Cerebral Hemodynamics and Metabolism Following Experimental Head Injury
01 Mar 1970-Journal of Neurosurgery (Journal of Neurosurgery Publishing Group)-Vol. 32, Iss: 3, pp 304-319
TL;DR: The present experiments were undertaken to clarify the nature of acute cerebral disorders resulting from head injury and based on experimental observations of concussion produced by a pendulum striking the freely moving head, it was concluded that this type of concussion was due to temporary paralysis of nervous function.
Abstract: T HE pathogenesis of cerebral concussion has long been debated. The present experiments were undertaken to clarify the nature of acute cerebral disorders resulting from head injury. Concussion was defined by Denny-Brown as a "transitory and reversible nervous reaction with immediate onset following physical stress of sufficient violence and brevity, and characterized by progressive recovery thereafter. ''~ There are two main theories concerning the pathogenesis of concussion: the excitation theory of Walker, e t al., 4a and the paralytic theory of Denny-Brown and Russell2 These two theories, which postulate opposite mechanisms, will be reviewed. Walker and his associates 43 observed the appearance of fast activity in the electroencephalogram (EEG) with little change in amplitude immediately after a compressive impact applied to the exposed dura and brain in experimental animals. This was followed by '"extinction." The EEG changes were frequently accompanied by tonic extension movements of the extremities. They suggested that this type of concussion resulted from excitation of the central nervous system. An opposite view was proposed by Denny-Brown and Russell. Based on experimental observations of concussion produced by a pendulum striking the freely moving head (acceleration concussion), they concluded that this type of concussion was due to temporary paralysis of nervous function. In man, concussion is characterized by transient loss of neural function, accompa-
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TL;DR: This study suggests thatPlayers with a history of previous concussions are more likely to have future concussive injuries than those with no history; 1 in 15 players with a concussion may have additional concussions in the same playing season; and previous concussion may be associated with slower recovery of neurological function.
Abstract: ContextApproximately 300 000 sport-related concussions occur annually
in the United States, and the likelihood of serious sequelae may increase
with repeated head injury.ObjectiveTo estimate the incidence of concussion and time to recovery after concussion
in collegiate football players.Design, Setting, and ParticipantsProspective cohort study of 2905 football players from 25 US colleges
were tested at preseason baseline in 1999, 2000, and 2001 on a variety of
measures and followed up prospectively to ascertain concussion occurrence.
Players injured with a concussion were monitored until their concussion symptoms
resolved and were followed up for repeat concussions until completion of their
collegiate football career or until the end of the 2001 football season.Main Outcome MeasuresIncidence of concussion and repeat concusion; type and duration of symptoms
and course of recovery among players who were injured with a concussion during
the seasons.ResultsDuring follow-up of 4251 player-seasons, 184 players (6.3%) had a concussion,
and 12 (6.5%) of these players had a repeat concussion within the same season.
There was an association between reported number of previous concussions and
likelihood of incident concussion. Players reporting a history of 3 or more
previous concussions were 3.0 (95% confidence interval, 1.6-5.6) times more
likely to have an incident concussion than players with no concussion history.
Headache was the most commonly reported symptom at the time of injury (85.2%),
and mean overall symptom duration was 82 hours. Slowed recovery was associated
with a history of multiple previous concussions (30.0% of those with ≥3
previous concussions had symptoms lasting >1 week compared with 14.6% of those
with 1 previous concussion). Of the 12 incident within-season repeat concussions,
11 (91.7%) occurred within 10 days of the first injury, and 9 (75.0%) occurred
within 7 days of the first injury.ConclusionsOur study suggests that players with a history of previous concussions
are more likely to have future concussive injuries than those with no history;
1 in 15 players with a concussion may have additional concussions in the same
playing season; and previous concussions may be associated with slower recovery
of neurological function.
1,450 citations
Cites background from "Cerebral Hemodynamics and Metabolis..."
...Animal studies have described an acute neurometabolic cascade involving accelerated glycolysis and increased lactate production immediately following concussion.(28-30,43-45) The increased lactate is believed to leave neurons more vulnerable to secondary ischemic injury and has been considered a possible predisposition to repeat injury....
