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Outcome of patients with diffuse axonal injury: the significance and prognostic value of MRI in the acute phase.

BACKGROUND: To compare the magnetic resonance imaging (MRI) findings in the acute phase with outcome in patients with diffuse axonal injury (DAI). METHODS: A group of 33 patients with closed head injury and discrepancy between the apparently normal computed tomographic scan findings and their neurologic statuses were studied with MRI during the first 48 hours. Among them, 24 were found to suffer from DAI-type lesions. According to the Glasgow Coma Scale (GCS), 19 patients suffered from severe head injury (GCS score <8) and 5 patients had moderate head injury (GCS score of 9-12). Four MRI sequences in various planes were applied. Patients were divided into three groups, according to staging described in the literature. RESULTS: In five patients, MRI demonstrated nonhemorrhagic DAI lesions stage 1. In 11 patients, findings were consistent with DAI lesions stage 2, eight nonhemorrhagic and three hemorrhagic. Eight patients showed DAI lesions stage 3, six of which were nonhemorrhagic. CONCLUSIONS: MRI is more sensitive compared with computed tomography in the detection of traumatic brain lesions, especially the nonhemorrhagic DAI. The presence of hemorrhage in DAI-type lesions and the association with traumatic space-occupying lesions is a poor prognostic sign. Isolated nonhemorrhagic DAI-type lesions are not associated with poor clinical outcome.

Adolescent↗

Magnetization transfer imaging of diffuse axonal injury following experimental brain injury in the pig: characterization by magnetization transfer ratio with histopathologic correlation.

PURPOSE: Our goal was to evaluate the use of the magnetization transfer ratio (MTR) in the detection of diffuse axonal injury (DAI) resulting from traumatic brain injury in a swine model. METHOD: DAI was created by applying a nonimpact, coronal plane, rotational acceleration to the heads of miniature swine (n = 4). GE imaging was performed with and without off-resonance MT saturation. Histologic correlation of axonal injury with MRI was performed 7 days postinjury. Thirty-one subcortical white matter regions and 10 deep white matter regions were selected for the direct comparison of histologic data and MTR measurements. RESULTS: Nineteen of 41 examined locations exhibited histologic evidence of axonal injury. The mean MTR in regions with axonal damage was significantly less than in regions without axonal damage. These changes were observed both in regions demonstrating high signal intensity on T2-weighted images (T2WI) (p <0.0001, n = 6) and in regions with no signal intensity change on T2WI (p < 0.05, n = 13). CONCLUSION: These results suggest that the measurement of MTR may have the potential for evaluation axonal damage in DAI following traumatic brain injury even when conventional T2WI does not demonstrate the lesion.

Animals↗

Diffuse axonal injury associated with multiple traumatic aneurysms of the distal anterior cerebral artery--case report.

A rare case of multiple traumatic aneurysms, arising from the distal anterior cerebral artery (ACA), associated with a diffuse axonal injury is presented. An 18-year-old male sustained a frontal impact injury in a traffic accident on February 19, 1988. He immediately lost consciousness and was transported to a local hospital where his Glasgow Coma Scale score was 6. A computed tomographic scan showed a traumatic subarachnoid hemorrhage extending from the corpus callosum to the left parietal lobe. With conservative treatment, he gradually regained consciousness and was referred to our hospital 12 days later. Skull x-rays revealed no fracture. A right common carotid angiogram revealed multiple aneurysmal dilatations on the right distal ACA. A left frontoparietal craniotomy was then performed to determine the nature of the aneurysmal dilatation, and to evacuate the intracerebral hematoma because his right hemiparesis persisted. Two aneurysmal dilatations on the distal ACA were tightly surrounded by clots and a hematoma extended from the corpus callosum to the parietal lobe. The ACA was trapped proximal and distal to the aneurysmal dilatations. The postoperative course was uneventful.

Adolescent↗

Diffuse axonal injury and traumatic coma in the primate.

Traumatic coma was produced in 45 monkeys by accelerating the head without impact in one of three directions. The duration of coma, degree of neurological impairment, and amount of diffuse axonal injury (DAI) in the brain were directly related to the amount of coronal head motion used. Coma of less than 15 minutes (concussion) occurred in 11 of 13 animals subjected to sagittal head motion, in 2 of 6 animals with oblique head motion, and in 2 of 26 animals with full lateral head motion. All 15 concussioned animals had good recovery, and none had DAI. Conversely, coma lasting more than 6 hours occurred in one of the sagittal or oblique injury groups but was present in 20 of the laterally injured animals, all of which were severely disabled afterward. All laterally injured animals had a degree of DAI similar to that found in severe human head injury. Coma lasting 16 minutes to 6 hours occurred in 2 of 13 of the sagittal group, 4 of 6 in the oblique group, and 4 of 26 in the lateral group, these animals had less neurological disability and less DAI than when coma lasted longer than 6 hours. These experimental findings duplicate the spectrum of traumatic coma seen in human beings and include axonal damage identical to that seen in sever head injury in humans. Since the amount of DAI was directly proportional to the severity of injury (duration of coma and quality of outcome), we conclude that axonal damage produced by coronal head acceleration is a major cause of prolonged traumatic coma and its sequelae.

