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PubMed1993

Concussive brain injury is associated with a prolonged accumulation of calcium: a 45Ca autoradiographic study.

In order to determine the extent and duration of calcium (Ca2+) flux following a lateral fluid percussion brain injury in the rat, 45Ca autoradiography was used to study animals immediately, 6, 24 and 96 h after the insult. In addition, cell suspension studies were conducted to determine the extent of cellular flux of 45Ca. Optical density and/or scintillation counting was utilized to provide a relative measure of 45Ca accumulation within 20 different structures. The results indicated that in animals who exhibited no gross morphological damage, 45Ca accumulation following injury was exhibited primarily within the ipsilateral cerebral cortex, dorsal hippocampus and striatum. This accumulation continued for several days returning to control levels by the 4th day after injury. In animals who sustained morphological damage, the contusion site exhibited a marked accumulation of 45Ca which did not resolve spontaneously over the course of 4 days. We conclude from this work that Ca2+ flux is a major component of this experimental model of traumatic injury. Furthermore, that depending on the extent of cell damage, the accumulation of Ca2+ is regionally different. Finally, that even in an injury which by itself does not produce gross morphological tissue damage, accumulation of Ca2+ can continue for at least 48 h.

Animals↗
PubMed1990

Changes in cortical extracellular levels of energy-related metabolites and amino acids following concussive brain injury in rats.

The aim of this study was to measure extracellular chemical changes in the cerebral cortex in response to compression contusion trauma in rats. Energy-related metabolites (i.e., lactate, pyruvate, adenosine, inosine, and hypoxanthine) and amino acids were harvested from the extracellular fluid (ECF) using microdialysis and analyzed by high-performance liquid chromatography. The measurements were performed in cortical tissue, where neuronal injury occurs in this model. The severity of the trauma was varied by using different depths of impact: mild trauma, 1.5 mm; severe trauma, 2.5 mm. The trauma induced a dramatic increase in the ECF levels of energy-related metabolites that was conditioned by the severity of the insult. The ECF level of taurine, glutamate, aspartate, and gamma-aminobutyric acid (GABA) also rose markedly, while other amino acids did not change significantly. The results suggest that the trauma induced a transient, profound focal disturbance of energy metabolism in the cortical tissue, probably as a result of mechanically induced disruption of ion homeostasis and reduced blood flow in combination. The data support the potential role of glutamate and aspartate as mediators of traumatic brain injury. However, the concomitantly released adenosine, GABA, and taurine may be protective and ameliorate excitotoxicity. In analogy with the reported cumulative damaging effects of repeated ischemic insults, the observed ECF changes may help explain the vulnerability of traumatized brain tissue to secondary ischemia.

Adenosine↗
PubMed1989

Increased plasma PGE2, 6-keto-PGF1 alpha, and 12-HETE levels following experimental concussive brain injury.

Previous investigations have shown that brain prostaglandin levels are transiently elevated following experimental fluid percussion brain injury. Associated with these increased prostaglandin levels there is free radical production and abnormalities in cerebral arteriolar function. The purpose of this study was to determine whether experimental fluid percussion brain injury in cats is associated with increased systemic levels of prostaglandins and the lipoxygenase product, 12-HETE. Blood samples were collected before and at various periods of time after 2.7 atm of fluid percussion brain injury was produced in adult cats. Prostaglandin and 12-HETE analysis was performed by radioimmunoassay after extraction of the plasma samples. The control levels for 6-keto-PGF1 alpha, PGE2, and 12-HETE were 477 +/- 42, 2,372 +/- 431, and 13,328 +/- 1,769 pg/ml, respectively. Following injury all three eicosanoids reached peak plasma levels by 1-5 min after injury. The percentile increases for all eicosanoids were similar and increased from 70 to 110%. The increases were sustained at up to 30 min postinjury and by 1 h after injury were at control levels. As in previous studies, hypertension following injury was maximal by 1 min postinjury and blood pressure had returned to near normal levels by 5 min postinjury. These studies demonstrate prolonged systemic increases in eicosanoids following injury. Since free radical production and vascular damage occur concomitantly with eicosanoid production, the prolonged increases in these products suggest that there is an attainable therapeutic window following injury during which administration of free radical scavengers may decrease radical damage and reduce the consequences of injury.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed2000

Inhibition of neocortical plasticity during development by a moderate concussive brain injury.

