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PubMed1999

Correlation of survival time with size of axonal swellings in diffuse axonal injury.

Widespread damage to axons in the white matter of the brain is a well-recognised consequence of non-missile head injury. This diffuse axonal injury is characterised by a gradual swelling of the axon associated with an accumulation of cellular organelles and proteins. We have investigated the relationship between the size of the swellings of the damaged axon with survival time in post-mortem brain tissue. Sixty-six cases of head injury with known length of post-traumatic survival were selected for study, and immunohistochemistry for beta-amyloid precursor protein (betaAPP) was carried out. The minimum diameter of the betaAPP-immunolabelled damaged axons was measured in micrometers using the IBAS image analysis system. There was a strong, positive and significant relationship between the mean size of axonal swelling and survival time which plateaued at around 85 h post injury. With longer survival times the situation becomes more complex. betaAPP immunolabelling of damaged axons can contribute evidence about trauma and post-injury survival time in the forensic setting but should always be assessed with other evidence.

Adolescent↗

PubMed1994

Distribution of forebrain diffuse axonal injury following inertial closed head injury in miniature swine.

Diffuse axonal injury (DAI) is one of the most frequently encountered types of brain damage resulting from closed head injury. This study was designed to verify whether DAI could be produced in miniature swine by rapid acceleration and deceleration of the head in the coronal plane. Hanford miniature swine (16-19 kg) were anesthetized with 3% isoflurane and their heads accelerated rapidly once through a 60-105 degrees arc in the coronal plane, producing only transient post-traumatic unconsciousness without prolonged coma. All animals made a good recovery and were sacrificed between 6 h and 10 days after injury. The response of forebrain projection systems to this injury was studied using neurofilament immunohistochemistry with antisera to nonphosphorylated (SMI-32) and phosphorylated (SMI-31) epitopes common to heavy (200 kDa) and medium (160 kDa) neurofilament proteins. In 9 of 12 animals, lesions characterized by foci of SMI-32 positive axonal retraction balls were present at the white matter/gray matter junction at the crests of gyri in the dorsolateral regions of the frontal, parietal, and temporal cortices and along margins of the lateral ventricles. A high density of pyramidal neuron perikarya in layers III and V within cortical gyri associated with subcortical DAI were intensely positive for SMI-31 immunohistochemistry. These results validate the use of miniature swine in studies of axonal injury and demonstrate that axonal injury analogous to that seen in the mildest form of DAI (grade I) can be produced in these animals without producing prolonged coma.

Animals↗

PubMed2002

Semiquantitative analysis of corpus callosum injury using magnetic resonance imaging indicates clinical severity in patients with diffuse axonal injury.

OBJECTIVE: To evaluate the hypothesis that the extent of corpus callosum injury indicates the depth of shearing lesions in the central brain structure and therefore relates to the clinical severity of diffuse axonal injury. METHODS: A simple and objective procedure for semiquantitative analysis of magnetic resonance images (MRI)-the maximum signal intensity ratio (MSIR)-was employed prospectively in 21 patients with diffuse axonal injury but without apparent injury to the ventral pons. All were diagnosed using serial combination MRI scans of fluid attenuated inversion recovery (FLAIR) and T2* weighted gradient echo imaging during the initial two weeks after the injury. The signal intensity ratio between the two regions of interest-the corpus callosum and the normal appearing ventral pons-was calculated serially in mid-sagittal and parasagittal FLAIR image sections in each patient. The MSIR during the study period was determined as a semiquantitative index of corpus callosum injury in each patient. The correlations between MSIR and the duration of unconsciousness, Glasgow outcome scale at six months, and the presence of apparent midbrain injury were investigated. RESULTS: The mean (SD) MSIR value was 1.12 (0.18) at 7.4 (3.1) days after the injury (n = 21). MSIR correlated strongly with the duration of unconsciousness (n = 19, R(2) = 0.74, p < 0.0001), and was higher in patients with both an unfavourable GOS outcome (p = 0.020) and apparent midbrain injury (p < 0.001). CONCLUSIONS: MSIR, which is a simple and objective procedure for semiquantitative analysis of corpus callosum damage in diffuse axonal injury, correlated with clinical severity. A high MSIR value may indicate the presence of concomitant midbrain injury.

Adolescent↗

PubMedDate not supplied

Diffusion-weighted imaging for the evaluation of diffuse axonal injury in closed head injury.

