Experimental Investigation of Cerebral Contusion: Histopathological and Immunohistochemical Evaluation of Dynamic Cortical Deformation

We used a new approach, termed dynamic cortical deformation (DCD), to study the neuronal, vascular, and glial responses that occur in focal cerebral contusions. DCD produces experimental contusion by rapidly deforming the cerebral cortex with a transient, nonablative vacuum pulse of short duration (...

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Veröffentlicht in:Journal of neuropathology and experimental neurology 1999-02, Vol.58 (2), p.153-164
Hauptverfasser: Shreiber, David I, Bain, Allison C, Ross, Douglas T, Smith, Douglas H, Gennarelli, T A, McIntosh, Tracy K, Meaney, David F
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container_issue 2
container_start_page 153
container_title Journal of neuropathology and experimental neurology
container_volume 58
creator Shreiber, David I
Bain, Allison C
Ross, Douglas T
Smith, Douglas H
Gennarelli, T A
McIntosh, Tracy K
Meaney, David F
description We used a new approach, termed dynamic cortical deformation (DCD), to study the neuronal, vascular, and glial responses that occur in focal cerebral contusions. DCD produces experimental contusion by rapidly deforming the cerebral cortex with a transient, nonablative vacuum pulse of short duration (25 milliseconds) to mimic the circumstances of traumatic injury. A neuropathological evaluation was performed on brain tissue from adult rats sacrificed 3 days following induction of either moderate (4 psi, n=6) or high (8 psi, n=6) severity DCD. In all animals, DCD produced focal hemorrhagic lesions at the vacuum site without overt damage to other regions. Examination of histological sections showed localized gross tissue and neuronal loss in the cortex at the injury site, with the volume of cell loss dependent upon the mechanical loading (p
doi_str_mv 10.1097/00005072-199902000-00005
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DCD produces experimental contusion by rapidly deforming the cerebral cortex with a transient, nonablative vacuum pulse of short duration (25 milliseconds) to mimic the circumstances of traumatic injury. A neuropathological evaluation was performed on brain tissue from adult rats sacrificed 3 days following induction of either moderate (4 psi, n=6) or high (8 psi, n=6) severity DCD. In all animals, DCD produced focal hemorrhagic lesions at the vacuum site without overt damage to other regions. Examination of histological sections showed localized gross tissue and neuronal loss in the cortex at the injury site, with the volume of cell loss dependent upon the mechanical loading (p&lt;0.001). Axonal pathology shown with neurofilament immunostaining (SMI-31 and SMI- 32) was observed in the subcortical white matter inferior to the injury site and in the ipsilateral internal capsule. No axonal injury was observed in the contralateral hemisphere or in any remote regions. Glial fibrillary acidic protein (GFAP) immunostaining revealed widespread reactive astrocytosis surrounding the necrotic region in the ipsilateral cortex. This analysis confirms that rapid mechanical deformation of the cortex induces focal contusions in the absence of primary damage to remote areas 3 days following injury. Although it is suggested that massive release of neurotoxic substances from a contusion may cause damage throughout the brain, these data emphasize the importance of combined injury mechanisms, e.g. mechanical distortion and excitatory amino acid mediated damage, that underlie the complex pathology patterns observed in traumatic brain injury.</description><identifier>ISSN: 0022-3069</identifier><identifier>EISSN: 1554-6578</identifier><identifier>DOI: 10.1097/00005072-199902000-00005</identifier><identifier>PMID: 10029098</identifier><identifier>CODEN: JNENAD</identifier><language>eng</language><publisher>Hagerstown, MD: American Association of Neuropathologists, Inc</publisher><subject>Animals ; Astrocytes - chemistry ; Biological and medical sciences ; Biomechanical Phenomena ; Brain Chemistry - physiology ; Brain Concussion - pathology ; Brain Concussion - physiopathology ; Cerebral Cortex - cytology ; Cerebral Cortex - pathology ; Cerebral Hemorrhage - pathology ; Cerebral Hemorrhage - physiopathology ; Disease Models, Animal ; Glial Fibrillary Acidic Protein - analysis ; Injuries of the nervous system and the skull. Diseases due to physical agents ; Male ; Medical sciences ; Necrosis ; Neurofilament Proteins - analysis ; Neurons - chemistry ; Rats ; Rats, Sprague-Dawley ; Traumas. 