Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PERCUSSION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMed2005

Early loss of the glutamate transporter splice-variant GLT-1v in rat cerebral cortex following lateral fluid-percussion injury.

Glutamate transporter proteins are essential for the control of interstitial glutamate levels, with an impairment of their function or levels being a major potential contributor to excitotoxicity. We have investigated the effects of lateral fluid percussion on the levels of the glutamate transporter proteins GLT-1alpha, its splice variant GLT-1v, GLAST, and EAAC1 in the rat in order to evaluate their pathogenetic role in this model of traumatic brain injury (TBI). Immunoblot analysis revealed neuronal loss in the cerebral cortex was accompanied by a 54% decrease in GLT-1v 6 h following the insult which progressed to an 83% loss of the transporter after 24 h. No changes in GLT-1alpha, GLAST, or EAAC1 were observed in this brain region at either time point. GLT-1v content was also decreased by 55% and 68% in the hippocampus and thalamus, respectively, at 6 h post-injury, but recovered fully after 24 h in both brain regions. In contrast, levels of GLT-1alpha were increased in the hippocampus at 6 h and 24 h post-TBI. These alterations in transporter protein content were also confirmed using immunohistochemical methods. Our results show for the first time a pattern of early, dynamic changes in the levels of GLT-1 transporter splice variants in different brain regions in this trauma model. In addition, correlation of GLT-1v levels with both neuronal cell loss and alpha-internexin content in the injured cortex suggests that loss of this novel glutamate transporter may be a key factor in determining cerebral vulnerability following this type of brain injury.

Alternative Splicing↗
PubMed1991

Surface coil spectroscopic imaging: time and spatial evolution of lactate production following fluid percussion brain injury.

Detailed temporal and spatial distributions of lactate production are presented for graded fluid-percussion brain injury in the rat. A one-dimensional proton spin-echo spectroscopic imaging (1D SESI) technique, performed with a surface coil, is presented and evaluated. This technique, which represents a practical compromise, provides spatially localized proton nuclear magnetic resonance (NMR) brain spectra from a series of small voxels (less than 0.15 cm3) in less than 10 min, thus enabling both spatial and temporal monitoring of lactate production. These high-resolution lactate maps are correlated with hyperintense regions observed in T2-weighted images taken 10 h after impact, which, in turn, correlate with histology. The data demonstrate that, following severe trauma there is delayed production and propagation of lactate to regions of the brain that are remote from the trauma site. The extent of lactate production depends on the severity of impact. More significantly, the data show that following severe trauma, local lactate concentrations exceed 15 mumol/g, the concentration that has been claimed as the threshold for brain injury. Therefore high lactate levels cannot be ruled out a priori as a possible factor in brain injury following severe head trauma.

Animals↗
PubMed1995

Comparison of effects of an intrapulmonary percussive ventilator to standard aerosol and chest physiotherapy in treatment of cystic fibrosis.

Impaired mucociliary clearance due to defective ion and water transport and the effects of chronic airway infections lead to stasis of secretions and progressive pulmonary damage in patients with cystic fibrosis (CF). Methods to improve removal of tenacious lung secretions in CF patients contribute to slowing the decline in respiratory function. We have evaluated an intrapulmonary percussive ventilator (IPV), which is a device designed to enhance airway clearance and preserve lung function. A previous pilot study by us had determined that the device was acceptable to patients and is safe. We undertook a 6 month parallel comparative trial of the IPV versus standard, manual chest physiotherapy in 16 CF children and adults. No significant differences in spirometric measures, numbers of hospitalizations, use of oral or IV antibiotics, or anthropometric measurements were detected between the standard aerosol/chest physiotherapy group and the IPV group over the duration of the trial. Patient acceptance, as determined by participant survey, was good. The device appeared to be safe and durable. It was concluded that the IPV is as effective as standard aerosol and chest physiotherapy in preserving lung function and anthropometric measures, and there was no difference in the use of antibiotics and hospitalizations.

Adolescent↗
PubMed1997

Fluid percussion injury causes disruption of the septohippocampal pathway in the rat.

