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PubMed1994

Diffuse brain swelling after head injury: more often malignant in adults than children?

A series of 118 patients with diffuse traumatic brain swelling was studied retrospectively in order to compare the clinical findings in children with those in adults, and to determine the occurrence of neurological deterioration and outcome. The computerized tomography (CT) picture of absent third ventricle and basal cisterns was used to identify the cases. Although this condition has been associated with children, we found the same number of children and adults (59 cases each). Secondary deterioration (decline in consciousness, the development of new focal neurological signs, or an increase in intracranial pressure) occurred in 40% of cases and was more common in adults than children. Features that were significantly associated with deterioration were the presence of prolonged coma (> 1 hour) after the injury, CT signs of diffuse axonal injury or subarachnoid hemorrhage, or a recorded episode of hypotension. A moderate or good recovery at 6 months was achieved by 70 patients (59%), but 45 patients had a poor outcome (severe disability in nine, vegetative state in three, and death in 33) and this was often a consequence of secondary deterioration. In three patients, the outcome was not known. The combination of a severe initial injury, secondary insult, and diffuse swelling is associated with a poor outlook, particularly in adults. The CT appearance of diffuse swelling may develop more readily in children because of the lack of cerebrospinal fluid available for displacement. In children, diffuse swelling may have a relatively benign course unless there is a severe primary injury or a secondary hypotensive insult.

Adolescent↗
PubMed1993

Fatal falls in childhood. How far must children fall to sustain fatal head injury? Report of cases and review of the literature.

The question of whether fatal head injuries may occur from short-distance falls is one that continues to cause controversy. The records of the Sacramento County Coroner's Office from 1983 to 1991 were reviewed for cases of fatal head injury in children aged < or = 5 years, where a history of a fall was initially given. During this 9-year period, three cases of witnessed falls from heights of > 10 ft (3 m) were found. At autopsy, all children had multiple complex calvarial skull fractures, basal fractures, or both; subdural and subarachnoid hemorrhage was found in all cases, and two showed severe cerebral contusion. None had retinal hemorrhage or axonal injury. These are compared with 19 fatalities initially alleged to have occurred from short falls of < or = 5-6 ft (1.5-1.8 m). As others have found, most of these "minor fall" fatalities occurred under circumstances where there were no unrelated witnesses to corroborate the initial history. Autopsy findings in these cases tended to be of unexpected severity for the initially proposed mechanism of injury, and a number of cases showed evidence of accelerative injury (retinal hemorrhage and/or diffuse axonal injury) where no such mechanism was accounted for by initial history. After sufficient investigation, most of these cases (74%) have ultimately been proven to represent inflicted trauma. A thorough literature review on the subject identifies two major viewpoints. One is that short falls have a significant potential for fatality. The other, more widely espoused view is that short falls rarely, if ever, cause serious injury or death.(ABSTRACT TRUNCATED AT 250 WORDS)

Accidental Falls↗
PubMed1999

Neuron-specific enolase as an effective immunohistochemical marker for injured axons after fatal brain injury.

Recently, it has been reported that a diagnosis of diffuse axonal injury in cases with a short survival period can be made with the use of immunolabelling for beta-amyloid precursor protein (APP). We examined whether immunostaining for neuron-specific enolase (NSE) can also be a useful marker for the detection of axonal injury in its early stages. Sections of the corpus callosum from 19 cases of head injury and from 9 cases of no head injury were immunostained for NSE and stained by the standard Holmes' silver method. For comparison, serial sections from several cases were immunostained for APP. Immunostaining for NSE as well as for APP, labelled injured axons in head injury cases with as early as 1.5 h survival where Holmes' staining failed to detect any changes of axons. Since NSE and APP labelled only injured axons but not normal axons, the results were readily interpretable. These findings indicate that NSE should be an effective marker for the detection of axonal injury in its early stages.

Adolescent↗
PubMed2003

Anthropomorphic simulations of falls, shakes, and inflicted impacts in infants.

