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PubMed2000

Immediate coma following inertial brain injury dependent on axonal damage in the brainstem.

OBJECT: Immediate and prolonged coma following brain trauma has been shown to result from diffuse axonal injury (DAI). However, the relationship between the distribution of axonal damage and posttraumatic coma has not been examined. In the present study, the authors examine that relationship. METHODS: To explore potential anatomical origins of posttraumatic coma, the authors used a model of inertial brain injury in the pig. Anesthetized miniature swine were subjected to a nonimpact-induced head rotational acceleration along either the coronal or axial plane (six pigs in each group). Immediate prolonged coma was consistently produced by head axial plane rotation, but not by head coronal plane rotation. Immunohistochemical examination of the injured brains revealed that DAI was produced by head rotation along both planes in all animals. However, extensive axonal damage in the brainstem was found in the pigs injured via head axial plane rotation. In these animals, the severity of coma was found to correlate with both the extent of axonal damage in the brainstem (p < 0.01) and the applied kinetic loading conditions (p < 0.001). No relationship was found between coma and the extent of axonal damage in other brain regions. CONCLUSIONS: These results suggest that injury to axons in the brainstem plays a major role in induction of immediate posttraumatic coma and that DAI can occur without coma.

Animals↗
PubMed2002

[Therapeutic possibilities in axonal injury caused by head trauma].

Traumatic brain injury is putting an extreme burden on societies all over the world. While surgical and neuro-intensive treatment is traditionally aimed at space occupying or focal lesions, traumatic brain injury is frequently associated with diffuse axonal injury, which significantly contributes to its morbidity and mortality. Current taught appreciates that diffuse axonal injury is a progressive event gradually evolving from focal alterations in axolemmal permeability and the underlying axonal ultrastructure to axonal disconnection, a process amenable of therapeutic interventions. This review is primarily focusing on the clinical/neuroradiological manifestation and our contemporary knowledge of the pathobiology of traumatically evoked (diffuse-) axonal injury with particular emphasize on recent- to date, primarily experimental-therapeutic approaches that in the future might offer potential aid to the head injured.

Accidents, Traffic↗
PubMed2002

Temporal characterisation of pro- and anti-apoptotic mechanisms following diffuse traumatic brain injury in rats.

Few studies have characterised apoptosis in a brain injury model that causes a significant degree of diffuse axonal injury. Such characterisation is essential from a clinical viewpoint since diffuse axonal injury is a major component of human head injury. The present study therefore, examines the expression of active and proactive caspase-3, and the bax, bcl-2 and bcl-x members of the bcl-2 family, to characterise the temporal profile of apoptosis in a model of traumatic brain injury in rats that produces significant diffuse axonal injury. Pentobarbital anaesthetised male Sprague-Dawley rats were injured using the 2m impact-acceleration model of diffuse traumatic brain injury. After injury, diffuse trauma resulted in an increased bax expression followed by induction of caspase-3. The increase in caspase-3 was simultaneous with an increase in anti-apoptotic bcl-2 expression. Bcl-x levels were increased after induction of caspase-3 and the increased levels of bcl-x were sustained to the end of the 5-day observation period. Increased active caspase-3 expression was associated with the appearance of TUNEL positive cells. These cells were detected in different brain regions at different times, with some regions showing no apoptotic cells until 3 days after injury. No TUNEL positive cells were detected at 7 and 14 days after injury. DNA electrophoresis confirmed that DNA fragmentation was maximal at 3 days after injury. Increased active caspase-3 levels were also significantly correlated with increased bcl-2 levels (r=0.80; P<0.001) suggesting that the apoptotic cascade after diffuse traumatic brain injury is a carefully controlled cellular homeostatic response. Pharmacological manipulation of this balance may offer a therapeutic approach for preventing cell death and improving outcome after diffuse traumatic brain injury.

Animals↗
PubMed1993

Pathobiology of traumatically induced axonal injury in animals and man.

