Experimental studies in head injury

Lindgren, S.; Rinder, L

doi:10.1007/bf01191611

Cited by 86 publications

(26 citation statements)

References 8 publications

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“…Fluid percussion has been widely used by a number of laboratories and produces many features of brain injury resembling the pathophysiologic responses in human head injury. These include brief pressure transients similar to those recorded in human cadaver skulls during sudden impact (Lindgren;1966, Lindgren andRinder, 1966), behavioral suppression and neurologic signs Hayes et al, 1984Hayes et al, , 1988a resembling unconsciousness in humans (Teasdale, 1976), reduction or abolition of cerebrovascular responsiveness to changes in Pco2 and Po2 (Saunders et al, 1979;Wei et al, 1980;Lewelt et al, 1982), loss of pressure, autoregulation (Lewelt et al, 1980), and immediate and late developing increases in intracranial pressure (Rosner and Becker, 1982). Fluid percussion injury in the rat Lyeth et al, 1988b) produces neurologic signs of areflexia, flaccid coma, and stupor similar to those reported in other species and humans.…”

Section: Surgical Preparation and Experimental Injurymentioning

confidence: 89%

Pretreatment with Phencyclidine, an N-Methyl-d-Aspartate Antagonist, Attenuates Long-Term Behavioral Deficits in the Rat Produced by Traumatic Brain Injury

Hayes

Jenkins

Lyeth

et al. 1988

Journal of Neurotrauma

193

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This study examined the effects of pretreatment with phencyclidine (PCP), a selective /V-methyl-D-aspartate (NMDA) antagonist, on behavioral and physiologic responses of the rat to experimental traumatic brain injury (TBI). For the behavioral experiments, rats were administered either saline or PCP (1.0, 2.0, or 4.0 mg/kg, intrapentoneally [IP] 15 min before TBI. Rats were ventilated as necessary following injury. The duration of acute suppression of several reflexes (pinna, corneal, righting, and flexion) and responses (escape, head support, and spontaneous locomotion) was recorded for up to 70 min after trauma. Longer-term behavioral assessments (beam walking, beam balance, inclined plane, ambulatory activity, and body weight) were made for up to 10 days after trauma. PCP did not significantly alter the duration of acute behavioral suppression. At a dosage of 1.0 mg/kg, PCP significantly attenuated all long-term deficits except beam walking. Maximal protection against beam walking deficits was provided by the 4.0 mg/kg dosage of PCP. Sixty-three percent of saline-treated animals died within 10 days after injury. For rats pretreated with 1.0, 2.0, and 4.0 mg/kg of PCP, 40%, 23%, and 33% died, respectively. In physiologic experiments, pretreatment with 4.0 mg/kg of PCP (IP) 15 min before injury did not significantly affect systemic cardiovascular responses, plasma glucose levels, or blood gas levels observed within 30 min after injury.While the possibility of effects mediated by other neurotransmitter systems cannot be excluded, these data suggest that NMDA agonist-receptor interactions contribute to the

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Section: Surgical Preparation and Experimental Injurymentioning

confidence: 89%

Pretreatment with Phencyclidine, an N-Methyl-d-Aspartate Antagonist, Attenuates Long-Term Behavioral Deficits in the Rat Produced by Traumatic Brain Injury

Hayes

Jenkins

Lyeth

et al. 1988

Journal of Neurotrauma

193

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“…First described by Lindgren and Rinder in a rabbit model of TBI (Lindgren and Rinder, 1966), the fluid percussion (FP) device has been used in several other animal species, including cats (Sullivan et al, 1976), rats (Dixon et al 1987; McIntosh et al, 1989), pigs (Armstead and Kurth, 1994), and mice (Carbonell et al, 1998). The FP device (Figure 1A) consists of a Plexiglas cylinder filled with physiologic saline and enclosed at one end by a male Luer-Lock fitting that is subsequently paired with a female fitting.…”

Section: Contemporary Laboratory Models Of Traumatic Brain Injurymentioning

confidence: 99%

Found in translation: Understanding the biology and behavior of experimental traumatic brain injury

Bondi

Semple

Noble-Haeusslein

et al. 2015

Neuroscience & Biobehavioral Reviews

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BONDI, C.O., B.D. Semple, L.J. Noble-Haeusslein, N.D. Osier, S.W. Carlson, C.E. Dixon, C.C. Giza and A.E. Kline. Found in translation: understanding the biology and behavior of experimental traumatic brain injury. NEUROSCI BIOBEHAV REV. The aim of this review is to discuss in greater detail the topics covered in the recent symposium entitled “Traumatic brain injury: laboratory and clinical perspectives,” presented at the 2014 International Behavioral Neuroscience Society annual meeting. Herein we review contemporary laboratory models of traumatic brain injury (TBI) including common assays for sensorimotor and cognitive behavior. New modalities to evaluate social behavior after injury to the developing brain, as well as the attentional set-shifting test (AST) as a measure of executive function in TBI, will be highlighted. Environmental enrichment (EE) will be discussed as a preclinical model of neurorehabilitation, and finally, an evidence-based approach to sports-related concussion will be considered. The review consists predominantly of published data, but some discussion of ongoing or future directions is provided.

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“…Extensive research on brain concussion has been in progress in various laboratories for several years. Experimental models, animals, and human cadavers have been used to achieve impact data (Danny-Brown andRussell, 1941: Edberg et al, 1963;Gurdjian et al, 1962;Holbourn, 1943;Lindgren, 1966;Ommaya et al, 1964;Ward, 1966), but the extrapolation to the living human brain has been difficult.…”

Section: Introductionmentioning

confidence: 99%

Association football injuries to the brain. A preliminary report.

Tysvaer¹,

Storli²

1981

Br J Sports Med

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In 1975 the authors sent a questionnaire to all players in the Norwegian First Division League Clubs to record the incidence of head injuries due to heading. The conclusion of the questionnaire is that there seems to be a low percentage of serious head injuries. None of the players had been operated on for epi-or subdural hematoma or other brain damage and only a few have had concussion due to heading. In sixty per cent of the players a full neurological examination and EEG recording was undertaken. The result of these studies will be published in a subsequent article.

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Experimental studies in head injury

Cited by 86 publications

References 8 publications

Pretreatment with Phencyclidine, an N-Methyl-d-Aspartate Antagonist, Attenuates Long-Term Behavioral Deficits in the Rat Produced by Traumatic Brain Injury

Pretreatment with Phencyclidine, an N-Methyl-d-Aspartate Antagonist, Attenuates Long-Term Behavioral Deficits in the Rat Produced by Traumatic Brain Injury

Found in translation: Understanding the biology and behavior of experimental traumatic brain injury

Association football injuries to the brain. A preliminary report.

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