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PubMed1994

Diffuse axonal injury with brainstem localisation: report of a case in a mild head injured patient.

The authors present the case of a 26-yrs-old woman admitted into our hospital after a severe polytrauma with a mild head injury. CT scanning disclosed two small hemorrhages located in her brainstem and mesial temporal lobe. After splenectomy the patient made a full recovery without neurological sequelae. Radiological signs of diffuse axonal injury even in the brainstem may be present in a clinically mild head injury.

Accidents, Traffic↗
PubMed1998

Diffuse axonal injury (DAI) is not associated with elevated intracranial pressure (ICP).

OBJECTIVE: Traditionally, intracranial pressure (ICP) monitoring has been utilized in all patients with severe head injury (Glasgow coma score of 3-8). Ventriculostomy placement, however, does carry a 4 to 10 percent complication rate consisting mostly of hematoma and infection. The authors propose that a subgroup of patients presenting with severe head trauma and diffuse axonal injury without associated mass lesion, do not need ICP monitoring. Additionally, the monitoring data from ICP, MAP, and CPP for a comparison severe head injury group, and subgroups of DAI would be presented. MATERIALS AND METHODS: Thirty-six patients sustaining blunt head trauma and fitting our strict clinical and radiographic diagnosis of DAI were enrolled in our study. Inclusion criteria were severe head injury patients who did not regain consciousness after the initial impact, and whose CT scan demonstrated characteristic punctate hemorrhages of < 10 mm diameter at the greywhite junction, basal ganglia, corpus callosum, upper brainstem, or a combination of the above. Patients with significant mass lesions and documented anoxia were excluded. Their intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were compared to a control group of 36 consecutive patients with severe non-penetrating non-operative head injury, using the Analysis for Variance method. RESULTS: Eighteen (50.0%), six (16.7%), and twelve (33.3%) patients had types I, II, and III DAI, respectively. The admission Glasgow Coma Score (GCS) was higher for types I and II than for type III DAI. ICP was monitored from 23 to 165 hours, with a mean ICP for 36 patients of 11.70 mmHg (SEM = 0.75) and a range from 4.3 to 17.3 mmHg. Of all ICP recordings, of which 89.7%, (2421/2698) were < or = 20 mmHg. Average mean arterial pressure (MAP) was 96.08 mmHg (SEM = 1.69), and 94.6% (2038/2154) of all MAP readings were greater than 80 mmHg. Average cerebral perfusion pressure (CPP) was 85.16 mmHg (SEM = 1.68), and 90.1% (1941/2154) of all CPP readings were greater than 70 mmHg. This is compared to the control group mean ICP, MAP, and CPP of 16.84 mmHg (p = 0.000021), 92.80 mmHg (p = 0.18), and 76.49 mmHg (p = 0.0012). No treatment for sustained elevated ICP > 20 mmHg was needed for DAI patients except in two; one with extensive intraventricular and subarachnoid hemorrhage who developed communicating hydrocephalus, and another with ventriculitis requiring intrathecal and intravenous antibiotic treatments. Two complications, one from a catheter tract hematoma, and another with Staph epidermidis ventriculitis, were encountered. All patients, except type III DAI, generally demonstrated marked clinical improvement with time. The outcome, as measured by Glasgow Coma Score (GCS) and Glasgow Outcome Score (GOS) was similarly better with types I and II than type III DAI. CONCLUSION: The authors conclude that ICP elevation in DAI patients without associated mass lesions is not as prevalent as other severe head injured patients, therefore ICP monitoring may not be as critical. The presence of an ICP monitoring device may contribute to increased morbidity. Of key importance, however, is an accurate clinical history and interpretation of the CT scan.

Adolescent↗
PubMed1997

Experimental diffuse axonal injury induces enhanced neuronal C5a receptor mRNA expression in rats.

Several studies suggest the involvement of the complement system in the pathophysiology of traumatic brain injury (TBI). Since the intrathecal generation of anaphylatoxin C5a has been shown to mediate inflammatory effects within the central nervous system, we sought to characterize the cellular expression of the mRNA for the C5a receptor (C5aR, CD88) in brains of rats with experimental diffuse axonal injury (DAI) by in situ hybridization. Infiltrating leukocytes expressing C5aR mRNA were seen in meninges and lateral ventricles as early as 4 h after induction of DAI. The number of infiltrating C5aR-positive cells increased gradually up to 24 h after trauma. Within the brain parenchyma, up-regulation of C5aR mRNA expression was first seen in cerebellar Purkinje cells within 8 h. At 24 h after TBI, expression of C5aR mRNA was widespread bilaterally throughout the cortex and cerebellum, the cellular expression being restricted to pyramidal neurons and Purkinje cells. The intensity of C5aR transcript signals on neurons increased further up to 96 h after trauma. Ligand binding of C5a to its receptor on neurons might mediate previously unknown functions, thus possibly leading to neurotoxicity and secondary neuronal damage after TBI.