STUDY OBJECTIVES: Although diffuse axonal injury is recognized as a consistent feature of traumatic brain injury, there is confusion regarding its pathogenesis. To provide insight into its pathogenesis, animal models of traumatic brain injury complemented by post mortem human analyses were used. DESIGN: In animals, anterograde tracers together with antibodies targeting the neurofilament subunits were used in light and electron microscopic analyses of axonal injury. In humans, antibodies to the neurofilament subunits also were used to follow diffuse axonal injury. Animals were followed from minutes to months after injury, whereas humans were studied from six hours to 59 days after injury. MEASUREMENTS AND MAIN RESULTS: In neither animals nor humans did traumatic brain injury cause direct axonal tearing. Instead, the traumatic brain injury triggered focal intra-axonal change in the 68-kd neurofilament subunit, which became disordered in its alignment and resulted in impaired axoplasmic transport. This caused axonal swelling and disconnection. The sequence of axonal change was similar in animals and man; however, its temporal progression was slower in humans. CONCLUSION: Traumatically induced axonal damage is triggered first by focal intra-axonal change involving the neurofilament subunits. This neurofilament change is due to either direct mechanical failure of the axonal cytoskeleton or the initiation of a biochemical event that causes neurofilament disassembly. In general, the temporal progression of the intra-axonal changes that lead to ultimate disconnection is influenced by the severity of the traumatic injury and the species evaluated.

Animals↗
PubMed1996

[Clinical features and CT diagnostic criteria for diffuse axonal brain injury].

The clinical and computed tomographic features of 117 patients with severe closed head injury were analysed. We put forward the CT diagnostic criteria of diffuse axonal injury (DAD)i.e. (1) single or multiple small intraparenchymal hemorrhages in the cerebral hemispheres (< 2 cm in diameter); (2) intraventricular hemorrhage; (3) hemorrhage in the corpus callosum; (4) small focal areas of hemorrhage adjacent to the third ventricle (< 2 cm in diameter); (5) brain stem hemorrhage. Our patients were divided into DAI group and non-DAI group according to the set of criteria. Traffic accidents were the main injury cause in patients with DAI. GCS on admission in patients with DAI were significantly lower than those in patients without DAI. The incidence of diffuse brain swelling in patients with DAI significantly higher than that in non-DAI patients, whereas the incidences of skull fracture and epidual hematoma were respectively significantly lower than those in non-DAI patients. There was no significant difference between the incidences of subarachnoid hemorrhage and subdual hematoma in the two groups. The incidence of poor outcome in DAI group was significantly higher than that in non-DAI group, although there was no significant difference between the mortalities in the two groups. Because DAI is a very important factor worsening the outcome of head-injured patient, it is very important to make a diagnosis as soon as we can. However, the clinical manifestations of DAI are not specific and DAI does not show directly on CT, so it is difficult to make a diagnosis. The CT diagnostic criteria of DAI we put forward now are practicable, though they are not perfect.

Adolescent↗
PubMed1986

Post-traumatic diffuse axonal brain injury. Analysis of 78 patients studied with computed tomography.

A group of 78 severe head injury patients showing computerized tomography (CT) findings of the so-called "diffuse axonal injury" is analyzed. These patients represent 20% of the authors' series of severe head injury. Twenty-three patients showed small intraparenchymal haemorrhages in the CT scan study, 15 intraventricular haemorrhage and 40 patients had both intraparenchymal and intraventricular haemorrhages. Signs of brainstem haemorrhagic contusion were seen in 29 (38%) patients. Generalized brain swelling superimposed on the above findings was present in 75% of the cases. Raised intracranial pressure, which was found in 50% of the patients, correlated with the presence of ventriculocisternal collapse in the CT scan and an unfavourable outcome. Only 4 patients in this series made a good recovery, 13 developed a moderate disability, 11 a severe disability, 12 became vegetative and 38 (49%) died. The prognosis with this post-traumatic lesion is the worst in the authors' severe head injury series after excluding cases with subdural haematoma.

Adolescent↗
PubMed2006

[Paroxysmal sympathetic storm after diffuse axonal head injury].

