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PubMed1998

The effect of human corticotrophin releasing factor on the formation of post-traumatic cerebral edema.

Controlled cortical impact is a well validated model of cortical contusion which is known to produce cerebral edema. Corticotrophin Releasing Factor (CRF) is a hypothalamic neuropeptide, which is known to inhibit transendothelial leakage of plasma derived fluid and tissue edema in response to injury. The aim of this study was to determine cerebral edema after controlled cortical impact and then compare the effect of high and low doses of CRF. We evaluated the effect of CRF in rats divided into groups of sham, trauma alone, and trauma treated with CRF at 50 micrograms/kg and 100 micrograms/kg. Animals were sacrificed at 24 hours and water content was determined. We found that CRF was effective in reducing cerebral edema associated with cortical contusion and propose that the action of CRF obviated barrier leakage.

Animals↗
PubMed1998

Brain ischemia detected by tissue-PO2 measurement and the lactate-oxygen index in head injury.

The aim of the study was to find out whether there is a correlation between the tissue-pO2 (ti-pO2) measurement and the lactate-oxygen index (mLOI). Both methods are to be considered as methods to detect brain ischemia. We studied 7 patients after severe head injury (GCS < 8) with a jugular bulb catheter and a tissue pO2 probe. Possible ischemia was defined with ti-pO2 below 10 mm Hg and mLOI above 0.08. 67 pairs of ti-pO2 and corresponding mLOI were found. In 5 cases out of the 7 cases with a ti-pO2 below 10 we found a pathological mLOI above 0.08. In 11 cases with pathological mLOI values, however, we found only 6 cases of decreased ti-pO2. The absolute values did not correlate. The sensitivity to predict normal values is above 85% with both methods. The specifity to predict ischemia is low (< 72%). The reason is the fact, that ti-pO2 is a local method in contrast to the mLOI values. In cases of diffuse brain injury without major contusions there should be a correlation between ti-pO2 and the mLOI.

Brain↗
PubMed1998

Cerebral oxygenation in contusioned vs. nonlesioned brain tissue: monitoring of PtiO2 with Licox and Paratrend.

Brain tissue PO2 in severely head injured patients was monitored in parallel with two different PO2-microsensors (Licox and Paratrend). Three different locations of sensor placement were chosen: (1) both catheters into non lesioned tissue (n = 3), (2) both catheters into contusioned tissue (n = 2), and (3) one catheter (Licox) into pericontusional versus one catheter (Paratrend) into non lesioned brain tissue (n = 2). Mean duration of PtiO2-monitoring with both microsensors in parallel was 68.1 hours. Brain tissue PO2 varied when measured in lesioned and nonlesioned tissue. In non lesioned tissue both catheters closely correlated (delta Licox/Paratrend: mean PtiO2 < 5 mm Hg) after 20 hours post insertion. In pericontusional tissue PtiO2 was reduced relative to non lesioned tissue (delta lesioned/non lesioned: mean PtiO2: 10.3 mm Hg). In contusioned brain tissue PtiO2 was always below the "hypoxic threshold" of 10 mm Hg, independent of the type of microsensor used. During a critical reduction in cerebral perfusion pressure (< 60 mm Hg), PtiO2 decreased measured with both microsensors. Elevation of inspired oxygen fraction, normally followed by a rapid increase in tissue PO2, only increased PtiO2 when measured in pericontusional and nonlesioned brain. To recognize critical episodes of hypoxia or ischemia, PtiO2-monitoring of cerebral oxygenation is recommended in nonlesioned brain tissue.

Adult↗
PubMed1998

Cortical extracellular sodium transients after human head injury: an indicator of secondary brain damage?

Animal studies indicate that elevated extracellular sodium can increase glutamate-induced excitotoxicity. Therefore, we investigated the relationship between sodium and glutamate and the effect of changes in sodium concentrations on the outcome of head-injured patients. Thirty-four (34) patients were selected for this study and divided into a group of patients having episodes (> or = 30-min) of high sodium in dialysates (> or = 200 mM; HIGH, n = 11) and a group of patients having no such episodes (NORMAL, n = 23). Levels for sodium (226 +/- 5.7 mM), glutamate (12.53 +/- 2.2 microM) and ICP (32.2 +/- 4.0 mm Hg,) were relatively high during the high sodium episodes. Overall, mean values for glutamate, ICP and outcome did not differ amono both groups. The mean dialysate sodium concentration, however, was significantly higher in the HIGH (178 +/- 6 mM) compared to the NORMAL group (158 +/- 3 mM; p < 0.01). Spearman rank correlation between sodium and glutamate or ICP were not significant. The HIGH sodium group did not have significantly more patients with poor outcome than the NORMAL group. The results indicated sodium concentrations did not affect the outcome of head-injured patients. However, other sodium monitoring techniques are desirable to elucidate these apparent potentially major sodium transients, which we have observed in the human cortex, after severe head injury.