Fluid percussion injury (FPI) causes memory deficits, loss of hippocampal neurons, and basal forebrain cholinergic immunoreactivity in rats. Basal forebrain septohippocampal projections terminate in specific hippocampal regions. The purpose of this study was to examine the effects of FPI on the septohippocampal pathway (SHP). Halothane-anesthetized rats received either a sham injury or a parasagittal FPI. To characterize the anatomical effects of FPI on the SHP, silver stains were performed on brains of animals at 1, 5, and 10 days following FPI and were compared to sham-injured preparations. To characterize the effects of FPI on retrograde transport in the SHP, a separate group of FPI and sham-injured animals with survival times of 2, 5, and 10 days received bilateral WGA-HRP injections into the hippocampal formation 24 h prior to sacrifice. Argyrophilic CA3 neurons were present 1 day following FPI. Five days following FPI, terminal degeneration was present in the inner third of the molecular layer of the dentate gyrus bilaterally that was not present 1 day after injury. Fiber and terminal degeneration was not observed in the basal forebrain until 10 days after FPI. WGA-HRP-labeled septal neurons decreased significantly (P < 0.05) ipsilateral to injury in animals sacrificed 5 and 10 days following FPI but not 2 days after injury. This investigation demonstrated that FPI produces focal injury in the hippocampal formation. In addition, the appearance of terminal degeneration in the dentate molecular layer correlated with the significant reduction in axonal transport 5 days following injury. This correlation illustrates the secondary processes that structurally damage the SHP up to 10 days after injury.

Animals↗
PubMed2001

Regional expression of Par-4 mRNA and protein after fluid percussion brain injury in the rat.

Regional levels of prostate apoptosis response-4 (Par-4) protein and mRNA were measured after lateral fluid percussion (FP) brain injury in rats. Immunochemical studies indicated that Par-4 immunoreactivity (ir) is present in cortical neurons and hippocampal CA1-CA3 pyramidal neurons in uninjured rats. Increases of Par-4-ir were observed in the CA3 neurons of the ipsilateral hippocampus (IH), but not in injured left cortex (IC) at 48 h after FP brain injury. Levels of the Par-4 mRNA measured by RT-PCR assay and protein measured by Western blot procedure were significantly increased in the injured IC and IH, but not in the contralateral right cortex and hippocampus after brain injury. Levels of both Par-4 protein and mRNA were significantly increased in the IC and IH as early as 2 h and stayed elevated at 24 and 48 h after injury. These data show that the induction of proapoptotic Par-4 mRNA and protein occurs only in the IC and IH that have been observed to undergo apoptosis and neuronal cell loss after lateral FP brain injury. Because increased expression of Par-4 has been observed to contribute to apoptosis and cell death in cultured neurons, the present temporal pattern of Par-4 expression is consistent with a role for Par-4 in apoptosis and neuronal cell death after traumatic brain injury.

Animals↗
PubMed2006

Unilateral spatial neglect and memory deficit associated with abnormal beta-amyloid precursor protein accumulation after lateral fluid percussion injury in Mongolian gerbils.

The purpose of this study was to investigate cognitive/memory dysfunctions and the pathological process contributing to such dysfunction following moderate lateral fluid percussion injury (LFPI) in Mongolian gerbils. Mongolian gerbils were subjected to moderate LFPI (1.3 1.6 atm). During 7 days post-trauma, spatial cognitive and memory dysfunctions were evaluated by T-maze test (TMT). At 6 hours, 24 hours, and 7 days post-injury, animals were sacrificed and the brains were prepared for Kluver-Barrera staining and immunostaining of beta-amyloid precursor protein (APP). In LFPI animals, the spontaneous alternation rate in the TMT remained below the random alternation rate (< 50%) on all post-injury test days. These animals also showed a transient tendency to choose only the right arm (ipsilateral to the injury) in the TMT at 6 hours and 24 hours after injury. Significant accumulation of APP was found widespread in the ipsilateral hemisphere including directly injured cortex, subcortical white matter, and hippocampal formation at 6 hours and 24 hours post-injury, while on day 7, the increased immunoreactivity of APP subsided. These results suggest that the widespread axonal degeneration of the white matter might contribute to the unilateral spatial neglect and memory deficit in the acute stage after LFPI.

