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PubMed1997

Cerebral perfusion changes in traumatic diffuse brain injury; IMP SPECT studies.

Diffuse brain injury (DBI) is characterized by axonal degeneration and neuronal damage which cause diffuse brain atrophy. We have investigated the time course of abnormalities in cerebral perfusion distribution in cases of DBI by using Iodine-123-IMP SPECT, and the relationship to the appearance of diffuse brain atrophy. SPECT scans were performed on eight patients with diffuse brain injury due to closed cranial trauma in acute and chronic stages. All patients showed abnormalities in cerebral perfusion with decreases in perfusion, even in non-depicted regions on MRI, and the affected areas varied throughout the period of observation. Diffuse brain atrophy appeared in all patients. In some patients, diffuse brain atrophy was observed at or just after the time when the maximum number of lesions on SPECT were seen. The abnormalities in cerebral perfusion in cases of DBI might therefore be related to axonal degeneration and neuronal damage which causes diffuse brain atrophy.

Adolescent↗
PubMed2001

Histopathologic response of the immature rat to diffuse traumatic brain injury.

The purpose of this study was to characterize the histopathologic response of rats at postnatal day (PND) 17 following an impact-acceleration diffuse traumatic brain injury (TBI) using a 150-g/2-meter injury as previously described. This injury produces acute neurologic and physiologic derangements as well as enduring motor and Morris water maze (MWM) functional deficits. Histopathologic studies of perfusion-fixed brains were performed by gross examination and light microscopy using hematoxylin and eosin, Bielschowsky silver stain, and glial fibrillary acidic protein (GFAP) immunohistochemistry at 1, 3, 7, 28, and 90 day after injury. Gross pathologic examination revealed diffuse subarachnoid hemorrhage (SAH) at 1-3 days but minimal supratentorial intraparenchymal hemorrhage. Petechial hemorrhages were noted in ventral brainstem segments and in the cerebellum. After 1-3-day survivals, light microscopy revealed diffuse SAH and intraventricular hemorrhage (IVH), mild edema, significant axonal injury, reactive astrogliosis, and localized midline cerebellar hemorrhage. Axonal injury most commonly occurred in the long ascending and descending fiber tracts of the brainstem and occasionally in the forebrain, and was maximal at 3 days, but present until 7 days after injury. Reactive astrocytes were similarly found both in location and timing, but were also significantly identified in the hippocampus, white matter tracts, and corpus callosum. Typically, TBI produced significant diffuse SAH accompanied by cerebral and brainstem astrogliosis and axonal injury without obvious neuronal loss. Since this injury produces some pathologic changes with sustained functional deficits similar to TBI in infants and children, it should be useful for the further study of the pathophysiology and therapy of diffuse TBI and brainstem injury in the immature brain.

Age Factors↗
PubMed2003

The morphological and neurochemical effects of diffuse brain injury on rat central noradrenergic system.

The central noradrenergic system is widely distributed throughout the brain and is closely related to spontaneous motility and level of consciousness. The study presented here evaluated the morphological as well as neurochemical effects of diffuse brain injury on the central noradrenergic system in rat. Adult male Sprague-Dawley rats were subjected to impact-acceleration brain injury produced with a weight-drop device. Morphological changes in locus coeruleus (LC) neurons were examined by using immunohistochemistry for dopamine-beta-hydroxylase, and norepinephrine (NE) turnover in the cerebral cortex was measured by high performance liquid chromatography with electrochemical detection. The size of LC neurons increased by 11% 24 h after injury but had decreased by 27% seven days after injury. Axons of noradrenergic neurons were swollen 24 h and 48 h after injury but the swelling had dwindled in seven days. NE turnover was significantly reduced seven days after injury and remained at a low level until eight weeks after injury. These results suggest that focal impairment of axonal transport due to diffuse brain injury causes cellular changes in LC and that the neurochemical effect of injury on the central noradrenargic system lasts over an extended period of time. Chronic suppression of NE turnover may explain the sustained behavioral and psychological abnormalities observed in a clinical situation.