Adult↗
PubMed1998

Indices for decreased cerebral blood flow control--a modelling study.

Time-dependent interactions between pressure, flow and volume of cerebral blood and cerebrospinal fluid were mathematically modelled. The model was designed to simulate blood inflow and storage, arteriolar and capillary blood circulation controlled by cerebral autoregulation, venous blood outflow and storage modulated by intracranial pressure, and cerebrospinal fluid production, storage and reabsorption. The software implementation of the model was used to calculate the response to a gradual decrease in cerebral perfusion pressure corresponding to either systemic hypotension or intracranial hypertension. We computed flow pulsatility index (PI) and short range correlation coefficients between systolic, diastolic and mean flow velocity (FVs,d,m) and mean cerebral perfusion pressure (CPP). In simulation, the changes in cerebral flow produced by intracranial hypertension and systemic hypotension were practically indistinguishable. The relationship between PI and CPP was reciprocal, independent of the state of autoregulation. The short range running correlation coefficients between FVs, FVm and CPP indicated both combined safe CPP range and preserved autoregulation, promising a clear clinical detection of "non-worsening" blood supply conditions. A similar procedure was applied to selected clinical data to illustrate the theoretical considerations.

Adolescent↗
PubMed1998

Incidence of intracranial hypertension after severe head injury: a prospective study using the Traumatic Coma Data Bank classification.

UNLABELLED: Intracranial hypertension (ICH) is a frequent finding in patients with a severe head injury. High intracranial pressure (ICP) has been associated with certain computerized tomography (CT) abnormalities. The classification proposed by Marshall et al. based on CT scan findings, uses the status of the mesencephalic cisterns, the degree of midline shift, and the presence or absence of focal lesions to categorize the patients into different prognostic groups. Our aim in this study was to analyze the ICP evolution pattern in the different groups of lesions of this classification. PATIENTS AND METHODS: We present the results of a prospective study in 94 patients with severe head injury, in whom ICP was monitored for at least 6 hours. ICP evolution was classified into three different categories: 1) ICP always < 20 mm Hg, 2) Intracranial hypertension at some time during monitoring, but controlled by medical or surgical treatment, 3) Uncontrollable ICP. The ICP pattern was correlated with the final CT diagnostic category. CONCLUSIONS: 3 patients had a normal CT scan, and none of them presented intracranial hypertension. In diffuse injury type II, the ICP evolution may be quite different. Patients with bilateral brain swelling (Diffuse Injury III) have a high risk of increased ICP (63.2%). Although in our study the frequency of Diffuse Injury IV was low, all patients in this category had a refractory ICP. In the category of evacuated mass lesions, two thirds of the patients presented an intracranial hypertension. In one third, ICP was refractory to treatment. 85% of patients with a non-evacuated mass lesion showed an increased ICP.

Adult↗
PubMed1998

Pathogenesis of the mass effect of cerebral contusions: rapid increase in osmolality within the contusion necrosis.

The non-hemorrhagic mass effect of cerebral contusions is commonly attributed to vasogenic edema and/or cytotoxic edema (cellular swelling). We propose that a marked increase in osmolality within the contusion necrosis proper, in which the cellular elements uniformly undergo shrinkage, disintegration and homogenation, represents an important and unique mechanism underlying the contusion edema. The present study demonstrates in a rat model of cerebral contusion, that 1) the osmolality of the contused brain tissue increases rapidly, 2) the increase in osmolality is not caused by changes in inorganic ion contents, suggesting a metabolic production of osmoles or release of idiogenic osmoles, and 3) the contused brain tissue strongly attracts water, provided that blood supply is maintained. We suggest that the primary driving force of water accumulation into contused brain tissue is the elevated colloid osmotic potential of contusion necrosis.

Animals↗
PubMed1998

Magnetic resonance imaging studies with cluster algorithm for characterization of brain edema after controlled cortical impact injury (CCII).