PURPOSE: The purpose of this work was to compare diffusion-weighted imaging (DWI) with conventional MRI in the detection of shearing injuries in acute closed head injuries. METHOD: Twenty-five patients (19 male, 6 female) were examined within 48 h of trauma. Conventional MRI included T2-weighted fast spin echo, fluid-attenuated inversion recovery (FLAIR), and T2*-weighted gradient echo sequences. Full tensor DWI with calculation of apparent diffusion coefficient (ADC) maps was also performed. Lesions were identified and compared on all sequences. RESULTS: Four hundred twenty-seven lesions were counted by the combined use of all sequences. DWI identified 70 lesions not seen on conventional MRI. DWI identified 310 shearing injuries, followed by T2/FLAIR (n = 248) and T2* (n = 202). The majority of DWI-positive lesions showed decreased diffusion (65%). CONCLUSION: DWI is valuable in closed head injury because it identifies additional shearing injuries not visible on T2/FLAIR or T2* sequences. Furthermore, DWI/ADC maps differentiate between lesions with decreased or increased diffusion. DWI is less sensitive than T2* imaging for detecting hemorrhagic lesions.

Adolescent↗

PubMed2000

[The role of diffuse axonal injury in psychiatric assessment of brain-head trauma].

The concept of diffuse axonal injury is presented and the relevance in medicolegal assessment of brain injured patients is discussed. The lesion pattern of diffuse axonal injury not only plays a significant role in the acute management and rehabilitation of brain injured patients but also in issues of litigation. Brain imaging techniques are most important in the evaluation of structural damage to the brain and play a pivotal role in the detection of diffuse axonal injury. While computer-tomography follow-up studies may be valuable for the detection of diffuse axonal injury, magnetic resonance imaging is superior due to better sensitivity and contrast-resolution. The article presents selected case studies and illustrates the different lesion patterns.

Axons↗

PubMed2001

Clinical features of diffuse axonal injury.

OBJECTIVE: To analyze the mechanism of diffuse axonal injury (DAI) and study the relationship between DAI and brain concussion, brain contusion, and primary brain stem injury. METHODS: The clinical data and iconographic characteristics of 56 patients with DAI were analyzed retrospectively. RESULTS: Traffic accidents were the main cause of DAI. Among t he 56 cases, 34 were injured for at least twice, and 71.43% of the patients were complicated with contusion. CONCLUSIONS: It is considered that DAI is a common pattern of primary brain injury, which is often underestimated. And DAI includes cerebral concussion and primary brain injury, and is often complicated by cerebral cortex contusion. Therefore, it is very simple and practical to divide primary brain injuries into local and diffuse injuries.

Adolescent↗

PubMed1987

Diffuse axonal injury by assault.

A case of diffuse axonal injury (DAI) by assault is reported. The majority of DAI cases documented have been due to traffic accidents and some due to falls from height. DAI is caused by angular or rotational acceleration of the victim's head. The condition is common and is the second most important head injury after subdural hematoma with regard to death. Its clinical picture is characterized by immediate and prolonged coma or demented state. Because of the subtle nature of histological changes in DAI, awareness and intentional search for the lesion is essential. The triad of DAI is as follows: focal lesions (hemorrhages and/or lacerations) in the corpus callosum and brain stem, and microscopic demonstration of axonal damage--retraction balls. The concept of DAI will elucidate and enhance the understanding of many head trauma cases.

Adult↗

PubMed2000

[Model of diffuse axonal injury and focal brain injury in rats].

OBJECTIVE: To establish a rather ideal experimental brain injury model in rats, in which diffuse axonal injury(DAI) and focal brain contusion were made concurrently. METHODS: The pathophysiological changes were monitored, and the histological changes were observed under naked eye, microscope and electric microscope. RESULTS: 1. The mortality in the group suffering from DAI with focal contusion(Group A) was much higher than that in DAI(Group B) and sham group(Group C); 2. The time of post-injury primary coma in Group A [(5.19 +/- 0.49) h] was longer than that in Group B [(2.75 +/- 0.16) h] and Group C [(2.77 +/- 0.20) h] significantly(P < 0.01); 3. Immunohistological examination showed that the diffuse axonal injury could be seen in several parts of the brain(subcortical, corpus callosum and brainstem) in Group A; 4. We observed in Group A under electric microscope that the axons were swollen and degenerated fragmently, neurofilaments ranged disorderly and there was vacuolation. CONCLUSION: The model is cheap, simple and can be easily repeated. Furthermore it can be used to research the changes of pathophysiology, histology and moleculobiochemistry of head injury in human beings.

Animals↗

PubMed2002

The effect of varying impact energy on diffuse axonal injury in the rat brain: a preliminary study.

