[Neurosurgery in the 21st century--neurotraumatology].
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Brain Injuries↗
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Results for “Diffuse Axonal Injury”
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Increase in the chronically monitored cerebrospinal fluid pressure after experimental brain injury in rats.
The early effects of experimental brain injury with diffuse axonal lesions on intracranial pressure (i.c.p.), mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) in rats have been already studied. The aim of this experiment was to examine the effects of brain injury on ICP, MAP and CPP during the first few days post-injury. In order to do that, an accurate technique of ICP measurement had to be developed. In a series of eight rats, a translumbar intrathecal catheter (TIC) was surgically introduced allowing repeated measurements of cerebrospinal fluid pressure (CSFP). Under anaesthesia, a second series of nine rats were equipped simultaneously with TIC and an intracranial fiberoptic device to measure ICP. Simultaneous measurements of CSFP and ICP were recorded for baseline values, than during and after jugular compression which was intended to induce an acute and significant increase in ICP. A third series of 53 rats having TIC received an experimental severe brain injury. MAP was measured non-invasively and CPP was calculated as CPP-MAP. CSFP, MAP and CPP were intermittently measured during 5-6 post-traumatic days and compared to the values obtained during ten control rats (SHAM). A clinical score was used to compare clinical condition. The results showed that the translumbar CSFP accurately measured ICP in rats having normal or acutely increased ICP. The experimental brain injury induced increased CSFP lasting up to 5-6 days, with increased MAP during the first 6 hours. CPP values were compromised at 24-48 hours. The clinical performance was reduced in the brain-injured rats. The translumbar technique of CSFP measurement reflected exact ICP in normal and acutely increased ICP in rats. Experimental brain injury with diffuse axonal lesions can increase lumbar CSFP in rats for many days.
Analysis of Variance↗
Thalamic proton magnetic resonance spectroscopy in vegetative state induced by traumatic brain injury.
OBJECTIVES: To determine whether proton magnetic resonance spectroscopy (MRS), a newer radiographic technology, would be useful in the evaluation of the thalamus of patients in vegetative states resulting from traumatic brain injury. METHODS: 14 victims of severe traumatic brain injury who were in the vegetative state and whose magnetic resonance images of the thalamus were normal underwent bilateral thalamic proton (MRS) studies. The N-acetyl aspartate to creatine (NAA:Cr) and choline to creatine (Cho:Cr) ratios were obtained for each patient. The proton thalamic MRS findings of patients who were in a persistent vegetative state (n = 8) and in patients who had regained awareness after being in the vegetative state (n = 6) were compared with proton thalamic MRS findings in five healthy volunteers. RESULTS: While conventional magnetic resonance imaging suggested that each patient had a normal thalamus, proton MRS indicated that the thalamus of each patient in the series was damaged. The NAA:Cr ratio was significantly lower in the thalami of both the patients who remained in a persistent vegetative state for the duration of the study and in those who regained awareness after being in the vegetative state (p < 0.001). In addition, NAA:Cr ratios were lower in the group of patients who remained in a persistent vegetative state than in the group of patients who regained awareness after being in the vegetative state (p < 0.001). CONCLUSIONS: Results suggest that the NAA:Cr ratio within the thalamus is significant and that thalamic MRS may be helpful when attempting to determine the degree of severity of neuronal and axonal injury in patients in the vegetative state.
Adolescent↗
Pathology of nonaccidental brain injury.
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Child Abuse↗
Diffuse axonal pathology detected with magnetization transfer imaging following brain injury in the pig.
This study was designed to evaluate with magnetization transfer imaging (MTI) and conventional magnetic resonance (MR) imaging the manifestation of diffuse axonal injury (DAI) in an animal model of injury via nonimpact coronal plane rotational acceleration. A second objective was to investigate the diagnostic use of quantitative MTR imaging based on statistical parameters in a single subject, as opposed to grouped analysis. Seven mini-swine were subjected to brain trauma known to produce isolated DAI and to MR imaging at two time points. Following sacrifice, the brains were harvested for histopathologic examination. Magnetization transfer ratio (MTR) maps were generated for double-blinded comparison of regions with abnormal MTR values and regions with documented DAI. Positive and negative predictive values for MTR detection of DAI were 67 and 56%, respectively, and in acute studies alone, 89 and 61%. Gains in sensitivity over conventional imaging for detection of DAI were demonstrated.