Amyloid beta-Protein Precursor↗
PubMed2006

Alteration of gap junction proteins (connexins) following lateral fluid percussion injury in rats.

Gap junctions are intercellular channels that mediate the cytoplasmic exchange of small hydrophilic molecules and are formed by a family of integral membrane proteins called connexins (Cxs). Cx43 is expressed predominantly in astrocytes, while Cx36 is expressed in neurons. In this study, we show alteration of Cx43 and Cx36 in the hippocampus after traumatic brain injury in rats. Adult male Sprague-Dawley rats were subjected to lateral fluid percussion injury of moderate severity. Brain coronal sections were used for immunohistochemistry with Cx43 and Cx36 antibodies. Cx43 immunoreactivity was increased in reactive astrocytes in the damaged hippocampus 24 hours after injury, and persisted for 72 hours. On the other hand, Cx36 immunoreactivity increased in CA3 neurons 1 hour after injury, and decreased later. These results indicate that gap junctions might participate in the pathophysiological process after traumatic brain injury.

Adaptation, Physiological↗
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

Evidence for lactate uptake after rat fluid percussion brain injury.

UNLABELLED: Traumatic brain injury (TBI) places enormous early energy demand on brain tissue to reinstate normal ionic balance. Glucose declines and lactate increases after TBI as demonstrated in clinical and lab studies, suggesting increased glycolysis. This led us to hypothesize that high extracellular fluid (ECF) lactate may be beneficial after TBI. We measured cerebral dialysate lactate and glucose, and arterial lactate and glucose, before & after rat Fluid Percussion Injury (FPI) (2.06 +/- 0.13 atm) with and without i.v. lactate infusion (100 mM x 4.5 hours) to test the hypotheses that arterial lactate determines ECF lactate. 14C-lactate autoradiography was also performed, to demonstrate whether lactate is taken up by traumatized brain. RESULTS: Dialysate lactate was always significantly higher than arterial. After lactate infusion, both the dialysate and the arterial lactate were significantly increased (P < 0.0001). Dialysate lactate increased within 10 min. following FPI, with significantly higher values in the lactate infusion group (82% higher with lactate infusion after FPI). Dialysate glucose fell following FPI, with a more severe decline in the saline group (129% lower), suggesting lactate infusion preserves or "spares" glucose in ECF. In our autoradiographic study, i.v. 14C-lactate accumulated at the injury site, with levels 2-4 times higher than in contralateral cortex. In conclusion, arterial lactate augmentation thus increases brain dialysate lactate and results in less reduction in ECF glucose, after FPI. Infused lactate accumulates at the injury site, where metabolism is probably the greatest.

Animals↗
PubMedDate not supplied

Serum extravasation and cytoskeletal alterations following traumatic brain injury in rats. Comparison of lateral fluid percussion and cortical impact models.

Disruption of the blood-brain barrier (BBB) and neuronal cytoskeletal damage were evaluated in two commonly used rat models of traumatic brain injury. Adult rats received a lateral cortical impact (CI) or lateral fluid percussion (FP) injury of mild or moderate severity or a sham procedure. Six hours after trauma, the brains were removed and analyzed with immunocytochemical techniques for alterations in the serum protein, IgG, and the cytoskeletal protein, microtubule-associated protein 2 (MAP2). Both models induced profound alterations in these proteins in the ipsilateral cortex and hippocampus compared to sham-injured controls. Following an injury of moderate severity, the CI injury resulted in greater IgG extravasation in the cortex and hippocampus than the FP injury. Conversely, after a mild injury, IgG extravasation in the hippocampus was greater for FP than CI. All of the animals in the CI group and most of the FP group showed a loss of MAP2 in the hippocampus. The specific subregions within the cortex and hippocampus that were affected by the injury varied between models, despite having identical impact sites. These data demonstrate that there are both similarities and differences between a CI and FP injury on vascular and neuronal cystoskeletal integrity, which should be considered when utilizing these animal models to study selected features of human head injury.

Animals↗
PubMed2000

Tissue tears in the white matter after lateral fluid percussion brain injury in the rat: relevance to human brain injury.

