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At least 433 records · Page 24Linked to original sources
PubMed1996

Progesterone rapidly decreases brain edema: treatment delayed up to 24 hours is still effective.

Cerebral edema is a serious side effect of traumatic brain injury. We have previously established that progesterone injections, initiated within 1 h after cortical contusion injury, reduced edema when assessed 3 days later. To determine how rapidly progesterone can reduce edema, male and female rats were given the hormone 1 h after damage to the medial frontal cortex, and edema levels were assessed between 2 h and 7 days postinjury. Progesterone decreased edema with 6 h of the injury and continued to be effective for the duration of treatment. In addition, we assessed whether progesterone injections are effective when delays are imposed between injury and initiation of treatment. Male and female rats received progesterone after postinjury delays 6, 24, or 48 h. Progesterone was effective in reducing edema when treatment was delayed until 24 h after injury.

Animals↗
PubMed2001

Differential working memory load effects after mild traumatic brain injury.

The objective of this study was to explore the effects of increasing working memory (WM) processing load on previously observed abnormalities in activation of WM circuitry shortly after mild traumatic brain injury (MTBI). Brain activation patterns in response to increasing WM processing load (auditory n-back: 0-, 1-, 2-, and 3-back conditions) were assessed with fMRI in 18 MTBI patients within 1 month of their injury and in 12 healthy controls. Performance accuracy on these tasks was also measured. Brain activation patterns differed between MTBI patients and controls in response to increasing WM processing loads. Controls maintained their ability to increase activation in regions of WM circuitry with each increase in WM processing load. MTBI patients showed disproportionately increased activation during the moderate processing load condition, but very little increase in activation associated with the highest processing load condition. Task performance did not differ significantly between groups on any task condition. MTBI patients showed a different pattern of allocation of processing resources associated with a high processing load condition compared to healthy controls, despite similar task performance. This suggests that injury-related changes in ability to activate or modulate WM processing resources might underlie some of the memory complaints after MTBI.

Adolescent↗
PubMed1983

Oxygen radicals and vascular damage.

The effects of topical application of agents which produce oxygen radicals on cerebral arterioles were studied in anesthetized cats. Xanthine oxidase plus xanthine, which produced superoxide anion radical, hydrogen peroxide, and hydrogen peroxide plus ferrous sulfate, which produced the free hydroxyl radical, induced sustained dilation, reduced responsiveness to the vasoconstrictor effect of hypocapnia, and destructive lesions of the endothelium and of the vascular smooth muscle. Similar effects were produced by arachidonate, 15-HPETE, and PGG2. The effect of arachidonate was inhibited by mannitol, a free hydroxyl radical scavenger, the effect of PGG2 was inhibited by SOD, the effect of 15-HPETE was inhibited by either catalase or SOD. These results suggest that these cerebral vascular abnormalities were produced by a single destructive free radical, probably the hydroxyl free radical, generated via interaction of superoxide and hydrogen peroxide. Cerebral vascular abnormalities similar to those produced by oxygen radicals were also seen after experimental concussive brain injury or after acute hypertension. After brain injury, activation of phospholipase C and increased brain prostaglandin concentration were demonstrated. The vascular effects of brain injury and acute hypertension were inhibited by free radical scavengers. The results suggest that, in these conditions, vascular damage is induced by oxygen radicals generated from arachidonate in association with increased prostaglandin synthesis.

Animals↗
PubMed1981

Acceleration induced head injury in the monkey. II. Neuropathology.

A comprehensive neuropathological study has been undertaken in 53 adult subhuman primates subjected to a single sagittal plane angular acceleration impulse. The types of injury produced correlated well with the input force and were very similar to those seen in fatal nonmissile head injuries in man. There was a fracture of the skull in 14 animals. Subdural haematoma occurred in 33 animals, contusions in the frontal and temporal regions of the brain in 39, and discrete intracerebral haematoma in 4. Brain shift and tentorial herniation were also seen. There was evidence of hypoxic brain damage in 22 animals, and central chromatolysis in Betz cells and in the motor nuclei of the brain stem in 16.

