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Results for “Concussion”

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At least 19 recordsLinked to original sources

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↗

PubMed2026

Investigating genetic susceptibility to concussion through rare variants in ion channel and neurotransmission genes.

Some individuals appear more susceptible to concussion or mild traumatic brain injury (mTBI) and the severity, range, and the persistence of post-concussion symptoms vary considerably between affected individuals. Genetic factors are likely to contribute to this variability. Symptomatic overlap of post-concussion syndrome with neurological conditions such as familial hemiplegic migraine (FHM) caused by rare pathogenic variants in ion channel and synapse protein genes, with high sensitivity to head trauma for some patients, suggests that variation in similar pathways may influence concussion susceptibility and recovery. To investigate this hypothesis, we performed whole exome sequencing in 93 unrelated individuals who had sustained a single or multiple concussions and examined rare protein-altering variants in FHM genes, other neuronal ion channel and transporter genes, and genes involved in neurotransmission. We identified 62 different rare missense variants across 24 genes in 59 participants (63%), with 26 individuals carrying 2 or more variants. The prevalence of specific likely damaging rare variants in the 16 ion channel-related genes that were identified was approximately fivefold higher than that observed from gnomAD population controls (Odds Ratio = 5.44, 95% CI [4.13,7.18], P < 0.0001). Notably, voltage-gated calcium and sodium channel genes, including SCN9A, together with neurotransmission-related genes such as SNCAIP, harboured multiple potentially deleterious variants. These findings suggest that rare deleterious variants in genes involved in ion homeostasis and neurotransmission may contribute to an individual's susceptibility to concussion or more severe post-concussion symptoms. This study provides a foundation for future genetic and functional investigations aimed at improving our understanding of concussion susceptibility and outcomes. Further validation in larger cohorts and mechanistic studies is warranted to determine their utility as biomarkers of concussion risk and prognosis.

Humans↗

PubMed1977

[Surgery of concussion foci in the cerebral hemispheres].

On the basis of observations in 144 patients operated on because of severe cerebral concussions, the importance of primary and secondary removal of the concussion focus is stressed. The diagnosis is made by means of EEG, angiography, and echo encephalography. Examinations of the concussion region with clearance etc. showed that the immediate vicinity of the cerebral lesion exhibits a considerably reduced blood flow which, due to the stimulus of the concussion, will further decrease within the following days. After six days, the blood supply stabilises in the zone of the oscillating reaction. The enlargement of the zone of necrosis intensifies the intracranial increase in pressure and can only be avoided by the removal of the concussion. Resection is carried out subpial in order to isolate the cerebral tissue from the dura mater. Lethality: With solitary concussion foci 22%, in case of combination with intracranial haematoma 60%, with multiple foci 67%, total 46%.

Action Potentials↗

PubMed2026

Near and distance vergence facility provides complementary clinical information in concussion-related convergence insufficiency.

PURPOSE: To compare near and distance vergence facility testing in adolescents and young adults with concussion-related convergence insufficiency and evaluate changes following office-based vergence/accommodative therapy (OBVAM). METHODS: This secondary analysis of the CONCUSS randomized clinical trial evaluated vergence facility at near (40 cm) and distance (4 m) using a 12Δ base out/3Δ base in prism flipper. Participants aged 11-25 years with concussion-related convergence insufficiency were randomized to immediate or 6 weeks delayed OBVAM. Vergence facility was assessed at baseline, outcome time 1 assessment (after 12 therapy sessions for the immediate group and 6 weeks of watchful waiting for the delayed group), and outcome time 2 assessment (after both groups completed 16 therapy sessions). Agreement between near and distance vergence facility classifications was evaluated, and treatment-related changes were compared between groups. RESULTS: Of the 106 enrolled participants, 102 completed all study visits. At baseline, the near and distance vergence facility classifications demonstrated substantial discordance. Among 101 participants with both measures available, 49 demonstrated reduced distance vergence facility despite normal near vergence facility, whereas only two showed the opposite pattern (Cohen's κ = 0.12; p < 0.0001). Vergence facility improved following therapy in both treatment groups, with larger early improvements in the immediate-treatment group. CONCLUSIONS: Near and distance vergence facility testing provided complementary rather than interchangeable clinical information in adolescents and young adults with concussion-related convergence insufficiency. Both measures improved following vergence/accommodative therapy, supporting consideration of both testing distances in clinical assessment.

Humans↗

PubMed1975

Cumulative effect of concussion.

Twenty young adults were studied after a second concussion. The rate at which they were able to process information was reduced more than in controls who had been concussed only once, and they took longer to recover than the controls. The effects of concussion seem to be cumulative, and this has important implications for sports where concussion injury is common.

Adolescent↗

PubMed1977

Exerimental head injury in the rat. Part 2: Regional brain energy metabolism in concussive trauma.