Animals↗
PubMed1989

[Diffuse axonal injury manifested as corpus callosum damage on magnetic resonance imaging. Case report].

A 26-year-old male was injured in a motorcycle accident and arrived unconscious at a local general hospital. Lack of improvement despite intensive care prompted his referral to the neurosurgical department, approximately 10 hours after the accident. On neurological examination his Glasgow Coma Scale score was 8, and mild right hemiparesis and right radial nerve palsy were noted. There was no skull fracture. Computed tomography disclosed intraventricular hemorrhage and small hemorrhagic foci in the prepontine area and the border between the gray and white matter. No hemorrhage was demonstrated in the corpus callosum. Magnetic resonance imaging (MRI) was performed 3 weeks after admission with a 0.5-tesla resistive Vista magnetic resonance scanner. The inversion recovery technique was used, with a repetition time (TR) of 2100 msec, an inversion time of 500 msec, and an echo time (TE) of 40 msec, for T1-weighted images. The spin-echo technique was used, with a TR of 2000 msec and a TE of 80 msec, for T2-weighted images. In the body and splenium of the corpus callosum, T1-weighted images showed a spotty area of low signal intensity with an irregular margin; this area was of high signal intensity on T2-weighted images. On repeat MRI performed 4 months after injury, T1-weighted images showed, in the same region, granular low signal intensity, while T2-weighted images showed high signal intensity. The MRI findings in the subacute and chronic stages of diffuse axonal injury are discussed.

Adult↗
PubMed1999

A patient with cerebral palsy whose mother had a traffic accident during pregnancy: a diffuse axonal injury?

A 16-year-old girl had spastic cerebral palsy (CP) with triplegia and focal epilepsy. The patient's past history included her mother's lower abdominal trauma caused by a traffic accident at the 7th month of gestation. Brain examination with magnetic resonance imaging (MRI) revealed encephalomalacia at the bilateral parieto-temporal lobes and the left caudate nucleus, segmental narrowing of the splenium of the corpus callosum, dilatation of the left lateral ventricle and an abnormally high intensity at the right posterior portion of the internal capsule. These findings might indicate a diffuse axonal injury (DAI), but not an asphyxic brain damage. In this patient, CP might be caused by an intrauterine DAI when her mother was involved in the accident.

Accidents, Traffic↗
PubMed1998

Imaging findings in diffuse axonal injury after closed head trauma.

Even in patients with closed head trauma, brain parenchyma can be severely injured due to disruption of axonal fibers by shearing forces during acceleration, deceleration, and rotation of the head. In this article we review the spectrum of imaging findings in patients with diffuse axonal injuries (DAI) after closed head trauma. Knowledge of the location and imaging characteristics of DAI is important to radiologists for detection and diagnosis. Common locations of DAI include: cerebral hemispheric gray-white matter interface and subcortical white matter, body and splenium of corpus callosum, basal ganglia, dorsolateral aspect of brainstem, and cerebellum. In the acute phase, CT may show punctate hemorrhages. The true extent of brain involvement is better appreciated with MR imaging, because both hemorrhagic and non-hemorrhagic lesions (gliotic scars) can be detected. The MR appearance of DAI lesions depends on several factors, including age of injury, presence of hemorrhage or blood-breakdown products (e. g., hemosiderin), and type of sequence used. Technical aspects in MR imaging of these patients are discussed. Non-hemorrhagic lesions can be detected with fluid attenuated inversion recovery (FLAIR), proton-density-, or T2-weighted images, whereas gradient echo sequences with long TE increase the visibility of old hemorrhagic lesions.

Adolescent↗
PubMed1995

Homicidal blunt head trauma, diffuse axonal injury, alcoholic intoxication, and cardiorespiratory arrest: a case report of a forensic syndrome of acute brainstem dysfunction.