To determine if a moderate traumatic brain injury (TBI) sustained early in life alters the capacity for developmental plasticity, 17-20-day-old rat pups received a lateral fluid percussion and then reared in an enriched environment for 17 days. Compared to sham-injured controls, this moderate TBI prevented the increase in cortical thickness (1.48 vs. 1.68 mm, p < 0.01) as well as the corresponding enhancement in cognitive performance in the Morris Water Maze (39 vs. 25 trials to criterion, p < 0.05). These injured animals exhibited no significant neuronal degeneration and no evidence of neurologic or motor deficits. These findings strongly support the conclusion that a diffuse brain injury is capable of inhibiting both anatomical and cognitive manifestations of experience-dependent developmental plasticity.

Animals↗
PubMedDate not supplied

[Short-latency brain-stem auditory evoked potentials in patients with a brain concussion].

The short-latent acoustic stem potentials were examined in 72 males aged 9 to 61 years (mean 32.3 +/- 10.2 years) with concussion of the brain in different early posttraumatic periods (0.5-15 days). The clinical picture of the victims was characterized by systemic cerebral and mild transient symptoms of involvement of stem regions of the brain. Two thirds of the patients were found to have decreased rates of conduction of electric pulses along the acoustic pathway of the brain stem. Moreover, a fourth of the victims had a retarded perception of acoustic stimuli, which implies that concussion of the brain led to the decreased function of the auditory nerve and all relay nuclei of the acoustic system of the brain. The normal pattern of short-latent acoustic stem evoked potentials was seen in 8.3%, their mild and moderate abnormal changes were observed in 40.3 and 51.4% of the patients. Prolongation of a latent period and interpeak intervals, the deformation and lack of waves were considered to be criteria for abnormal changes in short-latent acoustic stem evoked potentials.

Acoustic Stimulation↗
PubMed1990

Massive increases in extracellular potassium and the indiscriminate release of glutamate following concussive brain injury.

An increase in extracellular K+ concentration ([K+]c) of the rat hippocampus following fluid-percussion concussive brain injury was demonstrated with microdialysis. The role of neuronal discharge was examined with in situ administration of 0.1 mM tetrodotoxin, a potent depressant of neuronal discharges, and of 0.5 to 20 mM cobalt, a blocker of Ca++ channels. While a small short-lasting [K+]c increase (1.40- to 2.15-fold) was observed after a mild insult, a more pronounced longer-lasting increase (4.28- to 5.90-fold) was induced without overt morphological damage as the severity of injury rose above a certain threshold (unconscious for 200 to 250 seconds). The small short-lasting increase was reduced with prior administration of tetrodotoxin but not with cobalt, indicating that neuronal discharges are the source of this increase. In contrast, the larger longer-lasting increase was resistant to tetrodotoxin and partially dependent on Ca++, suggesting that neurotransmitter release is involved. In order to test the hypothesis that the release of the excitatory amino acid neurotransmitter glutamate mediates this increase in [K+]c, the extracellular concentration of glutamate ([Glu]c) was measured along with [K+]c. The results indicate that a relatively specific increase in [Glu]c (as compared with other amino acids) was induced concomitantly with the increase in [K+]c. Furthermore, the in situ administration of 1 to 25 mM kynurenic acid, an excitatory amino acid antagonist, effectively attenuated the increase in [K+]c. A dose-response curve suggested that a maximum effect of kynurenic acid is obtained at a concentration that substantially blocks all receptor subtypes of excitatory amino acids. These data suggest that concussive brain injury causes a massive K+ flux which is likely to be related to an indiscriminate release of excitatory amino acids occurring immediately after brain injury.