OBJECT: Rotational loading conditions have been shown to produce subdural hemorrhage and diffuse axonal injury. No experimental data are available with which to compare the rotational response of the head of an infant during accidental and inflicted head injuries. The authors sought to compare rotational deceleration sustained by the head among free falls, from different heights onto different surfaces, with those sustained during shaking and inflicted impact. METHODS: An anthropomorphic surrogate of a 1.5-month-old human infant was constructed and used to simulate falls from 0.3 m (1 ft), 0.9 m (3 ft), and 1.5 m (5 ft), as well as vigorous shaking and inflicted head impact. During falls, the surrogate experienced occipital contact against a concrete surface, carpet pad, or foam mattress. For shakes, investigators repeatedly shook the surrogate in an anteroposterior plane; inflicted impact was defined as the terminal portion of a vigorous shake, in which the surrogate's occiput made contact with a rigid or padded surface. Rotational velocity was recorded directly and the maximum (peak-peak) change in angular velocity (delta theta(max)) and the peak angular acceleration (theta(max)) were calculated. Analysis of variance revealed significant increases in the delta theta(max) and theta(max) associated with falls onto harder surfaces and from higher heights. During inflicted impacts against rigid surfaces, the delta theta(max) and theta(max) were significantly greater than those measured under all other conditions. CONCLUSIONS: Vigorous shakes of this infant model produced rotational responses similar to those resulting from minor falls, but inflicted impacts produced responses that were significantly higher than even a 1.5-m fall onto concrete. Because larger accelerations are associated with an increasing likelihood of injury, the findings indicate that inflicted impacts against hard surfaces are more likely to be associated with inertial brain injuries than falls from a height less than 1.5 m or from shaking.

Accidental Falls↗
PubMed1998

Paroxysmal sympathetic storms ("diencephalic seizures") after severe diffuse axonal head injury.

We describe a patient with a severe traumatic head injury who exhibited paroxysmal sympathetic storms, similar to those described in "diencephalic seizures." No epileptiform activity was evident on electroencephalography, and therapeutic levels of anticonvulsants failed to alter the spells; however, use of morphine sulfate abolished them. The features of this and several previously reported cases refute the primary roles of the diencephalon and seizures in this syndrome. Rather, in the setting of already compromised autonomic neuronal integrity, subtle fluctuations in intraventricular pressure or activation of reflexes triggered from muscle mechanoreceptors or chemoreceptors during episodes of hypertonia are more likely. "Paroxysmal sympathetic storms," a more appropriate descriptive term for these phenomena, should be recognized; thus, unnecessary diagnostic evaluations can be minimized, and appropriate therapy can be initiated.

Adolescent↗
PubMed2001

Sertraline to improve arousal and alertness in severe traumatic brain injury secondary to motor vehicle crashes.

OBJECTIVE: To establish whether or not the serotonin reuptake inhibitor (SSRI) sertraline can improve arousal and alertness of patients with traumatic brain injury (TBI) and associated diffuse axonal injury (DAI). Serotonin is a major inhibitory as well an excitatory neurotransmitter, and serotonergic neurons modulate the activity of brain regions responsible for motor control, arousal, attention, and emotional regulation. SETTING: Tertiary care inpatient rehabilitation centre directly attached to a university hospital level-one trauma centre. DESIGN: Prospective placebo-controlled randomized trial utilizing sertraline on admission to acute rehabilitation. DATA SET: Eleven subjects, post-high speed motor vehicle crash and post-severe TBI (GCS < or = 8) with presumed DAI randomized to receive either sertraline 100mg per day or placebo for 2 weeks. All subjects were within 2 weeks of acute injury. Outcome measures recorded were the Orientation Log (daily), Agitated Behaviour Scale (daily), and the Galveston Orientation and Amnesia Test (weekly). RESULTS: Both placebo and active medication groups demonstrated similar rates of improvement on all three scales. There was no difference in the rates of recovery for either study group (p > 0.05, ANOVA with repeated measures). The groups did not demonstrate a statistically significant negative effect on recovery either, although the size is too small for a statistically reliable beta-effect. CONCLUSION: This pilot study fails to establish whether the early use of sertraline may improve alertness, decrease agitation or improve cognitive recall of material. This may be due to the small size of the study group, the brief duration of treatment or by a skewed placebo group. Larger studies will be required to prove any efficacy. There were no complications with its use and sertraline did not demonstrate a detrimental effect on recovery. This indicates that sertraline may be safe to use in the treatment of psychiatric or behavioural complications attributable to TBI.