Diffuse axonal injury (DAI) is seen as widespread damage in the white matter of brain characterized by morphological changes to axons throughout the brain and brain stem. The current study attempted to investigate the effect of increasing impact energy on the presence and severity of DAI in corpus callosum (CC). DAI was induced in adult male Sprague-Dawley rats using an injury model adapted from Marmarou et al. in 1994. A 450-g cylindrical brass weight was dropped from three different heights (2.0 m, 1.5 m and 1.0 m) on to a metal helmet affixed to the skull of the rats. In the sham group, rats underwent a surgical procedure with no impact. After a 24-h survival period the animals were transcardially perfused. The brain was removed and the cerebral hemispheres were sectioned with a vibrotome and stained by silver impregnation technique. The CC of all the impacted rats showed DAI in the form of beaded axons, retraction balls and vacuole-like enlargements. The axonal injury was most severe in the 2-m group, while mildest in the 1-m group. In the sham group, axons appeared to be normal. This study demonstrates evidence of graded DAI depending on the impact energy. Such data is useful for mathematical modeling of axonal injury in rat brain using the same impact parameters and potential determination of injury thresholds for neural trauma.

Animals↗

PubMed1999

Diffuse axonal injury in infants with nonaccidental craniocerebral trauma: enhanced detection by beta-amyloid precursor protein immunohistochemical staining.

OBJECTIVE: Accurate identification of diffuse axonal injury is important in the forensic investigation of infants who have died from traumatic brain injury. beta-Amyloid precursor protein (beta-APP) immunohistochemical staining is highly sensitive in identifying diffuse axonal injury. However, the effectiveness of this method in brain-injured infants has not been well established. The present study was undertaken to assess the utility of beta-APP immunohistochemistry in detecting diffuse axonal injury in infants with either shaken baby syndrome or blunt head trauma. MATERIALS AND METHODS: Archival formalin-fixed, paraffin-embedded blocks from infants (<1 year old) with shaken baby syndrome (7 cases) and blunt head trauma (3) and blocks from 7 control cases that included nontraumatic cerebral edema (1), acute hypoxic-ischemic encephalopathy (1), and normal brain (5) were immunostained for beta-APP. A semiquantitative assessment of the severity of axonal staining was made. Corresponding hematoxylin-eosin-stained sections were examined for the presence of axonal swellings. RESULTS: Immunostaining for beta-APP identified diffuse axonal injury in 5 of 7 infants with shaken baby syndrome and 2 of 3 infants with blunt head trauma. Immunoreactive axons were easily identified and were present in the majority of the sections examined. By contrast, hematoxylineosin staining revealed axonal swellings in only 3 of 7 infants with shaken baby syndrome and 1 of 3 infants with blunt head trauma. Most of these sections had few if any visible axonal swellings, which were often overlooked on initial review of the slides. No beta-APP immunoreactivity was observed in any of the 7 control cases. CONCLUSIONS: Immunostaining for beta-APP can easily and reliably identify diffuse axonal injury in infants younger than 1 year and is considerably more sensitive than routine hematoxylin-eosin staining. We recommend its use in the forensic evaluation of infants with fatal craniocerebral trauma.

Adult↗

PubMed1997

[Shearing injuries of parasagittal white matter, corpus callosum and basal ganglia: possible radiological evidences of hemiplegia in diffuse axonal injury].

The relationship between spastic hemiplegia in diffuse axonal injury (DAI) and neuroradiological findings was studied in 100 cases. These cases were prospectively collected from the files of Automobile Insurance Rating Organization in Japan between 1993 from to 1996. Requirements for entry to this study were as follows: presence of initial unconsciousness after head injury without any lucid interval. Existence of CT scan or MRI film obtained within 12 hours of injury showing no significant mass effects, as well as follow-up CT scan or MRI film obtained more than 3 months after the injury. Psychosocial outcome was described both by the medical professional and the caregiver. The hemiplegia was rated severe, mild, or none. The outcome and diffuse ventriculomegaly were classified as reported by the authors previously. Spastic hemiplegia or quadriplegia was documented in the chronic stage in 63 cases, including 53 severe cases with difficulty in walking and 10 mild cases with only pyramidal signs detected. Chi-square analysis showed significant correlation between hemiplegia and the DAI outcome level or ventriculomegaly rating. Focal brain contusion was noticed in 33 cases, but did not correlate with the hemiplegia at all. Radiological findings included 25 cases of parasagittal white matter injury (gliding contusion), 20 cases of callosal injury, 19 cases of basal ganglionic region injury, 5 cases of brain-stem injury, and 3 cases of cerebellar injury. Chi-square analyses of hemiplegia and contralateral presence of these injuries were significant in the former three types of injury. Presence of at least one of these 3 lesions was defined as GCB injury. There were altogether 46 GCB injury cases which were significantly correlated with contralateral hemiplegia by chi-square analysis and by Spearman rank analysis. Partial correlation analysis with hemiplegia as the target variable indicated highly significant correlation only with GCB injury and outcome level. In conclusion, spastic hemiplegia in DAI is a manifestation of primary shear injury. Neuroradiological findings of GCB injury were statistically able to be significantly correlated with the presence of hemiplegia, and suggested pyramidal tract injury either at the corona radiata or the internal capsule level.