The term paroxysmal sympathetic storms is used to define episodic alterations in body temperature, blood pressure, heart and respiratory rate, size of pupil, and level of consciousness coinciding with hyperhidrosis, excessive salivation and extensor posturing. All the cases were presented after severe diffuse axonal head injury. We present two young patients with diffuse axonal head injury that develop in their evolution hypertension, tachycardia and fever without evidence during the episodes of epileptiform activity and without any infectious cause with excellent answer to the treatment with beta-blockers and morphine. We consider that the correct diagnosis of this entity minimizes the application of unnecessary studies allowing an appropriate treatment.

Adult↗
PubMed1988

MR imaging of head trauma: review of the distribution and radiopathologic features of traumatic lesions.

The distribution and extent of traumatic lesions were prospectively evaluated with MR imaging in 40 patients with closed head injuries. Primary intraaxial lesions were classified according to their distinctive topographical distribution within the brain and were of four main types: (1) diffuse axonal injury (48.2%), (2) cortical contusion (43.7%), (3) subcortical gray-matter injury (4.5%), and (4) primary brainstem injury (3.6%). Diffuse axonal injury most commonly involved the white matter of the frontal and temporal lobes, the body and splenium of the corpus callosum, and the corona radiata. Cortical contusions most frequently involved the inferior, lateral, and anterior aspects of the frontal and temporal lobes. Primary brainstem lesions were most commonly seen in the dorsolateral aspects of the rostral brainstem. The pattern and distribution of primary lesions seen by MR were compared with those expected from previous pathologic studies and found to be quite similar. Our data and review of the literature would also indicate that MR detects a more complete spectrum of traumatic lesions than does CT. Secondary forms of injury (territorial arterial infarction, pressure necrosis from increased intracranial pressure, cerebral herniation, secondary brainstem injury) were also visible by MR in some cases. The level of consciousness was most impaired in patients with primary brainstem injury, followed by those with widespread diffuse axonal injury and subcortical gray-matter injury. The best MR imaging planes, pulse sequences, and imaging strategies for evaluating and classifying traumatic lesions were evaluated, and the mechanisms by which traumatic stresses result in injury were reviewed. MR was found to be superior to CT and to be very effective in the detection of traumatic head lesions and some secondary forms of injury. While T2-weighted images were most useful for lesion detection, T1-weighted images proved to be most useful for anatomic localization and classification.

Adolescent↗
PubMed1987

Influence of lesions detected by computed tomography on outcome and neuropsychological recovery after severe head injury.

Outcome at 6 months after severe head injury was determined in 117 patients whose computed tomographic (CT) examinations demonstrated diffuse axonal injury (DAI), diffuse swelling (DS), or focal injuries. Neuropsychological sequelae were ascertained from two examinations in 30 of the conscious survivors within the 1st year after injury. Outcome differences varied with the type of CT lesion. DS and focal injuries resulted in more favorable (good recovery) outcomes. Mortality was higher after DAI. Neuropsychological outcome varied with the type of CT lesion and the function measured. Overall differences in memory and learning were revealed among the three CT lesion categories, whereas differences in intelligence and visuomotor functions were not significant. Levels of memory, learning, and visuomotor speed were higher after DS injuries, but improvement was less. Greater improvement of memory, learning, and visuomotor speed occurred after DAI. After focal injuries, visuomotor speed improved, but not recall and learning. The results suggest that the type of injury incurred differentially influences the outcome and the neuropsychological aftermath of severely head-injured adults.

Craniocerebral Trauma↗
PubMed1998

The persistent vegetative state after closed head injury: clinical and magnetic resonance imaging findings in 42 patients.