A standardized model of acceleration concussion in the rat was used for the study of cerebral energy metabolism during the acute concussive reaction. Impact velocities of 7 and 9 m/sec were used, and the cerebral metabolic state was determined 1, 4, and 15 minutes after the impact. A concussive response could be sustained with a normal energy state in the tissue, but with the more intense reaction to a 9 m/sec impact, energy depletion usually occurred. At 1 minute these changes were most pronounced in the brain-stem regions. At 4 minutes the reactions were more varied but a progression usually occurred during this time, while at 15 minutes restitution was indicated. Hypoxia due to neurogenic pulmonary edema aggravated the state. The findings are compatible with a high metabolic rate during concussion, but progressive changes indicate the rapid appearance of complicating factors, including hypoxemia and probably also ischemia.

Adenine Nucleotides↗

PubMed1977

Experimental head injury in the rat. Part 3: Cerebral blood flow and oxygen consumption after concussive impact acceleration.

Cerebral blood flow (CBF) and oxygen consumption (CMRO2) were determined during timmediate posttraumatic period in rats subjected to concussive impact acceleration. According to previous studies an impact of 9 m/sec velocity elicited typical and marked symptoms of experimental concussion and often a prolonged comatose state, accompanied by cerebral metabolic signs of energy failure. During the immediate concussive response there was an increase of the CBF, followed within the next few minutes by a decrease to about one-third of normal flow, and then by a tendency toward normalization of flow 20 to 40 minutes posttrauma. Simultaneous measurements of cerebral oxygen extraction indicated an increase of the CMRO2 during the first minute. During the ischemic phase oxygen extraction increased but the lowest CBF values were only partially compensated for, and normal oxygen availability could not be maintained. The combined data, including cerebrospinal fluid pressure measurements, indicated primary cerebrovascular effects of the concussive trauma. These vasomotor effects may induce critical cerebral ischemia and thus profoundly influence posttraumatic cerebral function, and cause irreversible damage.

Animals↗

PubMed1977

Rate of cerebral energy consumption in concussive head injury in the rat.

The metabolic rate was determined in the rat brain during the immediate concussive response to standardized impact accelerations of 7 and 9 m/sec velocity. In one series, the metabolic state was determined in freeze-clamped cortical and brain-stem tissue 20 seconds after the impact. The metabolic rate was calculated from the rate of energy depletion in the adjacent unclamped tissue during 10 seconds of total ischemia. The freeze-clamping procedure per se was shown to enhance the metabolic rate probably by inducing mechanical excitation. In another series, in situ freezing was used for tissue sampling in the same situation. A 10-second period of heart standstill induced a standardized period of ischemia. During the acute concussive response to impact acceleration at 7 m/sec velocity, there was an increase of the metabolic rate in the brain stem. A more intense concussive impact at 9 m/sec velocity further enhanced this reaction and also involved the cortex. It is concluded that the basis of the immediate concussive response is a mechanically elicited neuronal excitation. This may lead to energy depletion unless the increased metabolic demands are met.

Adenine Nucleotides↗

PubMed1977

Concussion.

We have observed the effects of concussion on nonanesthetized rats and humans. We believe the phenomenon in both to be identical. There are four obvious stages to concussion and the recovery therefrom: fourth stage--visceral (respiratory) and somatic immobility; third stage--return of irregular visceral (respiratory) mobility with continuing somatic immobility; second stage--normal visceral mobility with impaired somatic mobility; and first stage--normal somatic mobility with impaired performance. Zero stage is complete normality. Our method of testing detects no lingering or permanent change after a single concussion. This proves only that we must continue with open minds on the question, "Does concussion always leave permanent brain damage?"

Animals↗

PubMedDate not supplied

Concussion: comparison of humans and rats.

Concussion is the most primitive and probably the most simple central nervous system response to an outside agent. Although millions of neurons undergo a very rapid reversal with loss and restoration of function, many physicians argue that every knockout blow leaves some residual damage, i.e., some or all of these neurons stop short of recovery. Clinical experience shows a wide discrepancy in the appearance or persistence of certain signs and symptoms after all types of head injury, but particularly after concussing blows, when third party or grievance cases are involved. Using slow motion filmstrips of boxing ring knockouts, we established a grading system for concussion and duplicated these grades in nonanesthetized rats. When we compared the performance, learning, and memory of concussed rats with their preconcussion performance and with the performance of nonconcussed controls, we were unable to find any differences.

Animals↗

PubMed1979

The morphopathologic substrates of concussion?