Adolescent↗

PubMed1989

Diffuse axonal injury after severe head trauma. A clinico-pathological study.

Diffuse Axonal Injury (DAI) is a well known entity that affects many patients with severe head trauma. Classically DAI has been considered the pathological substrate of those cases rendered unconscious at the moment of impact and in which the CT scan does not show mass lesions. Diffuse axonal damage is almost always related to mechanisms of injury in which the rotational acceleration produces shear and tensile strains of high magnitude. In this paper we present a group of 24 patients with a severe head injury in whom the postmortem examination demonstrated unequivocal signs of DAI. Widespread axonal retraction balls, located preferentially in the centrum semiovale and internal capsule were the most constant histological finding. We divided the entire series into two subgroups. One group (15 cases), included all the patients in whom the CT scan did not demonstrate mass lesions. In the second group (9 patients) we considered patients with a diffuse axonal injury in whom the CT scan additionally demonstrated a mass lesion (6 acute subdural haematomas, 2 intracerebral and 1 extradural haematoma). The mean age of the entire group was 26 years. Twenty two patients were injured in a road traffic accident, the remaining two fell from a considerable height. All were rendered immediately unconscious on impact. Diffuse brain damage is a common finding in patients with a severe head injury and immediate coma in whom the CT scan does not show mass lesions. Diffuse axonal injury can also appear in connection with a wide spectrum of focal lesions (acute subdural haematoma, basal ganglia haematoma etc.).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1988

Acute subdural hematoma and diffuse axonal injury after severe head trauma.

The association of acute subdural hematoma (SDH) and diffuse axonal injury has received little attention in the literature. The authors report the clinicopathological findings in six patients who died of severe head injury in whom computerized tomography revealed acute SDH as the predominant lesion. All patients were injured in road traffic accidents and lost consciousness on impact. The mean total contusion index was 17.4 and sever contusions were seen in only two cases. All patients presented histological criteria of intracranial hypertension (pressure necrosis focus in one or both parahippocampal gyri). Hypoxic brain damage was evident in the postmortem examination of three patients. In three cases, macroscopic hematic lesions were observed in the corpus callosum. All patients had widespread axonal retraction balls disseminated in the white brain matter. Three patients who survived for more than 11 days had microglial clusters. In some patients with a head injury, acute SDH may be only an epiphenomenon of a primary impact lesion of variable severity: that is, a diffuse axonal injury. In these cases, the final outcome is fundamentally dependent on the severity of the subjacent diffuse axonal injury.

Acute Disease↗

PubMed1995

Impact acceleration-induced severe diffuse axonal injury in rats: characterization of phosphate metabolism and neurologic outcome.

Diffuse axonal injury (DAI) occurs in over half of all severe cases of traumatic brain injury and has been associated with the development of a persistent vegetative state. Although a number of studies have examined the biochemical and physiological events following brain trauma, none of these has concentrated on events associated with the occurrence of severe DAI. The present study has used phosphorus magnetic resonance spectroscopy (MRS) and the rotarod motor test to characterize metabolic and neurologic consequences of severe diffuse axonal injury in rats induced by impact acceleration. Traumatic brain injury was induced in male rats by dropping a 450-g brass weight a distance of 2 m onto a 10-mm stainless-steel disc (3 mm wide) attached to the closed skull. Changes in brain intracellular pH, free magnesium concentration, cytosolic phosphorylation ratio, and mitochondrial oxidative metabolism after injury were monitored by phosphorus MRS while neurologic motor outcome over 1 week was assessed using the rotarod test. Impact acceleration-induced injury resulted in a highly significant decline in free magnesium concentration, cytosolic phosphorylation ratio, and an increased rate of mitochondrial oxidative phosphorylation, but no significant change in pH. These changes were associated with the occurrence of a significant neurologic deficit over 1 week postinjury. The similarity in metabolic events associated with production of neurologic deficits in this and other models of traumatic brain injury suggests that these bioenergetic changes may be common to all models of brain trauma.

Animals↗

PubMedDate not supplied

[A case of postural and kinetic tremor caused by diffuse axonal injury].

