Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Diffuse Axonal Injury”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 361 records · Page 20Linked to original sources
PubMed2005

Rehabilitation interventions after mild head injury.

PURPOSE OF REVIEW: This review examines current management and rehabilitation strategies for mild traumatic brain injury, with emphasis on the need to address multiple potential causative factors in order to enhance outcomes and to conduct more controlled efficacy studies. RECENT FINDINGS: Whilst most individuals who sustain mild traumatic brain injury make a good recovery, a proportion experience significant ongoing disability. In some cases this is due to diffuse axonal injury and cognitive impairment, but in others symptoms are exacerbated by factors such as pain, stress, personality issues or litigation, or in children, previous head injury, behavioural or learning difficulties. Provision of information early after injury results in reduced symptom reporting in adults and children. There is also a need, however, to address these other factors in treatment. Psychological therapy using a cognitive behavioural approach may be helpful, but controlled evaluations of such interventions have been lacking. Recent uncontrolled studies have examined the impact of computer-mediated interventions to remediate visual and verbal processing and oculomotor problems and the impact of quantitative electroencephalography. More rigorous efficacy studies of these approaches are needed. Guidelines for management of sports-related concussion and timing of return to play also require a more solid scientific basis. SUMMARY: The evidence base for management of mild traumatic brain injury is still very limited. There is a need to conduct more carefully controlled prospective studies and examine the influence of factors not directly related to the brain injury as a basis for formulating more uniform management guidelines.

Cognition Disorders↗
PubMed2000

Diffusion-weighted imaging as a problem-solving tool in the evaluation of patients with acute strokelike syndromes.

This article addresses syndromes that clinically and/or radiologically resemble acute stroke. These syndromes generally fall into four categories. (1) Patients with acute neurological deficits with nonischemic lesions and no acute abnormality on diffusion-weighted images. These patients may have peripheral vertigo, migraines, seizures, dementia, functional disorders, amyloid angiopathy, or metabolic disorders. When these patients present, we can confidently predict that they are not undergoing infarction. (2) Patients with ischemic lesions with reversible clinical deficits. Nearly 50% of patients with transient ischemic attacks have lesions with restricted diffusion. Patients with transient global amnesia may have punctate lesions with restricted diffusion in the medial hippocampus, parahippocampal gyms, and corpus callosum. (3) Vasogenic edema syndromes that may mimic acute infarction clinically and on conventional imaging. These include eclampsia/hypertensive encephalopathy, other posterior leukoencephalopathies, human immunodeficiency virus encephalopathy, hyperperfusion syndrome following carotid endarterectomy, venous sinus thrombosis, acute demyelination, and neoplasm. These syndromes demonstrate elevated diffusion rather than the restricted diffusion associated with acute ischemic stroke. (4) Entities in which restricted diffusion may resemble acute infarction. These include pyogenic infections, herpes virus encephalitis, Creutzfeldt-Jakob disease, diffuse axonal injury, tumors with dense cell packing, and rare acute demyelinative lesions.

Diffusion↗
PubMed1987

Ataxia after severe head injury: the pathological substrate.

Ataxia is a common finding in patients who have recovered from severe head injury. This report delineates the clinical and pathological findings in a patient who recovered from a head injury but was left with ataxia of gait. A lesion of the superior cerebellar peduncle, demonstrated post mortem 2 1/2 years after injury, was the only explanation for the ataxia. This lesion is part of the spectrum of changes seen in diffuse axonal injury thought to be due to shearing forces which tear white matter at the time of the initial injury.

Accidents, Traffic↗
PubMed1989

Magnetic resonance imaging after closed head injury in children.

Magnetic resonance imaging (MRI) was performed in a series of 21 children and adolescents who had been hospitalized after sustaining closed head injuries of varying severity at least 6 months previously. Areas of high intensity in the parenchyma were present in 8 of the 11 severely injured patients, whereas MRI findings were normal in all 10 patients with mild-to-moderate head injuries. Lesions involving the subcortical white matter were confined to severely injured patients whose clinical features were compatible with diffuse axonal injury. Neuropsychological assessment disclosed deficits primarily in the severely injured patients; these deficits were significantly associated with persistent lesions visualized by MRI. Serial MRI and neurobehavioral assessment following early injury may be useful in documenting cognitive impairment in relation to structural alterations of the young brain.

