Lesions in the cerebral hemispheres after blunt head injury.

Strich, Sabina J.

doi:10.1136/jcp.s3-4.1.166

Cited by 61 publications

(15 citation statements)

References 20 publications

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“…Although patients with this type of presentation have been studied previously under a variety of titles, i.e. "diffuse degeneration in the cerebral white matter" [50], "shearing injury" [33,51,52], "diffuse damage to white matter of immediate impact type" [1] and "diffuse white matter shearing injury" [56], it was not until the early 1980s [2] that the underlying pathology of all these cases of diffuse brain injury was recognised to be widespread damage to axons and termed DAI. This unifying concept was rapidly appreciated to be the common neuropathological denominator for these various groups of patients, the short-surviving cases being characterised by evidence of widespread damage to axons (axonal swellings and bulbs) to be gradually replaced by microglia and macrophages (microglial clusters) and in cases surviving months or years loss of myelinated axons in ascending and descending fibre tracts (Wallerian degeneration).…”

Section: Discussionmentioning

confidence: 99%

Tissue tears in the white matter after lateral fluid percussion brain injury in the rat: relevance to human brain injury

Graham¹,

et al. 2000

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A characteristic feature of severe diffuse axonal injury in man is radiological evidence of the "shearing injury triad" represented by lesions, sometimes haemorrhagic, in the corpus callosum, deep white matter and the rostral brain stem. With the exception of studies carried out on the non-human primate, such lesions have not been replicated to date in the multiple and diverse rodent laboratory models of traumatic brain injury. The present report describes tissue tears in the white matter, particularly in the fimbria of Sprague-Dawley rats killed 12, 24, and 48 h and 7 days after lateral fluid percussion brain injury of moderate severity (2.1-2.4 atm). The lesions were most easily seen at 24 h when they appeared as foci of tissue rarefaction in which there were a few polymorphonuclear leucocytes. At the margins of these lesions, large amounts of accumulated amyloid precursor protein (APP) were found in axonal swellings and bulbs. By 1 week post-injury, there was macrophage infiltration with marked astrocytosis and early scar formation. This lesion is considered to be due to severe deformation of white matter and this is the first time that it has been identified reproducibly in a rodent model of head injury under controlled conditions.

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Section: Discussionmentioning

confidence: 99%

Tissue tears in the white matter after lateral fluid percussion brain injury in the rat: relevance to human brain injury

Graham¹,

et al. 2000

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“…The primary objectives of the current study were to examine the performance of the animals in a battery of sensorimotor as well as cognitive tasks over a 1-year period in order to determine: (1) if lasting behavioral deficits could be detected in a rodent model of TBI and (2) if different impact sites produce different patterns of sensorimotor and cognitive deficits in rats. Established models of frontal and lateral cortical contusion (Hoffman et al, 1994;Sutton et al, 1993) were used since the neuropathological sequelae of moderateto-severe TBI in humans frequently include epidural, subdural, subarachnoid, and/or intraparenchymal hemorrhages and contusion to frontal, temporal, and/or parietal cortices (Mitchell and Adams, 1973;Strich, 1970;Willmore, 1990). …”

Section: Introductionmentioning

confidence: 99%

Dissociable Long-Term Cognitive Deficits after Frontal versus Sensorimotor Cortical Contusions

Lindner¹,

Plone²,

Cain³

et al. 1998

Journal of Neurotrauma

107

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Cognitive deficits are the most enduring and disabling sequelae of human traumatic brain injury (TBI), but quantifying the magnitude, duration, and pattern of cognitive deficits produced by different types of TBI has received little emphasis in preclinical animal models. The objective of the present study was to use a battery of behavioral tests to determine if different impact sites produce different patterns of behavioral deficits and to determine how long behavioral deficits can be detected after TBI. Prior to surgery, rats were trained to criteria on delayed nonmatching to position, radial arm maze, and rotarod tasks. Rats received sham surgery (controls), midline frontal contusions (frontal TBI, 2.25 m/sec impact), or unilateral sensorimotor cortex contusions (lateral TBI, 3.22 m/sec impact) at 12 months of age and were tested throughout the next 12 months. Cognitive deficits were more robust and more enduring than sensorimotor deficits for both lateral TBI and frontal TBI groups. Lateral TBI rats exhibited transient deficits in the forelimb placing and in the rotarod test of motor/ambulatory function, but cognitive deficits were apparent throughout the 12-month postsurgery period on tests of spatial learning and memory including: (1)reacquisition of a working memory version of the radial arm maze 6-7 months post-TBI, (2) performance in water maze probe trials 8 months post-TBI, and (3) repeated acquisition of the Morris water maze 8 and 11 months post-TBI. Frontal TBI rats exhibited a different pattern of deficits, with the most robust deficits in tests of attention/orientation such as: (1) the delayed nonmatching to position task (even with no delays) 1-11 weeks post-TBI, (2) the repeated acquisition version of the water maze--especially on the first "information" trial 8 months post-TBI, (3) a test of sensorimotor neglect or inattention 8.5 months post-TBI, and (4) a DRL20 test of timing and/or sustained attention 11 months after surgery. These results suggest that long-term behavioral deficits can be detected in rodent models of TBI, that cognitive deficits seem to be more robust than sensorimotor deficits, and that different TBI impact sites produce dissociable patterns of cognitive deficits in rats.

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“…Since the amount of DAI was directly proportional t o the severity of injury (duration of coma and quality of outcome), we conclude that axonal damage produced by coronal head acceleration is a major cause of prolonged traumatic coma and its sequelae. [8, 28,42,[47][48][49] 521. This report describes the experimental production of diffuse axonal injury and its accompanying neurological deficits.…”

mentioning

confidence: 99%

Diffuse axonal injury and traumatic coma in the primate

Gennarelli¹,

Thibault²,

Adams³

et al. 1982

Annals of Neurology

1,327

627

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Traumatic coma was produced in 45 monkeys by accelerating the head without impact in one of three directions. The duration of coma, degree of neurological impairment, and amount of diffuse axonal injury (DAI) in the brain were directly related to the amount of coronal head motion used. Coma of less than 15 minutes (concussion) occurred in 11 of 13 animals subjected to sagittal head motion, in 2 of 6 animals with oblique head motion, and in 2 of 26 animals with full lateral head motion. All 15 concussioned animals had good recovery, and none had DAI. Conversely, coma lasting more than 6 hours occurred in one of the sagittal or oblique injury groups but was present in 20 of the laterally injured animals, all of which were severely disabled afterward. All laterally injured animals had a degree of DAI similar to that found in severe human head injury. Coma lasting 16 minutes to 6 hours occurred in 2 of 13 of the sagittal group, 4 of 6 in the oblique group, and 4 of 26 in the lateral group, these animals had less neurological disability and less DAI than when coma lasted longer than 6 hours. These experimental findings duplicate the spectrum of traumatic coma seen in human beings and include axonal damage identical to that seen in sever head injury in humans. Since the amount of DAI was directly proportional to the severity of injury (duration of coma and quality of outcome), we conclude that axonal damage produced by coronal head acceleration is a major cause of prolonged traumatic coma and its sequelae.

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Lesions in the cerebral hemispheres after blunt head injury.

Cited by 61 publications

References 20 publications

Tissue tears in the white matter after lateral fluid percussion brain injury in the rat: relevance to human brain injury

Tissue tears in the white matter after lateral fluid percussion brain injury in the rat: relevance to human brain injury

Dissociable Long-Term Cognitive Deficits after Frontal versus Sensorimotor Cortical Contusions

Diffuse axonal injury and traumatic coma in the primate

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