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DCD produces experimental contusion by rapidly deforming the cerebral cortex with a transient, nonablative vacuum pulse of short duration (25 milliseconds) to mimic the circumstances of traumatic injury. A neuropathological evaluation was performed on brain tissue from adult rats sacrificed 3 days following induction of either moderate (4 psi, n=6) or high (8 psi, n=6) severity DCD. In all animals, DCD produced focal hemorrhagic lesions at the vacuum site without overt damage to other regions. Examination of histological sections showed localized gross tissue and neuronal loss in the cortex at the injury site, with the volume of cell loss dependent upon the mechanical loading (p&lt;0.001). Axonal pathology shown with neurofilament immunostaining (SMI-31 and SMI- 32) was observed in the subcortical white matter inferior to the injury site and in the ipsilateral internal capsule. No axonal injury was observed in the contralateral hemisphere or in any remote regions. Glial fibrillary acidic protein (GFAP) immunostaining revealed widespread reactive astrocytosis surrounding the necrotic region in the ipsilateral cortex. This analysis confirms that rapid mechanical deformation of the cortex induces focal contusions in the absence of primary damage to remote areas 3 days following injury. Although it is suggested that massive release of neurotoxic substances from a contusion may cause damage throughout the brain, these data emphasize the importance of combined injury mechanisms, e.g. mechanical distortion and excitatory amino acid mediated damage, that underlie the complex pathology patterns observed in traumatic brain injury.</description><subject>Animals</subject><subject>Astrocytes - chemistry</subject><subject>Biological and medical sciences</subject><subject>Biomechanical Phenomena</subject><subject>Brain Chemistry - physiology</subject><subject>Brain Concussion - pathology</subject><subject>Brain Concussion - physiopathology</subject><subject>Cerebral Cortex - cytology</subject><subject>Cerebral Cortex - pathology</subject><subject>Cerebral Hemorrhage - pathology</subject><subject>Cerebral Hemorrhage - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Glial Fibrillary Acidic Protein - analysis</subject><subject>Injuries of the nervous system and the skull. Diseases due to physical agents</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Necrosis</subject><subject>Neurofilament Proteins - analysis</subject><subject>Neurons - chemistry</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Traumas. 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DCD produces experimental contusion by rapidly deforming the cerebral cortex with a transient, nonablative vacuum pulse of short duration (25 milliseconds) to mimic the circumstances of traumatic injury. A neuropathological evaluation was performed on brain tissue from adult rats sacrificed 3 days following induction of either moderate (4 psi, n=6) or high (8 psi, n=6) severity DCD. In all animals, DCD produced focal hemorrhagic lesions at the vacuum site without overt damage to other regions. Examination of histological sections showed localized gross tissue and neuronal loss in the cortex at the injury site, with the volume of cell loss dependent upon the mechanical loading (p&lt;0.001). Axonal pathology shown with neurofilament immunostaining (SMI-31 and SMI- 32) was observed in the subcortical white matter inferior to the injury site and in the ipsilateral internal capsule. No axonal injury was observed in the contralateral hemisphere or in any remote regions. Glial fibrillary acidic protein (GFAP) immunostaining revealed widespread reactive astrocytosis surrounding the necrotic region in the ipsilateral cortex. This analysis confirms that rapid mechanical deformation of the cortex induces focal contusions in the absence of primary damage to remote areas 3 days following injury. Although it is suggested that massive release of neurotoxic substances from a contusion may cause damage throughout the brain, these data emphasize the importance of combined injury mechanisms, e.g. mechanical distortion and excitatory amino acid mediated damage, that underlie the complex pathology patterns observed in traumatic brain injury.</abstract><cop>Hagerstown, MD</cop><pub>American Association of Neuropathologists, Inc</pub><pmid>10029098</pmid><doi>10.1097/00005072-199902000-00005</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record>
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source Oxford University Press Journals All Titles (1996-Current); MEDLINE; EZB-FREE-00999 freely available EZB journals; Journals@Ovid Complete
subjects Animals
Astrocytes - chemistry
Biological and medical sciences
Biomechanical Phenomena
Brain Chemistry - physiology
Brain Concussion - pathology
Brain Concussion - physiopathology
Cerebral Cortex - cytology
Cerebral Cortex - pathology
Cerebral Hemorrhage - pathology
Cerebral Hemorrhage - physiopathology
Disease Models, Animal
Glial Fibrillary Acidic Protein - analysis
Injuries of the nervous system and the skull. Diseases due to physical agents
Male
Medical sciences
Necrosis
Neurofilament Proteins - analysis
Neurons - chemistry
Rats
Rats, Sprague-Dawley
Traumas. Diseases due to physical agents
title Experimental Investigation of Cerebral Contusion: Histopathological and Immunohistochemical Evaluation of Dynamic Cortical Deformation
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