Adolescent↗
PubMed1987

The shaken baby syndrome. A clinical, pathological, and biomechanical study.

Because a history of shaking is often lacking in the so-called "shaken baby syndrome," diagnosis is usually based on a constellation of clinical and radiographic findings. Forty-eight cases of infants and young children with this diagnosis seen between 1978 and 1985 at the Children's Hospital of Philadelphia were reviewed. All patients had a presenting history thought to be suspicious for child abuse, and either retinal hemorrhages with subdural or subarachnoid hemorrhages or a computerized tomography scan showing subdural or subarachnoid hemorrhages with interhemispheric blood. The physical examination and presence of associated trauma were analyzed; autopsy findings for the 13 fatalities were reviewed. All fatal cases had signs of blunt impact to the head, although in more than half of them these findings were noted only at autopsy. All deaths were associated with uncontrollably increased intracranial pressure. Models of 1-month-old infants with various neck and skull parameters were instrumented with accelerometers and shaken and impacted against padded or unpadded surfaces. Angular accelerations for shakes were smaller than those for impacts by a factor of 50. All shakes fell below injury thresholds established for subhuman primates scaled for the same brain mass, while impacts spanned concussion, subdural hematoma, and diffuse axonal injury ranges. It was concluded that severe head injuries commonly diagnosed as shaking injuries require impact to occur and that shaking alone in an otherwise normal baby is unlikely to cause the shaken baby syndrome.

Battered Child Syndrome↗
PubMed1990

Characterization of axonal injury produced by controlled cortical impact.

Axonal injury and behavioral changes were evaluated 3-7 days after traumatic brain injury. Previous research from this laboratory demonstrated that clinical central nervous pathology is produced by dynamic brain compression using a stroke-constrained impactor. We wanted to determine if the technique also would produce diffuse axonal injury after recovery from the procedure. The experiments were performed at Wayne State University School of Medicine using aseptic techniques while assuring analgesic care. Impacts were performed at 4.3 m/sec or 8.0 m/sec, with congruent to 10% compression (2.5 mm). Extensive axonal injury was observed at 3 and 7 days postinjury using both velocity-compression combinations. Regions displaying axonal injury were the subcortical white matter, internal capsule, thalamic relay nuclei, midbrain, pons, and medulla. Axonal injury also was evident in the white matter of the cerebellar folia and the region of the deep cerebellar nuclei. Behavioral assessment showed functional coma lasting up to 36 h following 8.0 m/sec impacts, with impaired movement and control of the extremities over the duration of the postinjury monitoring time. These experiments confirm that the cortical impact model of traumatic brain injury mimics all aspects of traumatic brain injury in humans and can be used to investigate mechanisms of axonal damage and prolonged behavioral suppression.

Animals↗
PubMed1995

Traumatic intracerebral lesions without extracerebral haematoma in 218 patients.

218 of the 852 patients in the HIT-2 study of head injury had intracerebral lesions only. They were analysed to get more information on the optimal treatment of these severely injured patients. The initial CT scans were reviewed to exclude patients with extracerebral lesions, and to make a radiological diagnosis of contusion, contusion under a depressed fracture, diffuse axonal injury, or intracerebral haematoma. Deterioration after admission to hospital was seen in 71% of patients. Patients with contusions, and contusions from depressed fractures in particular showed a worse outcome than expected, while patients with diffuse injury had a tendency to improve rather than to deteriorate. Patients with intracerebral haematoma seemed to improve if the mass was evacuated. Nimodipine had an impact only in patients with contusions. Our findings mandate surgical evacuation of contusions and intracerebral haematomas in patients with lesions larger than 20 ml who also have radiological signs of a mass effect. Regardless of an apparently good clinical state in the early phase, intracerebral lesions larger than 50 ml seemed to benefit from surgery as compared to nonsurgical treatment. The findings indicated that a further refinement of diagnostic criteria may enable individually tailored head injury treatment to interfere with most important pathogenic mechanisms. More accurate diagnoses will improve head injury treatment and outcome, and are a prerequisite for making successful pharmaceutical trials of head injury in the future.

