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PubMed2002

Delayed changes in regional brain energy metabolism following cerebral concussion in rats.

Traumatic brain injury (TBI) results in an acute altered metabolic profile of brain tissue which resolves within hours of initial insult and yet some of the functional deficits and cellular perturbations persist for days. It is hypothesized that a delayed change in energy status does occur and is a factor in the neural tissue's ability to survive and regain function. Regional metabolic profile and glucose consumption were determined at either 1 or 3 days following two different intensities of parasagittal fluid-percussion (F-P). A significant decrease in both 1CMRgluc and levels of ATP and P-creatine was evident in the hemisphere ipsilateral to the trauma at 1 day after the insult. The effect was greater in the cortical than the subcortical regions and was more pronounced at the higher trauma intensity. Normalization of glucose consumption and energy levels was essentially complete by 3 days. It would appear that the delayed metabolic changes at 1 day postinsult cannot be explained by a secondary ischemia since the changes in the metabolite profile do not elicit an increase in the consumption of glucose. These changes in energy metabolites may account for and contribute to the chronic neurological deficits following TBI.

Adenosine Triphosphate↗
PubMed2002

[Brain concussion: risk factors].

AIM: Identification of risk factors for intracranial bleeding after minor traumatic brain injury. METHOD: The charts of 464 patients treated between January 1976 and December 1997 with the initial diagnosis of minor traumatic brain injury were reviewed. They were analyzed for clinical and diagnostic signs putting the patients at risk for intracranial bleeding. RESULTS: About two thirds of the patients (67.5%) were males, the average age being 36.1 years. Leading causes of accident were sudden falls (27.4%) and bike/autocycle crashes (24.8%). 30.4% of the patients were under the influence of alcohol. At the time of admission to the hospital 17.2% of the patients showed impaired consciousness and 12.5% presented neurologic signs. In ten patients an intracranial bleeding was found. All these bleedings were diagnosed at the primary investigation. DISCUSSION/CONCLUSIONS: Following groups of patients with traumatic brain injury have an increased risk for intracranial bleeding: Age > 60 and < 16 years, sudden falls, tachycardia, Glasgow-Coma-Scale < 15, impairment of consciousness, neurologic signs, fracture of the skull and patients suffering from coagulopathy. Drunk patients are difficult to judge; therefore, they should be handled as being at risk. Patients at increased risk should be observed on an intensive care unit whereas patients without those risk factors can be observed on a normal ward or, alternatively, discharged after reexamination and uneventful course after some hours.

Adolescent↗
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↗
PubMedDate not supplied

[Sonographic follow-up of pronounced brain concussion in a 3-week-old infant following trauma caused by shaking].

Cerebral sonography was performed in a 3 week old whiplash shaken baby who had no external marks of injury and no skull fracture. On the day of admission, increased echogenicity in the white matter could be correlated with hypodense contusional lesions in the cranial computerized tomography. Sonographic follow-up showed multiple cystic defects in the white matter and later on marked dilatation of the adjacent lateral ventricle. In all infants with open anterior fontanel presenting with unexplained clouding of consciousness and/or external marks of child abuse, cerebral sonography should be a basic diagnostic method.

Brain↗
PubMed1996

[Post-concussion occlusion of the central artery and vein of the retina].

BACKGROUND: Combined simultaneous occlusion of the central retinal artery and central retinal vein occurs very rarely and has been observed in patients with systemic disorders such as leukaemia. CASE REPORT: We report a case of a young man who suffered a combined retinal vascular occlusion with occlusion of the posterior ciliary arteries following blunt trauma to the face with massive haematoma of the lids. To our knowledge, this is the first time that such a sequence of events has been recorded.

Adult↗