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Results for “Diffuse Axonal Injury”

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PubMed2002

[Traumatic, infectious or degenerative pathology].

CRANIO-ENCEPHALIC TRAUMAS: Scanography remains the examination of choice. However, MRI can be useful in diagnosis of diffuse axional lesions, not clearly visualized with scanography, and for screening the subsequent lesions. INFECTIOUS OR INFLAMMATORY LESIONS: Some are very evocative with MRI: cerebral abscesses, notably herpetic encephalitis and Creutzfeldt-Jacob's disease. If multiple sclerosis is suspected, MRI is considered as the principle para-clinical examination able to confirm the diagnosis with the first episode. It also supplies data for the diagnosis of metabolic, toxic and degenerative diseases.

Brain↗
PubMed2004

Calcium overloading in traumatic axonal injury by lateral head rotation: a morphological evidence in rat model.

The study investigated morphologically axonal calcium overloading and its relationship with axonal structural changes. Twelve SD rats were divided into an injury and a sham group. The rat model of traumatic axonal injury (TAI) by lateral head rotation was produced. The oxalate-pyroantimonate technique for calcium localization was used to process the rat's medulla oblongata tissues with thin sections observed electron-microscopically for axonal structure and calcium precipitates on it. The axonal damage in medulla oblongata appeared at 2 h post-injury, gradually became diffuse and severe, and continued to exist at 24 hours. At 2 hours, calcium precipitates were deposited on separated lamellae and axolemma, but were rarely distributed in the axoplasm. At 6 hours, calcium precipitates occurred on separated lamellae and axolemma in much higher density, but on axoplasm in extremely small amounts. Some axons, though lacking structural changes of the myelin sheath, sequestered plenty of calcium deposits on their swollen mitochondria. At 24 hours, damaged axons presented with much more severe lamellae separation and calcium deposits. Axonal calcium overloading developed in rat TAI model using lateral head rotation. This was significantly related to structural damage in the axons. These findings suggest the feasibility of using calcium antagonists in cope the management of human DAI in its very early stage.

Animals↗
PubMed2005

Diffusion tensor imaging with three-dimensional fiber tractography of traumatic axonal shearing injury: an imaging correlate for the posterior callosal "disconnection" syndrome: case report.

OBJECTIVE: To demonstrate that magnetic resonance diffusion tensor imaging (DTI) with three-dimensional (3-D) fiber tractography can visualize traumatic axonal shearing injury that results in posterior callosal disconnection syndrome. METHODS: A 22-year-old man underwent serial magnetic resonance imaging 3 days and 12 weeks after blunt head injury. The magnetic resonance images included whole-brain DTI acquired with a single-shot spin echo echoplanar sequence. 3-D DTI fiber tractography of the splenium of the corpus callosum was performed. Quantitative DTI parameters, including apparent diffusion coefficient and fractional anisotropy, from the site of splenial injury were compared with those of a normal adult male volunteer. RESULTS: Conventional magnetic resonance images revealed findings of diffuse axonal injury, including a lesion at the midline of the splenium of the corpus callosum. DTI performed 3 days posttrauma revealed that the splenial lesion had reduced apparent diffusion coefficient and fractional anisotropy, reflecting a large decrease in the magnitude of diffusion parallel to the white matter fibers, which had partially recovered as revealed by follow-up DTI 12 weeks postinjury. 3-D tractography revealed an interruption of the white matter fibers in the posteroinferior aspect of the splenium that correlated with the patient's left hemialexia, a functional deficit caused by disconnection of the right visual cortex from the language centers of the dominant left hemisphere. CONCLUSION: DTI with 3-D fiber tractography can visualize acute axonal shearing injury, which may have prognostic value for the cognitive and neurological sequelae of traumatic brain injury.

Adult↗
PubMed2000

Cytochrome c release and caspase activation in traumatic axonal injury.

Axonal injury is a feature of traumatic brain injury (TBI) contributing to both morbidity and mortality. The traumatic axon injury (TAI) results from focal perturbations of the axolemma, allowing for calcium influx triggering local intraaxonal cytoskeletal and mitochondrial damage. This mitochondrial damage has been posited to cause local bioenergetic failure, leading to axonal failure and disconnection; however, this mitochondrial damage may also lead to the release of cytochrome c (cyto-c), which then activates caspases with significant adverse intraaxonal consequences. In the current communication, we examine this possibility. Rats were subjected to TBI, perfused with aldehydes at 15-360 min after injury, and processed for light microscopic (LM) and electron microscopic (EM) single-labeling immunohistochemistry to detect extramitochondrially localized cytochrome c (cyto-c) and the signature protein of caspase-3 activation (120 kDa breakdown product of alpha-spectrin) in TAI. Combinations of double-labeling fluorescent immunohistochemistry (D-FIHC) were also used to demonstrate colocalization of calpain activation with cyto-c release and caspase-3-induction. In foci of TAI qualitative-quantitative LM demonstrated a parallel, significant increase in cyto-c release and caspase-3 activation over time after injury. EM analysis demonstrated that cyto-c and caspase-3 immunoreactivity were associated with mitochondrial swelling-disruption in sites of TAI. Furthermore, D-IFHC revealed a colocalization of calpain activation, cyto-c release, and caspase-3 induction in these foci, which also revealed progressive TAI. The results demonstrate that cyto-c and caspase-3 participate in the terminal processes of TAI. This suggests that those factors that play a role in the apoptosis in the neuronal soma are also major contributors to the demise of the axonal appendage.