Animals↗
PubMedDate not supplied

Trauma radiology: Part IV. Imaging of acute craniocerebral trauma.

Diagnostic imaging has a key role in diagnosis and management of patients sustaining craniocerebral injuries from trauma. We review the current role of skull radiography, computed tomography (CT), and magnetic resonance (MR) in imaging patients sustaining craniocerebral trauma, and we describe the appearance of major forms of pathology as depicted by each modality. CT scan is used to assess quickly the extent of injury and to triage patients to observation, medical, or neurosurgical management. CT findings can be divided into primary craniocerebral injuries, including skull fractures; extraaxial hematomas (subdural and epidural); intraparenchymal injury, such as hematoma, contusion, and diffuse axonal shearing; and intraventricular or subarachnoid hemorrhage. Secondary manifestations of injury, such as cerebral edema and herniation, are also identified, and their course can be followed by serial CT. CT is crucial in assessing the outcome of surgical intervention and in identifying potential delayed complications of either head trauma or surgical intervention, including infection, delayed hemorrhage, cerebral infarction, and tension pneumocephalus. In recent years, MRI has been shown to be valuable in diagnosing cerebral injury. MRI has generally been shown to have greater overall accuracy than CT in identifying and characterizing most forms of traumatic cerebral pathology, but it is less accurate at demonstrating subarachnoid hemorrhage acutely, pneumocephalus, and calvarial fractures, particularly those involving the skull base. Moreover, MRI is still more difficult to perform than CT in critically ill patients, and it is generally far more time-consuming. However, MRI is unequivocally more accurate than CT at revealing certain lesions, particularly brainstem contusion, diffuse axonal shearing, predominantly nonhemorrhagic contusions, and thin collections of blood adjacent to bone, and it should be used selectively when these injuries are suspected.

Craniocerebral Trauma↗
PubMed1996

Detection of acute pathologic changes following experimental traumatic brain injury using diffusion-weighted magnetic resonance imaging.

Standard magnetic resonance imaging (MRI) has been shown to be remarkably insensitive to acute changes following traumatic brain injury. Because diffusion-weighted MRI has recently demonstrated excellent sensitivity to acute ischemic injury and other CNS abnormalities, we evaluated the use of diffusion MRI for the detection of pathologic changes in the rat brain during the first hours following parasagittal fluid percussion brain injury. Diffusion MRI was able to demonstrate a significant diffusion decrease in the primary cortical contusion injury and a comparable decrease in the ipsilateral thalamus. Tissue damage in the thalamus region is much weaker than in the cortex, but the thalamus is a primary site of axonal and dendritic injury in this model. T2 imaging in the same subjects showed slight enhancement in the neighborhood of the injured cortex but was unable to demonstrate injury elsewhere. Diffusion imaging was superior to T2 at demonstrating injury and the prominent diffusion decrease in the thalamus suggests that diffusion MRI is preferentially sensitive to axonal or dendritic injury.

Animals↗
PubMed1991

Neurotrophic factors in regeneration.

Nerve growth factor, fibroblast growth factor, and ciliary neurotrophic factor can protect selected populations of neurons from some of the degenerative changes that otherwise follow axonal injury or other insults. The function of diffusible neurotrophic factors in axonal regeneration is still unclear, however. Knowledge of the nerve growth factor congeners, brain-derived neurotrophic factor and neurotrophin-3, is advancing rapidly as is the identification of neurotrophin receptors, several of which are membrane-bound tyrosine kinases.

Animals↗
PubMed1997

Numerical model for calculation of apparent diffusion coefficients (ADC) in permeable cylinders--comparison with measured ADC in spinal cord white matter.