A characteristic feature of severe diffuse axonal injury in man is radiological evidence of the "shearing injury triad" represented by lesions, sometimes haemorrhagic, in the corpus callosum, deep white matter and the rostral brain stem. With the exception of studies carried out on the non-human primate, such lesions have not been replicated to date in the multiple and diverse rodent laboratory models of traumatic brain injury. The present report describes tissue tears in the white matter, particularly in the fimbria of Sprague-Dawley rats killed 12, 24, and 48 h and 7 days after lateral fluid percussion brain injury of moderate severity (2.1-2.4 atm). The lesions were most easily seen at 24 h when they appeared as foci of tissue rarefaction in which there were a few polymorphonuclear leucocytes. At the margins of these lesions, large amounts of accumulated amyloid precursor protein (APP) were found in axonal swellings and bulbs. By 1 week post-injury, there was macrophage infiltration with marked astrocytosis and early scar formation. This lesion is considered to be due to severe deformation of white matter and this is the first time that it has been identified reproducibly in a rodent model of head injury under controlled conditions.

Amyloid beta-Protein Precursor↗
PubMed2006

Structural and functional alterations of cerebellum following fluid percussion injury in rats.

Cerebellum was shown to be vulnerable to traumatic brain injury (TBI) in experimental animals. However, the detailed pathological and functional changes within the cerebellum following TBI are not known. Using our established cerebellum fluid percussion injury (FPI) model, we characterized the temporal pattern and the nature of structural damage following FPI, as well as the functional changes of Purkinje cells in response to climbing fiber activation. Our results showed that 60% of Purkinje cells died within the first 24 h following moderate FPI. In contrast, clusters of densely stained shrunken granule cells were stained positive for terminal deoxynucleotidyl transferase-mediated UTP nick end labeling (TUNEL) in 1, 3 or 7 days following FPI animals. We also observed an accompanying structural damage to the cerebellar white matter tract. Disconnected axonal fibers appeared 1 day post-FPI, and loss of white matter fibers were visible 3 and 7 days post-FPI. Massive accumulation of beta-amyloid precursor protein (betaAPP) was found in the white matter tracts and molecular layer in the cerebellum of 1, 3 or 7 days FPI animals. Our functional study showed that the majority of Purkinje cells from 1 day and all cells from 3 to 7 days post-FPI had distorted membrane potential and synaptic responses to climbing fiber activation. These results suggested that there is a co-related structural and functional deterioration with a specific temporal pattern in the cerebellum following FPI. These observations provide a basis for future mechanistic investigations aiming to realize neuroprotection from cerebellar neuronal death and loss of cerebellar functionality.

Amyloid beta-Peptides↗
PubMed2001

Immunomorphological sequelae of severe brain injury induced by fluid-percussion in juvenile pigs--effects of mild hypothermia.

Severe traumatic brain injury (TBI) often leads to a bad outcome with considerable neurological deficits. Secondary brain injuries due to a rise of intracranial pressure (ICP) and global hypoxia-ischemia are critical and may be reduced in extent by mild hypothermia. A porcine animal model was used to study the effect of severe TBI, induced by fluid percussion (FP; 3.5+/-0.3 atm) in combination with a secondary insult, i.e., temporary blood loss with hypovolemic hypotension. Six-week-old juvenile pigs were subjected to this kind of severe TBI; one group was then submitted to moderate hypothermia at 32 degrees C for 6 h, starting 1 h after brain injury. Animals were killed after 24 h. TBI and hypothermia-associated alterations in the brains were investigated by immunohistochemistry with antibodies against microtubule-associated protein 2 (MAP-2) and beta-amyloid precursor protein (betaAPP). In addition, DNA fragmentation was investigated by the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) method. Seven of the 13 normothermic TBI animals developed a secondary increase in ICP (TBI-NT-ICP) after an interval of several hours. None of the animals in the hypothermic trauma (TBI-HT) group exhibited a secondary ICP increase, indicating a protective effect of the treatment. TBI-HT animals showed significantly higher levels of MAP-2 immunoreactivity, lower levels of betaAPP immunoreactivity and less DNA fragmentation than the TBI-NT-ICP animals. Differences between the TBI-HT group and normothermic animals without an ICP increase (TBI-NT) were less marked. A considerable decrease in MAP-2 outside the site of TBI-FP administration was seen only in the TBI-NT-ICP animals. MAP-2 immunohistochemistry was thus a reliable marker of diffuse brain damage. Axonal injury was present in all TBI groups, indicating its special significance in neurotrauma. Thus, severe TBI caused by FP, combined with temporary blood loss, consistently produced traumatic axonal injury and focal brain damage. Mild hypothermia was able to prevent a secondary increase in ICP and its sequelae of diffuse hypoxic-ischemic brain injury. However, hypothermia did not afford protection from traumatic axonal injury.

