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Results for “Diffuse Axonal Injury”

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PubMed1997

[Immunohistochemical methods in the diagnosis of diffuse axonal injury].

Diffuse axonal injury (DAI) was diagnoses according to axonal reaction proved as balls by Palmgren's silver impregnation and axonal lesions by immunohistochemical investigation of ubiquitin and low molecular weight neurofilaments (68 kD). Diffuse axonal injury was found in 16 cases from a group of 36 persons deceased of craniocerebral trauma (44%). Diagnosis was based on the presence of axonal retraction balls in 15 cases; the balls showed also a striking positivity with antibodies against ubiquitin and low molecular neurofilaments as well. In the last patient who died 10 hours after a head injury, too early for axonal retraction balls to be formed, diagnosis of DAI could be settled because of the presence of axonal swellings immunohistochemically positive for ubiquitin and neurofilaments. A control groups of 6 persons after sudden death showed both axonal widenings and swellings but their immunohistochemistry was negative. Immunohistochemical methods of proving ubiquitin and low molecular weight neurofilaments represent substantial contribution to diagnosis of diffuse axonal injury. Earlier phase of axonal lesions than in simple histology can be observed and histological diagnosis of axonal injury independently confirmed.

Adolescent↗

PubMed1984

Diffuse axonal injury.

Diffuse axonal injury is a distinct form of head injury, induced by direct external forces at the time of the trauma, and not produced by secondary changes due to a primary injury. This type of lesion may be without conspicuous findings on gross brain examination, or may be found with coexisting conventional types of brain injuries. It is characterized by diffuse retraction balls (axonal swellings), hemorrhage or laceration of the corpus callosum, and hemorrhages in the brain stem. It is of utmost importance for forensic pathologists to be aware of this little-recognized entity. Five illustrative cases are presented.

Adolescent↗

PubMed1990

[Computed tomography in diagnosis of diffuse axonal injury].

Diffuse axonal injury (DAI) has been described in instances of prolonged traumatic coma on the basis of the neuropathological findings, but the same findings are also found in patients with cerebral concussion. Experimental studies confirm that the quality of survivors following trauma is directly proportional to the amount of primarily injured-axon. When the injured axon lies in a widespread area of the brain, outcome for the patient is always poor. In a series of 260 severely head-injured patients, based on their poor outcome, 69 (27%) were diagnosed as DAI. Because of their relatively good outcome, eighty-two patients (32%) were classified into non-DAI group. The predominant CT finding of DAI patients was intraparenchymal deep-seated hemorrhagic lesion. This was observed in 28 patients (41%). Normal CT was also observed in 11 patients (16%). On the other hand, 8 of the non-DAI group (10%) manifested deep-seated lesions. Diffuse cerebral swelling (DCS) appeared in both groups in the same incidence. Subarachnoid hematoma in the perimesencephalic cistern (SAH (PMC] and intraventricular hematoma (IVH) were observed in 64% of the DAI group, and in 23% of the non-DAI group. The available evidence indicates that various types of hematoma seen in the deep-seated structures of the brain do not have an absolute diagnostic value, but the frequency of hematoma is thought to increase in proportion to the amount of injured-axon.

Adolescent↗

PubMedDate not supplied

Diffuse axonal injury.

Diffuse axonal injury (DAI) is a severe form of traumatic brain injury that is seen almost exclusively following motor vehicle accidents. It is associated with immediate coma lasting from six hours to prolonged coma. The author reviews the mechanism of injury, significant neurological findings, neuropathology, and diagnostic criteria. Priorities for nursing care in the emergency department, critical care, and inpatient and rehabilitation units are outlined.

Accidents, Traffic↗

PubMed1995

[An autopsy case of traumatic subdural hematoma from arterio-venous malformation with diffuse axonal injury].

Diffuse axonal injury (DAI) is defined as widespread damage to axons in the white matter of the brain without focal injury such as contusion and acute subdural hematoma. A case of traumatic subdural hematoma from arterio-venous malformation accompanied by DAI is reported. A 58-year-old man was assaulted, and immediately lost consciousness, and remained unconscious during about 44 hours until his death. The autopsy revealed acute subdural hematoma (about 160 g) on left temporal lobe and left cingular, uncal and cerebellar tonsillar herniation, and tear and hemorrhage of the corpus callosum. Under this subdural hematoma, gray-whitish vascular lesion with subarachnoid hemorrhage was found. Histologically, this lesion was diagnosed as the arterio-venous malformation. Neuropathological examination of the corpus callosum, dorsolateral part of midbrain and superior cerebellar peduncle revealed DAI findings, such as swelling and ballooning of the myelin fibers, swelling and waving of axons, and retraction balls. Axon degenerations were also observed immunohistochemically by anti-200 kD neurofilament antibody. From the results, his unconsciousness from the moment of impact might be occurred from not only subdural hematoma but also DAI.

