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At least 19 recordsLinked to original sources
PubMed1994

alpha-Phenyl-tert-butyl-nitrone inhibits free radical release in brain concussion.

Traumatic brain injury (TBI) is one of the important causes of mortality and morbidity. The pathogenesis of the underlying brain dysfunction is poorly understood. Recent data have suggested that oxygen free radicals play a key role in the primary and secondary processes of acute TBI. We report direct electron spin resonance (ESR) evidence of hydroxyl (.OH) radical generation in closed-head injury of rats. Moderate brain concussion was produced by controlled and reproducible mechanical, fixed, closed-head injury. A cortical cup was placed over one cerebral hemisphere within 20 min of the concussion, perfused with artificial cerebrospinal fluid (aCSF) containing the spin trap agent pyridyl-N-oxide-tert-butyl nitrone (POBN, 100 mM), and superfusate samples collected at 10 min intervals for a duration up to 130 min post brain trauma. In addition, POBN was administered systemically (50 mg/kg body wt.) 10 min pretrauma and 20 min posttrauma to improve our ability to detect free radicals. ESR analysis of the superfusate samples revealed six line spectra (alpha N = 15.4 G and alpha beta H = 2.5 G) characteristic of POBN-OH radical adducts, the intensity of which peaked 40 min posttrauma. The signal was undetectable after 120 min. Administration of alpha-phenyl-tert-butyl-nitrone (PBN), a spin adduct forming agent systemically (100 mg/kg body wt. IP 10 min prior to concussion) alone or along with topical PBN (100 mM PBN in aCSF), significantly (p < 0.001) attenuated the ESR signal, suggesting its possible role in the treatment of TBI.

Animals↗
PubMedDate not supplied

[Brain concussion--a minor craniocerebral injury].

INTRODUCTION: Brain concussion is a brain dysfunction without any macroscopic structural damage, caused by mechanical force. This research paper presents the occurrence and basic characteristics of patients with brain concussion without skull fracture. The second aim of this paper is to answer questions, related to this problem, neurosurgeons are most often asked by doctors of other specialties. MATERIAL AND METHODS: Posttraumatic amnesia (patient unable to remember events before and/or after injury) was a condition to diagnose the brain concussion. In 1995 there were 240 patients with brain concussions without skull fracture at the Department of Urgent Surgery of our Institute. Eighty of them (33%) have been admitted to the Neurosurgical Clinic for observation and/or treatment. In all patients with brain concussion the following diagnostic procedure was applied: personal history, physical and neurological examination, basic blood tests and skull x-rays. CT imaging of the brain is not a routine because of our economic and technical circumstances. RESULTS: 240 patients were examined; 67% were males. Glasgow coma score (GSC) was 13-15 in all patients, while in nonhospitalized patients it was 15 (GSC = 15). 54% of patients were 15-40 years old; 35% were 41-60 years old and 11% were older than 60 years of age. Average hospitalization lasted for 3.48 days. According to the Glasgow outcome scale all patients had a good recovery. DISCUSSION: Patients with brain concussion have always amnesia with normal neurologic status. Legal and clinical definition of the minor head injury are not completely equal. Brain concussion is legally always a minor head injury. Patients with organic damage of brain (legally severe injury) can clinically look like having minor injury initially or till the end of the illness. Risk for brain damage in patients with amnesia is about 3%. Posttraumatic amnesia is always established by asking patients to remember events and not asking them if they were unconscious. Brain concussion is often associated with headache, vegetative or/and psychotic difficulties. Diagnostic protocol should comprise at least personal history, physical and neurological examination and skull x-ray. Consultation of a neurosurgeon and hospitalization are not indicated in all cases. In our series it was done in 33% according to indications which are established. In these cases patients should be transported with documents describing the type of injury, diagnostic results and treatment performed. The therapy is symptomatic. After brain concussion gradual return to everyday activities is indicated. Sick leave of 7-10 days is usually sufficient. Postconcussion syndrome (headache, vegetative or psychotic disturbances) occurs often and may last for a long period of time. CONCLUSION: We tried to describe a doctrine for diagnostic and treatment of patients suffering from brain concussion most appropriate according to our technical and economical circumstances.

Adolescent↗
PubMed1997

A synergistic interaction between dopamine D1 and D2 receptor subtypes in the memory impairments induced by concussive brain injury (CBI) in mice.