Adult↗
PubMed1997

Loss of axonal microtubules and neurofilaments after stretch-injury to guinea pig optic nerve fibers.

Axonal swellings, characterized by focal accumulations of membranous organelles at presumed sites of interrupted axonal transport, occur in diffuse axonal injury (DAI) in human, blunt head injury and in animal models of nondisruptive axonal injury. Membranous organelles are transported by fast axonal transport in association with microtubules. Although loss of microtubules has been documented at levels of injury severe enough to result in permeabilization of the axolemma to tracers such as horseradish peroxidase, there has been no detailed analysis of responses by microtubules in less severe or milder forms of nondisruptive axonal injury. To test the hypothesis that in less severe forms of axonal injury there is a rapid response by axonal microtubules that might provide an explanation for loss of fast axonal transport, we have carried out a morphometric analysis of microtubules in CNS axons after stretch-injury. There is loss of microtubules at nodes of Ranvier with nodal blebs within 15 min of injury, and in internodal axonal swellings between 2 and 4 h. There is a return to control values at nodes of Ranvier by 4 h, and at the internode by 24 h. There is no loss of microtubules at paranodes, although there is a reduction in their density in the first 2 h after injury. The greatest loss of microtubules occurs at sites of axolemma infolding. Hypothetical mechanisms that might lead to this loss resulting in focal disruption of fast axonal transport and the formation of axonal swellings are discussed.

Analysis of Variance↗
PubMed1999

The possible role of hypoxia in the formation of axonal bulbs.

AIMS: To assess the possible role of hypoxia in the formation of axonal bulbs. METHODS: Study material comprised sections from 28 brains showing evidence of cerebral hypoxia with no history of head injury, four with a history of head trauma but no evidence of hypoxic change, eight with a history of head trauma and hypoxic change, and four from control brains originally described as "diffuse axonal injury." These were subjected to microwave antigen retrieval and immunohistochemistry using monoclonal antibodies to beta amyloid precursor protein (beta APP), glial fibrillary acid protein (GFAP), and CD68-PGM1. RESULTS: Positive staining for beta APP was seen in all four controls, all four cases of head injury only, seven of eight cases of head injury and hypoxic changes, and 12 of 28 cases of hypoxia without history of head injury; 22 of 25 cases who had been ventilated showed positive staining. The majority of cases showed evidence of cerebral swelling. CONCLUSIONS: Axonal bulbs staining positively for beta APP may occur in the presence of hypoxia and in the absence of head injury. The role of hypoxia, raised intracranial pressure, oedema, shift effects, and ventilatory support in the formation of axonal bulbs is discussed. The presence of axonal bulbs cannot necessarily be attributed to shearing forces alone.

Adult↗
PubMed2001

Concussion: the history of clinical and pathophysiological concepts and misconceptions.

Concussion is a well-recognized clinical entity; however, its pathophysiologic basis remains a mystery. One unresolved issue is whether concussion is associated with lesser degrees of diffuse structural change seen in severe traumatic brain injury, or is the mechanism entirely caused by reversible functional changes. This issue is clouded not only by the lack of critical data, but also by confusion in terminology, even in contemporary literature. This confusion began in ancient times when no distinction was made between the transient effects of concussion and severe traumatic brain injury. The first clear separate recognition of concussion was made by the Persian physician, Rhazes, in the 10th century. Lanfrancus subsequently expanded this concept as brain "commotion" in the 13th century, although other Renaissance physicians continued to obscure this concept. By the 18th century, a variety of hypotheses for concussion had emerged. The 19th century discovery of petechial hemorrhagic lesions in severe traumatic brain injury led to these being posited as the basis of concussion, and a similar logic was used later to suggest diffuse axonal injury was responsible. The neuropathology and pathophysiology of concussion has important implications in neurology, sports medicine, medicolegal medicine, and in the understanding of consciousness. Fresh approaches to these questions are needed and modern research tools, including functional imaging and experimental studies of ion-channel function, could help elucidate this puzzle that has evolved over the past 3,000 years.