Acceleration↗
PubMed1979

CKBB-isoenzymes as a sign of cerebral injury.

CKBB-isoenzymes in serum and CSF have been shown to be raised in patients after head injury with objective signs of damaged brain tissues (contusio cerebri), but not in the absence of these signs (commotio cerebri).

Brain Concussion↗
PubMed1983

Head injury in man and experimental animals: clinical aspects.

Clinical studies have demonstrated that, with regard to death, the two worst types of head injury are subdural haematoma (SDH) and diffuse axonal injury (DAI). These two have different mechanisms of causation; SDH occurs much more commonly in non-vehicular injuries, especially falls, while DAI is caused, almost exclusively by vehicular mechanisms. The production of these two types of injury in non-impact acceleration models helps to explain these causal differences, but also shows that both injuries share a common mechanical cause, differing only in degree. SDH is due to vascular injury that is caused by relatively short duration angular acceleration loading at high rates of acceleration. These are the circumstances that occur in falls where the head rapidly decelerates because of impact to firm, unyielding surfaces. DAI is also due to angular acceleration of the head, but occurs most readily when the head moves coronally and it only occurs when the acceleration duration is longer and the rate of acceleration lower than conditions that produce SDH. These conditions are met in vehicle occupants where impact to deformable or padded surfaces lengthens the deceleration and decreases its rate. In DAI the principal mechanical damage is to the brain itself (mainly to axons) while in SDH the primary damage occurs to surface blood vessels. Now that models of the two most important types of head injury have been created in the laboratory, it is hoped that a better understanding of their pathophysiology will result in new strategies to affect protection from their occurrence and in improved treatment when they do occur.

Accidents, Traffic↗
PubMed1983

Head injury in man and experimental animals: neuropathology.

All of the principal types of brain damage that occur in man as a result of a non-missile head injury, viz. cerebral contusions, intracranial haematoma, raised intracranial pressure, diffuse axonal injury, diffuse hypoxic damage, and diffuse swelling have been produced in subhuman primates subjected to inertial, i.e. non-impact, controlled angular acceleration of the head through 60 degrees in the sagittal, oblique and lateral planes.

Animals↗
PubMed2000

1H-MR spectroscopic monitoring of posttraumatic metabolism following controlled cortical impact injury: pilot study.

Proton magnetic resonance spectroscopy (1H-MRS) has been increasingly utilised in experimental traumatic brain injury for characterisation of posttraumatic metabolic dysfunction. Following human brain injury pathological findings correlated with outcome measures. Combined with conventional T2-weighted MR imaging MRS is a sensitive tool to evaluate metabolic changes in brain tissue following trauma. Studies have been restricted so far to diffuse axonal injury models and fluid percussion injury. Using a high resolution scanner at 4.7 T, MRI combined with 1H-MRS was applied in a pilot study to the controlled cortical impact injury model of experimental brain contusion (CCII). Eight Sprague-Dawley rats were investigated, of which two served as controls. Four animals were injured 24 h after craniotomy, two investigated at 72 h post craniotomy. MRS/MRI indicated a transient brain oedema development and metabolic changes induced by the craniotomy itself. Following CCII MRI demonstrated that the area of contusion as well as the surrounding brain oedema increased twofold in size within 24 h (p < 0.05). MRS showed an immediate increase of N-acetylaspartate (NAA) and glutamate ipsilateral to the contusion and a drop of NAA on the contralateral side. MRS/MRI investigations in the CCII model demonstrated a potential to further elucidate the pathophysiology following traumatic brain contusion.

Animals↗
PubMed2000

Heterogeneous mechanisms of early edema formation in cerebral contusion: diffusion MRI and ADC mapping study.