Age Factors↗
PubMed1996

Temporal and spatial characterization of neuronal injury following lateral fluid-percussion brain injury in the rat.

The pattern of neuronal injury following lateral fluid-percussion (FP) brain injury in the rat was systematically characterized at sequential time points to identify selectively vulnerable regions and to determine the temporal contribution of primary and delayed neuropathological events. Male Sprague-Dawley rats (n = 28) were killed 10 min, 2 h, 12 h, 24 h, 4 days, and 7 days following a lateral FP brain injury of moderate severity (2.2 atm), or 24 h after a sham injury. Brain sections were stained and analyzed using Nissl, acid fuchsin, and silver staining methods to identify regions with injured neurons or with visible lesions. Extensive numbers of acid fuchsin or silver-stained neurons were observed as early as 10 min after the FP brain injury in regions extending from the caudate/putamen to the pons. The frequency of injured neurons was greatest in the ipsilateral cortex, hippocampus, and thalamus, and a visible loss of Nissl-stained neurons was observed in these regions beginning at 12 h after the FP brain injury. Acid fuchsin-stained neurons were restricted to the same brain regions for all of the survival periods and gradually decreased in numbers between 24 h and 7 days after injury. These findings suggest that lateral FP brain injury in the rat produces a combination of focal cortical contusion and diffuse subcortical neuronal injury, which is present within minutes of the impact, progresses to a loss of neurons by 12 h, and does not markedly expand into other brain regions with survival periods up to 7 days. Furthermore, the acute onset and rapid evolution of the neuronal injury process may have important implications when considering a window of opportunity for pharmacological intervention.

Animals↗
PubMed1989

Experimental fluid percussion brain injury: vascular disruption and neuronal and glial alterations.

Because of the potential relationship between vascular disturbances and secondary tissue damage, we identified areas of brain which exhibited hemorrhage and leakage of protein during the acute stage after experimental brain injury and subsequently studied the development of pathologic changes, including cavity formation, neuronal necrosis, and gliosis within these regions. The development of pathologic changes was evaluated at 1, 6, and 24 h and 1, 2, and 4 weeks after lateral, fluid percussion (FP) brain injury of moderate severity in the rat. Vascular disruption in the acute stages, as evidenced by hemorrhage and leakage of Evans blue albumin, was most prominent 6 h postinjury and was maximal in the parieto-occipital cortex. From 1 to 24 h after injury, regions of the injured hemisphere, including the cortex and hippocampus, exhibited abnormal neurons which stained with acid fuchsin and Alizarin red, histochemical markers for injured neurons and calcium, respectively. These same regions suffered significant neuronal cell loss from 1 to 4 weeks after injury. The distribution of reactive astrocytes was also evaluated by immunocytochemical localization of glial fibrillary acidic protein (GFAP). By 2 weeks postinjury, a prominent cavity was present in the frontoparietal and occipital cortices. Although astrogliosis was most pronounced in the cortex surrounding the cavity, prominent reactive astrocytes were widely distributed throughout the injured hemisphere. This study characterized the pathological changes which occur after experimental traumatic brain injury. In particular, we propose that neuronal cell injury in the hippocampus serves as a useful 'window' to assess beneficial efficacy of pharmacological intervention in the treatment of brain injury.

Animals↗
PubMed1993

Biochemical and histological alterations induced by fluid percussion brain injury in the rat.