Animals↗
Screening for differentially expressed genes in the rat inner retina and optic nerve after optic nerve crush.
Limited optic nerve crush is a model of diffuse mechanical axon injury, the most prevalent cause of secondary neurodegeneration after closed head neurotrauma. In this report, a protocol is presented which allows for the rapid screening of differential gene expression in the inner retina, as well as the optic nerve, in response to partial nerve crush. To prove the reliability of the method, prototypically, the differential expression profiles of three candidate genes (kinesin light chain, ferritin, RYB-A) were verified. The method seems to be suitable to address the question of how differential gene expression contributes to degeneration, survival and axonal repair after partial nerve crush.
Animals↗
All roads lead to disconnection?--Traumatic axonal injury revisited.
Traumatic brain injury (TBI) evokes widespread/diffuse axonal injury (TAI) significantly contributing to its morbidity and mortality. While classic theories suggest that traumatically injured axons are mechanically torn at the moment of injury, studies in the last two decades have not supported this premise in the majority of injured axons. Rather, current thought considers TAI a progressive process evoked by the tensile forces of injury, gradually evolving from focal axonal alteration to ultimate disconnection. Recent observations have demonstrated that traumatically induced focal axolemmal permeability leads to local influx of Ca2+ with the subsequent activation of the cysteine proteases, calpain and caspase, that then play a pivotal role in the ensuing pathogenesis of TAI via proteolytic digestion of brain spectrin, a major constituent of the subaxolemmal cytoskeletal network, the "membrane skeleton". In this pathological progression this local Ca2+ overloading with the activation of calpains also initiates mitochondrial injury that results in the release of cytochrome-c, with the activation of caspase. Both the activated calpain and caspases then participate in the degradation of the local axonal cytoskeleton causing local axonal failure and disconnection. In this review, we summarize contemporary thought on the pathogenesis of TAI, while discussing the potential diversity of pathological processes observed within various injured fiber types. The anterograde and retrograde consequences of TAI are also considered together with a discussion of various experimental therapeutic approaches capable of attenuating TAI.
Axons↗
The postconcussion syndrome after mild head trauma: is brain damage overdiagnosed? Part 1.
UNLABELLED: Many investigators attribute the postconcussion syndrome following mild closed head injury to permanent brain damage. The evidence supporting this conclusion is reviewed, including the force necessary to cause permanent brain damage; the basis for determining whether the patient was exposed to sufficient force in the accident to permanently damage the brain; the basis for determining whether the patient actually has permanent brain damage (not just brain dysfunction) traceable to the accident; and whether the location and severity of brain damage is sufficient to account for the postconcussion syndrome. CONCLUSION: the evidence for permanent traumatic brain damage as the cause of the postconcussion syndrome following mild closed head injury is weak.
Brain Damage, Chronic↗
Script knowledge after severe traumatic brain injury.
Severe diffuse traumatic brain injury (TBI) may impair the performance of daily-life complex activities. The aim of the present study was to assess whether these difficulties are related to a representational impairment of action knowledge. Two tasks requiring the manipulation of scripts were used. The first (script reconstitution) required subjects to sort cards describing actions belonging to 4 different scripts, presented in a random order. The second (script generation) required subjects to generate actions belonging to a given script. The results showed that TBI patients had preserved access to goal representation and action knowledge. However, they demonstrated (1) significant impairments when they had to deal with simultaneous competing sources of information and (2) a lack of inhibitory control on routine overlearned skills. Patients' performance was significantly correlated with behavioral modifications in everyday life. These data suggest that action impairment in severe TBI patients cannot be attributed to an impairment of action knowledge per se. As previously suggested by Schwartz et al., a restriction of limited-capacity processing resources may account for the observed deficits.