Animals↗
PubMed1981

Inhibition by free radical scavengers and by cyclooxygenase inhibitors of pial arteriolar abnormalities from concussive brain injury in cats.

We studied the role of prostaglandins and free radicals in the induction of the functional and morphological pial arteriolar abnormalities produced by concussive brain injury. Anesthetized cats equipped with a cranial window for the observation of the pial microcirculation were subjected to concussive brain injury using a fluid-percussion device following administration of cyclooxygenase inhibitors (indomethacin or AHR-5850) or the vehicle for the solution of these agents (NaCl or Na2CO3 solution). Pial arterioles from vehicle-treated animals displayed sustained dilation, reduced responsiveness to the vasoconstrictor effect of arterial hypocapnia, and a high density of endothelial lesions. Animals pretreated with cyclooxygenase inhibitors showed less pronounced vasodilation, normal responsiveness to hypocapnia, and a significantly reduced number of lesions. The vasodilation and reduced responsiveness to the vasoconstrictor effects of hypocapnia after brain injury also were inhibited by topical application of free radical scavengers (nitroblue tetrazolium, superoxide dismutase, or mannitol). The vessels from cats pretreated with free radical scavengers also had a lower density of endothelial lesions than controls. The results support the view that the immediate cause of cerebral arteriolar damage in concussive brain injury is the generation of free oxygen radicals associated with increased prostaglandin synthesis.

Animals↗
PubMed1999

[The status of adaptive-compensatory mechanisms after the brain concussion in children].

80 children of preschool age were observed after concussion of the brain. In follow-up from 6 months 3 years clinical-anamnestic and neuropsychologic methods were used. The functions of autonomic nervous system were evaluated according to the results of estimation of initial autonomic tonus, autonomic reactivity, autonomic maintenance of the activity and the data of cardiointervalography. The state of nonspecific systems of the brain was studied with day time polygraphic research with a visual EEG evaluation, construction of histogramms by Fora method, estimation of speed and order of the fading of the components of a rough response. Psychovegetative stress was the ground for neurologic disorders in posttraumatic period. The disorders of adaptive regulation were manifested in exhausting of ergotropic systems with compensatory overstrain of trophotropic mechanisms, resulted in predominance of inhibiting influences with an inadequate response of synchronization on EEG during functional loads. Severity of clinical manifestations and disorders of adaptive regulation were more pronounced in children 1-3 year-old and with hypoxic-traumatic damages of the brain in anamnesis. Disintegration of cerebral activity correlated with the remote period. In the first 6-12 months after the concussion of the brain changes of vegetative reactivity prevailed, after 18 months the alterations in vegetative maintenance progressed.

Brain Concussion↗
PubMed1997

Brain concussion produces transient hypokalemia in children.

Hyperglycemia and hypokalemia caused by catecholamine discharge have been reported to occur in patients after severe head trauma. The aim of this prospective study was to evaluate whether a similar neuroendocrine and metabolic response is found in children after minor head trauma such as brain concussion (Glasgow Coma Scale (GCS) > or = 13). One hundred fifty patients aged 2 to 14 years (average, 6 years) were divided into three groups (n = 50 in each group). Group 1 included patients admitted to the emergency department for brain concussion (Glasgow Coma Scale (GCS) > or = 13); group 2 included patients admitted for fractures of long bones without head injury; and group 3 were control patients electively admitted for hernia repair. All patients had complete physical and neurological examinations. Complete blood count and blood chemistry were obtained on admission. All blood tests were repeated at 6, 12, and 24 hours in patients belonging to group 1. An electrocardiogram was obtained in selected patients and catecholamine levels were measured in some patients. Statistical analysis was performed using analysis of variance (ANOVA). Serum potassium and sodium levels in patients with brain concussion (group 1) were 3.6 +/- 0.6 and 136 +/- 3 mEq/L, respectively and were significantly lower (P < 0.01) than those in patients belonging to group 2, 4 +/- 0.4 and 138 +/- 3, respectively, and the controls (group 3), 4.2 +/- 0.5 and 140 +/- 2, respectively. Serum glucose level was 124 +/- 34 and 118 +/- 32 mg% in groups 1 and 2 and was significantly higher than that of the controls (group 3), 90 +/- 23 mg%. There was no correlation between serum electrolytes and GCS. No electrocardiogram changes or elevation of serum catecholamines were found. Hypokalemia resolved spontaneously within 24 hours. All patients recovered without neurological sequalae. Transient hypokalemia frequently occurs in children even with minor head trauma. This hypokalemia resolves spontaneously, without treatment and within 24 hours.