We have implemented a numerical method for calculation of the apparent diffusion coefficient (ADC) in spinal cord injury, which takes into account the distribution of axon diameters and permeability found in spinal cord white matter, as well as relative axonal volume. We propose a procedure for determining the status of axonal integrity from measured ADC values. These methods have been applied to a well characterized rat spinal cord injury model, affording a prediction of the increase in axonal permeability which is presumed to be closely related to functional deficit. ADC values are compared to those calculated from analytical formulas in the literature, and possible factors underlying the ADC behavior are explored. Calculated results indicate both axonal swelling and cell membrane permeability to be important factors contributing to ADC in traumatic spinal cord injury.

Animals↗
PubMed2006

Differential sensitivity of in vivo and ex vivo diffusion tensor imaging to evolving optic nerve injury in mice with retinal ischemia.

Decreased axial (lambda(||)) and increased radial (lambda( perpendicular)) diffusivity have been shown to reflect axonal and myelin injury respectively. In the present study, evolving white matter injury within the optic nerves of mice with retinal ischemia was examined by in vivo and ex vivo measurements of lambda(||) and lambda( perpendicular). The results show that at 3 days after retinal ischemia, a 33% decrease in vivo and a 38% decrease ex vivo in lambda(||) without change in lambda( perpendicular) was observed in the injured optic nerve compared to the control, suggestive of axonal damage without myelin injury. At 14 days, both in vivo and ex vivo measured lambda( perpendicular) increased significantly to 220-240% of the control level in the injured optic nerve suggestive of myelin damage. In contrast, the axonal injury that was clearly detected in vivo as a significantly decreased lambda(||) (33% decrease) was not as clearly detected by ex vivo lambda(||) (17% decrease). The current findings suggest that ex vivo lambda( perpendicular) is comparable to in vivo lambda( perpendicular) in detecting myelin injury. However, the structural changes resulting from axonal damage causing the decreased in vivo lambda(||) may not be preserved ex vivo in the fixed tissues. Despite the accurate depiction of the pathology using lambda(||) and lambda( perpendicular) in vivo, the use of ex vivo lambda(||) to extrapolate the status of axonal injury in vivo would require further investigation.

Algorithms↗
PubMed2000

Proton MR spectroscopy in multiple sclerosis.

Axonal injury in multiple sclerosis (MS) is focal and diffuse, and is directly responsible for irreversible disability. Acute inflammatory events can be associated with reversible disability that may parallel reversible axonal injury. This in part accounts for the remission following relapses early in the disease. By the time there is clinical disability, substantial axonal injury already has occurred. This provides a strong rationale for the early limitation of inflammation and its consequences.

Aspartic Acid↗
PubMed1998

Focal brain injury and its effects on cerebral mantle, neurons, and fiber tracks.

Following a mild cortical impact injury delivered by a piston to the right sensorimotor cortex of the anesthetized rat, we evaluated mantle loss, neuronal changes, and fiber track degeneration by deOlmos silver stains up to 8 weeks after injury. Darkened neurons indicating damage (chromatolysis) occurred widely throughout both hemispheres and were seen from 1 h to 8 weeks after injury. This effect might have occurred from pressure wave damage from piston impact, brain displacement or deafferentation. Cerebral mantle loss was variable but fiber track degeneration related to projection and corticofugal descending tracks associated with the right sensorimotor system was rather constant. Unexpectedly, considerable fiber track degeneration occurred within the cerebellum, especially the inferior vermis. Cells directly under the piston face were surprisingly well-preserved but axon degeneration studies showed that these apparently intact neuronal cell bodies were surrounded by a dense network of degenerating fiber tracks. The intact cells, therefore, may have been functionally cut off from the rest of the brain owing to interruption of their efferents and afferents. The increased susceptibility of axons compared to cell bodies seen with this focal injury is similar to that observed with diffuse brain injury. The early appearing, severe and widespread axon damage we observed suggests that amelioration of focal traumatic brain injury will have to be directed promptly to the preservation of axons as well as cell bodies.

Animals↗
PubMed1998

Magnetic resonance spectroscopy of diffuse brain trauma in the pig.