Profound latent learning and memory deficits with increased monoamine levels in the brain following concussive brain injury (CBI) have been documented in our previous work. The purpose of the present study was to determine the role of dopamine (DA) receptor subtypes in the memory deficits associated with CBI. Profound latent learning and memory impairments were observed in the vehicle-treated CBI mice. SCH-23390 administered 15 min post-injury had no significant effects on the impairments of latent learning and memory in the CBI mice. Sulpiride significantly improved the impairments of latent learning and memory in a dose-dependent manner, indicating that activation of dopaminergic neuronal function is involved in the CBI-induced amnesia. Interestingly, co-administration of sulpiride and SCH-23390, at doses which alone has no significant effect, significantly ameliorated the impairments of latent learning and memory. These results strongly suggested that D1 and D2 receptor subtypes are synergistically involved in the dysfunction of learning and memory associated with CBI.

Animals↗
PubMed2005

Temporal window of vulnerability to repetitive experimental concussive brain injury.

OBJECTIVE: Repetitive concussive brain injury (CBI) is associated with cognitive alterations and increased risk of neurodegenerative disease. METHODS: To evaluate the temporal window during which the concussed brain remains vulnerable to a second concussion, anesthetized mice were subjected to either sham injury or single or repetitive CBI (either 3, 5, or 7 days apart) using a clinically relevant model of CBI. Cognitive, vestibular, and sensorimotor function (balance and coordination) were evaluated, and postmortem histological analyses were performed to detect neuronal degeneration, cytoskeletal proteolysis, and axonal injury. RESULTS: No cognitive deficits were observed in sham-injured animals or those concussed once. Mice subjected to a second concussion within 3 or 5 days exhibited significantly impaired cognitive function compared with either sham-injured animals (P < 0.05) or mice receiving a single concussion (P < 0.01). No cognitive deficits were observed when the interconcussion interval was extended to 7 days, suggestive of a transient vulnerability of the brain during the first 5 days after an initial concussion. Although all concussed mice showed transient motor deficits, vestibulomotor dysfunction was more pronounced in the group that sustained two concussions 3 days apart (P < 0.01 compared with all other groups). Although scattered degenerating neurons, evidence of cytoskeletal damage, and axonal injury were detected in selective brain regions between 72 hours and 1 week after injury in all animals sustaining a single concussion, the occurrence of a second concussion 3 days later resulted in significantly greater traumatic axonal injury (P < 0.05) than that resulting from a single CBI. CONCLUSION: These data suggest that a single concussion is associated with behavioral dysfunction and subcellular alterations that may contribute to a transiently vulnerable state during which a second concussion within 3 to 5 days can lead to exacerbated and more prolonged axonal damage and greater behavioral dysfunction.

Animals↗
PubMedDate not supplied

[Brain stem auditory evoked potentials in the early period after a brain concussion].

Acoustic truncal evoked potentials (ATEP) were studied in 24 patients in the first 48 hours after concussion of the brain. The absolute peak latency of components 1, 3, and 5, the interpeak intervals 1-3, 3-5, and 1-5, and the interaural difference were determined. The results were compared with those of examination of a control group of 24 healthy individuals. Individual and group appraisal failed to reveal any significant differences from normal values in none of the studied parameters in patients with brain concussion. The informativeness of the method in mild craniocerebral trauma is discussed.

Adolescent↗
PubMed2003

[A study on the expression of C-FOS protein after experimental rat brain concussion].

OBJECTIVE: To study the relationship between expression of C-FOS protein and brain concussion and find a sensitive marker of diagnosis of the brain concussion. METHODS: Fifty-five rats were randomly divided into brain concussion groups and control group. The expression of C-FOS protein was microscopically observed by immunohistochemical method. RESULTS: There were negative expression of C-FOS protein in control group. In brain concussion group, however, positive expression of C-FOS protein in some neurons was seen at 15 min after brain concussion, and reach to the peak at 6 h after brain concussion, then decreased gradually. CONCLUSION: These findings suggest that detection of C-FOS protein could be an index of diagnosis of brain concussion and a sensitive marker of timing of injury after brain concussion.

Animals↗
PubMed2006

[The expression of GFAP after brain concussion in rats].

OBJECTIVE: To study the expression of GFAP and pathologic changes after rats brain concussion, so that to provide evidence on brain concussion for forensic identification. METHODS: Forty-five SD rats were divided into 3, 6, 12, 24 h and 2, 4, 7, 10 d and normal control groups in terms of different wounding time after brain concussion model established, and the expression of GFAP after rats brain concussion were then observed by using SP immunohistochemical method. RESULTS: In normal control brain, low-level GFAP expressions could be observed. After six hours' brain concussion, GFAP positive cells increased obviously. The trend reached to the peak at 7d, partly declined at 10d, then decreased gradually. CONCLUSION: Brain concussion induced the expression of GFAP. The detection of GFAP could be useful for diagnosis of brain concussion on forensic pathology, and could be a reference index for timing of injury after brain concussion.

Animals↗
PubMed1992

Administration of excitatory amino acid antagonists via microdialysis attenuates the increase in glucose utilization seen following concussive brain injury.