Animals↗
PubMed1999

Brain free magnesium concentration is predictive of motor outcome following traumatic axonal brain injury in rats.

A number of studies have supported a role for brain free magnesium as an important secondary injury factor in the development of neurologic deficits following traumatic brain injury. Despite this, few studies have characterised free magnesium changes in diffuse models of brain injury relevant to clinical trauma, and none have critically examined the association between brain free magnesium concentration and degree of neurologic deficit following graded trauma. In the present study, a combination of nuclear magnetic resonance spectroscopy and rotarod motor function tests were used to characterise the relationship between brain free magnesium concentration and neurologic motor function following graded traumatic axonal brain injury in rats. Induction of moderate or severe impact-acceleration induced traumatic brain injury resulted in a profound decline (p < 0.01) in brain free magnesium concentration that persisted for a minimum of 4 days post-trauma in both injury groups. Posttraumatic rotarod deficits assessed on a daily basis after injury were linearly correlated with brain free magnesium concentration measured in the same animals immediately after the motor tests were performed (r = 0.87; p < 0.001). These results suggest that brain free magnesium declines following graded diffuse axonal brain injury and that the concentration of the ion after trauma may be a prognostic indicator of motor outcome following.

Animals↗
PubMed2006

True hemicranial decompression for severe pediatric cranial trauma: a short series of 4 cases and literature review.

BACKGROUND: Traumatic acute SDH in pediatric patients is a life-threatening situation. There is a severe increase in ICP caused by acute SDH or diffuse brain swelling or secondary to ischemic brain damage. In certain situations, conventional measures may fail to control such a rapid increase in ICP. CASE DESCRIPTION: The cases of 4 pediatric patients with cranial trauma with raised ICP, in whom hemicranial decompression was performed, are described. All patients had acute SDH with diffuse brain injury; in addition, 2 of them had associated massive infarcts. Three of them survived and had a favorable outcome. CONCLUSIONS: In certain situations, pediatric patients with cranial trauma may be offered hemicranial decompression as a surgical option. These children may have a better long-term outcome despite massive infarcts.

Accidental Falls↗
PubMed1999

Latent structure of the Wisconsin Card Sorting Test after pediatric traumatic head injury.

The performance of 80 pediatric patients with traumatic head injury (THI) on the Wisconsin Card Sorting Test (WCST; Heaton, Chelune, Talley, Kay, & Curtiss, 1993) was examined to determine the underlying latent structure. Exploratory factor analysis with oblique rotation identified three factors: response accuracy, failure to self-monitor, and learning. The response accuracy factor was directly affected by both age and length of coma. Level of performance on this factor also covaried with post-injury psychometric intelligence. It is concluded that interpretation of the WCST results of children with THI should consider the multifactorial nature of the instrument in combination with injury severity characteristics and demographic variables.

Adolescent↗
PubMed2006

Changes in white matter late after severe traumatic brain injury in childhood.

Severe traumatic brain injury in childhood, particularly that complicated by raised intracranial pressure, has significant long-term effects on the brain. Since magnetic resonance imaging provides a means of visualizing neuroanatomic structure in exquisite detail, the scope of this review is to revisit the pathology of traumatic brain injury described in recent clinical imaging studies. Acute imaging provides insight into the acute mechanism of focal and diffuse injury. There is some reduction in threshold for white matter pathology in the hemisphere ipsilateral to injury. After injury, there may be long-term effects on white matter architecture and the potential for brain growth. In this context, the pattern of hippocampal rather than parahippocampal gyrus tissue loss provides insight into the likely cause of white matter injury being cerebral hypoperfusion.

Atrophy↗
PubMedDate not supplied

Impaired motor learning and diffuse axonal damage in motor and visual systems of the rat following traumatic brain injury.