The acute metabolic events linked to the evolution of selective axonal pathology in the white matter following diffuse brain injury have not previously been evaluated due to the paucity of relevant experimental models. Here, we utilized a new model of inertial brain injury in the pig that selectively damages axons in the white matter, and applied proton and phosphorous magnetic resonance spectroscopy (MRS) to noninvasively monitor the temporal course of metabolic changes following trauma. Evaluating four pigs with MRS prior to injury, within 1 h and 3 and 7 days postinjury, we found that widespread axonal injury was produced in the absence of changes in pH, PCr/Pi, or the concentrations of ATP, and lactate. However, we did observe an acute 60% loss of intracellular Mg2+ levels, which gradually resolved by 7 days postinjury. In addition, we found that the levels of the neuron marker, N-acetylaspartate (NAA), acutely dropped 20% and remained persistently decreased for at least 7 days postinjury. Moreover, the changes in Mg2+ and NAA were found with MRS in the absence of abnormalities with conventional magnetic resonance imaging (MRI). These results show that (1) profound alterations in intracellular metabolism occur acutely following diffuse axonal pathology in the white matter, but in the absence of indicators of ischemia, and (2) axonal pathology may be evaluated with high sensitivity utilizing noninvasive MRS techniques.

Adenosine Triphosphate↗
PubMed2000

Regional axonal loss in the corpus callosum correlates with cerebral white matter lesion volume and distribution in multiple sclerosis.

Previous imaging studies have suggested that there is substantial axonal loss in the normal-appearing white matter (NAWM) of brains from multiple sclerosis patients and that this axonal loss may be an important determinant of disability. Recently, substantial axonal loss in the NAWM has been confirmed directly in post-mortem tissue. Whether the NAWM changes occur as a consequence of damage to axons traversing lesions or to a more diffuse injury process is uncertain. Using formalin-fixed brains of eight multiple sclerosis patients and eight age-matched controls, we examined the relationship between demyelinating lesion load in three volumes of the cerebral white matter and the loss of axons in NAWM of the corresponding three projection regions (anterior, middle, posterior) in the corpus callosum (CC). There was a significant loss of calculated total number of axons crossing the CC in each of the three regions relative to the non-multiple sclerosis controls. Strong correlations were found between the regional lesion load and both the axonal density (r = -0.673, P: = 0.001) and the total estimated number of axons crossing the corresponding projection area in the CC (r = -0. 656, P: = 0.001) for the patients. This suggests that Wallerian degeneration of axons transected in the demyelinating lesions makes a major contribution to the substantial, diffuse loss of axons in the NAWM in multiple sclerosis. These findings emphasize the need to consider the consequences of multiple sclerosis lesions in terms of both local and distant effects in functionally connected regions of the brain.

Adult↗
PubMed2006

Possible axonal regrowth in late recovery from the minimally conscious state.

We used diffusion tensor imaging (DTI) to study 2 patients with traumatic brain injury. The first patient recovered reliable expressive language after 19 years in a minimally conscious state (MCS); the second had remained in MCS for 6 years. Comparison of white matter integrity in the patients and 20 normal subjects using histograms of apparent diffusion constants and diffusion anisotropy identified widespread altered diffusivity and decreased anisotropy in the damaged white matter. These findings remained unchanged over an 18-month interval between 2 studies in the first patient. In addition, in this patient, we identified large, bilateral regions of posterior white matter with significantly increased anisotropy that reduced over 18 months. In contrast, notable increases in anisotropy within the midline cerebellar white matter in the second study correlated with marked clinical improvements in motor functions. This finding was further correlated with an increase in resting metabolism measured by PET in this subregion. Aberrant white matter structures were evident in the second patient's DTI images but were not clinically correlated. We propose that axonal regrowth may underlie these findings and provide a biological mechanism for late recovery. Our results are discussed in the context of recent experimental studies that support this inference.

Adolescent↗
PubMed2001

Future applications of DWI in MS.