OBJECT: In this retrospective study, the authors analyzed the frequency, anatomical distribution, and appearance of traumatic brain lesions in 42 patients in a posttraumatic persistent vegetative state. METHODS: Cerebral magnetic resonance (MR) imaging was used to detect the number of lesions, which ranged from as few as five to as many as 19, with a mean of 11 lesions. In all 42 cases there was evidence on MR imaging of diffuse axonal injury, and injury to the corpus callosum was detected in all patients. The second most common area of diffuse axonal injury involved the dorsolateral aspect of the rostral brainstem (74% of patients). In addition, 65% of these patients exhibited white matter injury in the corona radiata and the frontal and temporal lobes. Lesions to the basal ganglia or thalamus were seen in 52% and 40% of patients, respectively. Magnetic resonance imaging showed some evidence of cortical contusion in 48% of patients in this study; the frontal and temporal lobes were most frequently involved. Injury to the parahippocampal gyrus was detected in 45% of patients; in this subgroup there was an 80% incidence of contralateral peduncular lesions in the midbrain. The most common pattern of injury (74% in this series) was the combination of focal lesions of the corpus callosum and the dorsolateral brainstem. In patients with no evidence of diffuse axonal injury in the upper brainstem (26% in this series), callosal lesions were most often associated with basal ganglia lesions. Lesions of the corona radiata and lobar white matter were equally distributed in patients with or without dorsolateral brainstem injury. Moreover, cortical contusions and thalamic, parahippocampal, and cerebral peduncular lesions were also similarly distributed in both groups. CONCLUSIONS: The data indicate that diffuse axonal injury may be the major form of primary brain damage in the posttraumatic persistent vegetative state. In addition, the authors demonstrated in this study that MR imaging, in conjunction with a precise clinical correlation, may provide useful supportive information for the accurate diagnosis of a persistent vegetative state after traumatic brain injury.

Adolescent↗
PubMedDate not supplied

Posttraumatic diffuse cerebral lesions. Relationship between clinical course, CT findings and ICP.

One hundred and fifty patients with posttraumatic diffuse cerebral lesions were reviewed. Criteria of inclusion were immediate coma and CT appearance of diffuse lesions, that were classified as follows: (a) Diffuse axonal injury (70 cases): patients with normal CT scan (50 cases) and patients with shearing injury (focal hemorrhages in corpus callosum, basal ganglia and brain stem; gliding contusions) (20 cases); (b) Diffuse brain swelling (80 cases): reduced or absent lateral ventricles, absence of 3rd ventricle and basal cisterns. Many of these patients had either subarachnoid haemorrhage or subdural blood effusion. Clinical course and mortality rate were in a ranking order in the considered groups. Patients with normal CT had a less severe coma and a better outcome than patients with shearing injury and diffuse brain swelling. There was evidence of high intracranial pressure in 75% of the patients with brain swelling, whereas no patient with normal CT had ICP elevation. Diffuse axonal injury represents a primary posttraumatic diffuse lesion. Secondary vascular involvement, due to hypoxia, shock and other unknown causes, is responsible for the appearance of vasoparesis, hyperemia and diffuse brain swelling.

Adult↗
PubMed1999

Quantification of axonal damage in traumatic brain injury: affinity purification and characterization of cerebrospinal fluid tau proteins.

Diffuse axonal injury is a primary feature of head trauma and is one of the most frequent causes of mortality and morbidity. Diffuse axonal injury is microscopic in nature and difficult or impossible to detect with imaging techniques. The objective of the present study was to determine whether axonal injury in head trauma patients could be quantified by measuring levels of CSF tau proteins. Tau proteins are structural microtubule binding proteins primarily localized in the axonal compartment of neurons. Monoclonal antibodies recognizing the form of tau found in the CSF of head trauma patients were developed by differential CSF hybridoma screening using CSF from head trauma and control patients. Clones positive for head trauma CSF tau proteins were used to characterize this form of tau and for ELISA development. Using the developed ELISA, CSF tau levels were elevated >1,000-fold in head trauma patients (mean, 1,519 ng/ml of CSF) when compared with patients with multiple sclerosis (mean, 0.014 ng/ml of CSF; p < 0.001), normal pressure hydrocephalus (nondetectable CSF tau), neurologic controls (mean, 0.031 ng/ml of CSF; p < 0.001), or nonneurologic controls (nondetectable CSF tau; p < 0.001). In head trauma, a relationship between clinical improvement and decreased CSF tau levels was observed. These data suggest that CSF tau levels may prove a clinically useful assay for quantifying the axonal injury associated with head trauma and monitoring efficacy of neuroprotective agents. Affinity purification of CSF tau from head trauma patients indicated a uniform cleavage of approximately 18 kDa from all six tau isoforms, reducing their apparent molecular sizes to 30-50 kDa. These cleaved forms of CSF tau consisted of the interior portion of the tau sequence, including the microtubule binding domain, as judged by cyanogen bromide digestion. Consistent with these data, CSF cleaved tau bound taxol-polymerized microtubules, indicating a functionally intact microtubule binding domain. Furthermore, epitope mapping studies suggested that CSF cleaved tau proteins consist of the interior portion of the tau sequence with cleavage at both N and C terminals.