Objective of this study was the characterization of traumatic brain injury induced by a "Controlled Cortical Impact" with magnetic resonance imaging techniques. The impact was applied to the intact dura of the left hemisphere in Sprague-Dawley rats. The pneumatic impactor was accelerated to a velocity of 7 m/s contusing the left temporo-parietal hemisphere to a depth of 2 mm. Posttraumatic hemispheric swelling and water content were determined gravimetrically, Evans Blue extravasation photometrically, and volume of ischemia by TTC-staining and planimetry. Magnetic resonance imaging was performed by a Bruker biospec 24/40, 90 min, 24 and 72 h post trauma using a T2w RARE sequence, a T1w sequence, before and after application of contrast agent, and a set of diffusion weighted images for calculation of ADC-maps. Data analysis was performed using a cluster algorithm enabling to interpret corresponding image pairs simultaneously. T2w imaging indicates the maximum edema about 24 h post trauma. Blood-brain barrier damage, detected by T1w imaging, is more predominant in the early posttraumatic phase. The cluster algorithm detects different edema components: from the necrotic core to the perifocal vasogenic rim. MRI in combination with the cluster algorithm will hopefully be a valuable tool in testing neuroprotective agents.

Animals↗
PubMed2002

Mechanisms of the mass effect of cerebral contusion: ICP monitoring and diffusion MRI study.

OBJECTIVE: Cerebral contusion is sometimes associated with a non-hemorrhagic mass effect which progresses rapidly within 12-48 hours post-trauma. In order to determine the mechanisms underlying such a mass effect, we analyzed data obtained from ICP monitoring and diffusion MRI in a total of 38 patients with cerebral contusion. METHODS: Diffusion imaging and ADC mapping were performed employing 1.5 T echo planar MRI. ADC values were expressed as a ratio relative to the values of intact brain areas. RESULTS: In 6 patients, ICP became uncontrollable medically and surgical resection of the contused brain tissue was eventually performed. Within 24 hours post-trauma, diffusion images revealed a low intensity core and a high intensity rim in the contusion. The ADC ratio increased in the central area (1.13 +/- 0.21) and decreased in the peripheral area (0.67 +/- 0.14). A crescent-shaped zone of very high ADC ratio (1.45 +/- 0.14) was observed at the border between these two areas during the period of 24-48 hours. CONCLUSIONS: It appears that the capacitance of edema fluid accumulation is elevated by cellular disintegration in the central area, whereas the resistance to edema fluid propagation is elevated by cellular swelling in the peripheral area. We suggest that such events facilitate extracellular edema fluid accumulation within contused brain tissue and contribute, together with cellular swelling itself, to the non-hemorrhagic mass effect of cerebral contusion.

Brain Concussion↗
PubMed2002

Experimental models of head trauma.

Traumatic brain injury is one of the most common causes for chronic disability in young people. Despite this there are currently no widely available modes of therapy that would limit the extent of brain damage secondary to trauma. Therefore, new insights into the pathological mechanisms involved in head trauma possibly leading to the identification of new therapeutic targets are urgently needed. In order to attain these goals adequate animal models for traumatic brain injury are needed. In the following paper the authors will review the various animal models for head trauma and emphasize their potential strengths and weaknesses.

Animals↗
PubMed1997

Antioxidant, OPC-14117, attenuates edema formation and behavioral deficits following cortical contusion in rats.

Oxygen free radicals may contribute to tissue injury processes in the central nervous system following ischemia or trauma. Recent studies have suggested that inhibition of free radicals improves the outcome in experimental models involving such conditions, and antioxidant therapy appears promising. In the present study, behavioral changes and edema formation in rat cortical contusion model were investigated, and the effects of a superoxide radical scavenger, OPC-14117, were tested. Wistar rats were anesthetized with halothane inhalation. Cortical contusion was induced in the parietal cortex employing a controlled cortical impact device. Immediately following injury induction, OPC-14117 was administered (300 mg/kg, p.o.). Edema formation was assessed in the center and peripheral areas of the contusion by the specific gravity method. Behavioral changes were evaluated by the Morris water maze test and the habituation of exploratory activity. The results revealed that the vehicle-administered control showed progressive edema formation and behavioral deficits following the injury. These changes were significantly attenuated by the OPC-14117 treatment (p < 0.05). Further, OPC-14117 reduced the size of contusional necrosis (p < 0.05). These findings suggest that superoxide free radicals are involved in contusion-induced edema formation, necrosis formation, and behavioral deficits, and that OPC-14117 has a therapeutic potential to prevent secondary cell damage following traumatic brain injury.

Animals↗
PubMed1986

Aspects on pathology and neuropathology in head injury.

