH.
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Journal of neurotrauma · Jun 2001
Age-Dependent vasopressinergic modulation of Noc/oFQ-induced impairment of NMDA cerebrovasodilation after brain injury.
This study was designed to characterize the role of vasopressin in nociceptin/orphanin FQ (NOC/oFQ)-induced impairment of NMDA cerebrovasodilation after fluid percussion brain injury (FPI) as a function of age in newborn (1-5 days old) and juvenile (3-4 weeks old) pigs equipped with a closed cranial window. Previous studies have observed that NOC/oFQ is released into CSF and contributes to impaired NMDA induced pial artery dilation following FPI to a greater extent in newborn versus juvenile pigs. Topical vasopressin (40 pg/mL), a concentration approximating that observed in CSF following FPI in the newborn, increased CSF NOC/oFQ from 69 +/- 3 to 102 +/- 8 pg/mol under non-FPI conditions. ⋯ The greater release of vasopressin following FPI in the newborn contributes to the corresponding greater release of NOC/oFQ in the newborn versus the juvenile. Moreover, vasopressin also contributes to the impairment of NMDA cerebrovasodilation after brain injury to a greater extent in newborn versus juveniles. These data suggest that vasopressin modulates NOC/oFQ-induced impairment of NMDA cerebrovasodilation after brain injury in an age-dependent manner.