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Results for “Diffuse Axonal Injury”

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PubMed2001

The neuropsychology of blunt head injury in the early postacute stage: effects of focal lesions and diffuse axonal injury.

This investigation evaluated the neuropsychological symptoms in the early posttraumatic period following blunt head injury and their correlation to routine imaging data in a consecutive series of TBI patients (Magdeburg Neurotrauma Databank). Of 135 consecutive patients, 68 could be assessed neuropsychologically 8-21 days after trauma. In 61 patients, routine clinical CT data were sufficient for neuroradiological analysis focusing on the presence or absence of CT signs of diffuse axonal injury (DAI) or focal traumatic injury. In these patients, the initial GCS score was significantly correlated with the presence of DAI but not with focal pathology. The presence of DAI was correlated with behavioral and cognitive symptoms of frontal lobe dysfunction, especially in interference tasks (Go/NoGO and Stroop reaction times) and semantic fluency. The presence of local frontal or temporal traumatic lesions was associated with deficits in concept formation, fluency tasks and behavioral symptoms, but not with increased interference. Patients with frontal contusions were impaired in a task of visuomotor planning and performance (Block design). Our data indicate that both traumatic DAI and focal lesions result in frontal lobe symptoms. We conclude that, even in clinically "mild" TBI, brain imaging should be used to identify patients with substantial brain damage. These should be assessed neuropsychologically for possible posttraumatic cognitive or behavioral impairment. In consideration of its easy accessibility, the refined use of the CT is considered a promising and valid tool for patient stratification. The application of MRI and biochemical markers may further improve prognostic predictions.

Adolescent↗

PubMed1994

Prevalence of MR evidence of diffuse axonal injury in patients with mild head injury and normal head CT findings.

PURPOSE: To assess the prevalence of MR evidence for diffuse axonal injury at 1.5 T in patients with normal head CT findings after mild head injury. METHODS: Twenty consecutive patients with mild head injury (Glasgow Coma Scale, 13 to 15; no subsequent deterioration, loss of consciousness < 20 minutes) and normal head CT findings were examined with MR at 1.5 T. Pulse sequences included a conventional T2-weighted spin-echo sequence (2500-3000/30,80/1[repetition time/echo time/excitations]) and a T2*-weighted gradient-echo sequence (750/40/2, 10 degrees flip angle). Each sequence was read independently by two blinded readers. RESULTS: The readers agreed that abnormalities compatible with diffuse axonal injury were present in the white matter of 6 (30%) of 20 patients (95% confidence interval, 12% to 54%). Both readers agreed that foci of high signal intensity were present on the T2-weighted spin-echo sequence in 3 (15%) of the 20 cases (95% confidence interval, 3% to 38%) and that foci of hypointensity compatible with hemorrhagic shear injury were present on the T2*-weighted sequence in 4 (20%) of the 20 patients (95% confidence interval, 6% to 44%). Both types of abnormality were noted by the readers in one patient. CONCLUSIONS: MR shows evidence of diffuse axonal injury in some patients with normal head CT findings after mild head injury. These lesions may represent the pathologic substrate underlying the postconcussion syndrome that occurs in many patients with moderate to severe head injury.

Adolescent↗

PubMed1998

Relation between diffuse axonal injury and internal head structures on blunt impact.

Diffuse axonal injury (DAI) is a severe head injury, which exhibits symptoms of consciousness disturbance and is thought to occur through rotational angular acceleration. This paper analyzes the occurrence of DAI when direct impacts with translational accelerations are applied to two-dimensional head models. We constructed a human model reproducing the human head structure, as well as modified human models with some internal head structures removed. Blunt direct impacts were applied from a lateral direction to the bottom of the third ventricle, considered to be the center of impact, using an impactor. The analysis was done by comparing the macroscopic manifestation of DAI with the shear stress as the engineering index. In the analytical data obtained from the human model, shear stresses were concentrated on the corpus callosum and the brain stem, in the deep area. This agrees with regions of the DAI indicated by small hemorrhages in the corpus callosum and the brain stem. The analytical data obtained by the modified human models show that the high shear stress on the corpus callosum is influenced by the falx cerebri, while the high shear stress on the brain stem is influenced by the tentorium cerebelli and the shape of the brain. These results indicate that DAI, generally considered to be influenced by angular acceleration, may also occur through direct impact with translational acceleration. We deduced that the injury mechanism of DAI is related to the concentration of shear stress on the core of the brain, since the internal head structures influence the impact stress concentration.

