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- Hamberger, Anders, 1937, et al.
(author)
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Concussion in Professional Football: Morphology of Brain Injuries in the Nfl Concussion Model-Part 16
- 2009
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In: Neurosurgery. - 0148-396X. ; 64:6, s. 1174-1182
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Journal article (peer-reviewed)abstract
- OBJECTIVE: An animal model of concussions in National Football League players has been described in a previous study. It involves a freely moving 300-g Wistar rat impacted on the side of the head at velocities of 7.4 to 11.2 m/s with a 50-g impactor. The impact causes a 6% to 28% incidence of meningeal hemorrhages and 0.1- to 0.3-mm focal petechiae depending on the impact velocity. This study addresses the immunohistochemical responses of the brain. METHODS: Twenty-seven tests were conducted with a 50-g impactor and velocities of 7.4, 9.3, or 11.2 m/s. The left temporal region of the helmet-protected head was hit 1 or 3 times. Thirty-one additional tests were conducted with a 100-g impactor. Diffuse axonal injury in distant regions of the brain was assessed with immunohistochemistry for NF-200, the heaviest neurofilament subunit, and glial fibrillary acidic protein, an intermediate filament protein in astrocytes. Hemorrhages were analyzed by unspecific peroxidase. There were 10 controls. RESULTS: A single impact at 7.4 and 9.3 m/s velocity with the 50-g impactor causes minimal neuronal injury and astrocytosis. Repeat impacts with 11.2 m/s velocity and more than 9.3-m/s impacts with 100 g cause diffuse axonal injury and distant injury bilaterally in the cerebral cortex, the subcortical, the white matter, the hippocampus CA1, the corpus callosum, and the striatum, as indicated by NF-200 accumulation in neuronal perikarya 10 days after impact. It also causes reactive astrocytosis in the midline regions of the cerebral cortex and periventricularly. Regions with erythrocyte-loaded blood capillaries indicated brain edema in regions of the cerebral cortex, the brainstem, and the cerebellum. CONCLUSION: When the immunohistochemical results are extrapolated to professional football players, concussions result in no or minimal brain injury. Repeat impacts at higher velocity or with a heavier mass impactor cause extensive and distant diffuse axonal injury. Based on this model, the threshold for diffuse axonal injury is above even the most severe conditions for National Football League concussion. Copyright (C) by the Congress of Neurological Surgeons
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- Säljö, Annette, et al.
(author)
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Exposure to short-lasting impulse noise causes microglial and astroglial cell activation in the adult rat brain.
- 2001
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In: Pathophysiology : the official journal of the International Society for Pathophysiology / ISP. ; 8:2, s. 105-111
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Journal article (peer-reviewed)abstract
- Exposure to impulse noise, i.e. pressure waves, is above a certain intensity, harmful to auditory function. Intense, short-lasting impulse noise of 198 or 202 dB affects the heavy subunit of neurofilament proteins in neuronal perikarya of the cerebral cortex and hippocampus. There was as well an increased expression of immediate early gene products and induction of neuronal apoptosis. Here, we show that this range of exposure also affects glial cells. We identified microglial cells with an antibody against the complement receptor type 3 (OX-42) and astrocytes with an antibody against the glial fibrillary acidic protein (GFAP). The pattern of damage included microglial activation as early as 2 h after exposure to 202 dB. The activation increased further at 18 h. There was a significant increase of the area occupied by microglial cells in the anterior and posterior hypothalamus and in the lateral septal nucleus. Astrogliosis was observed in the cerebral cortex, the dentate gyrus and in the pyramidal cell layers as well as in white matter of the hippocampus. Both the microglial and astrocytic reactivities remained at 21 days. Exposure to 198 dB, caused similar, but less prominent activation in both cell types.
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| 6. |
- Säljö, Annette, et al.
(author)
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Exposure to short-lasting impulse noise causes neuronal c-Jun expression and induction of apoptosis in the adult rat brain.
- 2002
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In: Journal of neurotrauma. - : Mary Ann Liebert Inc. - 0897-7151 .- 1557-9042. ; 19:8, s. 985-91
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Journal article (peer-reviewed)abstract
- Exposure to impulse noise, above a certain intensity, is harmful to auditory function. Effects of impulse noise on the central nervous system (CNS) are largely unexplored, and there is little information on critical threshold values and time factors. We have recently shown that neurofilament proteins are affected in the cerebral cortex and the hippocampus. Now we show that impulse noise induces expression of the immediate early gene c-Jun products, proposed to play a role in the initiation of neuronal death, and apoptosis as revealed by TUNEL staining. Rat brains were investigated immunohistochemically 2 h to 21 days after exposure to impulse noise of 198 dB or 202 dB. c-Jun was expressed in neuronal perikarya in layers II-VI of the temporal cortex, the cingulate and the piriform cortices at 2 h to 21 days after both exposure levels. Granule neurons of the dentate gyrus and the CA1-3 in the hippocampus pyramidal neurons were similarly affected. The elevated expression of c-Jun products remained high at all postexposure times. TUNEL staining was positive among the same nerve cell populations 6 h after exposure and persisted even at 7 days at both exposure levels.