Acceleration↗

[Clinicopathological studies of diffuse axonal injury--five autopsy cases].

In severe head injuries, delayed intracerebral hematoma appearing lately is noted due to the spread use of serial CT scan. The authors experienced the autopsy of 5 cases who presented diffuse axonal injury (DAI) among these new lesions in repeated CT scan findings and report the pathohistological findings. Subjects were as follows: The age range of the patients was 15 to 25 years. The consciousness levels of the 5 cases on admission were 6 or less by the Glasgow coma scale. CT findings of DAI were revealed hemorrhage of the corpus callosum, basal ganglia, tegmentum of pons, intraventricular, and acute brain swelling. Total clinical courses were 2 to 29 days, but most of them were 9 or less days. In the macroscopic findings, marked congestion and edema revealed mainly in deep part of the white matter of the frontal lobe in all 5 cases. Callosal disruption and hematoma adjacent the corpus callosum revealed in 4 out of 5 cases. Cerebral contusion with hemorrhage revealed in 3 out of 5 cases. Intraventricular hemorrhage and traumatic subarachnoid hemorrhage revealed in 2 out of 5 cases. Hemorrhage of basal ganglia and base of pons revealed in 2 cases. Microscopic examination of all 5 cases revealed pallor of myelin in the corpus callosum and white matter surrounding hemorrhagic lesion, and abnormal tortuous, swelling and fragmentation of axons in stained preparation. Axonal retraction ball was recognized in 3 out of 5 cases. In conclusion, five autopsied cases who presented acute brain swelling and hemorrhage of corpus callosum and tegmentum of pons in serial CT scan were examined.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

The diagnosis of diffuse axonal injury in routine autopsy practice.

A 40-year-old pedestrian was involved in a road traffic accident. He lost consciousness immediately and remained comatose for 6 months until he died of a bronchopneumonia. Examination of the fixed brain revealed the late results of diffuse axonal injury. Not all the features were readily visible macroscopically, but required a limited number of histological sections from readily predictable sites for demonstration. Special stains played only a confirmatory role. This case illustrates some of the problems in diagnosing one of the commoner patterns of brain damage in head injury, and shows how the problem may best be approached in practice.

Accidents, Traffic↗

Cognitive dysfunction and histological findings in rats with chronic-stage contusion and diffuse axonal injury.

The Morris water maze (MWM) technique is well known as a prominent method of evaluating learning acquisition and memory retention impairments in rats. We previously reported on a modified fluid percussion device that is able to consistently produce experimental cortical contusion (CC) and diffuse axonal injury (DAI) in separate groups of rats. The purpose of the present protocol is to evaluate the differences in learning acquisition and memory retention impairments between these two types of injured rats in the chronic stage using the MWM technique. CC and DAI rats are respectively induced by lateral and midline fluid percussion. We also compare the histological differences between these two different types of traumatic brain injury. The results show statistically significant differences in learning acquisition impairment between the sham and CC rats and between the sham and DAI rats. However, a difference in memory retention impairment was expected to be seen only between the sham and DAI rats. Histologically, the loss of CA3 pyramidal cells in the hippocampus was observed ipsilaterally in the CC and bilaterally in DAI. Neuronal cell loss was observed in bilaterally in layer II of the entorhinal cortex in DAI, but not in CC.

Animals↗

Intra-axonal overloading of calcium ion in rat diffuse axonal injury and therapeutic effect of calcium antagonist.

OBJECTIVE: Exploring the intra-axonal overloading of calcium ion (Ca(2+)) in brain diffuse axonal injury (DAI) and the therapeutic effect of calcium antagonist(Nimotop) on DAI. METHODS: Fourteen SD rats were divided into injury group, treatment group and control group. The DAI model of rats was produced by using a head-instant-axial-rotation device. Tissues from the medulla oblongata of rats were taken 2-24 h post-injury and processed for electron microscopic observation by a cytochemical technique for calcium ion. RESULTS: In the injured rats there was evidence of local disruption of myelin sheath,lucent spaces between myelin sheath lamellae, separation of axolemma from the inner layer of myelin sheath, peripheral accumulation of organellae, intra-axonal formation of vacuoles and reduction of mitochondria. A large number of fine calcium deposits were seen on the affected myelin sheath. The severity of the myelin sheath lesion was related positively to the number of calcium deposits on it. In the later post-injury period the coarse calcium particles appeared within the damaged axon. Neuronal somas and microvascular endotheliums showed a lot of vacuoles and some fine calcium deposits. Many microvilli formed on the luminal aspect of endothelium. In the treatment group myelin sheath tended to be injured locally, and axoplasmic mitochondria were nearly normal in number, structure, and distribution. Few calcium deposits were found in axons. Vacuolization was obviously reduced in neuronal soma and endothelium. CONCLUSIONS: In DAI there exists an intra-axonal overloading of calcium ion, which is a key factor to the occurrence and development of DAI. Early use of Nimotop can alleviate DAI.

Journal Article↗

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↗

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↗

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↗

[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↗

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↗

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↗

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↗

[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↗