Axons↗

PubMed1992

Diffuse axonal injury caused by assault.

The case reports of 50 fatal head injuries caused by assault and managed at the Institute of Neurological Sciences, Glasgow, were reviewed. Fifteen cases had diffuse axonal injury. Diffuse axonal injury is a well recognised type of brain damage brought about by a head injury, usually as a result of a road traffic accident or fall from a height. It does not seem to be widely appreciated that it may also occur as a result of an assault. This has important medicolegal implications.

Adolescent↗

PubMed2002

Amantadine to improve neurorecovery in traumatic brain injury-associated diffuse axonal injury: a pilot double-blind randomized trial.

BACKGROUND: Traumatic brain injury (TBI) caused by a high-speed transportation accident results in a mechanism of injury commonly described as diffuse axonal injury (DAI), which is associated with a reduction in dopamine turnover in the brain. Because of its affect on both dopamine and N-methyl-D-aspartate (NMDA) channels, amantadine has been the subject of considerable interest and clinical use in acute TBI. PARTICIPANTS: In this study, 35 subjects, who had a TBI in a transportation accident and were initially seen with a Glasgow Coma Scale score of 10 or less within the first 24 hours after admission, were randomly assigned to a double-blind, placebo-controlled, crossover design trial. MAIN OUTCOME MEASURES: Amantadine, 200 mg, or placebo was each administered for 6 weeks (12 weeks total) to patients who were recruited consecutively. RESULTS: There was an improvement in the Mini-Mental Status (MMSE) scores of 14.3 points (P =.0185), Disability Rating Scale (DRS) score of 9.8 points (P =.0022), Glasgow Outcome Scale (GOS) score of 0.8 points (P =.0077), and in the FIM Cognitive score (FIM-cog) of 15.1 points (P =.0033) in the group that received amantadine during the first 6 weeks (group 1), but there was no improvement in the second 6 weeks on placebo (P >.05). In group 2 (active drug second 6 weeks), there was an improvement in the MMSE of 10.5 points, in the DRS of 9.4 points (P =.0006), in the GOS of 0.5 points (P =.0231), and in the FIM-cog of 11.3 points (P =.0030, Wilcoxon signed rank) spontaneously in the first 6 weeks on placebo (P =.0015). However, group 2 gained a statistically significant additional 6.3 points of recovery in the MMSE (P =.0409), 3.8 points in the DRS (P =.0099), 0.5 points in the GOS (P =.4008), and 5.2 points in the FIM-cog (P =.0173, Wilcoxon signed rank) between the sixth week and the twelfth week of treatment on the active drug. CONCLUSIONS: There was a consistent trend toward a more rapid functional improvement regardless of when a patient with DAI-associated TBI was started on amantadine in the first 3 months after injury.

Accidents, Traffic↗

PubMed1995

Biomechanical analysis of experimental diffuse axonal injury.

The purpose of this paper is to present results from methodologies used in our laboratory that are targeted toward identifying specific brain injury thresholds. Results from studying one form of brain injury, diffuse axonal injury, are presented in this report. Physical models, or surrogates, of the skull-brain complex are used to estimate the relationship between inertial loading and brain deformation. A porcine model of diffuse axonal injury, developed with information from these physical models and earlier in vitro tissue modeling studies, is used to correlate histologic and radiologic evidence of axonal injury to predicted regions of injury from the experimental and theoretical analysis. These results form the basis for developing improved diffuse brain injury tolerance levels, as well as identifying new means of diagnostic and treatment techniques for diffuse axonal injury.

Animals↗

PubMed1999

A comparison of manual and semi-automated methods in the assessment of axonal injury.

Diffuse axonal injury (DAI) in the central nervous system is a common cause of post-traumatic coma and may result in varying degrees of disability up to and including the vegetative state. Experimental studies in man and animals have previously relied upon semi-quantitative grading systems for determining the relationship between the extent of DAI and the clinical features of patients. Using beta-amyloid precursor protein immunocytochemistry for the detection of DAI in sections of corpus callosum from 15 cases of fatal head injury, we have developed a quantitative image analysis technique for the assessment of axonal injury. This new method is objective and reproducible and should allow better correlation with biomechanical, radiological, and clinical parameters to increase our understanding of DAI.

Adolescent↗

PubMed1992

A proposed tolerance criterion for diffuse axonal injury in man.