Cognitive-motor functioning or motor skill learning is impaired in humans following traumatic brain injury. A more complete understanding of the mechanisms involved in disorders of motor skill learning is essential for any effective rehabilitation. The specific goals of this study were to examine motor learning disorders, and their relationship to pathological changes in adult rats with mild to moderate closed head injury. Motor learning deficits were determined by comparing the ability to complete a series of complex motor learning tasks with simple motor activity. The extent of neuronal damage was determined using silver impregnation. At all post-injury time points (day 1 to day 14), statistically significant deficits were observed in parallel bar traversing, foot placing, ladder climbing, and rope climbing. Performance improved with time, but never reached control levels. In contrast, no deficits were found in simple motor activity skills tested with beam balance and runway traverse. Histologically, axonal degeneration was widely distributed in several brain areas that relate to motor learning, including the white matter of sensorimotor cortex, corpus callosum, striatum, thalamus and cerebellum. Additionally, severely damaged axons were observed in the primary visual pathway, including the optic chiasm, optic tract, lateral geniculate nuclei, and superior colliculus. These findings suggest that motor learning deficits could be detected in mild or moderate brain injury, and this deficit could be attributed to a diffuse axonal injury distributed both in the motor and the visual systems.

Animals↗
PubMed2006

[The undetected brain lesion in sports. Minor traumatic brain injury and its sequelae].

The minor traumatic brain injury (mTBI) in sports is often looked at as a bagatelle. The treating physician underestimates the severity of the injury suspecting that a mTBI is a nonstructural lesion with an overall excellent prognosis in the majority of the cases. This paper shows that the minor traumatic brain injury may be a structural brain lesion with potentially life-threatening dangers. The therapy should follow exactly defined guidelines, e.g., stepwise protocol of the Concussion in Sports (CIS-) Group. Return to sports activities should happen only when all physical but also cognitive symptoms have subsided. All mTBIs that have been sustained prior to the actual injury have to be recorded properly because repeated mTBIs may cause chronic degenerative brain damage. Neuropsychological testing will aid in the correct diagnosis of a mTBI and is a useful parameter in the course of the injury. In the future biochemical markers may serve as indicators of the severity of the brain injury and may also aid in predicting the outcome after TBI. Today biochemical markers do not serve as a substitute for neuroimaging.

Adolescent↗
PubMed2002

Brain stem lesions after head injury.

There is little knowledge on the morphology of the brain stem in survivors of head injury, as CT fails to shown brain stem lesions, and neuropathological data is only available from autopsies. As magnetic resonance imaging (MRI) sheds new light on morphological lesions of the brain, the authors investigated 100 patients with a severe head injury. MRI was performed in a prospective study within the first seven days after head injury while the patients were still in coma and on ventilation. Relating the location of the lesions as depicted by MRI with the initial CT scan and outcome, death appeared to be closely linked to the phenomenon of bilateral pontine lesions. The extent of supratentorial lesions had no bearing on survival at all in the absence of brain stem lesions. Altogether the brain stem was affected in 52%. Obviously the occurrence of bilateral upper pontine lesions is of highest predictive value for a fatal outcome. Severe destruction of supratentorial white matter as demonstrated by MRI is not related to increased mortality, as long as the brain stem is spared.

Adolescent↗
PubMed2006

Microarray analysis of gene expression patterns in adult spinal motoneurons after different types of axonal injuries.

Three experimental models of axonal injuries in adult rat spinal motoneurons were established to investigate changes of gene expression in response to such injuries. We took advantage of cDNA microarray analysis to determine the differential expression of genes in injured motoneurons following distal axotomy or root avulsion in the absence or presence of BDNF. The major finding was that, in response to proximal axonal injury (avulsion), expression of genes that are known to facilitate neuronal survival and axonal regeneration (e.g., IGFRII, PI3K, IGFBP-6, GSTs, GalR2) were down-regulated; but following treatment with BDNF they were up-regulated. In addition, the expression of genes known to be involved in apoptosis and DNA damage (e.g., ANX5, TS, ALR) were down-regulated in BDNF-treated animals with avulsion. Furthermore, many functional families of genes previously shown to play roles in the pathophysiology of axonal injury, including SNAP-25A, SV2B, Ras-related ras3a/4b, ERK1/2, 14-3-3 proteins, proteasome proteins, oncogenes, GAP-43, and NMDAR1, were altered after either distal axotomy or avulsion injury. Some of the changes in gene expression, including Lim-2, FRAG1, GlaR2, GSTs, ALR, TS, ANX3/5, and nhe1/2, are first reported here in injured motoneurons. The differential expression of genes identified by the expression arrays was confirmed by gene-specific RT-PCR for eight genes (GAP-43, IGFR II, Lim-2, MIF, NDAP1, TS, PCC3, and FRAG1) and by in situ hybridization for Lim-2. These results suggest that abnormal regulation of particular biochemical pathways may induce motoneuron death after ventral root avulsion in adult animals. This study presents an approach for selecting specific genes and their products that may be involved in motoneuron degeneration following axonal injuries.