Accidents, Traffic↗
PubMed2001

Neuropathology of inflicted head injury in children. II. Microscopic brain injury in infants.

There are very few reports in the literature dealing with the neuropathology of infant head injury, and the question of whether diffuse traumatic brain damage [diffuse axonal injury (DAI)] occurs in such children has not yet been reliably established by detailed neuropathological studies. We report the findings in the brains of a series of 37 infants aged 9 months or less, all of whom died from inflicted head injuries, and 14 control infants who died of other causes. Axonal damage was identified using immunohistochemistry for beta-amyloid precursor protein. Full clinical details were available for each case, the most constant of which in the study cohort was an episode of significant apnoea at presentation, found to have been recorded in 75% of cases. Global hypoxic damage was the most common histological finding. Widespread axonal damage, interpreted as vascular, was present in 13 cases, but widespread traumatic axonal injury was found in only two children, both of whom had severe head injuries with multiple skull fractures. Epidural cervical haemorrhage and focal axonal damage to the brainstem and the spinal nerve roots, found in 11 cases but not in controls, indicate that the craniocervical junction is vulnerable in infant head injury, the neuropathology being that of stretch injury from cervical hyperextension/flexion. Damage to this region could account for the observed apnoea, which could in turn lead to hypoxic damage and brain swelling. The observation that the predominant histological abnormality in cases of inflicted head injury in the very young is diffuse hypoxic brain damage, not DAI, can be explained in one of two ways: either the unmyelinated axon of the immature cerebral hemispheres is relatively resistant to traumatic damage, or in shaking-type injuries the brain is not exposed to the forces necessary to produce DAI.

Amyloid beta-Protein Precursor↗
PubMed1999

Axonal cytoskeletal responses to nondisruptive axonal injury and the short-term effects of posttraumatic hypothermia.

In human diffuse axonal injury (DAI), axons are exposed to transient tensile strain. Over the ensuing several hours, injured axons enter a "pathological cascade" of events that lead to secondary axotomy. Use of animal models of traumatic axonal injury (TAI) has allowed description of a number of pathological changes before axotomy occurs, including structural and functional changes in the axolemma, disorientation, and/or loss of microtubules, either compaction and/or dispersion of neurofilaments together with focal compaction at sites where continuity of the axolemma is lost. Recent literature suggests that use of hypothermia may improve behavioral outcomes or reduce the number/density of injured axons in which axonal transport is altered after TAI. But there is presently no ultrastructural, pathological explanation as to how hypothermia may act at the level of the axon to reduce posttraumatic loss of axoplasmic transport. In this study, we tested the hypothesis that posttraumatic hypothermia may ameliorate (a) alteration of axonal transport and (b) early pathological changes in the axonal cytoskeleton prior to secondary axotomy. We have undertaken a pilot study within 4 h of stretch injury to adult guinea pig optic nerve axons as a model of TAI and applied stereological techniques to assess differences in pathology in animals either maintained at 37.5 degrees C or cooled to 32-32.5 degrees C for 2 or 4 h after injury. We provide quantitative evidence that posttraumatic hypothermia significantly reduces the number of axons labelled for beta-APP, a marker for disruption of fast axonal transport, and reduces the loss of microtubules and compaction of neurofilaments, which occurs in normothermic animals over the first 4 h after injury.

Amyloid beta-Protein Precursor↗
PubMed1999

Experimental axonal injury triggers interleukin-6 mRNA, protein synthesis and release into cerebrospinal fluid.