We reported a 25-year-old woman with postural and kinetic tremor caused by diffuse axonal injury. The patient demonstrated consciousness disturbance, left oculomotor palsy and tetraparesis because of an automobile accident. T2-weighted and FLAIR MRI showed features of diffuse axonal injury. Hyperintense lesions appeared in the corpus callosum, fornix, dorsal portion of midbrain, right cerebral peduncle, and bilateral internal capsules. About 3 weeks later, head tremor and left hemiparesis appeared with improvement of consciousness. Administration of trihexyphenidyl decreased the tremor. Ten weeks after the accident, a coarse tremor in the head and right upper extremity developed after withdrawal of trihexyphenidyl. Tremor in the right upper limb predominantly occurred while maintaining an upright posture and with intended movements. Re-administration of trihexyphenidyl decreased the tremors. The dentatothalamic pathway is one of the lesions responsible for posttraumatic tremor. Our patient demonstrated lesions of diffuse axonal injury involving the dentatothalamic pathway. We considered that these lesions were associated with postural and kinetic tremor in our case. The tremor occurred at least 3 weeks after the accident. This finding suggested that the tremor was caused by transsynaptic alternations of thalamus or the extrapyramidal system secondary to involvement of the dentatothalamic pathway.

Accidents, Traffic↗

PubMed1999

[Functional outcome after diffuse axonal injury in childhood traumatic brain injury].

We investigated the functional prognosis after traumatic diffuse axonal injury in children. We evaluated the status of the acute stage, as well as the functional independence measure (FIM) and intelligence quotient (IQ) at 4, 12, and 24 months after the injury. Physical disabilities persisted in all but 1 case, but 5 cases could walk by themselves after 1 year. IQ at 2 years after the injury was 64 in one case, but between 81 and 100 in others. Concerning the higher cortical function, all cases showed memory disturbance. None developed epilepsy. All cases showed abnormalities on cerebral MRI. Five of the 7 cases showed EEG abnormalities. As to the course of recovery scaled by FIM and IQ, marked improvement was seen in 4 cases during the first 4 months, 3 cases during the first 1 year. After 1 year, the degree of improvement became slower in all. All cases showed learning disability at school.

Activities of Daily Living↗

PubMed2003

Diffuse vascular injury in fatal road traffic accident victims: its relationship to diffuse axonal injury.

The authors have reported a macro- and microscopic study of brain lesions in 120 victims of fatal road traffic accidents, independent of the survival time. Diffuse vascular injury (DVI) was found in 14 patients (11.7%). All patients with DVI died within 24 h after the accident. The 14 patients with DVI also showed severe (Grade 2 or 3) diffuse axonal injury (DAI). Since DVI is restricted to road traffic accidents and incompatible with life, the high frequency observed in our series could be explained by the fact that all 120 patients were victims of road traffic accidents, and 69.2% had died within 24 h after the accident. The association between DVI and severe DAI (Grades 2 and 3) suggests that both lesions depend on the same mechanism, with the degree of axonal and vascular damage being determined by the intensity of the head acceleration. Our results show a relationship between DVI and DAI that suggest there may be a spectrum or at least a continuum between these entities as distinct from DVI being a separate entity.

Accidents, Traffic↗

PubMed1989

Axonal injury in the optic nerve: a model simulating diffuse axonal injury in the brain.

A new model of traumatic axonal injury has been developed by causing a single, rapid, controlled elongation (tensile strain) in the optic nerve of the albino guinea pig. Electron microscopy demonstrates axonal swelling, axolemmal blebs, and accumulation of organelles identical to those seen in human and experimental brain injury. Quantitative morphometric studies confirm that 17% of the optic nerve axons are injured without vascular disruption, and horseradish peroxidase (HRP) studies confirm alterations in rapid axoplasmic transport at the sites of injury. Since 95% to 98% of the optic nerve fibers are crossed, studies of the cell bodies and terminal fields of injured axons can be performed in this model. Glucose utilization was increased in the retina following injury, confirming electron microscopic changes of central chromatolysis in the ganglion cells and increased metabolic activity in reaction to axonal injury. Decreased activity at the superior colliculus was demonstrated by delayed HRP arrival after injury. The model is unique because it produces axonal damage that is morphologically identical to that seen in human brain injury and does so by delivering tissue strains of the same type and magnitude that cause axonal damage in the human. The model offers the possibility of improving the understanding of traumatic damage of central nervous system (CNS) axons because it creates reproducible axonal injury in a well-defined anatomical system that obviates many of the difficulties associated with studying the complex morphology of the brain.

Animals↗