The head injury criterion (HIC) is currently the government-accepted head injury indicator. The HIC is not injury-specific, does not relate to injury severity, nor does it take into account variations in the brain mass or load direction. This report focuses on one type of inertial brain injury, diffuse axonal injury (DAI), and utilizes animal studies, physical model experiments, and analytical model simulations to determine the kinematics of DAI in the subhuman primate and to scale these results to man. A human injury tolerance for moderate to severe DAI, which includes the influences of rotational loads and brain mass, is proposed.

Acceleration↗

PubMed1995

[A case of closed head injury with diffuse axonal injury, and oculomotor nerve avulsion and midbrain infarction].

We report an autopsy case of 66-year-old woman with closed head injury due to a fall from stairs. She had recovered after a half day period of coma following the fall. Severe right peripheral oculomotor nerve palsy was noted from the beginning. MRI demonstrated lesions in the corpus callosum and right midbrain. She had died of suffocation due to sputum impaction after 50 hours after the fall. Autopsy examination revealed traumatic subarachnoidal hemorrhage, partial tearing and petechial hemorrhage of the corpus callosum, and many axonal retraction balls scattered in the cerebral white matter. Avulsion of the right oculomotor nerve root and fresh midbrain infarct with hemorrhage in the territory of right paramedian artery were observed. Axonal retraction balls were densely distributed in the periphery of midbrain infarct. The distribution pattern of axonal retraction balls in the cerebrum was similar to that of damage due to shear strain in Holbourn's gelatin model of closed head injury. The midbrain infarct and oculomotor nerve avulsion may be due to both mechanical and ischemic damage during and after the fall. All of the lesions described above may be closely related to the rotatory force from the right forehead.

Aged↗

PubMed1994

Ultrastructural studies of diffuse axonal injury in humans.

Diffuse axonal injury (DAI) is observed commonly in traumatically brain injured humans. However, traditional histologic methods have proven of limited use in identifying reactive axonal change early (< 12 h) in the posttraumatic course. Recently, we have reported, in both humans and animals, that antibodies targeting neurofilament subunits are useful in the light microscopic recognition of early reactive change. In the present study, we extend our previous efforts in humans by analyzing the progression of traumatic brain injury (TBI)-induced axonal change at the ultrastructural level. This effort was initiated to follow the subcellular progression of reactive axonal change in humans and to determine whether this progression parallels that described in animals. Two commercially prepared antibodies were used to recognize reactive axonal change in patients surviving from 6 to 88 h. The NR4 antibody was used to target the light neurofilament subunit (NF-L), and the SMI32 antibody was used to target the heavy neurofilament subunit (NF-H). Plastic-embedded tissue sections were screened for evidence of reactive axonal change, and once identified, this reactive change was analyzed at the ultrastructural level. At 6 h survival, focally enlarged, immunoreactive axons with axolemmal infolding or disordered neurofilaments were seen within fields of axons exhibiting no apparent abnormality. By 12 h, some axons exhibited continued neurofilamentous misalignment, pronounced immunoreactivity, vacuolization, and, occasionally, disconnection. At later stages, specifically 30 and 60 h survival, further accumulation of neurofilaments and organelles had led to the further expansion of the axis cylinder, and clearly disconnected reactive swellings were recognized. These contained a dense core of disordered immunoreactive neurofilaments partially encompassed by a cap of less densely aggregated organelles. At 88 h, the reactive axons were larger and elongated, consistent with the continued delivery of organelles by axoplasmic transport. At the later time points, considerable heterogeneity was observed, with focally enlarged disconnected axons being observed in relation to axons showing less advanced reactive change. Our findings suggest that neurofilamentous disruption is a pivotal event in axonal injury.

Adult↗

PubMedDate not supplied

[Transcranial Doppler sonography in neurotraumatology: hemodynamic monitoring of diffuse axonal injury].

Six patients with diffuse axonal injury, ranging in age 8 to 29 years, hospitalized in emergency in our Polyclinic with a Glagow coma score under 8, were examined. Patients were intubated and connected to an automatic respirator. They underwent serial cranial CT and transcranial Doppler sonography recordings using the temporal window with insonation of the two middle cerebral arteries. During the period of observation, the metabolic processes and systemic hemodynamics were maintained within the limits of homeostasis. In all cases and at different times, osmotic diuretics (18% mannitol), barbiturates and hyperventilation therapy were administered. In 5 patients over 6 (80%) increased blood flow, variously sensitive to barbiturates, was detected associated to increased resistance index secondary to intracranial hypertension. Based on Doppler findings four patients underwent surgical treatment: ventriculostomy for monitoring of intracranial pressure or decompressive craniectomy. According to this experience, the use of transcranial Doppler US is mandatory for a correct identification of the hemodynamic injury associated to diffuse axonal injury, for planning the medical and/or surgical approach and for assessment of the successful results of therapeutic management.