Diffuse axonal injury is a frequent pathologic sequel of head trauma, which, despite its devastating consequences for the patients, remains to be fully elucidated. Here we studied the release of interleukin-6 (IL-6) into CSF and serum, as well as the expression of IL-6 messenger ribonucleic acid (mRNA) and protein in a weight drop model of axonal injury in the rat. The IL-6 activity was elevated in CSF within 1 hour and peaked between 2 and 4 hours, reaching maximal values of 82,108 pg/mL, and returned to control values after 24 hours. In serum, the levels of IL-6 remained below increased CSF levels and did not exceed 393 pg/mL. In situ hybridization demonstrated augmented IL-6 mRNA expression in several regions including cortical pyramidal cells, neurons in thalamic nuclei, and macrophages in the basal subarachnoid spaces. A weak constitutive expression of IL-6 protein was shown by immunohistochemical study in control brain. After injury, IL-6 increased at 1 hour and remained elevated through the first 24 hours, returning to normal afterward. Most cells producing IL-6 were cortical, thalamic, and hippocampal neurons as confirmed by staining for the neuronal marker NeuN. These results extend our previous studies showing IL-6 production in the cerebrospinal fluid of patients with severe head trauma and demonstrate that neurons are the main source of IL-6 after experimental axonal injury.

Animals↗
PubMed2002

Traumatic axonal injury after closed head injury in the neonatal pig.

Closed head injury is the leading cause of morbidity and mortality in infants and children, and results in pathologies such as diffuse axonal injury (DAI) and subarachnoid hematoma (SAH). To better understand the mechanical environment associated with closed head injury in the pediatric population, animal models that include salient features of human infant brain must be utilized. Based on detailed information regarding the parallels between brain development in the pig and the human, the 3-5-day-old piglet was used to represent the infant at less than 3 months of age. Anesthetized piglets (n = 7) were subjected to rapid, inertial (nonimpact) rotation of the head about its axial plane and sacrificed at 6 h postinjury. Immediately following injury, five of seven piglets were apneic, with an absence of pupillary and pain reflexes. All piglets exhibited severe coma immediately postinjury, but recovered by sacrifice time. Blood was present on the surface of the frontal lobes, cerebellum, and brainstem, and subarachnoid hemorrhage was evident in the frontal cortex. In six of seven brain-injured piglets, accumulation of the 68-kDa neurofilament protein was evident in contiguous axons (swollen) and occasionally in disconnected axons (axonal bulbs), suggestive of traumatic axonal injury (TAI). Mapping of the regional pattern of TAI revealed injured axons predominantly in central and peripheral white matter tracts in the frontal and temporal lobes and in the midbrain. The number of injured axons was equivalent in both hemispheres, and did not correlate to the load applied to the head. Together, these data demonstrate that rapid rotation of the piglet head without impact results in SAH and TAI, similar to that observed in children following severe brain trauma.

Animals↗
PubMed1997

[A lateral fluid percussion model for the experimental severe brain injury and a morphological study in the rats].

Few morphological studies have been reported on fluid-percussion experimental models using mechanically induced severe brain injury have been reported. This study was initiated to evaluate microscopic and immunohistochemical findings in severe brain injury models using rats. The experimental rats and the methods used were the same as described for a fluid-percussion model. Fluid-percussion models of traumatic brain injury were produce by rapidly injecting fluid volume into the epidural space of the temporal lobe. We used 5 rats which sustained various degrees of injury by high (7.0 atm), medium (5.6 atm) and low (3.5 atm) magnitudes of impact and sham control. The rats were sacrificed and perfused transcardially with buffer solution followed by 2.5% glutaraldehyde at intervals of 24 hours, 3 days, and 7 days, and there were normal and sham control groups. In this immunohistochemical study, monoclonal antibody to 70 kilodalton neurofilament subunit was used in a standard Avidin-Biotin Complex Kit (DAKO). Microscopic findings revealed subarachnoid hemorrhage, lateral IIIrd ventricular hemorrhage, and rarefaction and petechial hemorrhage of the local contusional lesion. In the medium level injury, there was a marked petechial hemorrhage in the corpus callosum and subependymal area. In the high level injury, there was marked edema in the white matter of the ipsi- and contralateral cerebral hemisphere, and multiple petechial hemorrhage in the brain stem and cerebellum. Microscopic findings in the corpus callosum, subependyma and brain stem in the vicinity of petechial hemorrhage revealed a large number of axonal swellings, but in these specimens only a few typical axonal retraction balls were seen with Bodian and immunohistochemical stains. In conclusion, this experimental model seems to simulate local and diffuse shearing injury, showing various morphological characteristics of diffuse axonal injury.

