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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↗

Successful treatment by spinal cord stimulation for gait disturbance in a patient with diffuse axonal injury.

The authors present a case of diffuse axonal injury (DAI) treated by cervical spinal cord stimulation (C-SCS) for gait disturbance. The patient had right hemiparesis of moderate degree, mild ataxia, ideational apraxia and gait disturbance, when admitted to our hospital for rehabilitation. He could not walk by himself, nevertheless neurorehabilitation was done for four months. Xenon-CT was examined by C-SCS loading and the changes of regional cerebral blood flow were significantly increased in both hemispheres, especially in the thalamus. C-SCS was performed continuously on condition of 25 Hz, 200 microsec and 0.5 V, daily for a month. Neurological deficits, especially gait disturbance due to ideational apraxia, were gradually improved after initiation of C-SCS, and the patient could walk by himself. We speculate that C-SCS played a role in triggering improvement of gait disturbance at the chronic stage in our case, and SCS may be helpful for neurorehabilitation of focal symptoms after DAI.

Adult↗

[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↗

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↗

Prediction of recovery from a post-traumatic coma state by diffusion-weighted imaging (DWI) in patients with diffuse axonal injury.

INTRODUCTION: To determine whether diffusion-weighted magnetic resonance (MR) imaging findings combined with initial clinical factors indicate the depth of shearing lesions in the brain structure and therefore relate to coma duration in diffuse axonal injury (DAI). METHODS: A total of 74 adult patients (48 male and 26 female) with DAI were examined with conventional MR imaging and diffusion-weighted MR imaging between 2 hours and 20 days after injury. Apparent diffusion coefficient (ADC) maps were obtained and the mean ADC values of each region of interest (ROI) were measured using MRI console software. The involvement of the brainstem, deep gray matter, and corpus callosum was determined for each sequence separately as well as for the combination of all sequences. The correlations between MR imaging findings indicating the presence of apparent brain injury combined with initial clinical factors were determined. RESULTS: Clinical characteristics, such as initial score on the Glasgow coma scale (GCS), age and number of all lesions, and ADC scores were predictive of the duration of coma. CONCLUSION: It was possible to predict post-traumatic coma duration in DAI from cerebral MR imaging findings combined with clinical prognostic factors in the acute to subacute stage after head injury. Age, ADC scores, GCS score and number of lesions were highly significant in predicting coma duration. The technique presented here might provide a tool for in vivo detection of DAI to allow the prediction of the coma duration during the early stages in patients with traumatic brain injury.

Accidents, Traffic↗

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↗

[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↗

Wall-eyed bilateral internuclear ophtalmoplegia presenting as monocular alternating nystagmus: a non-epileptic phenomenon in a case of diffuse axonal injury.

A 15-year-old male in a persistent vegetative state due to diffuse axonal injury presented with seizures and spontaneous alternating monocular nystagmus. The cranial MRI revealed diffuse axonal injury involving supratentorial and infratentorial structures, and the splenium of the corpus callosum. The monocular alternating nystagmus was thought to be independent of seizures and occurred as a result of diffuse axonal injury affecting the medial longitudinal fasciculus bilaterally.

Accidents, Traffic↗

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↗

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↗

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↗

[Expression of beta-amyloid precursor protein in diffuse axonal injury of rats].

OBJECTIVE: To explore an method for diffuse axonal injury (DAI) diagnosis and injury time estimation, the changes of beta-APP immunoreactivity and to observe the morphology of axonal in different parts of brain after experimental DAI injury. METHODS: The animal models of DAI was established according to the Marmarou's method. Immunohistochemistry and Gless staining were performed to observe the changes of beta-APP expression and the morphology of axon with the time elapsed after the DAI injury. RESULTS: In the brain injury group, the morphologic changes of axon in brain stem were showed as twisted, broken and swellen at 0.5 h, and the myelin sheaths broken could be observed, the retraction ball was found at 12 h. Those morphology changes further progressed at 12h, reached to peack up to 1 d, then repaired at 3 d, and recovered at 10 d; Meanwhile the analysis of beta-APP immunoreactivity was also showed a time-dependent difference as fellows: beta-APP expression begin at 3h, increased its immunoreactivity at 12h, reached to maximize at 1 d, decreased after 3 d, returned to basal level at 10 d. CONCLUSIONS: The results suggest that beta-APP immunohistochemistry combine with Gless staining be sensitive methods for DAI diagnosis, they could discover the time-dependent changes of the axonal morphology.The changes beta-APP are quite regular and could be used for timing DAI injury.

Amyloid beta-Protein Precursor↗

[Magnetic resonance in moderate and severe head injury: comparative study of CT and MR findings. Characteristics related to the presence and location of diffuse axonal injury in MR].

INTRODUCTION: Cranial CT has been the most extended evaluation means for patients suffering head trauma. However, it has low sensitivity in the identification of diffuse axonal injury and posterior fossa lesions. Cranial MR is a potentially more sensitive test but difficult to perform in these patients, a fact that has hampered its generalised use. OBJECTIVE: To compare the identification capability of traumatic intracranial lesions by both diagnostic tests in patients with moderate and severe head injury and to determine which radiological characteristics are associated with the presence of diffuse injury in MR and their clinical severity. MATERIAL AND METHODS: 100 patients suffering moderate or severe head injury to whom a MR had been performed in the first 30 days after trauma were included. All clinical variables related to prognosis were registered, as well as the data from the initial CT following Marshall et al., classification. The MR was blindly evaluated by two neuroradiologists that were not aware of the initial CT results or the clinical situation of the patient. All lesions were registered as well as the classification following the classification of lesions related to DAI described by Adams et al. CT and MR findings were compared evaluating the sensitivities of each test. Factors related to the presence of diffuse injury in MR were studied by univariate analysis using chi2 test and simple correlations. RESULTS: MR is more sensitive than CT for lesions in cerebral white matter, corpus callosum and brainstem. It also detects a greater number of cerebral contussions. The presence of diffuse axonal injury depends on the mechanism of the trauma, being more frequent in higher energy trauma, specially in traffic accidents. Among the radiological characteristics associated to DAI the most clearly related is intraventricular haemorrhage. The presence of a deeper injury and a higher score in the scales of Adams is associated with a lower score in the GCS and motor GCS, and so with a worse level of consciousness and bigger severity of injury, confirming Ommaya's model.

Adolescent↗

[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↗

Delayed presentation of diffuse axonal injury: a case report.

This report highlights a case of delayed onset of diffuse axonal injury in the apparent absence of direct head trauma. This case questions the appropriate observation period for patients with signs of diffuse axonal injury presenting after a high-velocity crash.

Accidents, Traffic↗

[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↗

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↗

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↗