Animals↗
PubMed2000

Cell activation and inflammatory response following traumatic axonal injury in the rat.

In a rat model of traumatic brain injury cell activation was characterized immunohistochemically from 2 h up to 2 weeks. Reactive astrocytosis became apparent perivascularly and in the grey matter within 4h after trauma. Increased OX42 immunoreactivity indicated microglial activation in cortex and hippocampus as early as 4 h, whereas up-regulation of MHC class II (OX6) was evident in white matter tracts at 24 h. Although macrophage (ED1) numbers increased in the meninges and perivascularly, brain infiltration appeared marginal. Accumulation of lymphocytes and granulocytes was not observed. Our results show that traumatic axonal injury induces a rapid and sustained glial activation in the absence of leukocyte infiltration. Thus, cell activation following diffuse trauma strongly differs from that found after focal brain damage, awaiting further functional characterization.

Animals↗
PubMed1999

Calpain activation and cytoskeletal protein breakdown in the corpus callosum of head-injured patients.

Calpain-mediated breakdown of the cytoskeleton has been proposed to contribute to brain damage resulting from head injury. We examined the corpus callosum from patients who died after a blunt head injury in order to determine if there was evidence of these pathophysiological events in a midline myelinated commissure that is susceptible to damage after human head injury. Western blotting revealed marked reductions in the levels of neurofilament triplet proteins 200 and 68kDa in the corpus callosum of head-injured patients compared with control subjects. Neurofilament 200kDa levels were significantly reduced as detected by either phosphorylation-dependent or -independent antibodies. In contrast, there were minimal changes in the levels of beta-tubulin or the microtubule-associated protein, tau, in the head-injured patients, although amyloid precursor protein immunostaining demonstrated axonal damage in 9 of the 10 patients. The inactive 800kDa and active 76kDa subunits of mu-calpain were present in control subjects and head-injured patients. However, there was a significant increase in the levels of calpain-mediated spectrin breakdown products in head-injured patients compared with the control subjects. The results demonstrate that following human blunt head injury, there is a significant degradation of neurofilament proteins and increased levels of calpain-mediated spectrin breakdown products within the corpus callosum. Therefore, our data support the hypothesis that calpain-mediated breakdown of the cytoskeleton may contribute to axonal damage after head injury.

Adult↗
PubMed2002

Traumatic brain injury and subarachnoid hemorrhage: in vivo occult pathology demonstrated by magnetic resonance spectroscopy may not be "ischaemic". A primary study and review of the literature.

OBJECTIVES: To look for evidence of early ischaemic neurochemical changes in patients suffering severe traumatic brain injury (TBI) and severe subarachnoid haemorrhage (SAH). Proton metabolite concentrations were measured in normal and abnormal areas of brain on T2 MR imaging, in regions considered particularly vulnerable to ischaemic injury. METHODS: Intensive care patients underwent T2 weighted imaging in a 1.5 Tesla MR scanner and proton magnetic resonance spectroscopy (single voxel or chemical shift imaging). Metabolite values in areas that appeared 'normal' and 'abnormal' on T2 MR imaging were compared with those obtained from normal controls. RESULTS: 18 TBI and 6 SAH patients were imaged at 1 to 26 days. N-acetyl aspartate (NAA) was lower in TBI and SAH patients compared to controls in both T2 normal and T2 abnormal areas (p<0.0005). SAH, but not TBI patients also had increased choline and creatine compared to controls in the T2 normal (p<0.02, p<0.02 respectively) and T2 abnormal (p=0.0003, p=0.003) areas. No lactate was found in TBI or SAH patients. CONCLUSIONS: Significant loss of normal functioning neurones was present in TBI and SAH, but no evidence of anaerobic metabolism using lactate as a surrogate marker, questioning the role of 'ischemia' as a major mechanism of damage. Increased choline and creatine were found in SAH patients suggestive of increased cell-wall turnover. Current theories of brain injury after TBI or SAH do not explain these observed neurochemical changes and further research is required.

Adolescent↗
PubMed2002

The minimally conscious state in children.

The minimally conscious state (MCS) is a condition of severely altered consciousness in which minimal but definite behavioral evidence of self- or environmental awareness is shown. Diagnostic criteria recently have been proposed for entry into and emergence from the MCS. We present clinical and neuroimaging data on 5 children diagnosed with MCS and discuss the limited information available concerning its epidemiology, etiology, pathology, and prognosis. Issues related to the evaluation and care of children suspected of having MCS are also reviewed as well as current ethical and legal controversies.

Adolescent↗