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At least 19 recordsLinked to original sources
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↗
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↗
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↗
PubMed1990

[Psychotherapy of patients with a history of brain concussion].

The author presents data on 168 patients: 75 during the acute period of brain concussion and 93 in the remote period of brain concussion. Age of the patients from 15 to 75 years. Drug treatment in these patients was combined with psychotherapy. Data are reported on the methods of psychotherapy including patients that suffered of concomitant chronic neurological and somatic diseases.

Adolescent↗
PubMed1992

[Brain concussion in patients with chronic vascular, gastrointestinal and pulmonary diseases].

Examined were 317 patients with brain concussion ranging in age from 16 to 75 years. Of them in 133 (41.91%), chronic diseases (I-II degree chronic insufficiency of cerebral circulation, arterial hypertension, chronic cholecystitis, gastric and duodenal ulcer disease, chronic bronchitis, bronchial asthma) were revealed. Peculiarities of the course of brain concussion in these patients are noted. The author stresses that it is necessary to take into account chronic diseases when observing and treating the sufferers with brain concussion.

Adolescent↗
PubMed1992

[The comprehensive diagnosis of patients with the sequelae of a brain concussion].

As many as 140 patients aged 16 to 75 years with a history of brain concussion were under observation. The observation periods were from 1 to 2 months after the acute period elapse up to 25 years. In addition to neurological examinations, the patients were subjected to echoencephalography, computer-aided tomography of the brain (38 patients), ultrasound tomoscopy of the brain (40 patients and 30 healthy subjects). It has been shown that the use of echoencephalography, computer-aided tomography and ultrasound tomoscopy of the brain makes it possible to identify, in some cases, different disorders on the part of the brain. The role of these methods in the diagnosis of brain concussion consequences increases, provided they are used combined or jointly with the data obtained during clinical examination and observation.

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↗
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↗
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↗
PubMed1990

[Long-term transcranial Doppler ultrasound monitoring in increased cerebrospinal fluid pressure caused by brain concussion].

Blood flow velocities of the basal cerebral arteries were studied by transcranial Doppler sonography in a 6 year old girl, comatous after cerebral contusion. Under progressive increase of cerebral pressure, Doppler sonographic long-term monitoring of the middle cerebral artery was performed parallel to the intracranial pressure until dissociated brain death. The results correlated closely with the cerebral perfusion pressure. Even before onset of the excessive increase in cerebral pressure no hyperventilation effect was seen in the contusion foci. Transcranial Doppler sonography represents an additional monitoring method for further improvement of treatment of severe head injuries.

Blood Flow Velocity↗
PubMed1991

[The superoxide dismutase activity of the brain and liver tissues in a rabbit with an experimental brain concussion].

A study is presented of the activity of superoxidedismutase and catalase in the brain and liver in the dynamics of mild head injury in experiments on rabbits. It was established that the activity of catalase in the brain show a three-times reduction within 15 minutes after the injury. The catalase activity in the liver remains practically unchanged. The activity of superoxidedismutase in the liver in the posttraumatic period does not differ from control values. In the brain superoxidedismutase activity reduces by 38% only on the 7 and 14 days after injury.

Animals↗