Animals↗
PubMed1997

Temporal and regional patterns of axonal damage following traumatic brain injury: a beta-amyloid precursor protein immunocytochemical study in rats.

Diffuse axonal injury (DAI) is an important consequence of human head trauma. This experimental investigation utilized the immunocytochemical visualization of beta-amyloid precursor protein (beta-APP) to document regional patterns of axonal injury after traumatic brain injury (TBI) and to determine the importance of injury severity on the magnitude of axonal damage. Rats underwent moderate (1.84-2.11 atm) or severe (2.38-2.52 atm) parasagittal fluid-percussion (F-P) brain injury or sham procedures. At 1, 3, 7 or 30 days after TBI, rats were perfusion-fixed and sections immunostained for the visualization of beta-APP. A regionally specific axonal response to TBI was documented after moderate F-P injury. Within the dorsolateral striatum, an early increase in beta-APP-positive axonal profiles at 24 hours (h) was followed by a significant decline at subsequent survival periods. In contrast, the frequency of reactive profiles was initially low within the thalamus, but increased significantly by day 7. Within the external capsule at the injury epicenter, numbers of immunoreactive axons increased significantly at 24 h and remained elevated throughout the subsequent survival periods. At multiple periods after TBI, selective cortical and thalamic neurons displayed increased staining of the perikarya. A significant increase in the overall frequency of beta-APP profiles was documented in the severe vs moderately injured rats at 72 h after TBI. These data indicate that parasagittal F-P brain injury (a) results in widespread axonal damage, (b) that axonal damage includes both reversible and delayed patterns, and (c) that injury severity is an important factor in determining the severity of the axonal response to TBI.

Amyloid beta-Protein Precursor↗
PubMed1987

The postmortem diagnosis of diffuse cerebral injuries, with special reference to the importance of brain fixation.

In 3 cases of head injury the main finding was the diffuse axonal injury pattern of brain damage. This is characterised post mortem by focal lesions in the corpus callosum and rostral (anterior) brainstem, together with diffuse damage to white matter. In order to diagnose this and other forms of diffuse injury, the importance of fixing the brain before examination is stressed. In addition, microscopic examination is often required, though of relatively few sections from readily predictable anatomical locations. A suggested method of approach is proposed, which will greatly facilitate diagnosis of this surprisingly common condition.

Adult↗
PubMed2005

Cortical demyelination and diffuse white matter injury in multiple sclerosis.

Focal demyelinated plaques in white matter, which are the hallmark of multiple sclerosis pathology, only partially explain the patient's clinical deficits. We thus analysed global brain pathology in multiple sclerosis, focusing on the normal-appearing white matter (NAWM) and the cortex. Autopsy tissue from 52 multiple sclerosis patients (acute, relapsing-remitting, primary and secondary progressive multiple sclerosis) and from 30 controls was analysed using quantitative morphological techniques. New and active focal inflammatory demyelinating lesions in the white matter were mainly present in patients with acute and relapsing multiple sclerosis, while diffuse injury of the NAWM and cortical demyelination were characteristic hallmarks of primary and secondary progressive multiple sclerosis. Cortical demyelination and injury of the NAWM, reflected by diffuse axonal injury with profound microglia activation, occurred on the background of a global inflammatory response in the whole brain and meninges. There was only a marginal correlation between focal lesion load in the white matter and diffuse white matter injury, or cortical pathology, respectively. Our data suggest that multiple sclerosis starts as a focal inflammatory disease of the CNS, which gives rise to circumscribed demyelinated plaques in the white matter. With chronicity, diffuse inflammation accumulates throughout the whole brain, and is associated with slowly progressive axonal injury in the NAWM and cortical demyelination.

Acute Disease↗
PubMed2005

Stretch-associated injury in cervical spondylotic myelopathy: new concept and review.