Adolescent↗
PubMedDate not supplied

[Inconsistencies between clinical and forensic recognition of brain concussion in the material of the Department of Forensic Medicine of the Medical Academy in Bydgoszcz].

The material contains 128 cases of brain concussion diagnosed by physicians since 1995 to 2000. The bases of diagnosing and the rules of opinionating of brain concussion after trauma of the head were discussed. Inconsistencies between clinical diagnosis and forensic medical opinionating were observed in 69.53%. In the group of patients who were intoxicated at the moment of head trauma disagreement was observed in 91.30%.

Academic Medical Centers↗
PubMed2005

[Headache occurrence and assessment of regional blood flow after brain concussion in children].

BACKGROUND AND PURPOSE: Headaches which can last for many months and even years belong to the most frequent consequences of closed head injuries in children. The method which makes it possible to demonstrate the presence and extent of the nervous tissue damage caused by trauma is the regional cerebral blood flow (rCBF) evaluation with single photon emission computerized tomography (SPECT). In the present study the regional cerebral blood flow (rCBF) was assessed 10-15 days after trauma, 3 months and one year in cases of brain concussion. We tried to establish whether there was a correlation between changes in rCBF and the occurrence of posttraumatic headache. MATERIAL AND METHODS: SPECT was applied in 32 children, aged 6-16, 10-15 days, and then 3 and 12 months after brain concussion. In all children no changes were found in CT and MRI examinations. RESULTS: In the studied group in the early period after trauma, blood flow impairment was found in 21 children, mostly in frontal areas. One year after trauma the rCBF improved in 11 children, in 10 cases the pattern was normal. In a group of 4 children with headache one year after brain concussion, three of them still presented the impairment of blood flow. CONCLUSIONS: SPECT shows a great sensitivity and usefulness in the assessment of consequences of head trauma and it can explain some posttraumatic complaints in children.

Adolescent↗
PubMed1980

Physiological effects of controlled concussive brain trauma.

Utilizing a fluid percussion device, we measured the physiological effects of brain trauma in cats exposed to controlled levels of injury. Concussive brain injury at 3-4 atm of intensity led to profound elevations of the mean systemic arterial blood pressure from 128 +/- 26 to 229 +/- 33 mmHg, left ventricular end-diastolic pressure from 4 +/- 2 to 24 +/- 15 mmHg, and pulmonary wedge pressures (PWP) from 5 +/- 3 to 27 +/- 17 mmHg and a relatively moderate increase in intracranial pressure (ICP) from 6 +/- 3 to 38 +/- 31 mmHg (all P < 0.001). Pulmonary edema was evidenced by a significant increase in lung tissue wet-to-dry weight ratios to 3.74 +/- 0.81 as compared with a control group of 2.29 +/- 0.23 (P < 0.001). There was poor correlation between wet-to-dry weight ratios and PWP. Approximately 60% of all spontaneously breathing animals become permanently apneic within 6 min after injury, while the remaining 40% developed transient apnea. Arterial O2 or CO2 pressure alterations, in contrast to pretreatment with phentolamine did not affect the hemodynamic or edemogenic response to trauma. Phentolamine did not block the apneic response or increase in ICP. Comparative studies using intravenous levarterenol without trauma produced responses similar to trauma. Concussive brain injury of 3-4 atm results in pulmonary edema, apnea, sympathetically mediated peripheral vasoconstriction and left ventricular failure effect.

Animals↗