Activities of Daily Living↗
Regionally distinct patterns of calpain activation and traumatic axonal injury following contusive brain injury in immature rats.
Impact-induced head injury in infants results in acute focal contusions and traumatic axonal injury (TAI) that are associated with chronic holohemispheric cortical and white matter atrophy and may contribute to poor outcome in brain-injured children less than 4 years of age. Contusive brain trauma in postnatal day (PND) 11 or PND 17 rat pups, ages neurologically equivalent to a human infant and toddler, respectively, leads to cortical tissue loss and white matter atrophy which are associated with cognitive deficits. In adult models of brain trauma and in brain-injured humans, acute and sustained activation of the calpain family of calcium-activated neutral proteases has been implicated in neuronal death and TAI. PND 11 or PND 17 rat pups were subjected to closed head injury over the left hemisphere using the controlled cortical impact device and sacrificed at 6 h, 24 h or 3 days. Hemorrhagic contusions and tissue tears in the cortex and white matter were visible at 6 h, and neuronal loss was evident by 3 days. Calpain activation was observed in cell soma and dendrites of injured neurons at 6 h, and in degenerating dendrites and atrophic neurons at 24 h after injury at both ages. Axonal accumulation of amyloid precursor protein, indicative of TAI, was observed in the corpus callosum and lateral aspects of the white matter below the site of impact, and in the thalamus in PND 11 rats only. Intra-axonal calpain activation was observed to a limited extent in the corpus callosum and subcortical white matter tracts in both brain-injured PND 11 and PND 17 rats. Collectively, these results provide evidence that calpain activation may participate in neuronal loss in the injured cortex, but may not contribute to the pathogenesis of TAI following contusive brain trauma in the immature rat.
Aging↗
Improved identification of axonal shear injuries with gradient echo MR technique.
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Adult↗
Characterization of a prolonged regenerative attempt by diffusely injured axons following traumatic brain injury in adult cat: a light and electron microscopic immunocytochemical study.
Traumatic brain injury in animals and humans is well known to cause axonal damage diffusely scattered throughout the brain without evidence of other brain parenchymal change. This observation has prompted some to posit that such damaged axons are well positioned to mount a regenerative attempt. The present study uses an immunocytochemical marker specific for regenerating neurites to explore this issue. Further, in an attempt to expedite and enhance any potential regenerative effort, this study evaluates the efficacy of intrathecally applied nerve growth factor. Three sets of experiments were performed in adult cats. One group of animals was subjected to moderate fluid percussion brain injury and followed for 7 or 14 days post injury, with the continuous intraventricular infusion of nerve growth factor delivered by implanted osmotic pumps. These animals were compared to a second group of time-matched, sham-operated animals receiving artificial cerebrospinal fluid infusion. To assess axonal damage immunohistochemical staining for the low molecular weight neurofilament subunit (NF-L) was carried out using an NR4 monoclonal antibody. To localize axons exhibiting a regenerative response immunohistochemical staining for the growth associated protein GAP43 was employed. In sham controls, at the light microscopic level NF-L-immunoreactive axonal swellings were numerous at 7 days, but by 14 days post injury their frequency declined markedly. In contrast, GAP43-immunoreactive, disconnected reactive axonal swellings were rarely observed at 7 days but were numerous at 14 days. Ultrastructural analysis at 14 days post injury of carefully matched sections revealed reactive axons demonstrating sprouting consistent with a regenerative effort. Analysis of tissue from animals of 14 days of survival indicated that supplementation with nerve growth factor did not appear to enhance the capacity of damaged brain axons to mount a regenerative attempt. Rather, it appears that regenerative efforts seen reflect a spontaneous response. A third group of adult cats, subjected to the same injury but not subjected to osmotic pump implantation, was allowed to survive for 22-28 days. Animals in this group also demonstrated GAP43 immunoreactivity in reactive axonal swellings in the brain stem. This study demonstrates that diffusely injured axons can mount a sustained regenerative attempt that is associated with a reorganization of their cytoskeleton and accompanied by an up-regulation of growth-associated proteins.