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01 Jan 2003
TL;DR: Departments of Exercise andSport Science (Drs Guskiewicz and Cantu), Ortho-paedics, Orthopaedics and Epidemi-ology (Dr Marshall), and Injury Prevention ResearchCenter (Dr Onate), University ofNorth Carolina at Chapel Hill; Neuroscience Center,Waukesha Memorial Hospital, Waukeha, Wis (DrMcCrea); Department of Neurology, Medical Collegeof Wisconsin, Milwaukee (Dr McCrea); NeurosurgeryService, Emerson Hospital, Concord, Mass(Dr Cantu); Chicago Neurological Institute (D
Abstract: Departments of Exercise andSport Science (Drs Guskiewicz and Cantu), Ortho-paedics (Drs Guskiewicz and Marshall), and Epidemi-ology (Dr Marshall), and Injury Prevention ResearchCenter (Drs Guskiewicz and Marshall), University ofNorth Carolina at Chapel Hill; Neuroscience Center,Waukesha Memorial Hospital, Waukesha, Wis (DrMcCrea); Department of Neurology, Medical Collegeof Wisconsin, Milwaukee (Dr McCrea); NeurosurgeryService, Emerson Hospital, Concord, Mass(Dr Cantu); Chicago Neurological Institute (Drs Ran-dolph and Kelly) and Department of Neurology,Northwestern University Feinberg School of Medicine(Dr Kelly), Chicago, Ill; Department of Neurology,Loyola University Medical School, Maywood, Ill (DrRandolph); Department of Neurology, New YorkUniversity School of Medicine, New York (Dr Barr);and Department of Rehabilitation Sciences AthleticTraining Program, Sargent College of Health andRehabilitation Sciences, Boston University, Boston,Mass (Dr Onate).
1,439 citations
Journal Article•
TL;DR: Improved guidelines for clinical management of concussion may be formulated as the functional significance and duration of these postinjury neurometabolic derangements are better delineated.
Abstract: OBJECTIVE: To review the underlying pathophysiologic processes of concussive brain injury and relate these neurometabolic changes to clinical sports-related issues such as injury to the developing brain, overuse injury, and repeated concussion DATA SOURCES: Over 100 articles from both basic science and clinical medical literature selected for relevance to concussive brain injury, postinjury pathophysiology, and recovery of function DATA SYNTHESIS: The primary elements of the pathophysiologic cascade following concussive brain injury include abrupt neuronal depolarization, release of excitatory neurotransmitters, ionic shifts, changes in glucose metabolism, altered cerebral blood flow, and impaired axonal function These alterations can be correlated with periods of postconcussion vulnerability and with neurobehavioral abnormalities While the time course of these changes is well understood in experimental animal models, it is only beginning to be characterized following human concussion CONCLUSIONS/RECOMMENDATIONS: Following concussion, cerebral pathophysiology can be adversely affected for days in animals and weeks in humans Significant changes in cerebral glucose metabolism can exist even in head-injured patients with normal Glasgow Coma Scores, underscoring the need for in-depth clinical assessment in an effort to uncover neurocognitive correlates of altered cerebral physiology Improved guidelines for clinical management of concussion may be formulated as the functional significance and duration of these postinjury neurometabolic derangements are better delineated
1,318 citations
TL;DR: A randomized, controlled trial compared the effects of moderate hypothermia and normothermia in 82 patients with severe closed head injuries and found thatHypothermia may limit some of the deleterious metabolic responses of traumatic brain injury.
Abstract: Early reports of therapeutic hypothermia for severe traumatic brain injury can be traced back to the first half of the 20th century. It is only within the last two decades that clinical studies have demonstrated that therapeutic moderate hypothermia for brief durations can improve patient outcomes following brain injury. The historical background, recent clinical experience, and mechanisms of action of moderate hypothermia are reviewed.
1,212 citations
TL;DR: It is concluded that this simple model is capable of producing a graded brain injury in the rodent without a massive hypertensive surge or excessive brain-stem damage.