Immediately following concussive brain injury, cells exhibit an increase of energy demand represented by the activation of glucose utilization. We have proposed that this trauma-induced hypermetabolism reflects the effort of cells to restore normal ionic balance disrupted by massive ionic fluxes through transmitter-gated ion channels. In the present study, changes in local CMRglc following fluid-percussion concussive injury were determined using [14C]2-deoxy-D-glucose autoradiography, and the effects of in situ administration (via microdialysis) of excitatory amino acid (EAA) antagonists [kynurenic acid (KYN), 2-amino-5-phosphonovaleric acid (APV; 100 microM, 1 mM, and 10 mM), and 6-cyano-7-nitroquinoxaline-2,3-dine (CNQX; 300 microM, 1 mM, and 10 mM] on glucose utilization were investigated. Animals that did not receive dialysis showed a remarkable increase (up to 181% of normal control) in cortical glucose utilization following injury. In contrast, this high demand for glucose was reduced in areas infiltrated with KYN, APV, and CNQX. These results indicate that EAA-activated ion channels are involved in the posttraumatic increase in glucose utilization, reflecting the energy demand of cells required to drive pumping mechanisms against an ionic perturbation seen immediately following the concussive injury. The effects of KYN, APV, and CNQX suggest that although all subtypes of the glutamate receptor appear to be involved in this phenomenon, N-methyl-D-aspartate-activated channels may play a major role.

2-Amino-5-phosphonovalerate↗
PubMedDate not supplied

[Current views on brain concussion].

Modern views on brain concussion are reviewed by the authors who present also the evolution of the views on this problem in the last five decades. Owing to devising of an experimental model of light craniocerebral injuries the presence of structural changes in the central nervous system developing after concussion has been demonstrated. Using the modern diagnostic imaging techniques (SPECT) in clinical practice persistent disturbances of regional cerebral blood flow were found following such head injuries. The mechanism, which could explain the development of cerebral perfusion changes, could produce also axonal disorders, breakdown of the blood-brain barrier, atrophy of hippocampal neurons which lesions had been noted previously in experiments. The results of SPECT investigations put in doubt the presence of a "pure" functional brain damage following slight craniocerebral injury and provide evidence for the existence will aim at correlating of electrophysiological phenomena, vascular changes and biochemical disturbances with lesions leading to disorders of behaviour observed in the so called postconcussion syndromes.

Atrophy↗
PubMed2006

[Expression of c-myc protein on rats' brains after brain concussion].

OBJECTIVE: To study the changes of expression of c-myc protein on rats' brains after brain concussion. METHODS: sixty rats were randomly divided into brain concussion groups and control group. The expression of c-myc protein was microscopically observed by immunohistochemical method. RESULTS: No expression of c-myc protein in control group were observed. However, positive expression of c-myc protein in some neurons was seen at 20 min after brain concussion, and reach to the peak at 8h after brain concussion and then decreased gradually. CONCLUSION: These findings suggest that the detection of c-myc protein could be an index of diagnosis of brain concussion.

Animals↗
PubMed2003

Traumatic cerebral vascular injury: the effects of concussive brain injury on the cerebral vasculature.

In terms of human suffering, medical expenses, and lost productivity, head injury is one of the major health care problems in the United States, and inadequate cerebral blood flow is an important contributor to mortality and morbidity after traumatic brain injury. Despite the importance of cerebral vascular dysfunction in the pathophysiology of traumatic brain injury, the effects of trauma on the cerebral circulation have been less well studied than the effects of trauma on the brain. Recent research has led to a better understanding of the physiologic, cellular, and molecular components and causes of traumatic cerebral vascular injury. A more thorough understanding of the direct and indirect effects of trauma on the cerebral vasculature will lead to improvements in current treatments of brain trauma as well as to the development of novel and, hopefully, more effective therapeutic strategies.

Animals↗
PubMed1976

[Autoradiographic investigations in repeated experimental brain concussion (author's transl)].

Single brain concussion in rabbits causes an increased proliferation of glial and mesenchymal cells. Repeated experimental concussions in rabbits (3 times at intervals of 24 h) led to an increased incorporation of H3-thymidine in glial and mesenchymal cells with a maximum at 48 h after the third concussion. This is interpreted as an indication of increased cell proliferation. The first and the second concussion did not cause a comparable reaction, thus suggesting that concussions may inhibit DNA synthesis under the conditions of our experimental setup. When the concussions were induced at an interval of 48 h the result was different: 48 h after each concussion we found an increase of labeled cells compared with the controls. After the second concussion the reaction was still more enhanced compared with the reaction following the first concussion. In contrast to this the number of labeled cells after the third concussion was significantly decreased compared with those after the second one. Parallels with pugilistic encephalopathy are discussed.

Animals↗