Acceleration↗

PubMed1997

The diagnosis of diffuse axonal injury: implications for forensic practice.

The diagnosis of diffuse axonal injury (DAI), which may be of considerable importance in forensic medicine, necessitates widespread sampling of the brain for histology. Because a limited sampling method for screening brains for axonal damage would be of value for medico-legal work, the authors have tested the findings of an earlier study which suggested that a standard set of three blocks from above and below the tentorium could reliably be used in routine practice as a basis for the diagnosis of DAI. A series of 22 previously diagnosed cases of DAI, with a range of survival times, was studied using immunohistochemistry with antibodies to beta-amyloid precursor protein (beta APP), the microglial-associated antigen CD68 (PG-M1) and for GFAP. Strict histological criteria were used to assess traumatic damage, and the evolution of the histological changes with increasing survival is described. In four cases, the sampling scheme employed yielded evidence of axonal damage in only one block, and a diagnosis of DAI could have been made in only 13/22 cases. In six of the shortest surviving cases, beta APP positivity in the corpus callosum and brainstem outlined areas of early ischaemia, as well as of traumatic damage, so that interpretation of immunolabelling was not always clearcut The findings suggest that DAI cannot be reliably diagnosed on a restricted number of blocks from vulnerable areas, and that the use of beta APP and PG-M1 immunocytochemistry may bring interpretative problems that can only be resolved by taking a larger series of tissue samples for histology.

Adolescent↗

PubMed2000

Controlled study of nimodipine in treatment of patients with diffuse axonal injury.

OBJECTIVE: To determine the efficacy and safety of early intervention with nimodipine treatment in diffuse axonal injury. METHODS: Based on the characteristic radiological signs and criteria for diffuse axonal injury (DAI), 89 patients with the diagnosis of DAI were enrolled in this randomized, double-blind, placebo-controlled trial. RESULTS: Nimodipine proved to be safe and well tolerated. With TCD sonography we found that there was a higher incidence of cerebral vasospasm in this series (38.2%). Overall, Nimodipine produced a better clinical result than placebo, but there was no statistically significant difference in favorable outcome at 3 months after injury (P=0.11) between the two groups. A trend toward a favorable effect was suggested by the analyses in two small subgroups, either in the patients suffering from clinical Grade III DAI (P=0.04), or in those with the TCD-evidence of cerebral vasospasm during clinical observation (P=0.049). CONCLUSIONS: We postulate that a clinically valuable benefit is possible with nimodipine treatment in DAI patients. However, the effects on outcome should be verified by further controlled study.

Journal Article↗

PubMed2000

Acute and late changes in N-acetyl-aspartate following diffuse axonal injury in rats: an MRI spectroscopy and microdialysis study.

N-acetyl-aspartate (NAA) measured by proton nuclear magnetic resonance spectroscopy (1H-NMR) has been used as a marker of neuronal injury in many cerebral pathologies. Therefore, we evaluate the roles of microdialysis vs. 1H-NMR as techniques to assess NAA (NAAd; NAA/Creatine ratio) in the living brain, and compare the results with whole brain NAA (NAAw), analyzed by HPLC after diffuse traumatic brain injury (TBI). Acute (4 h post-injury survival) and late (48 h survival) changes were studied in a sham-operated group (Sham, n = 4), and two injured groups (TBI/4 h, n = 8; TBI/48 h, n = 7). Baseline NAAd was 8.17 +/- 1 microM, and there was no significant difference between groups. There was only a small (twice of control), but transient increase in NAAd in the TBI/4 h group after trauma. Baseline NAA/Cr ratio was 1.35 +/- 0.2, which did not change significantly between baseline, 1, 2, 3, 4 and 48 h or between groups after TBI. Whole brain NAAw (baseline 8.5 +/- 0.5 mmol kg-1 wet weight) did not differ significantly between groups before and after TBI. Diffuse TBI did not produce long-term changes in NAA, assessed by three different methods. These results may indicate that NAA is not a sensitive marker of the severity of diffuse axonal damage. However, further studies are needed to evaluate whether confounding factors such as microdialysis probe, voxel position and non-regional tissue homogenization might have influenced our data.