Animals↗
Cerebellar atrophy after severe traumatic head injury in children.
OBJECT: The purpose of this study was to describe late neuropathological MRI findings in pediatric severe head injury and to explore the relationship between these lesions and cognitive sequelae. METHODS: Thirteen infants with severe head trauma (Glasgow 6) were included in this investigation. Clinical examination, a battery of tests designed to assess neurophysiological status, and MRI investigations of the brain were obtained in periods ranging between 8 and 20 months after the accident. Hemosiderin deposits, encephalomalacia, and cerebellar atrophy were the most frequent traumatic sequelae. The lesions were located in frontal lobes, the basal ganglia, and the cerebellum. Six patients had cerebellar atrophy associated with frontal or temporal postraumatic lesions. Cerebellar clinical dysfunction was observed in only 3 of these patients. Performance on tests evaluating frontal lobe functions was depressed in 5 of them. CONCLUSIONS: Late MRI after severe head trauma in our pediatric population showed unexpected cerebellar atrophy. Its correlation with prefrontal dysfunction is difficult to confirm because of its association with other parenchymal post-traumatic lesions. Further research involving a larger sample of patients with brain injury of varying severity is in progress, to investigate whether cerebellar atrophy could be a consequence of severe head trauma.
Adolescent↗
Changes of mGluR4 and the effects of its specific agonist L-AP4 in a rodent model of diffuse brain injury.
OBJECTIVE: Excessive release of glutamate from nerve terminals following diffuse brain injury (DBI) is thought to contribute to neuronal calcium overload leading to calcium-mediated cell damage. Metabotropic glutamate receptor subtype 4 (mGluR4) is regarded as one of the neuroprotective receptors in mammalian brains. Therefore, the mGluR4 specific agonists might exert neuroprotective effects after DBI. The focus of this study is to examine the changes of expression of mGluR4 after DBI and the role of its specific agonist L-AP4 in vivo. METHODS: One hundred and sixty-one male SD rats were randomized into two groups. Group A included normal control, sham-operated control and DBI group. DBI was produced by Marmarou's diffuse head injury model. The mRNA expression of mGluR4 was detected by hybridization in situ. Group B included DBI alone, DBI treated with normal saline and DBI treated with L-AP4. All DBI rats were trained in a series of performance tests, following which they were subjected to DBI. At 1 and 12 h, animals were injected intracerebroventricularly with L-AP4 (100 mM, 10 microl) or normal saline, respectively. The rats were tested for motor and cognitive performance at 1, 3, 7, 14 days post-injury and the damaged neurons were detected. RESULTS: There was no significant difference between the normal control group and sham-operated group in the expression of mGluR4 (P>0.05). The animals exposed to DBI showed a significant increased expression of mRNA of mGluR4 compared with that of the sham-operated animals 1 h after injuries (P<0.05). At 6 h, the evolution of neuronal expression of mGluR4 in the trauma alone group was relatively static. Compared with saline-treated control animals, rats treated with L-AP4 showed decreased number of damaged neurons and a better motor and cognitive performance. CONCLUSIONS: The increased expression of mGluR4 is an important process in the pathophysiological of DBI and its specific agonist L-AP4 can provide a remarkable neuroprotection against DBI not only at the histopathological level but also in the motor and cognitive performance.
Aminobutyrates↗
Optimizing screening for blunt cerebrovascular injuries.