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| 7. |
- Säljö, Annette, et al.
(author)
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Expression of c-Fos and c-Myc and deposition of beta-APP in neurons in the adult rat brain as a result of exposure to short-lasting impulse noise.
- 2002
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In: Journal of neurotrauma. - : Mary Ann Liebert Inc. - 0897-7151 .- 1557-9042. ; 19:3, s. 379-85
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Journal article (peer-reviewed)abstract
- There is increasing evidence that impulse noise causes brain damage, but little is known about the mechanisms and extent of the response. Here, rat brains were investigated immunohistochemically for the expression of c-Fos, c-Myc, and beta-APP during the first 3 weeks postexposure to impulse noise of 198 or 202 dB. The expression of c-Fos and c-Myc increased at 2 h after exposure in neurons of the cerebral cortex, thalamus, and hippocampus, and this c-Fos immunoreactivity remained elevated for the entire observation period. The c-Myc immunoreactivity peaked at 18 h in both neurons and astrocytes but returned to control levels at 7 days. Abnormal deposition of beta-APP was evident within 6 h in the same brain regions. The beta-APP immunoreactivity was most prominent at 18 h and remained increased over the 21-day period assessed. The observed effects were similar to those described in humans following traumatic brain injury and in Alzheimer's disease. We conclude that impulse noise influences the brain in a fashion similar to that in cases with progressive CNS degeneration.
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| 8. |
- Säljö, Annette, et al.
(author)
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Low-level blast raises intracranial pressure and impairs cognitive function in rats: prophylaxis with processed cereal feed
- 2010
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In: Journal of Neurotrauma. - : Mary Ann Liebert Inc. - 0897-7151 .- 1557-9042. ; 27:2, s. 383-389
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Journal article (peer-reviewed)abstract
- There is increasing evidence that even low levels of blast cause brain injury, but little is known about their thresholds and mechanisms. Exposure of rats to 10-60 kPa blasts elevate intracranial pressure (ICP) in a dose-dependent manner and impair cognitive function. We have evaluated a prophylactic measure against these brain injuries in a rat animal model, consisting of feeding them processed cereal. This type of feed is known to ameliorate disturbances in secretion of body fluids and to have anti-inflammatory effects. In humans, intake of processed cereals is effective against intestinal diarrhea and also reduces the symptoms of Ménière's disease. Rats were given either standard laboratory feed or processed cereal feed for 2 weeks before exposure to blast in a shock tube. The ICP was monitored at different time points up to 1 week after exposure to a 60-kPa blast, and for up to 24 h after exposure to a 30-kPa blast. Maximal ICP elevation was reached at 10 h in both groups. In the group of rats on standard feed exposed to 60 kPa, an ICP increase of 145% was noted at 10 h, and the corresponding increase in the rats fed processed cereal feed was only 50%. In rats exposed to a 30-kPa blast, those fed standard feed and processed cereal feed demonstrated increases of ICP of 80% and 40%, respectively. Cognitive function as measured by the Morris water maze was assessed in other groups of rats at 2 days after exposure to 10- or 30-kPa blasts. Their performance was significantly impaired at both exposure levels in rats on standard feed, but no functional impairment was seen in rats fed processed cereal feed.
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| 10. |
- Säljö, Annette, et al.
(author)
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Mechanisms and pathophysiology of the low-level blast brain injury in animal models
- 2011
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In: NeuroImage. - 1053-8119. ; 54:Suppl 1
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Journal article (peer-reviewed)abstract
- The symptoms of primary blast-induced mTBI, posttraumatic stress disorder and depression overlap. Evidence of an organic basis for these entities has been scarce and controversial. We present a review of animal studies demonstrating that low-level blast causes pathophysiological and functional changes in the brain. We monitor a time period from minutes to approximately 1 week after blast exposure from multiple modes (air, underwater, localized and whole body). The most salient findings observed were (1) the peak pressures (P(max)) in the brain, elicited from the blast from the firing of military weapons (P(max) 23-45 kPa), have a similar magnitude as that registered in air close to the head. Corresponding measurements during the detonation pulse from explosives under water show a P(max) in the brain, which is only 10% of that in water outside the head. (2) The rise time of the pressure curve is 10 times longer in the brain as compared with the blast in air outside the head during firing of military weapons. (3) The lower frequencies in the blast wave appear to be transmitted more readily to the brain than the higher frequencies. (4) When animals are exposed to low levels of blast, the blast wave appears mostly transmitted directly to the brain during air exposure, not via the thorax or abdomen. (5) Low levels of blast cause brain edema, as indicated by increased bioelectrical impedance, an increase in the intracranial pressure, small brain hemorrhages and impaired cognitive function.
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