Animals↗

PubMed1998

[Diagnosis of early phase diffuse axonal injury using immunohistochemical methods].

Histologic and immunohistochemical investigation of the brain aimed at diagnosis of diffuse axonal injury (DAI) was performed in a group of 12 persons deceased of craniocerebral injury. Traumatic axonal change was visualized by immunohistochemical positivity of ubiquitin, low-molecular neurofilaments, beta-amyloid precursor protein and neuron-specific enolase. In addition, H-E stain and silver impregnation of axons according to Palmgren were performed. Diffuse axonal injury was found in 7 cases (58%). In persons surviving more than 12 hours, morphological diagnosis of DAI was based on the finding of so called retraction balls. In person deceased in the first hours after injury, the retraction balls had not been formed yet and DAI was diagnosed according to histochemistry of axonal lesion. The earliest diagnosis of DAI was established 2 hours after injury when axonal lesion showed an immunohistochemical positivity with anti-neuron-specific enolase. In a control group of 6 sudden death cases, axonal oedema was also found but lacking immunohistochemical positivity. Immunohistochemical proof, specially of neuron-specific enolase, seems to be inevitable for diagnosis of early phase DAI when the traumatic etiology of axonal deformities is to be distinguished from possible artificial lesions.

Adolescent↗

PubMed2001

Apoptotic change and NOS activity in the experimental animal diffuse axonal injury model.

Although nitric oxide (NO) plays an important role in the pathophysiological process of cerebral ischemia or severe traumatic brain injury, its contribution to the pathogenesis of moderate diffuse axonal injury (mDAI) remains to be clarified. The alterations in nitric oxide synthase (NOS) activity and the histopathological response after mDAI was investigated. Forty anesthetized Sprague-Dawley adult rats were injured with a Marmarou's weight-drop device through a Plexiglas guide tube. These rats were divided into 8 groups (control, 1 hr, 2 hr, 3 hr, 6 hr, 12 hr, 24 hr, 48 hr after trauma). The temporal pattern of apoptosis in the adult rat brain after mDAI was characterized using TUNEL histochemistry. In addition, the cDNA for NOS activity was amplified using RT-PCR. The PCR products were electrophoresed on a 2% agarose gel. eNOS activity was not detected, but nNOS activity was expressed after 3 hr and continuously 48 hr after impact, which was approximately double that of the control group at 12 and 24 hr. Subsequently, there was a decrease in activity after 48 hr. The iNOS activity increased dramatically after 12 hr and was constant for a further 12 hr followed by a dramatic decrease below the level of the control group. Significant apoptotic changes occurred 12 and 24 hr. after insult. nNOS and iNOS activity were affected after moderate diffuse axonal injury in a time-dependent manner and there was a close relation between the apoptotic changes and NOS activity. Although the nNOS activity was expressed early, its activity was not stronger than iNOS, which was expressed later.

Animals↗

PubMed2003

[Cognitive dysfunction in 32 diffuse axonal injury cases].

In acute stage of traumatic brain injury, it is not easy to diagnose diffuse axonal injury (DAI) by computer imaging. Even in chronic stage, DAIs occasionally show no remarkable abnormality by ordinal CT or MRI images. We retrospectively studied 32 DAI cases by the Functional Independence Measure (FIM), a battery of neuropsychological tests and CT or MRI films of acute and chronic phase. The result showed decrease of cognitive function in 32 DAI cases. The degree of enlargement of the ventricles in chronic stage did not correlate with cognitive dysfunction.

Adult↗

PubMed1998

Diffuse axonal injury without direct head trauma and with delayed onset of coma.

A 16-year-old female was involved in a jet ski (water craft) accident resulting in bilateral lower extremity fractures but no loss of consciousness or any other evidence of head trauma. Thirty hours later she became comatose. Magnetic resonance imaging was consistent with diffuse axonal injury. She recovered after several weeks without any clinical sequelae. This patient demonstrates an unusual example of diffuse axonal injury without direct head trauma and with delayed onset of symptoms. The authors recommend that patients involved in high-velocity accidents, even without immediate evidence of head injury, be observed for signs of diffuse axonal injury.