Severe cerebral contusion is sometimes associated with early edema formation within 24-48 hours post-trauma, and this frequently results in progressive ICP elevation and clinical deterioration. To investigate the underlying mechanisms of such severe contusion edema, diffusion imaging and ADC mapping were performed in 20 patients with cerebral contusion, employing 1.5 T echo planar MRI. Within 24 hours post-trauma, the diffusion images demonstrated a low intensity core in the central area and a high intensity rim in the peripheral area of contusion. The ADC value increased in the central area (ADC ratio (contusion/normal brain) = 1.13 +/- 0.13) and decreased in the peripheral area (ADC ratio = 0.83 +/- 0.13). This suggested that intra- and extracellular components underwent disintegration and homogenization within the central area, whereas cellular swelling was predominant in the peripheral area. A crescent-shaped zone of very high ADC value (ADC ratio = 1.38-1.61) was observed at the border between these two areas during the period of 24-48 hours post-trauma in some cases, apparently indicating that edema fluid was accumulated within a space formed by homogenization. The ADC values in the peripheral area shifted to an increase after 48-72 hours post-trauma. These findings imply that multiple mechanisms operate in early edema formation in cerebral contusion. It appears that the capacity for edema fluid accumulation increases in the central area and resistance for edema fluid propagation is elevated by cellular swelling in the peripheral area. We suggest that a combination of such events facilitates edema fluid accumulation in the central area and contributes, together with the cellular swelling in the peripheral area, to the mass effect of contusion edema. Diffusion MRI and ADC mapping represent powerful tools for investigating spatially as well as temporally heterogeneous mechanisms of contusion edema.

Brain↗
PubMed2000

The permissive nature of blood brain barrier (BBB) opening in edema formation following traumatic brain injury.

The contribution of blood brain barrier opening to traumatic brain edema is not known. This study compares the course of traumatic BBB disruption and edema formation, with the hypothesis that they are not obligately related. Sprague-Dawley rats were divided into three groups: Group A (n = 47)--Impact Acceleration (IAM); Group B (n = 104)--lateral cortical impact (CCI); Group C (n = 26)--IAM + hypoxia & hypotension (THH). BBB integrity was assessed using i.v. markers (Evan's Blue, or gadolinium-DTPA). Edema formation was evaluated with gravimetry, and T1-weighted MRI. In IAM, BBB opened immediately but closed rapidly, and remained closed for at least the next 36 hours whilst 24-hour hemispheric water content (HWC) rose by 0.9% (p < 0.01). In CCI, BBB opened in both hemispheres for up to 4 hours; four hour HWC in the uninjured hemisphere was indistinguishable from Sham, where HWC in the injured hemisphere rose by approximately 1.5% (p < 0.005). We distinguished two THH animals based on Apparent Diffusion Coefficient (ADC) recovery: in ADC-recovery animals 4 hour cortical water content (CWC) was 80.4 +/- 0.6%, cf 81.4 +/- 1.3% in ADC-non-recovery (p < 0.05). In all animals the BBB was open, however two populations of permeability were seen which likely related to flow-limited extravasation of gadolinium. In IAM edema forms despite only brief BBB opening. Although there is diffuse BBB opening with lateral contusion, edema only forms in the injured hemisphere. In THH, edema formation in the face of a widely permeable barrier is driven by ADC changes or cell swelling. Edema formation clearly does not correspond with BBB opening and an open BBB is clearly not required for edema formation. However we hypothesize that a permeable BBB permissively worsens the process, by acting as a low resistance pathway for ion and water movement. These findings are consistent with our general hypothesis that edema formation after TBI is mainly cytotoxic.

Animals↗
PubMed2000

Metabolic changes in pericontusional oedematous areas in mild head injury evaluated by 1H MRS.