Neuronal inundation with i.v. infused horseradish peroxidase was studied following concussive brain injury by means of both light and electron microscopy. In animals sustaining mechanical brain injury of insufficient intensity as to elicit either microscopic intraparenchymal hemorrhage or other neuropathological change, yet of sufficient intensity as to provoke a physiological concussive response, vascular peroxidase exudation concomitant with neuronal peroxidase inundation occurred throughout the raphe and reticular core. Initially such inundated neurons were totally flooded with the tracer and as such appeared reminiscent of cells visualized in Golgi preparations. However, over the course of a 24-h period these peroxidae flooded neurons apparently organized the peroxidase into vesicles and vacuoles which assumed a perinuclear position from where the peroxidase ultimately reached both the nucleus and nucleolus. It was remarkable that these events occurred without any evidence of subcellular alteration. We interpret such initial inundation with this protein tracer, its ultimate reorganization, and its nuclear and nucleolar uptake as being consistent with some form of subtle and transient neuronal perturbation. We speculate that as such this neuronal perturbation may constitute a morphological correlate of the concussive episode.

Animals↗

PubMed1979

Experimental cerebral concussion. A histochemical study.

The activity of mitochondrial enzymes (succinic dehydrogenase and cytochrome oxidase) and enzymes associated with blood-brain barrier function (butyrylcholinesterase and alkaline phosphatase) in the CNS of rats was studied from 5 minutes to 62 hours after cerebral concussion. There was a transient increase in succinic dehydrogenase activity during the first hour after concussion in the neurons of the structures close to the impact. The alkaline phosphatase activity, strongly positive in the walls of normal blood vessels, decreased within five minutes after concussion; it virtually disappeared in 15 minutes but returned to normal level after 62 hours. These findings are in good correlation with previous electron microscopic observations. Their significance is discussed.

Alkaline Phosphatase↗

PubMed1992

Concussion is completely reversible; an hypothesis.

It is hypothesized that there is an entity properly called 'concussion', a transient loss of neuronal function without permanent neuronal damage, as defined years ago by Derek-Denny Brown. This implies that multiple concussions leave no deficit. n +1 times zero is still zero. Arguments are presented indicating that there is a margin of safety between the acceleration inducing 1-10 s loss of function (concussion) and that inducing permanent damage (contusions, lacerations).

Boxing↗

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↗

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

Light microscopic response of neuronal somata, dendrites and axons to post-mortem concussive head injury.

Forty anesthetized rats were cooled below 3 degrees C by 30-min transcardial perfusion of chilled physiological saline before a concussive head injury. The animals were then perfusion-fixed with a buffered formaldehyde-glutaraldehyde solution. Another forty rats were fixed by 30-min transcardial perfusion of the same fixative before a similar concussive head injury. In brain sections of both groups of animals a new silver method stained, in a Golgi-like fashion, a number of neurons and long axonal segments scattered among unstained ones. The similarity between these findings and those obtained following in vivo concussive head injuries described in accompanying papers suggests that the formation of traumatically induced argyrophilic neuronal damage is independent of metabolic processes, i.e., it may be a primary morphopathological process.

Animals↗

PubMed1992

An immediate light microscopic response of neuronal somata, dendrites and axons to contusing concussive head injury in the rat.

Thirty-four rats were killed by transcardial perfusion fixation 1 min after a contusing concussive head injury, and 17 rats 1 day later. From the results obtained with a new silver method demonstrating traumatically damaged neuronal somata, dendrites and axons the following conclusions were drawn: (1) outside the contused territories all features of traumatically induced neuronal argyrophilia are similar to those found in non-contusing concussive head injury, as reported in an accompanying paper; (2) within contused territories the neuronal argyrophilia is abolished by some substance released either from damaged blood vessels or damage parenchymal cells, while the neuronal damage otherwise underlying the induction of argyrophilia is present; (3) different phenotypes of neurons are vulnerable to different values of the parameters of the intracranial pressure wave generated by the trauma; (4) some of the neurons may recover from the traumatically induced argyrophilic damage; (5) traumatically induced inundation of neurons with extracellular tracers, as reported by other authors, and somato-dendritic argyrophilia may be different manifestations of one and the same phenomenon; and (6) diffuse primary traumatic axonal injury in human neuropathology may be closely correlated to axonal argyrophilia.

Animals↗

PubMed1992

Changes in hippocampal monoamine concentration following halothane anesthesia and concussion.

The concentration of norepinephrine in the hippocampus of rats anesthetized with halothane (Wyeth-Ayerst, Philadelphia, Pa) is found to be markedly increased, presumably due to the stress of handling and administering the anesthetic. This increased norepinephrine concentration persists for about 50 minutes but is obliterated when the anesthetized rat is concussed. This 50-minute period corresponds to the time it takes for a rat (or human), comatose for 1-2 seconds following concussion, to regain normal memory. No changes in 3,4-dihydroxybenzene-acetic acid (DOPAC), 3-(3,4-dihydroxyphenyl) alanine (L-DOPA), and 3,4-dihydroxybenzylamine (DHBA) were noted. 5-Hydroxy indole acetic acid (HIAA) showed a depression at 5 minutes and again at 30 minutes, changes that were consistent but not considered statistically significant.

Anesthesia, Inhalation↗