In the present study we have characterized the time-course of the histopathological and biochemical alterations resulting from mechanical brain injury caused by lateral fluid percussion centered over the parietal cortex in the rat. The injury device used was an HPLC pump coupled to a solenoid valve which delivered a constant and short lasting (10 ms) impact pressure (1.6 atm). This traumatic procedure resulted in an accumulation of blood in the subarachnoid space and cortical edema at 4-24 h post-trauma. From 4 h after injury, cortical neurons exhibited a pathologic appearance and phagocytic cells invaded the brain parenchyma. At 3 and 7 days post-injury, complete neuronal loss was observed in the parietal cortex around the impact site. In the ipsilateral cortex, the time-course of histologically assessed neuronal loss and phagocytic/glial activation paralleled the time-course of the loss of omega 1-2 (benzodiazepine) sites (a neuronal marker) and of the increase in p sites (peripheral-type benzodiazepine binding sites; a glial/macrophage marker). Neuronal loss and increase in the density of the glial/macrophage biochemical marker were also observed in the hippocampus but not in the contralateral cortex or in other subcortical structures, suggesting a selective vulnerability of the hippocampus to this traumatic procedure. There was a very good spatial correlation between the histological alterations and the changes in the density of the neuronal and glial/macrophage biochemical markers (as assessed by autoradiography). The volume of the lesion, integrated from the surface of the lesion measured at 10 coronal levels cut at a 1 mm interval and stained with haemalum and eosin, represented 32.9 +/- 1.7 mm3.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Interleukin-1 receptor antagonist inhibits neuronal damage caused by fluid percussion injury in the rat.

Increased expression of the cytokine interleukin-1 (IL-1) has been observed in rodent and human brain after injury, and IL-1 has been implicated in ischaemic and excitotoxic brain damage in the rat. These data suggest that neurodegeneration caused by brain injury may be mediated by local IL-1 production and action. This hypothesis was tested by studying the effects of central injection of recombinant human interleukin-1 receptor antagonist (rhIL-1ra) on brain damage (assessed histologically, H and E stain) induced by fluid percussion trauma in the rat. Injection of rhIL-1ra (10 micrograms, i.c.v.) 15 min and 2, 4, 6, 8, 24 and 48 h after injury significantly reduced, by 44%, the extent of damage measured 3 days later. Similar protection was observed in animals killed 7 days after injury. Delayed administration of rhIL-1ra (4, 6, 8, 24 and 48 h) after injury also significantly reduced (by 28%) neuronal damage. These data indicate that endogenous IL-1 mediates damage caused by traumatic brain injury and that rhIL-1ra offers significant protection even when treatment is delayed.

Animals↗
PubMed1996

Prolonged and extensive IgG immunoreactivity after severe fluid-percussion injury in rat brain.

The relationships between protein extravasation, morphological changes in neurons, and reactive changes in axons were evaluated in rats subjected to right lateral fluid-percussion injury to the brain (4.8-5.6 atm, 20 ms). Serial sections of the brain were immunostained with antibodies to rat immunoglobulin G (IgG) and 68-kDa neurofilament at 1 h to 2 weeks after injury or sham injury. Ischemic changes in neurons were noted in the injured cortex at 6-48 h after injury, and macroscopic hemorrhages were noted in the right corpus callosum and external capsule at 1 h to 1 week after injury. Extracellular IgG immunostaining was observed in the right cortex and right hippocampus at 1 h to 1 week after injury, and in the cortices and hippocampi bilaterally at 2 weeks after injury, but was most prominent in those regions at 24 h after injury. Intracellular IgG staining was noted in the neurons of cortices, hippocampi, brainstem, and cerebellum at 1 h to 2 weeks after injury. The number of IgG immunoreactive neurons was greatest at 1 week after injury. Thickened IgG immunoreactive axons and reactive axonal changes seen with neurofilament immunostaining were both in the similar region of the brainstem at 1 h to 1 week after injury. It appears that prolonged and widespread breakdown of the blood-brain barrier to plasma protein occurs after severe concussive brain injury and that this breakdown is not always accompanied by morphological changes. Intra-axonal IgG immunostaining provides additional clues to the pathogenesis of axonal damage following diffuse brain injury.

Animals↗