Some principal differences of the head injury materal available to clinicians, hospital pathologists and forensic pathologists are discussed with reference to the primary and secondary findings at focal and diffuse brain injury and intracranial injuries after trauma. The importance of cooperative understanding between the different disciplines is stressed in order to cover the whole head injury pattern. Examples are given. The importance of intracranial arterial hemorrhages is stressed and may also be the cause of a particular group of acute subdural hematomas; it may be of special prognostic importance because of their probable availability to successful surgery in the acute stage. The cause may be a tearing of arterial connections between the peripheral branches of the middle cerebral artery and the dura. The diagnosis of different types of primary diffuse brain injury is discussed with particular reference to the non-satisfactory common histological methods of investigation early after trauma. Diffuse brain injury due to hypoxia at the trauma can be serious but give few macroscopical findings; disseminated intravasal coagulation can appear isolated in the brain or be part of a systemic manifestation.

Brain↗
PubMed1990

Posttraumatic epilepsy. Incidence and prophylaxis.

A detailed review, based on the literature and the author's own series, is given of the incidence of both early and late epilepsy following head injury related to age, severity and other specific features of the injury and clinical sequelae. Use of prophylactic anti-convulsant therapy, following head injury, remains controversial despite positive results of animal experiments. Hence, the author recommends that antiepileptic medication should be restricted to patients who have had at least two epileptic fits during the first two years after injury.

Anticonvulsants↗
PubMed1990

Controversies in posttraumatic epilepsy.

In civilian accidents the factors involved in the origin of posttraumatic epilepsy are controversial. In this study of 506 consecutive head trauma patients and 101 epileptic patients developing seizures after head trauma, we have examined the importance of the duration of coma, type of seizure and drug therapy, time to first seizure, age and focal lesions and compared our results with the literature. The importance is stressed of focal lesions and of neurological deficits for the origin of posttraumatic seizures.

Adolescent↗
PubMed1990

Blood-brain barrier damage in traumatic brain contusions.

Plasma proteins were used as an endogenous marker of blood-brain barrier damage in 19 patients dying with traumatic cortical contusions. Patients survived for a few hours to 31 days after head injury. Eight proteins (M WT 61-2,500 x 10(3) were demonstrated with standard immunohistochemical techniques. Proteins were not found in "control" brains or in macroscopically normal parasagittal cortex in the head injury patients. Proteins were found in all of the macroscopic contusion in all brains. Protein leakage appeared to be from the contusion itself. Protein staining around histologically normal vessels was unusual. There was a gradient of staining from the macroscopic contusion into the surrounding brain. There was a trend for staining to be most marked between 3 and 8 days survival after head injury. There was no gradient of leakage by molecular size of the protein.

Blood Proteins↗
PubMed1990

Oedema fluid formation within contused brain tissue as a cause of medically uncontrollable elevation of intracranial pressure: the role of surgical therapy.

In patients with focal cerebral contusions, medical therapies have generally been advocated unless haemorrhages significantly contributing to the elevated intracranial pressure (ICP) exist. We report here several lines of clinical evidence which indicate that (1) enormous amount of extracellular oedema fluid is formed within contused brain tissue, (2) the formation of extracellular oedema fluid within contused brain tissue alone can be a cause of medically uncontrollable elevation of ICP and (3) surgical excision of the contused brain tissue provides excellent control of the elevated ICP in such patients. The excision of contused brain tissue appears to be the only therapy currently available to alleviate the formation of extracellular oedema fluid in cerebral contusions. We believe that, if ICP is elevated primarily by extracellular oedema due to cerebral contusions and the elevated ICP is medically uncontrollable, surgical excision of contused brain tissue should be carried out without delay regardless of the size of associated haemorrhages.

Body Fluids↗
PubMed1990

The time course of vasogenic oedema after focal human head injury--evidence from SPECT mapping of blood brain barrier defects.

We have tomographically mapped changes in the blood brain barrier (BBB) (99 mTc Pertechnetate) in 20 patients with acute contusions, and four with acute subdural haematomas in situ. The changes were related to regional CBF, (99 mTc HMPAO SPECT) T2 weighted MRI scans, CT abnormalities and the clinical features. Seventy-five percent of contusions were accompanied by a BBB abnormality, usually a "halo" around the lesion, which was more common in scans made after the second day. All contusions demonstrated "oedema" as a zone of "T2" signal on MRI or a zone of lucency on CT, and all were accompanied by a focal zone of low CBF on SPECT. Early contusional oedema appears to be cytotoxic but in certain cases, delayed blood brain barrier lesions develop, suggesting a vasogenic component.

Acute Disease↗