BACKGROUND: The recognition that early diagnosis and intervention, prior to ischemic neurologic injury, has the potential to improve outcome following blunt cerebrovascular injuries (BCVI), led to a policy of aggressive screening for these injuries. The resultant epidemic of BCVI has created a dilemma, as widespread screening is impractical. We sought to identify independent predictors of BCVI, to focus resources. METHODS: Cerebral arteriography was performed based on signs or symptoms of BCVI, or in asymptomatic patients with high-risk mechanisms (hyperextension, hyperflexion, direct blow) or injury patterns. Logistic regression analysis identified independent predictors. RESULTS: A total of 249 patients underwent arteriography; 85 (34%) had injuries. Independent predictors of carotid arterial injury were Glasgow coma score < or =6, petrous bone fracture, diffuse axonal brain injury, and LeFort II or III fracture. Having one of these factors in the setting of a high-risk mechanism was associated with 41% risk of injury. Of patients with cervical spine fracture, 39% had vertebral arterial injury. CONCLUSIONS: Patients sustaining high-risk injury mechanisms or patterns should be screened for BCVI. In the face of limited resources, screening efforts should be focused on those with high-risk predictors.
Adult↗
Diffusion-weighted imaging demonstrates transient cytotoxic edema involving the corpus callosum in a patient with diffuse brain injury.
Reversible T2 hyperintense signal abnormality in the corpus callosum, although frequently seen after diffuse brain injury, has not been well clarified. With some accumulated evidence, we report a case of diffuse brain injury in a 24-year-old man. Magnetic resonance imaging (MRI) demonstrated T2 hyperintense signals in the trunk and the splenium of the corpus callosum 12 days postinjury. Echo-planar diffusion-weighted imaging was also performed on the same day, which revealed decreased diffusion (hyperintense signals) in the same site and almost the same size as T2 hyperintense signals. T1-weighted images were normal. Neuropsychological examination of the patient did not show callosal syndrome, namely hemialexia, unilateral agraphia and unilateral apraxia. Repeat MRI on day 20 demonstrated a signal decrease of both T2-weighted images and diffusion-weighted images (DWI) in the lesion. Follow-up MRI at 6 months showed complete resolution of the T2 signal abnormalities and of the corresponding decreased diffusion. Considering that diffusion-weighted imaging showed transient decreased diffusion, the lesion in the corpus callosum indicated the existence of cytotoxic edema. Also, transient DWI hyperintensity, namely cytotoxic edema, in the trunk and the splenium of the corpus callosum does not necessarily reveal callosal deficits.
Adult↗
Differentiation of mechanism and prognosis of traumatic brain stem lesions detected by magnetic resonance imaging in the acute stage.
We retrospectively evaluated the MRI from 17 patients with primary brain stem injury obtained in the acute stage. Clinical and radiological findings were analyzed in these 17 patients. T2-weighted imaging proved to be most sensitive and specific for the diagnosis of primary brain stem injury. We found two patterns of brain stem injury. The good prognosis group showed ventral brain stem lesions or dorsal superficial brain stem lesions. On the other hand the poor prognosis group showed deep dorsal brain stem lesions. These acute stage findings are seen only temporally in many cases so that it is most important to examine MRI findings in the acute stage to evaluate the prognosis of the patient. MRI was valuable in predicting the outcome. The possible mechanism of brain stem injury in patients with head injury is briefly discussed.
Acute Disease↗
Multimodal neuroimaging approaches to disorders of consciousness.
Advances in neuroimaging techniques hold significant promise for improving understanding of disorders of consciousness arising from severe brain injuries. We review neuroimaging studies of the vegetative state (VS) and minimally conscious state (MCS), and findings in an unusual case of late emergence from MCS. Multimodal neuroimaging studies using positron emission tomography techniques, functional magnetic resonance imaging, and quantitative electroencephalography and magnetoencephalography quantify variations of residual cerebral activity across these patient populations. The results suggest models to distinguish the pathophysiologic basis of VS and MCS. Less clear are potential brain mechanisms underlying late recovery of communication in rare MCS patients. Diffusion tensor magnetic resonance imaging studies and recent experimental findings suggest that structural remodeling of the brain following severe injury may play a role in late functional recoveries. More generally, relatively long time courses of recovery following severe brain injury emphasize the need to develop markers for identifying patients who may harbor potential for further meaningful recovery. Introduction of neuroimaging into the clinical evaluation process will require developing frameworks for longitudinal assessments of cerebral function. Although limited in number, available studies already provide important insights into underlying brain mechanisms that may help guide development of such assessment strategies.
Arousal↗