Adult↗

PubMed2002

Diffusion-weighted MRI in diffuse axonal injury of the brain.

The goal of this study was to identify and describe the different types and patterns of tissue injury which are encountered by diffusion-weighted imaging (DWI) in diffuse axonal injury (DAI) of the brain. The DWI data sets of 98 patients who suffered from a closed-head injury were retrospectively evaluated. Medical records were reviewed to rule out pre-existing neurological diseases. Lesions were studied for their DWI signal characteristics and lesion size or extension. Traumatic lesions were classified into three categories depending on their signal characteristica on DWI and apparent diffusion coefficient (ADC) maps: type 1, DWI- and ADC-hyperintense most likely representing lesions with vasogenic edema; type 2, DWI-hyperintense, ADC-hypointense indicating cytotoxic edema; type 3, central hemorrhagic lesion surrounded by an area of increased diffusion. According to the size and extent of lesions, injury was classified into three groups: group A, focal injury; group B, regional/confluent injury; and group C, extensive/diffuse injury. Our study showed that diffusion-weighted imaging differentiates between lesions with decreased and increased diffusion in patients with DAI. Different degrees of tissue injury extent were noticed. Future prospective studies should study if this additional information can be used as a predictor of injury reversibility, final outcome and prognosis.

Adolescent↗

PubMed1987

Diffuse axonal injury in early infancy.

Diffuse axonal injury typified by retraction balls and axonal swellings was identified in the brains of a series of infants, 5 months old and younger, who had suffered closed head injuries. These axonal discontinuities were shown by using Nauomenko and Feigin's silver method, which is particularly useful for showing fine axons such as those found in the developing brain. Diffuse axonal injury in early infancy may occur in the same way as that described in adults. The low incidence of intracerebral haematomata suggests that recurrent trauma to the head from a combination of direct contact and shaking results in axonal damage to the poorly myelinated axons and that blood vessels are rarely damaged.

Axons↗

PubMed1996

[Clinical analysis of diffuse axonal injury].

Sixty cases of diffuse axonal injury were analysed in this paper. All cases were caused by traffic accident; the mortality was 53.12%. Clinical manifestations were post-traumatic immediate and continuous coma with severe dysfunction of brain stem. MRI is helpful for clinical diagnosis. Pathological findings include the diffuse axonal injury of cortical while matter, corpus callosum, brain stem, and focal hemorrhage and infarction. The early use of hyperbaric oxygen combined with neuro-growth factor as an effective therapy is recommended.

Accidents, Traffic↗

PubMed1999

1H spectroscopic imaging of acute head injury--evidence of diffuse axonal injury.

Using single slice two-dimensional spectroscopic imaging (SI), nine acute head injury patients and six controls have been successfully scanned. The problems presented by the need for ITU monitoring of these patients during MR scanning was overcome using MR compatible monitoring equipment. In previous studies of head injury which used proton spectroscopy, single voxel localisation procedures have meant that the spatial extent of the spectral data has been limited. With spectral data from a whole axial slice, we have been able to identify NAA abnormalities in regions remote to any T2 visible lesions. This suggests that SI (of NAA in particular) will be useful for the diagnosis of diffuse axonal injury.

Adult↗

PubMed2002

Diffusion tensor MR imaging in diffuse axonal injury.

BACKGROUND AND PURPOSE: Disruption of the cytoskeletal network and axonal membranes characterizes diffuse axonal injury (DAI) in the first few hours after traumatic brain injury. Histologic abnormalities seen in DAI hypothetically decrease the diffusion along axons and increase the diffusion in directions perpendicular to them. DAI therefore is hypothetically associated in the short term with decreased diffusion anisotropy. We tested this hypothesis by measuring the diffusion characteristics of traumatized brain tissue with use of diffusion tensor MR imaging. METHODS: Five patients with mild traumatic brain injuries and 10 control subjects were studied with CT, conventional MR imaging, and diffusion tensor imaging. All patients were examined within 24 hours of injury. In each participant, diffusion tensor indices from homologous normal-appearing white matter regions of both hemispheres were compared. These indices were also compared between homologous regions of each patient and the control group. In two patients, diffusion tensor images from the immediate post-trauma period were compared with those at 1 month follow-up. RESULTS: Patients displayed significant reduction of diffusion anisotropy in several regions compared with the homologous ones in the contralateral hemisphere. Such differences were not observed in the control subjects. Significant reduction of diffusion anisotropy was also detected when diffusion tensor results from the patients were compared with those of the controls. This reduction was often less evident 1 month after injury. CONCLUSION: White matter regions with reduced anisotropy are detected in the first 24 hours after traumatic brain injury. Therefore, diffusion tensor imaging may be a powerful technique for in vivo detection of DAI.

Adult↗