Alzheimer Disease↗
PubMed1999

Improved motor outcome in response to magnesium therapy received up to 24 hours after traumatic diffuse axonal brain injury in rats.

OBJECT: The goal of this study was to establish the therapeutic window during which delayed therapy with MgSO4 improves neurological motor outcome in rats that have suffered severe traumatic axonal brain injury. METHODS: Severe brain injury was induced in male Sprague-Dawley rats by using the impact-acceleration model of severe traumatic diffuse axonal brain injury. Injured animals were subsequently treated with MgSO4 (750 micromol/kg) infused intramuscularly at 30 minutes or at 8, 12, or 24 hours after trauma and were tested for neurological motor outcome during the following week by using the rotarod test. Injured untreated (control) animals demonstrated highly significant (p < 0.001) neurological motor deficits that were sustained over the 1-week assessment period. Animals treated with MgSO4 at 30 minutes or at 8 or 12 hours postinjury demonstrated significantly improved motor outcomes compared with untreated control animals at all time points (0.001 < p < 0.05). Animals treated with MgSO4 at 24 hours had motor scores that were similar to those of untreated control animals early in the week, but demonstrated a significantly more rapid recovery in function and, by the end of the assessment period, they demonstrated significantly improved motor scores (p < 0.01). Repeated administration of MgSO4 over the 1-week observation period did not further improve outcome. CONCLUSIONS: The present results demonstrate that Mg++ plays a neuroprotective role following severe diffuse traumatic axonal brain injury. Moreover, Mg++ therapy significantly improved motor outcome when administered up to 24 hours after injury, with early treatments providing the most significant benefit. Repeated administration beyond 24 hours postinjury did not provide additional neuroprotection.

Animals↗
PubMed1998

Anoxic and ischemic injury of myelinated axons in CNS white matter: from mechanistic concepts to therapeutics.

White matter of the brain and spinal cord is susceptible to anoxia and ischemia. Irreversible injury to this tissue can have serious consequences for the overall function of the CNS through disruption of signal transmission. Myelinated axons of the CNS are critically dependent on a continuous supply of energy largely generated through oxidative phosphorylation. Anoxia and ischemia cause rapid energy depletion, failure of the Na(+)-K(+)-ATPase, and accumulation of axoplasmic Na+ through noninactivating Na+ channels, with concentrations approaching 100 mmol/L after 60 minutes of anoxia. Coupled with severe K+ depletion that results in large membrane depolarization, high [Na+]i stimulates reverse Na(+)-Ca2+ exchange and axonal Ca2+ overload. A component of Ca2+ entry occurs directly through Na+ channels. The excessive accumulation of Ca2+ in turn activates various Ca(2+)-dependent enzymes, such as calpain, phospholipases, and protein kinase C, resulting in irreversible injury. The latter enzyme may be involved in "autoprotection," triggered by release of endogenous gamma-aminobutyric acid and adenosine, by modulation of certain elements responsible for deregulation of ion homeostasis. Glycolytic block, in contrast to anoxia alone, appears to preferentially mobilize internal Ca2+ stores; as control of internal Ca2+ pools is lost, excessive release from this compartment may itself contribute to axonal damage. Reoxygenation paradoxically accelerates injury in many axons, possibly as a result of severe mitochondrial Ca2+ overload leading to a secondary failure of respiration. Although glia are relatively resistant to anoxia, oligodendrocytes and the myelin sheath may be damaged by glutamate released by reverse Na(+)-glutamate transport. Use-dependent Na+ channel blockers, particularly charged compounds such as QX-314, are highly neuroprotective in vitro, but only agents that exist partially in a neutral form, such as mexiletine and tocainide, are effective after systemic administration, because charged species cannot penetrate the blood-brain barrier easily. These concepts may also apply to other white matter disorders, such as spinal cord injury or diffuse axonal injury in brain trauma. Moreover, whereas many events are unique to white matter injury, a number of steps are common to both gray and white matter anoxia and ischemia. Optimal protection of the CNS as a whole will therefore require combination therapy aimed at unique steps in gray and white matter regions, or intervention at common points in the injury cascades.