Sudden death can occur in drunk individuals who are severely beaten about the face. The structural basis for this forensic syndrome is unknown. We herein describe the case of an intoxicated 23-year-old man (blood alcohol 234 mg%, 51 mmol/l) who was involved in an altercation and received blows and kicks to his head. A cardiorespiratory arrest occurred during the assault. He was resuscitated in hospital 23 min later but died 90 h after admission of severe ischemic encephalopathy and bronchopneumonia. Postmortem examination revealed diffuse scalp bruising, no evidence of a skull fracture, multiple small hemispheric contusions, severe cerebral edema secondary to ischemic encephalopathy, and axonal swellings in the corpus callosum, subcortical white matter, midbrain, right rostral inferior cerebellar peduncle, and medulla. This case of near sudden death confirms that blunt head trauma sustained during an assault can cause mild diffuse axonal injury. In addition, it is possible that sudden, alcohol intoxication-associated, craniofacial traumatic death is caused by acute dysfunction of the brainstem cardiorespiratory centers, whose capacity to correct potentially fatal dysrhythmias or apnea, induced by injury to their afferent axons, can be compromised by alcohol ingestion.

Adult↗
PubMed1991

[Diffuse axonal injury (DAI) in an autopsy case of head trauma with long survival].

The authors reported a clinico-pathological case survived 11 months after a traffic accident. A 41-year-old man had been hit by a motor car and was found in a state of semicoma. On admission, his consciousness level was III-100 to 200 (Japan Coma Scale). Pupils were isocoric; light reflex was present. Linear fracture of occipital bone was disclosed by Skull X-ray and subarachnoid hemorrhage was revealed on CT scan. This comatose state, lasting 24 hours, slowly improved and eventually he presented the so-called Korsakoff's syndrome until his death. He could not recognized his relatives, only uttered some meaningless words. He was unable to obey simple verbal orders. The patient was incontinent and right pyramidal sign was positive. On repeated CT scans, cerebral ventricles gradually increased in size; especially the enlargement of the fourth ventricle was remarkable. He expired of septic shock caused by bed sores. At autopsy brain weighed 1190 g. Old gloss contusional scars were observed on the bilateral frontal lobes including the orbital area and on the left temporal pole. Gliding contusions were revealed in the subcortical white matter beneath the left superior frontal convolution. Fibrillary gliosis was noted in this region, the deep white matter underlying the left temporal pole and the tissue surrounding the anterior horn of the left lateral ventricle. Nerve fibers were fragmented and lacerated at corpus callosum, anterior commissure and posterior limb of the left internal capsule. Bilateral pyramidal tracts showed mild myelin pallor at the brainstem. Loss of Purkinje cells were observed. This case would correspond to mile type of diffuse axonal injury proposed by Adams and Gennarelli. (ABSTRACT TRUNCATED AT 250 WORDS)

Accidents, Traffic↗
PubMed1995

[A case of diffuse brain injury involving the medial part of the brain--its difference from diffuse axonal injury].

A 30-year-old male clinico-pathological case survived for 1 year and 9 months after being hit by a truck while riding on his motorbike on Aug. 21, 1988. On admission, his consciousness level was 5 according to the Glasgow Coma Scale, and a traumatic intraventricular hemorrhage and cerebral contusion were revealed by CT scanning. He underwent immediately an operation in order to drain blood from the ventricles at which time a right side dominant quadriplegia was noted. He made a gradual improvement and by January 1989 was able to tell us his name and address correctly. However, he remained incontinent and bedridden owing to the contracture of joints. He was put on rehabilitation exercises in March 1989 which trained him to operate a wheelchair. In April 1990 he regained urinary control, but was remarkably devoid of will power, perseverance and memory. He expired of pneumonia on May 11, 1990. At autopsy, his brain weighed 1180g. The cerebral convexity was discolored, especially the rectal gyri and bilateral olfactory bulbs were brownish-yellow. Old gross contusional scars were observed on the left rectal and orbital gyri, and the 3rd ventricle and inferior horns of the lateral ventricles were enlarged. Holzer's method revealed fibrillary gliosis in the corpus callosum, fornix, cingulate gyrus and a part of the caudate nucleus adjacent to the thalamus. Microscopically, axons were seen to be disrupted in the corpus callosum as well as in the anterior commissure, having the appearance of macrophages. (ABSTRACT TRUNCATED AT 250 WORDS)

Axons↗
PubMed2004

The conformation of the brain plays an important role in the distribution of diffuse axonal injury in fatal road traffic accident.