Brain Concussion↗
PubMed1996

[Psychiatric sequelae of craniocerebral trauma--a review of the literature].

In a brief review psychiatric aspects of head-injured patients are discussed. The topic is put into a historical perspective. Examples of recent developments in head-trauma research are given. Differentiation between focal and diffuse brain injury is suggested to be of clinical relevance. Little is known as yet about the neuropsychologic and psychiatric sequelae of diffuse axonal injury to the brain.

Brain Concussion↗
PubMed2001

Neuronal free Ca(2+)and BBB permeability and ultrastructure in head injury with secondary insult.

OBJECTIVE: To study changes in free calcium (Ca(2+)), neuronal and blood-brain barrier (BBB) permeability and ultrastructure in brain after diffuse axonal injury (DAI) with secondary brain insults (SBIs). METHOD: One hundred and twenty Sprague-Dawley (SD) rats were randomised into control, DAI alone and DAI with SBI groups which were sub-divided into 5 groups that were 0.5 h, 2 h, 12 h, 24 h, 48 h post trauma. The animal models of DAI and DAI with SBI have been described before (2). Fluorescence probe Fluo-3/Am was used to measure free Ca(2+)in neurons. Laser scan microscopy was used to detect fluorescence intensity. After the animals were anesthetized, Lanthanum nitrate liquid was used for intracardiac perfusion to assess BBB permeability. Under the transmission electron microscope, changes in cerebral ultrastructure and BBB permeability were observed. RESULTS: The fluorescence intensity was weak in the control. The concentration of free Ca(2+)in neurons was obviously increased at 30 min after brain injury, reached a peak at 12 h-24 h (P< 0.01), and appeared to decrease at 48 h after injury. In the DAI alone group, BBB tight junction opening with particles of Lanthanum nitrate outside the vessels was found at 30 min after injury, and peaked at 24 h. In DAI with SBI, the changes in ultrastructure and BBB permeability were more severe than that in the DAI alone group at the same time interval. The shape of the fluorescence concentration curve was basically the same for both kinds of brain injury. The intensity of fluorescence in DAI with SBI was higher than that in the DAI alone group at the same time interval (P< 0.05). CONCLUSION: In DAI alone and DAI with SBI, Ca(2+)overload and BBB permeability changes interact and both play important roles in the aggravation of brain damage.

Animals↗
PubMed1992

The cerebrovascular response to experimental lateral head acceleration.

A number of microvascular changes, such as the development of astrocyte lucency, increased endothelial pit/vesicle activity, development of crater like lesions, and endothelial microvilli have been reported after injury to the brain. Lateral head acceleration in the non-human primate, however, still provides the best experimental model for human diffuse axonal injury. No attempt has yet been made to document the spatial extent or time course of the microvascular response to acceleration injury to the head. We have examined the brains of baboons 1, 4, 6, and 12 h and 7 days after acceleration injury to the head to analyse the microvascular response. In the experimental animals there was a short-term rise in intracranial pressure followed by a long-term resolution, and a reduction in both mean arterial blood pressure and cerebral perfusion pressure which, however, never dropped below 75% of baseline for more than 5 min after injury in any animal. We found evidence for extravasation of blood in a small number of blood vessels in all parts of the brain. Interendothelial tight junctions are not disrupted. Pit/vesicle activity rises in the 1st h in the occipital cortex, but not until 4 h in the frontal cortex, and remains elevated for at least 7 days. There is little change in the thalamus. Development of microvilli is most rapid in the frontal cortex with peak values at 1 h, but slower in the thalamus and occipital cortex where peak values are only obtained at 6 h. Highest numbers of microvilli occur in parasagittal regions of the brain.(ABSTRACT TRUNCATED AT 250 WORDS)

Acceleration↗
PubMed1997

Severe head trauma. Review of the factors influencing the prognosis.