Animals↗
PubMed1998

Immunohistochemical diagnosis and significance of forensic neuropathological changes.

Immunohistochemistry is very useful when investigating the cause of death. Ischemic cell changes in the hippocampal neurons were not obvious in the brains damaged by hypoxic injury. However, it is suggested that even a moderate hypoxia, which may affect the neuronal proteins and metabolism, induced astrocytosis in the CA3 and CA4 regions, and that in patients with a history of hypoxic attacks neuronal damage may be severe even several hours after ischemic injury. Furthermore, hsp70 expression was found in the CA2, CA3 and CA4 regions of long-term survivors after severe hypoxic/ischemic injury. In forensic practice, detailed information about the duration and extent of a hypoxic/ischemic injury is often unavailable, so that immunohistochemical detection of hsp70 and glial cell staining can be of great value in diagnosing not only the hypoxic/ischemic injury during the process of death but also the victim's past history of hypoxic attacks. In diffuse axonal injury, degeneration of axon and myelin, such as swelling and waving, were observed in survivors of more than 8 hours. Retraction balls appeared in survivors of more than 1 days. In longer term survivors, such as 3 or 5 months, breakdown of myelin and fat-granule cells were observed. In addition, retraction balls were also found. Immunohistochemical staining of 200 kD neurofilament was a very useful method to examine axonal changes, because antisera is specific for degenerative neurofilaments. In our study, all cases which had pathological findings of diffuse axonal injury (DAI) were associated with focal head injuries. From the immunohistochemical staining of neurons in the hippocampus, it was suggested that neurons in the hippocampus were injured by diffuse brain damage. Furthermore, repairing and protective mechanisms occurred especially from CA2 to CA4. It was considered that neuronal damage in diffuse brain injury was elucidated not only morphologically but also functionally. Therefore, in cases of suspected diffuse brain damage, it is recommended to examine the neuronal changes in addition to observing the findings of diffuse axonal injury. Immunohistochemical staining of the carotid body is potentially very useful for necropsy diagnosis, since it provides a method to detect evidence of mechanical asphyxia in suspected cases of manual and/or ligature strangulation.

Biomarkers↗
PubMed2002

Traumatic injuries: imaging of head injuries.

Due to the forces of acceleration, linear translation, as well as rotational and angular acceleration, the brain undergoes deformation and distortion depending on the site of impact of traumatizing force direction, severity of the traumatizing force, and tissue resistance of the brain. Linear translation of accereration in a closed-head injury can run along the shorter diameter of the skull in latero-lateral direction causing mostly extra-axial lesions (subdural hematoma,epidural hematoma, subarachnoidal hemorrhage) or quite pronounced coup and countercoup contusions. Contusions are considerably less frequently present in medial or paramedial centroaxial blows (fronto-occipital or occipito-frontal). The centroaxial blows produce a different pattern of lesions mostly in the deep structures, causing in some cases a special category of the brain injury, the diffuse axonal injury (DAI). The brain stem can also be damaged, but it is damaged more often in patients who have suffered centroaxial traumatic force direction. Computed tomography and MRI are the most common techniques in patients who have suffered brain injury. Computed tomography is currently the first imaging technique to be used after head injury, in those settings where CT is available. Using CT, scalp, bone, extra-axial hematomas, and parenchymal injury can be demonstrated. Computed tomography is rapid and easily performed also in monitored patients. It is the most relevant imaging procedure for surgical lesions. Computed tomography is a suitable method to follow the dynamics of lesion development giving an insight into the corresponding pathological development of the brain injury. Magnetic resonance imaging is more sensitive for all posttraumatic lesions except skull fractures and subarachnoidal hemorrhage, but scanning time is longer, and the problem with the monitoring of patients outside the MRI field is present. If CT does not demonstrate pathology as can adequately be explained to account for clinical state, MRI is warranted. Follow-up is best done with MRI as it is more sensitive to parenchymal changes. In routine MR protocol gradient-recalled-echo sequences should be included at any other time after a traumatic event since they are very sensitive in detection of hemosiderin as well as former hematoma without hemosiderin. The MR signal intensity varies depending on sequences and time scanning after trauma.