In order to define metabolic brain changes associated with mild traumatic brain injury, proton magnetic resonance spectroscopy (MRS) was performed in patients with regional brain contusion and 13-15 of initial GCS score. The authors measured N-acetylaspartate(NAA)/creatine(Cr) ratio and lactate signal on in vivo proton MRS, which indicated cell loss and ischaemic dAmage respectively, in pericontusional oedematous areas (region of interest; ROI) adjacent to traumatic brain contusion on brain MRI to determine possible metabolic changes. The metabolic ratio of NAA/Cr and lactate/Cr peaks was measured both in the ROI and a corresponding region of the contralateral hemisphere (ROC) in seven patients and twenty-five normal control. In initial NAA/Cr ratios, the values of ROIs were significantly lower than those of the control (p = 0.009), but there was no difference either between ROI and ROC (p = 0.410) or between ROC of patients and the control (p = 0.199). In lactate/Cr ratios, the ROI in all seven patients and the ROC in two showed increased lactate signals. The lacate/Cr ratios of the ROIs were significantly elevated as compared to those of the ROCs (p = 0.02) and the control (p = 0.015). In 2-month follow up, lactate signals were absent or significantly reduced (p = 0.015). In no patients, clinical or radiological deterioration has been observed. Our results demonstrate that there is significant neuronal dysfunction in pericontusional oedematous areas as indicated by NAA/Cr ratios in the patients with mild head injury at both early and late stages. And there are significant ischaemic changes as indicated by increase of lactate level in ROI at early stage. These findings suggest that pericontusional oedematous areas can be vulnerable to secondary brain insults even in the patients with mild head injury.

Adolescent↗
PubMed2000

The effects of dopamine on edema formation in two models of traumatic brain injury.

The risk of vasopressors worsening cerebral edema has been raised. Previously we have reported that dopamine was able to restore cerebral blood flow in a model of monotonically rising intracranial pressure. In this study the effects of dopamine on cortical contusion and diffuse injury with secondary insult are examined. Adult male rats were divided into two groups: group 1 (n = 32)--Impact Acceleration Injury (IAM) with 30 minutes hypoxia and hypotension; group 2 (n = 12)--controlled cortical impact (6.0 m/sec, 3 mm depth). Dopamine was administered 2 hours post-injury (10-60 micrograms/kg/min i.v.). Cerebral water content and apparent diffusion coefficients (ADC) values were measured at baseline and four hours post-injury using MRI. Preinjury water content was the same in each group. Group 1 was subdivided into Groups 1A & 1B based on the ADC profile. Post-injury water content in Group 1A did not differ between saline or dopamine treated animals. Water content was higher in Group 1B-dopamine (83.4 +/- 1.1%) than Group 1B-saline animals (81.4 +/- 1.3%, p = 0.006). Contusion caused significant edema formation, however there was no significant difference between the dopamine treated or untreated group when considering either ipsilateral or contralateral cortex. Dopamine however significantly worsened edema in ipsilateral and contralateral hippocampus and both temporal cortices. ADC remained unchanged except in the contralateral hippocampus where both water content and ADC rose with dopamine suggesting precipitation of a vasogenic edema. In this study dopamine clearly worsened edema formation in two models of traumatic brain injury, and we conclude that there may be analogous clinical situations; therefore pressors should not be considered a 'blanket' therapy for all patients with a low cerebral perfusion pressure.

Animals↗
PubMed2000

Bradykinin 2 receptor antagonist LF 16-0687Ms reduces posttraumatic brain edema.

Activation of the kallikrein-kinin system contributes to traumatic brain edema formation. Inhibition of bradykinin 2 (B2) receptors has been shown to successfully reduce brain edema formation. The purpose of this study was to investigate the protective effect of the novel nonpeptide B2 receptor antagonist LF 16-0687Ms in brain-injured rats. Contusion was produced in forty rats by controlled cortical impact injury. Five minutes after trauma rats received a single dose of 0, 3, or 30 mg/kg of LF 16-0687Ms. After 24 hours brain swelling and hemispheric water content were determined. Brain swelling was significantly decreased by 25% in the low and 27% in the high dose group compared to controls (p < 0.03). Water content of the traumatized hemisphere tended to be decreased (80.2 +/- 0.1 vs. 80.4 +/- 0.1%) while water content of the non-traumatized hemispheres tended to be increased after administering LF 16.0687Ms (79.3 +/- 0.1 vs. 79.0 +/- 0.1%). Single administration of the novel nonpeptide B2 receptor antagonist LF 16-0687Ms significantly reduces brain swelling. The missing significant reduction in water content of the traumatized hemisphere, however, could be related to an unspecific increase in water content due to LF 16.0687Ms as suggested by increased water content in the non-traumatized hemisphere.