Diffusion imaging is a noninvasive technique for measuring the movement of water molecules. Although it has had its greatest impact thus far in the area of stroke imaging, the information garnered from diffusion experiments can provide an indication of myelin injury and perhaps axonal integrity. In this paper, we describe some current and potential future applications of diffusion imaging in multiple sclerosis. These include the use of global indices such as diffusion trace and anisotropy, as well as implementation of axonal fiber tracking methodologies for assessment of axonal integrity and connectivity between cortical regions.

Diffusion↗
PubMed2005

Demyelination increases radial diffusivity in corpus callosum of mouse brain.

Myelin damage, as seen in multiple sclerosis (MS) and other demyelinating diseases, impairs axonal conduction and can also be associated with axonal degeneration. Accurate assessments of these conditions may be highly beneficial in evaluating and selecting therapeutic strategies for patient management. Recently, an analytical approach examining diffusion tensor imaging (DTI) derived parameters has been proposed to assess the extent of axonal damage, demyelination, or both. The current study uses the well-characterized cuprizone model of experimental demyelination and remyelination of corpus callosum in mouse brain to evaluate the ability of DTI parameters to detect the progression of myelin degeneration and regeneration. Our results demonstrate that the extent of increased radial diffusivity reflects the severity of demyelination in corpus callosum of mouse brain affected by cuprizone treatment. Subsequently, radial diffusivity decreases with the progression of remyelination. Furthermore, radial diffusivity changes were specific to the time course of changes in myelin integrity as distinct from axonal injury, which was detected by betaAPP immunostaining and shown to be most extensive prior to demyelination. Radial diffusivity offers a specific assessment of demyelination and remyelination, as distinct from acute axonal damage.

Algorithms↗
PubMed1990

[Symptoms of disconnection of cerebral hemispheres and brain stem in severe cranio-cerebral injuries].

Based on an analysis of 56 cases with diffuse axonal lesions the authors describe symptoms of dissociation of the brain hemispheres and brain stem. Such symptoms occur on transformation of long coma to a steady or transitory vegetative state and are characterized by chaotic activation of the subcortical and stem formations remaining intact and dynamic manifestation of a complex of postural and generalized motor reactions, complex pathological reflexes, oral, oculomotor, pupillary and cerebrospinal automatisms, paroxysmal vegeto-visceral abnormalities along with functional silence of the cortex.

Adolescent↗
PubMedDate not supplied

Diffusion-weighted imaging of acute corticospinal tract injury preceding Wallerian degeneration in the maturing human brain.

BACKGROUND AND PURPOSE: Wallerian degeneration, the secondary degeneration of axons from cortical and subcortical injury, is associated with poor neurologic outcome. Since diffusion-weighted (DW) imaging is sensitive to early changes of cytotoxic edema, DW imaging may depict the acute injury to descending white matter tracts that precedes Wallerian degeneration; this injury is not visible on conventional CT or MR images in the maturing human brain. METHODS: Two neuroradiologists retrospectively analyzed clinical MR images in six children (aged 3 days to 5 months) with DW findings consistent with acute injury of the descending white matter tract due to territorial anterior or middle cerebral artery infarction. In five patients, images were obtained as a part of routine clinical evaluation. The remaining patient was a part of a prospective study of brain injury. Imaging findings were correlated with clinical outcomes. RESULTS: In all six patients, DW imaging performed 2-8 days after the onset of ischemia depicted injury to the descending white matter tract ipsilateral to the territorial infarct. Conventional MR images of the ipsilateral descending white matter tracts were abnormal in three patients. In all five patients for which follow-up results were available, the presence of DW changes was correlated with persistent neurologic disability. CONCLUSION: As shown in this retrospective analysis, DW imaging can depict acute injury to the descending white matter tract in neonates and infants, when conventional MR imaging may show normal findings. These DW findings likely precede the development of Wallerian degeneration, and they may portend a poor clinical outcome.

Acute Disease↗