OBJECTIVE: A study was made of the brain lesions in 120 random victims of fatal road traffic accidents to determine the frequency and topographic distribution of diffuse axonal damage (DAI) in relation to the midline brain structures. METHOD: The identification of axons was carried out with a mouse antibody anti-neurofilament proteins 70-, 160-, and 210-kD. RESULTS: DAI was identified in 96 (80%) brains and classified as Grade 1 in 21.9%, as Grade 2 in 51%, and as Grade 3 in 27.1% of the patients. In spite of the diffuse distribution that is characteristic of DAI, damage occurred preferentially in the interhemispheric formations (corpus callosum and fornix) and rostral portion of the brainstem, usually to one side of the midline. CONCLUSION: From a mechanical point of view, the interhemispheric formations and the rostral portion of the brainstem act as fixating structures for the cerebral hemispheres during rotational acceleration of the head. It is known that the motion of the cerebral hemispheres is delayed at the points of fixation, where greater stress would be produced, particularly on the side subjected to greater displacement. The frequent involvement by DAI of deep, center-medial brain structures, usually to one side of the midline, supports the mechanism proposed above.

Accidents, Traffic↗
PubMed1985

Metabolic complications associated with severe diffuse brain injury.

Diffuse axonal injury (DAI), the severest form of diffuse brain injury, causes extensive damage throughout the cerebrum, diencephalon and brainstem. The effects of this injury, however, are not isolated to the brain. This paper discusses diffuse axonal injury, the metabolic complications to be anticipated from the systems' response to cerebral trauma in general, and the nursing implications.

Brain Injuries↗
PubMed2000

Diffuse axonal injury with or without an evacuated intracranial hematoma in head injured patients. Are they different lesions?

The general classification of head injury proposed by Marshall et al., based on admission CT scan findings, might mask a group of patients who have Diffuse Brain Injury (DI) in addition to intracranial haematomas. The aim of this study was to assess possible differences in outcome with respect to the level of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) between a group of patients with DI: III-IV (Marshall's classification) after the evacuation of an intracranial haematoma (group A) and another group with DI: III-IV in the absence of a mass lesion (group B). We prospectively studied 129 patients with isolated and closed severe head injury (GCS < 9). In group A (n = 61), the median percentage of hours with ICP > 20 mmHg and CPP < 70 mmHg was 42.8 and 18, respectively and 17 (28%) survived with GOS 4-5. In group B (n = 68), median values of 20 and 5.5 hours were obtained for ICP > 20 and CPP < 70 respectively, whilst 39 (57.3%) survived with favourable outcomes. When we analysed the effects of the DI: III-IV in both groups of patients, we found that the differences in percentage of time with ICP > 20 and CPP < 70 were statistically significant (p < 0.01) and patients in group A had a higher morbidity and mortality (p < 0.05). This study has demonstrated that the levels of ICP, morbidity and mortality in patients with DI: III-IV and an evacuated mass lesion were higher than in patients with DI: III-IV without a mass lesion.

Adolescent↗
PubMed2002

Ultrastructural observation of effect of moderate hypothermia on axonal damage in an animal model of diffuse axonal injury.

OBJECTIVE: To investigate the effect of moderate hypothermia on responses of axonal cytoskeleton to axonal injury in the acute stage of injury. METHODS: Of fifteen adult guinea pigs, twelve animals were subjected to stretch injury to the right optic nerves and divided into the normothermic group (n = 6) in which the animal's core temperature was maintained at 36.0-37.5 degrees C and the hypothermia group (n = 6) in which the core temperature was reduced to 32.0-32.5 degrees C after stretch injury. Remaining three animals sustained no injury to the right optic nerves and served as control group. Half of injured animals (n = 3) of either normothermic group or hypothermic group were killed at either 2 hours or 4 hours after injury. The ultrastructural changes of axonal cytoskeleton of the right optic nerve fibers from the animals were examined under a transmission electron microscope and analyzed by quantitative analysis with a computer image analysis system. RESULTS: At 2 hours after stretch injury, there was a significant reduction in the mean number of microtubules (P < 0.001), and a significant increase in the mean intermicrotubule spacing (P < 0.05 or P < 0.01) in axons of all sizes in normothermic animals. The mean number of neurofilaments also decreased statistically (P < 0.01) in large and medium subgroups of axons in the same experimental group at 2 hours. By 4 hours, the large subgroup of axons in normothermic animals still demonstrated a significant decline in the mean number of microtubules (P < 0.01) and an increase in the mean intermicrotubule spacing (P < 0.05), while the medium and small subgroups of axons displayed a significant increase in the mean number of neurofilaments (P < 0.05) and reduction in the mean interneurofilament spacing (P < 0.05). On the contrary, either the mean number of microtubules and the mean intermicrotubule spacing, or the mean number of neurofilaments and interneurofilament spacing in axons of all sizes in hypothermic stretch-injured animals was not significant different from the mean values of sham-operated animals. CONCLUSIONS: Posttraumatic moderate hypothermia induced immediately after axonal injury results in substantial protection of axonal cytoskeleton and ameliorates axonal damage.

Animals↗