Polymorphonuclear (PMN) elastase in patients after severe traumatic brain injury.

BACKGROUND: Data on PNM elastase levels in cerebrospinal fluid following traumatic brain injury (TBI) in humans are not available in the literature. Therefore, the aim of this prospective study was to evaluate the dynamics of PMN elastase in the cerebrospinal fluid (CSF) of patients after TBI. METHODS: Patients suffering from isolated, closed TBI, presenting with an initial Glasgow coma score ≤ 8 and with intracerebral hemorrhage on the initial cranial computed tomography scan (performed within 90 min after TBI) were enrolled. CSF and blood samples were obtained immediately, 12 h, 24 h, 48 h, and 72 h after admission. ELISA testing was used to quantify the PMN elastase levels in CSF. In addition, the ratio of CSF albumin to serum albumin was calculated to evaluate the role of the blood-cerebrospinal fluid barrier (BCSFB). As controls, CSF samples were taken from patients receiving spinal anesthesia for elective orthopedic surgery of the lower extremity. RESULTS: Twenty-three patients meeting the inclusion criteria and ten control patients were enrolled. The PMN elastase showed a significant elevation at 48 and 72 h after TBI. When comparing the PMN elastase levels of patients with intact BCSFB to patients with defective BCSFB, there was no significant difference for the respective observation points. CONCLUSIONS: This is the first study to demonstrate that the PMN elastase levels in CSF significantly increased in the early posttraumatic phase (48 h and 72 h after TBI) in patients. The function of the BCSFB showed no significant influence on the PMN levels.

Cerebrospinal s100-B: a potential marker for progressive intracranial hemorrhage in patients with severe traumatic brain injury.

OBJECTIVE: Traumatic brain injury (TBI) is associated with cerebrovascular dysfunction and changes of the blood-brain barrier (BBB) function. Although knowledge about the function of the BBB would be of high interest, non-invasive neurodiagnostic tools are still lacking. In this context it has been shown, that the astrocytic protein S100-B is a significant parameter for neuronal damage. However, there is only poor knowledge about the dynamics of S100-B in cerebrospinal fluid (CSF) and serum of patients with severe TBI. Therefore, the aim of this study was to analyze intrathecal and systemic concentrations of S100-B in patients with severe TBI in correlation to the development of progressive intracranial hemorrhage (PIH) as well as to the CSF/serum albumin ratio (Q subsetalb), as functional parameter of the BBB. PATIENTS AND METHODS: In patients, suffering from severe TBI (GCS =or<8pts) and respectively healthy control patients, albumin for calculating the CSF/serum albumin ratio (Q subsetalb) as well as S100-B protein were analyzed in CSF and serum. Samples were collected immediately after placement of a ventricular catheter and 12h, 24h, 48 h and 72 h after TBI. S100-B was quantified using Elecsys S-100 superset assay (Roche superset Diagnostics; Mannheim, Germany). Volume measurements of focal mass lesions based on CT images taken during the first 72 h after TBI were obtained according to the Cavalieri's Direct Estimator method. RESULTS: 21 TBI-patients and respectively 10 healthy controls were enrolled. In patients exhibiting a mean ICP >15 mmHg (n = 15) CSF levels of S100-B were significantly increased on admission (819 +/- 78 pg/ml) compared to patients with ICP =or<15 mmHg (n = 6, 175 +/- 12 pg/ml) as well as to the control group (n = 10, 0.8 +/- 0.09 pg/ml). In the group with ICP >15 mmHg 8 patients developed PIH A positive correlation was found between CSF S100-B and ICP (r2 = 0.925, p<0.001). Furthermore a positive correlation between serum S100-B and Q subsetalb was found for each sampling point (r superset2 = 0.793, p<0.001). CONCLUSIONS: The cerebrospinal and serum concentration of S100-B in patients with severe TBI was evaluated. Monitoring cerebrospinal S100-B might help to prospectively identify patients with PIH.

[Changes in regional meningeal immunity in local immunomodulating therapy in patients with acute traumatic intracranial hematomas].

A clinicomorphological study of 660 patients with acute traumatic intracranial hematomas has shown that pneummonia develops in 56% of cases, intracranial complications (purulent meningitis) in 14%.Pyoinflammatory complications were 1.5-1.7 times less common in small-sized hematomas, their total rate and the rate of pneumonias was twice higher in left cerebral hemispheric lesion. On the contrary, intracranial complications were twice more common in right cerebral hemispheric lesion. The structural bases of the regional meningeal immunity system were as follows: the pathways of blood and spinal fluid circulation and dural arachnoidal intercellular fluid; cellular cooperation of the meninx and tissue of the brain; the network of lymph vessels of the dura mater encephali and adventitia of large blood vessels and middle and inferior jugular (regional) lymph nodes. Morphodunctional changes in the local meningeal immunity system in patients with hematomas point to the development of secondary immunodeficiency. Inclusion of regional immunotherapy with T-activin into multimodality treatment decreases the incidence of extra- and intracranial pyoinflammatory complications and mortality.