Adolescent↗

PubMed1998

Clinical studies on diffuse axonal injury in patients with severe closed head injury.

OBJECTIVE: To discuss the clinical criteria for diagnosing diffuse axonal injury (DAI). METHODS: Clinical and computed tomographic features of 117 patients with severe closed head injury were analyzed. The authors preliminarily put forward CT diagnostic criteria of DAI, that is, 1) single or multiple small intraparenchymal hemorrhages in the cerebral hemispheres (< 2 cm in diameter); 2) intraventricular hemorrhage; 3) hemorrhage in the corpus callosum; 4) small focal areas of hemorrhage adjacent to the third ventricle (< 2 cm in diameter); and 5) brain stem hemorrhage. All patients were divided into two groups, DAI and non-DAI group, according to the criteria. There were 42 patients in the DAI group and 75 patients in the non-DAI group. The injury causes, Glasgow coma scale (GCS) scores on admission, coexisting injuries and outcomes were compared between the two groups. The relationship between DAI and the outcomes in the patients with severe head injury was analyzed. RESULTS: Traffic accident was the main injury cause in the cases of DAI. GCS scores on admission in patients with DAI were significantly lower than those in patients without DAI. The incidence of diffuse brain swelling (DBS) in the DAI group was significantly higher than that in the non-DAI group, whereas the incidences of both skull fracture and epidural hematoma (EDH) in the DAI group were significantly lower than those in non-DAI group. There was no significant difference between the incidence of subarachnoid hemorrhage (SAH) and subdural hematoma (SDH) in the two groups. The incidence of poor outcome in the DAI group was significantly higher than that in the non-DAI group, although there was no significant difference between the mortalities in the two groups. CONCLUSIONS: Because DAI is a very important factor worsening the outcome of patients with head injury, it is essential to make a diagnosis as soon as possible. The clinical manifestations of DAI, however, are not specific and DAI does not show directly on CT scans, so it is difficult to make a definite diagnosis. The CT diagnostic criteria of DAI put forward in this article are practicable, though they are by no means perfect.

Adolescent↗

PubMed2000

Diffuse axonal injury due to lateral head rotation in a rat model.

OBJECT: The authors investigated the ramifications of producing diffuse axonal injury (DAI) by lateral head rotation in a rat model. METHODS: Using a special injury-producing device, the rat's head was rapidly rotated 90 degrees in the coronal plane at an angular velocity of at least 753.13 rad/second and an angular acceleration of at least 1.806 x 10(5) rad/second2; the rotation was complete within 2.09 msec. There were no statistically significant changes in PO2, PCO2, pH, or blood pressure values at 5, 15, or 60 minutes after head rotation compared with their respective preinjury baseline values. The rats exhibited posttraumatic behavior suppression for an average of 12.6 minutes. The mortality rate was 17%. The rats that survived had diffuse subarachnoid hemorrhage around the brainstem and upper cervical cord, but no obvious brain contusion. In sections stained with silver or hematoxylin and eosin, axonal swelling and bulblike protrusions at the axonal axis were observed in the medulla oblongata, midbrain, upper cervical cord, and corpus callosum between 6 hours and 144 hours postinjury. The axonal injuries were most severe in the brainstem and were accompanied by parenchymal bleeding. The density of bulblike axonal protrusions peaked 6 hours postinjury in the medulla oblongata and 24 hours postinjury in the midbrain. CONCLUSIONS: Rapid lateral head rotation can produce DAI characterized by severe damage to the rat brainstem.

Animals↗

PubMed1994

Diffuse axonal injury in craniocerebral trauma. A comparative histologic and immunohistochemical study.

Axonal swellings are the major histologic hallmark of diffuse axonal injury in craniocerebral trauma. In this study, we compared conventional histologic and immunohistochemical methods for demonstrating axonal swellings in 11 cases of head trauma. Brain regions known to be susceptible to diffuse axonal injury were examined with conventional hematoxylin-eosin and silver (Bodian) stains and immunohistochemical markers for neurofilaments, ubiquitin, and tau and beta/A4-amyloid. A quantitative assessment of the axonal swellings visualized with each stain was made. In all but one case, axonal swellings were identified with the hematoxylin-eosin stain. By contrast, both the silver and neurofilament stains demonstrated fewer axonal swellings and were often difficult to interpret due to staining of normal axons. In the majority of cases, the ubiquitin stain revealed the greatest number of axonal swellings. Axonal swellings were not visualized with the tau or beta/A4-amyloid antibodies. We conclude that the standard hematoxylin-eosin stain remains a reliable method for the detection of axonal swellings in craniocerebral trauma and is superior to the Bodian and neurofilament stains. Identification and quantitative assessment of diffuse axonal injury is aided by the use of immunocytochemical staining for ubiquitin.