Animals↗
PubMed2000

Real time monitoring of glutamate following fluid percussion brain injury with hypoxia in the rat.

In this study, extracellular glutamate (Glu) was monitored in real time using a biosensor following traumatic brain injury (TBI) either with or without inducing hypoxia in the rat Fluid-percussion model. We also measured the cortical contusion volume at 3 days after the insult. The animals were divided into 3 groups. Group 1 was subjected to TBI only, Group 2 to TBI followed by 20 min of moderate hypoxia (FiO2: 10%) and Group 3 to 20 min of moderate hypoxia without TBI. The surge increase in the extracellular Glu concentration occurred immediately after TBI in Groups 1 and 2. Group 2 showed a prolonged efflux of Glu during hypoxia. Group 3 Glu showed low continuous steady levels. The contusion volume in Group 2 was significantly larger than in Group 1. To test the possible involvement of apoptosis in Groups 1 and 2, rats were sacrificed at 1, 6, 24 and 72 h after TBI. Immunohistochemical studies showed an increased number of both CPP32 positive cells at 24 h and TUNEL cells at 72 h in Group 2. These results suggest that TBI with moderate hypoxia induced a prolonged efflux of Glu that resulted more cortical damage due to necrosis and apoptosis.

Animals↗
PubMed2000

The synergistic effect of acute subdural hematoma combined with diffuse traumatic brain injury on brain edema.

It is well-documented that acute subdural hematoma (ASDH) following diffuse traumatic brain injury (dTBI) contributes to severe disability and high mortality. The objective of this study was to characterize edema formation in a model of ASDH and ASDH following dTBI. Eighteen Sprague-Dawley rats were separated into three groups: Sham operated (n = 6), ASDH (n = 6), ASDH following dTBI (n = 6). Diffuse TBI was produced via the Impact-Acceleration Model [10]. ASDH was induced in the left hemisphere using the well-described method [11]. Total tissue water content was determined 4 hours after TBI utilizing wet-weight/dry-weight assessment. Our results show that ASDH causes a significant increase in tissue water content in the left hemisphere (79.2 +/- 0.7%) compared with the contralateral hemisphere (78.5 +/- 0.5%, p = 0.009). Animals exposed to ASDH following dTBI had significantly greater edema formation than those with ASDH (right: 80.9 +/- 0.4%, left: 80.5 +/- 0.7, p = 0.008). There was no significant difference between the left and right hemisphere. We conclude that edema formation in ASDH is worsened by the combination of dTBI and ASDH. Furthermore a diffuse and focal injury in combination retain the features of the diffuse injury, but with increased severity. Further studies are required to elucidate the synergistic mechanisms involved in these pathological processes.

Animals↗
PubMed2000

Morphological presentation of posttraumatic vasospasm.

Posttraumatic vasospasm is a well-recognized sequela of head injury. The risk factors associated with posttraumatic vasospasm have not been well defined. We studied 119 consecutive patients with head injury to determine the risk factors for posttraumatic vasospasm. Posttraumatic vasospasm was detected in 32 (35.6%) of 90 patients. Among these patients, 29 (90.6%) had severe head injury and 3 (9.4%) had moderate head injury. None of the patients with mild head injury suffered posttraumatic vasospasm. In most cases, the onset of posttraumatic vasospasm began on the fifth day and lasted 1 to 9 days. In 8 (25%) patients, posttraumatic vasospasm began within the first three days of the head injury. Clinical deterioration was documented in two (2.5%) patients. Morphologically, posttraumatic vasospasm resembled features of aneurysmal vasospasm. We found increased corrugation of the internal elastic lamina and increased amounts of connective tissue in the subendothelial layer. These findings showed that posttraumatic vasospasm, although clinically more mild, demonstrated the same morphological changes as did aneurysmal vasospasm.

Adult↗