Abstract: This report describes the development of an experimental head injury model capable of producing diffuse brain injury in the rodent. A total of 161 anesthetized adult rats were injured utilizing a simple weight-drop device consisting of a segmented brass weight free-falling through a Plexiglas guide tube. Skull fracture was prevented by cementing a small stainless-steel disc on the calvaria. Two groups of rats were tested: Group 1, consisting of 54 rats, to establish fracture threshold; and Group 2, consisting of 107 animals, to determine the primary cause of death at severe injury levels. Data from Group 1 animals showed that a 450-gm weight falling from a 2-m height (0.9 kg-m) resulted in a mortality rate of 44% with a low incidence (12.5%) of skull fracture. Impact was followed by apnea, convulsions, and moderate hypertension. The surviving rats developed decortication flexion deformity of the forelimbs, with behavioral depression and loss of muscle tone. Data from Group 2 animals suggested that the cause of death was due to central respiratory depression; the mortality rate decreased markedly in animals mechanically ventilated during the impact. Analysis of mathematical models showed that this mass-height combination resulted in a brain acceleration of 900 G and a brain compression gradient of 0.28 mm. It is concluded that this simple model is capable of producing a graded brain injury in the rodent without a massive hypertensive surge or excessive brain-stem damage.
1,193 citations
References
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TL;DR: In this paper, it was shown that reticular activation is associated with the activation of the reticular formation of the brain stem, and that reticulus activation can be induced by low frequency stimulation of the diffuse thalamic projection system, rather than intra-cortical spread following the arrival of afferent impulses at the sensory receiving areas of the cortex.
4,014 citations
905 citations
TL;DR: In shock state associated with a reduced or maintained blood flow, an important proportion of muscle lactate release is regulated by a "2 receptor stimulation and not secondary to a reduced oxygen availability", demonstrating that lactate production during shock states is related, at least in part, to increased NaK-ATPase activity under "2 stimulation.
Abstract: During septic shock, muscle produces lactate by way of an exaggerated NaKYadenosine triphosphatase (ATPase)Ystimulated aerobic glycolysis associated with epinephrine stimulation possibly through \"2 adrenoreceptor involvement. It therefore seems logical that a proportion of hyperlactatemia in low cardiac output states would be also related to this mechanism. Thus, in low-flow and normal-to-highYflow models of shock, we investigate (1) whether muscle produces lactate and (2) whether muscle lactate production is linked to \"2 adrenergic stimulation and Na K-ATPase. We locally modulated the adrenergic pathway and NaK-ATPase activity in male Wistar rats’ skeletal muscle using microdialysis with nonselective and selective \" blockers and ouabain in different models of rodent shock (endotoxin, peritonitis, and hemorrhage). Blood flow at the probe site was evaluated by ethanol clearance. We measured the difference between muscle lactate and blood lactate concentration, with a positive gradient indicating muscle lactate or pyruvate production. Epinephrine levels were elevated in all shock groups. All models were associated with hypotension and marked hyperlactatemia. Muscle lactate concentrations were consistently higher than arterial levels, with a mean gradient of 2.5 T 0.3 in endotoxic shock, 2.1 T 0.2 mM in peritonitis group, and 0.9 T 0.2 mM in hemorrhagic shock (P G 0.05 for all groups). Muscle pyruvate concentrations were also always higher than arterial levels, with a mean gradient of 260 T 40 2M in endotoxic shock, 210 T 30 2M in peritonitis group, and 90 T 10 2M in hemorrhagic shock (P G 0.05 for all groups). Despite a decrease in blood flow, lactate formation was decreased by all the pharmacological agents studied irrespective of shock mechanism. This demonstrates that lactate production during shock states is related, at least in part, to increased NaK-ATPase activity under \"2 stimulation. In shock state associated with a reduced or maintained blood flow, an important proportion of muscle lactate release is regulated by a \"2 receptor stimulation and not secondary to a reduced oxygen availability. KEYWORDS—Sepsis, animal model, hypoxia, glycolysis, lactic acid, epinephrine
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