Adolescent↗

PubMed1993

[Diffuse axonal injuries and other closed injuries of the brain. Suggestions for a classification scheme].

The author presents a brief account of recent findings pertaining to different types of closed brain injuries. He supplements classical types of injuries by the concept of diffuse axonal injuries and brain swelling. The classification is based on diagnosis by the CT picture and clinical symptoms. The suggested schema of classification of different injuries alters Petit's classification of closed brain injuries.

Brain Injuries↗

PubMed1998

A case report of remarkable improvement of motor disturbances with L-dopa in a patient with post-diffuse axonal injury.

A 9-year-old girl with rigidospastic quadriplegia as post-traumatic sequela was reported. The distribution of lesions observed on a MRI implied diffuse axonal injury; involvement of the substantia nigra was also detected. L-Dopa administration was remarkably effective for relief of the rigidity. As a result, she became able to walk on her knees and communicate by writing letters. L-Dopa administration should be considered for patients who show rigidity as sequela of diffuse axonal injury with involvement of the substantia nigra.

Accidents, Traffic↗

PubMed1992

Pathological study of diffuse axonal injury patients who died shortly after impact.

It is generally considered that axonal injury is apparent only on electron microscopy in the very early stage after a closed head injury. To clarify the pathological findings in head injury patients dying very shortly after the impact, we analyzed 8 fatal cases of diffuse axonal injury (DAI) who underwent medicolegal autopsy at the Department of Forensic Medicine of Kyoto Prefectural University of Medicine. Seven cases died within one hour after injury and another one case died 3 days after injury. We studied these cases macroscopically, microscopically, and electron microscopically. Macroscopically all cases showed the typical findings of diffuse axonal injury. Microscopical study of the cases who died within one hour revealed no characteristic findings of DAI such as appearance of retraction balls or microglia. On the other hand, in the case who died only 3 days after injury it showed the typical retraction balls. Electron microscopic study showed the remarkable destruction of cytoskeletal structure of axons in all cases. From our results, it is reasonable to speculate that DAI may be common among head injury patients who die very soon after the impact.

Adolescent↗

PubMed1982

Diffuse axonal injury due to nonmissile head injury in humans: an analysis of 45 cases.

Forty-five cases of diffuse axonal injury (DAI) brought about by nonmissile head injury in humans are analyzed and compared with 132 cases of fatal head injury without DAI. All cases were subjected to a comprehensive neuropathological study. In the patients with DAI a statistically significant lower incidence of lucid interval, fracture of the skull, cerebral contusions, intracranial hematoma, and evidence of high intracranial pressure were found, with a higher incidence of head injury due to road traffic accident. Brain swelling and hypoxic brain damage were not statistically different in the two groups. The features of DAI in humans are compared with the DAI that has been produced in subhuman primates by pure inertial loading brought about by angular acceleration of the head. The available evidence indicates that DAI in human beings occurs at the time of head injury and is not due to complicating factors such as hypoxia, brain swelling, or raised intracranial pressure.

Adolescent↗

PubMed1998

Extradural haematoma and diffuse axonal injury in victims of fatal road traffic accidents.

Seven cases of victims of road traffic accidents with extradural haematoma (EH) and diffuse axonal injury (DAI) are reported. Such cases are part of a total of 120 victims of fatal road traffic accidents that were subjected to pathological study. The association of the two lesions occurred in 5.8% of the patients and all cases of EH were associated with DAI. The latter explains the immediate coma (absence of lucid interval) and the grave prognosis for all seven patients. It was noted that EH is relatively infrequent in road traffic accidents, but in such cases it is more severe since it is frequently associated with DAI and immediate coma.

Accidents, Traffic↗