A series of 72 severely head injured patients are reported, 24 (33%) with surgical intracranial hematomas. All patients were intensively cared for under the same therapeutic regime; intracranial pressure (ICP) was monitored and treated if increased. The series mortality was 39%. Uncontrollable increase of ICP (UI-ICP), always fatal, was observed in 18% of patients and in 13 of 28 deaths (46%); the incidence of UI-ICP among deaths was higher in patients less than in those more than 40 years old (55% vs 25%). Patients with UI-ICP were frequently deeply comatose and with arterial hypotension on admission; almost all died in the first days. Patients directly admitted from the scene with well staffed Life Flight Helicopter Emergency Care compared with those directly admitted from the scene with different type of ambulance service (paramedics, police, firemen and private) had a mortality rate significantly less (20% vs 54%) and an incidence of UI-ICP strongly lower both among patients (5% vs 29%) and among deaths (25% vs 54%). Thus in this small series intensive care after admission was not effective to obtain good results if patients had received poor preadmission emergency care. Review of the literature on main clinical predictors of outcome in severe head injury, have made possible some observations. Ischemic and intracranial hypertension brain lesions were generally present in patients killed by head trauma; while diffuse axonal injury, frequently responsible for vegetative, severe disability survival and late deaths, was observed only in 20-30% of postmortem examinations. Old age, poor neurological status and cardiocirculatory and respiratory disturbances prior to and upon admission positively worsened the outcome, while intracranial hematomas had a more variable predictive value. Intracranial hypertension was a definitively ominous predictor only if very high when the risk to be or become uncontrollable seems to be much elevated. UI-ICP, often fatal despite any aggressive therapy, was the single most frequent killer after severe head injury, responsible for about half of all deaths after admission. The different outcome among severe head injury series could be conceivably related to a different frequency of UI-ICP. Besides the severity of head injury and delay and mode of admission, we suggest that preadmission respiratory and cardiocirculatory and the quality of emergency medical system could strongly affect the incidence of uncontrollable increase of ICP in admitted patients and thus the mortality rate and favorable recovery of the series. The advanced preadmission emergency care service with intensive care after admission could significantly explain the better results often observed in severe head injury series.

Adolescent↗
PubMed2006

Posttraumatic infarction in the territory supplied by the lateral lenticulostriate artery after minor head injury.

BACKGROUND: Occlusion of the intracranial arteries due to blunt head traumas has been less frequently observed in patients with minor head injuries. CASE REPORT: A 4-year-old boy presented with speech disturbance 2 h after minor head injury. An initial computed tomography (CT) scan showed a questionable finding of a focal punctate high density in the left basal ganglia. Hemiparesis developed on the right limbs 8 h post-injury, and a subsequent CT scan revealed a discrete low-density change around the focal high density. Diffusion-weighted images revealed a clearly demarcated high-signal intensity lesion in similar area on T2-weighted and fluid-attenuated inversion recovery sequences images, compatible with infarcted tissues on the territory supplied by the lateral lenticulostriate artery. His hemiparesis improved gradually, and by post-trauma day 10 he was able to walk briefly without assistance. He was discharged on foot at post-trauma day 14. DISCUSSION AND CONCLUSION: Children with minor head trauma who have normal findings on initial CT scan may rarely have basal ganglionic infarction resulting from arterial spasm or thromboembolism of the perforating arteries. Hospital admission and careful observation should be considered for patients with minor head injury and persistent neurologic deficits despite normal CT findings. Magnetic resonance study is valuable for the evaluation of posttraumatic infarction, differentiating from hemorrhagic diffuse axonal injuries.

Child, Preschool↗
PubMed2006

Findings in older children with abusive head injury: does shaken-child syndrome exist?

Shaken-baby syndrome (SBS) has been hypothesized to occur after shaking by an adult during the first 2 years of life. We wondered whether it is possible to achieve rotational forces sufficient to cause SBS-like injuries in children >2 years of age. The present study describes cases of child abuse in older children who presented with the classic ophthalmologic and intracranial findings of SBS. In this case series, 4 cases of older children (2.5-7 years old; 11.8-22 kg) who died from abusive head injuries and who had diffuse retinal hemorrhages identified antemortem were selected for review. The cases were abstracted from hospital charts, records from autopsies, coroners' and district attorneys' offices, and court transcripts. In all 4 cases the history provided by the primary caregiver did not match the severity of the injuries. Three case subjects presented with patterned bruises. Multilayered retinal hemorrhages and acute subdural hematoma were observed in all 4 cases. At autopsy, diffuse axonal injury was evident in 3 of the 4 cases; all 4 cases had optic nerve sheath hemorrhages. None of the victims had skeletal fractures on radiologic examination or at autopsy. This case series demonstrates that it is possible to observe SBS-like retinal and central nervous system findings in the older and heavier child. Our findings underscore the need for providers to consider intentional shaking as a mechanism of injury in the evaluation of abusive head injury in older children.