The simple pathoanatomic concept that a narrowed spinal canal causes compression of the enclosed cord, leading to local tissue ischemia, injury, and neurological impairment, fails to explain the entire spectrum of clinical findings observed in cervical spondylotic myelopathy. A growing body of evidence indicates that spondylotic narrowing of the spinal canal and abnormal or excessive motion of the cervical spine results in increased strain and shear forces that cause localized axonal injury within the spinal cord. During normal motion, significant axial strains occur in the cervical spinal cord. At the cervicothoracic junction, where flexion is greatest, the spinal cord stretches 24% of its length. This causes local spinal cord strain. In the presence of pathological displacement, strain can exceed the material properties of the spinal cord and cause transient or permanent neurological injury. Stretch-associated injury is now widely accepted as the principal etiological factor of myelopathy in experimental models of neural injury, tethered cord syndrome, and diffuse axonal injury. Axonal injury reproducibly occurs at sites of maximal tensile loading in a well-defined sequence of intracellular events: myelin stretch injury, altered axolemmal permeability, calcium entry, cytoskeletal collapse, compaction of neurofilaments and microtubules, disruption of anterograde axonal transport, accumulation of organelles, axon retraction bulb formation, and secondary axotomy. Stretch and shear forces generated within the spinal cord seem to be important factors in the pathogenesis of cervical spondylotic myelopathy.

Biomechanical Phenomena↗
PubMed2000

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

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.

Amyloid beta-Protein Precursor↗
PubMed2002

Both MK801 and NBQX reduce the neuronal damage after impact-acceleration brain injury.

To understand the pathogenesis of diffuse axonal injury, we investigated the temporal and spatial profiles of neuronal degeneration in impact-acceleration injury in rats using Fluoro-Jade (FJ) staining. Impact-acceleration injury was produced in Wistar rats by the method described by Marmarou et al. with some modifications. Animals were sacrificed 1, 2, 7, 14, or 28 days after injury. Paraffin-embedded coronal sections were stained with HE or FJ, or analyzed immunohistochemically for GFAP or amyloid precursor protein (APP). FJ-positive degenerative neurons were found primarily in the dorsal brainstem and thalamus from 1 to 2 days following injury and these were associated with GFAP expression. However, FJ-positive cells were rarely found after 7 days. In all rats, significant expression of APP was observed primarily in the cingulum, cerebral peduncle and pontomedullary junction. FJ also stained these injured axons. Intrathecal administration of both NMDA and AMPA/kinate glutamate receptor antagonists MK-801 and NBQX, respectively, reduced the neuronal injury. NBQX showed more significant effects on axonal injury than MK-801. These observations indicate that not only axonal damage, but also primary neuronal damage occurs in this impact-acceleration injury model. It is also suggested that NBQX can act both directly on neuronal cells and white matter and that NMDA could have a significant protective effect against not only neuronal, but also axonal injury.

Amyloid beta-Protein Precursor↗
PubMed1993

[Recent advances in the study on the mechanism of brain injury].

A cerebral contusion and DAI (diffuse axonal injury) are practically very important in a medico-legal case of the closed head injury. In this paper, we will report the epitome of the recent advances in the study on the mechanism of them. Coup contusion can be mainly attributed to the skull inbending and/or the skull fracture which develop in the impact region. As to the mechanism of the contrecoup contusion, several theories are reported. During rotational movement of the head, intracerebral shear strains would be produced because of brain lag (Holbourn's rotation theory). Anatomical features of the skull plays an important role (Gurdjian). Relative movement between a brain and a skull induces intracranial cavitation due to pressure gradient (Gross's cavitation theory). Brain is injured by deformation pressure induced by skull deformation and acceleration one done by a movement of the head (Lindenberg). The last one is Courville's transmitted waves of force theory. As to DAI, there is Gennarelli's theory. During a rotational movement of a brain caused by high rate of angular acceleration operating for a long period, intracerebral shear strains occur and injure a brain. As to the brain injuries which include a cerebral contusion and DAI, two theories are reported. Centripetal progression of strains to the core of a brain injuries the brain (Ommaya). Natural frequency of impact determines the nature of resulting injury to the brain (Willinger).

Biomechanical Phenomena↗