Adolescent↗
PubMed2004

Diffusion-weighted MR imaging in closed head injury: high correlation with initial glasgow coma scale score and score on modified Rankin scale at discharge.

PURPOSE: To determine whether diffusion-weighted magnetic resonance (MR) imaging findings and conventional MR imaging findings correlate with initial Glasgow Coma Scale score and score on modified Rankin scale at discharge. MATERIALS AND METHODS: Twenty-six patients (18 male and eight female patients; mean age, 25.2 years; age range, 4-72 years) with diffuse axonal injury were examined with diffusion-weighted MR imaging and with fluid-attenuated inversion recovery, T2-weighted fast spin-echo, and T2*-weighted gradient-echo sequences. All images were evaluated by two neuroradiologists in consensus. Tissue volume with trauma-related signal-intensity abnormality on images from each sequence, number of lesions for each sequence, number of lesions for all sequences, and number of lesions with reduced apparent diffusion coefficient were correlated with scores on Glasgow Coma Scale and modified Rankin scale. Involvement of brainstem, deep gray matter, and corpus callosum were also correlated with clinical scores. Spearman rank correlation coefficients (r) were calculated. RESULTS: The strongest correlation was between signal-intensity abnormality volume on diffusion-weighted images and modified Rankin score (r = 0.772, P <.001). The strength of this correlation did not improve when only volume of lesions with decreased apparent diffusion coefficient was considered. For lesion number, the strongest correlation was between lesion number on images acquired with all sequences and modified Rankin score (r = 0.662, P <.001). For lesion location, the strongest correlation was between lesion location in the corpus callosum and modified Rankin score (r = 0.513, P =.007). CONCLUSION: Volume of lesions on diffusion-weighted MR images provides the strongest correlation with a score of subacute on modified Rankin scale at discharge. Total lesion number also correlates well with modified Rankin score. In future, diffusion-weighted images may be useful in determining treatment strategies for acute head injury.

Adolescent↗
PubMed1994

Modification of the cortical impact model to produce axonal injury in the rat cerebral cortex.

Diffuse axonal injury (DAI) is a form of brain injury that is characterized by morphologic changes to axons throughout the brain and brainstem. Previous biomechanical studies have shown that primary axonal dysfunction, ranging from minor electrophysiologic disturbances to immediate axotomy, can be related to the rate and level of axonal deformation. Some existing rodent head injury models display varying degrees of axonal injury in the forebrain and brainstem, but the extent of axonal damage in the forebrain has been limited to the contused hemisphere. This study examined whether opening the dura mater over the contralateral hemisphere could direct mechanical deformation across the sagittal midline and produce levels of strain sufficient to cause a more widespread, bilateral forebrain axonal injury following cortical impact. Intracranial deformation patterns produced by this modified cortical impact technique were examined using surrogate skull-brain models. Modeling results revealed that the presence of a contralateral craniotomy significantly reduced surrogate tissue herniation through the foramen magnum, allowed surrogate tissue movement across the sagittal midline, and resulted in an appreciable increase in the shear strain in the contralateral cortex during the impact. To evaluate the injury pattern produced using this novel technique, rat brains were subjected to rigid indentor impact injury of their left somatosensory motor cortex (1.5 mm indentation, 4.5-4.9 m/sec velocity, and 22 msec dwell time) and examined after a 2-7 day survival period. Neurofilament immunohistochemistry revealed numerous axonal retraction balls in the subcortical white matter and overlying deep cortical layers in the right hemisphere beneath the contralateral craniotomy. Retraction balls were not seen at these positions in normals, sham controls, or animals that received cortical impact without contralateral craniotomy and dural opening. The results from these physical modeling and animal experiments indicate that opening of the contralateral dura mater permits translation of sufficient mechanical deformation across the midline to produce a more widespread pattern of axonal injury in the forebrain, a pattern that is distinct from those produced by existing fluid percussion and cortical impact techniques.

Animals↗