Child↗
PubMed2003

Dose-response of cyclosporin A in attenuating traumatic axonal injury in rat.

Cyclosporin A has emerged as a promising therapeutic agent in traumatic brain injury (TBI), although its precise neuroprotective mechanism is unclear. Cyclosporin A, given as a single-dose intrathecal bolus, has previously been shown to attenuate mitochondrial damage and reduce axonal injury in experimental TBI. We assessed the effect of a range of intravenous cyclosporin A doses upon axonal injury attenuation to determine the ideal dose. Rats were subjected to experimental TBI and given one of five intravenous doses of cyclosporin A. At 3 h post-injury, brains were processed for brain tissue cyclosporin A concentration. In a second set of animals, at 24 h postinjury, brains were processed for amyloid precursor protein immunoreactivity, a widely used marker of axonal injury. Intravenous administration produced therapeutic levels of cyclosporin A in brain parenchyma. Higher concentrations were achieved with equivalent doses given intrathecally; this is consistent with the reported poor blood-brain barrier permeability of cyclosporin A. Cyclosporin A 10 mg/kg i.v. produced the greatest degree of neuroprotection against diffuse axonal injury; cyclosporin A 50 mg/kg i.v. was toxic. Intravenous cyclosporin A administration achieves therapeutic levels in brain parenchyma and 10 mg/kg is the most effective dose in attenuating axonal damage after traumatic brain injury.

Amyloid beta-Protein Precursor↗
PubMed2000

Early hyperthermia after traumatic brain injury in children: risk factors, influence on length of stay, and effect on short-term neurologic status.

OBJECTIVES: a) To determine the risk factors for early hyperthermia after traumatic brain injury in children; b) to identify the contribution of early hyperthermia to neurologic status at pediatric intensive care unit (PICU) discharge and to PICU length of stay in head-injured children. STUDY DESIGN: Observational cohort study. SETTING: PICU at a tertiary care, university medical center. PATIENTS: Children (n = 117) admitted to a PICU from July 1995 to May 1997 with traumatic brain injury. These children had a median age of 5.4 yrs (3 wks to 15.2 yrs old), and 33.4% were girls. MEASUREMENTS AND MAIN RESULTS: Early hyperthermia (temperature >38.5 degrees C within the first 24 hrs of admission) occurred in 29.9% of patients admitted to the PICU with traumatic brain injury. Risk factors predicting early hyperthermia included Glasgow Coma Scale score in the emergency department < or =8, pediatric trauma score < or =8, cerebral edema or diffuse axonal injury on initial head computed tomography scan, admission blood glucose >150 mg/dL (8.2 mmol/L), admission white cell count >14,300 cells/mm3 (14.3 x 10(9) cells/L), and systolic hypotension. The presence of early hyperthermia significantly increased the risk for Glasgow Coma Scale score <13 at PICU discharge (odds ratio [OR] 9.7, 95% confidence interval [CI] 2.8, 24.4) and PICU stay > or =3 days (OR 13.8, CI 5.1, 37.5). When we used multiple logistic regression models including injury severity and hypotension, early hyperthermia remained an independent predictor of lower Glasgow Coma Scale score at PICU discharge (OR 4.7, CI 1.4, 15.6) and longer PICU length of stay (OR 8.5, CI 2.8, 25.6). CONCLUSIONS: Early hyperthermia is independently associated with a measure of early neurologic status and resource utilization in children with traumatic brain injury serious enough to require PICU admission. These results support the prevention of hyperthermia in the management of traumatic brain injury in children. Further research is required to understand the mechanisms of this response and to identify appropriate preventive or therapeutic interventions.

Adolescent↗