Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Diffuse Axonal Injury”

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

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

At least 685 records · Page 38Linked to original sources
PubMed1994

Electrophysiologic assessment of intracerebral contusions in closed head injury.

To determine whether intracerebral contusions should be evacuated in severe closed head injuries, patients with Glasgow Coma Scale scores < or = 8 and with radiologic evidence of midline shift on computed tomography admitted from 1987 through 1993 to our intensive care unit were monitored with median nerve somatosensory evoked potentials (SSEPs). A total of 44 patients and 84 hemispheres were included in the study. Initial SSEPs, calculated by a quantitative peak-peak amplitude method, were not significantly different between hemispheres that contained localized contusions > or = 2.5 cm, those that had evidence of diffuse injury or punctate lesions < 2.5 cm not considered suitable for surgical evacuation, and those without evidence of parenchymal hemorrhage (mean 14.64 microV, p = 0.43). The SSEPs deteriorated 41.2% from initial baseline levels in diffusely injured and 22.6% in contused hemispheres, whereas in normal-appearing hemispheres, SSEPs improved 51.1% (p = 0.01). The difference in SSEPs, however, was not significant between the contused and diffusely injured hemispheres. The results suggest that in severe closed head injury, cerebral hemispheres without radiologic evidence of structural damage have a high likelihood of improving after initial impact injury. Furthermore, hemispheres with localized contusions showed no more deterioration than those with more diffuse injury, implying that hemispheric electrical deterioration is not related to size of localized contusions but rather to underlying axonal damage. This indicates that surgical evacuation of localized contusions unless accompanied by mass effect is probably not warranted.

Adolescent↗
PubMed2006

Chronic progressive external ophthalmoplegia: MR spectroscopy and MR diffusion studies in the brain.

OBJECTIVE: The purpose of our study was to show how, despite pathognomonic signs of cerebral involvement in chronic progressive external ophthalmoplegia (CPEO), mitochondrial respiratory chain insufficiency is associated with increased lactate and reduced N-acetylaspartate. CPEO and mitochondrial myopathy are caused by mitochondrial DNA mutations leading to impaired oxidative phosphorylation. Cortical and subcortical metabolites, cerebral diffusivity, and structural MRI were assessed to characterize possible subclinical cerebral pathology in CPEO. SUBJECTS AND METHODS: Ten patients with CPEO (n = 8), mitochondrial myopathy (n = 1), and Kearns-Sayre syndrome (n = 1) and 13 control group volunteers were studied by MRI, both long TE (144) proton MR spectroscopic imaging (1H MRSI), and diffusion-weighted imaging. Relative concentrations of N-acetylaspartate, choline, creatine, and lactate were estimated by Linear Combination of Model Spectra (LCModel) in healthy-appearing white matter, gray matter, and white matter hyperintensities. RESULTS: Of five patients with cortical atrophy, it was moderate in three and severe in two. One patient had severe and four had moderate cerebellar atrophy. Six of 10 patients showed unspecific white matter lesions, whereas the remainder had hyperintensities in the pyramidal tract (n =2) and middle cerebellar peduncle (n = 1) despite clinical signs. No basal ganglia lesions were found. Physiologic metabolite ratios were normal and lactate was absent in supratentorial healthy-appearing cortex and subcortical white matter. Global diffusion histogram metrics revealed no abnormalities. CONCLUSION: Normal spectroscopic imaging in radiologic unaffected brain and healthy global brain parenchymal diffusion findings do not support the hypothesis of a generalized cerebral energy loss in CPEO. Bilateral structural alteration of central motor pathways in two patients without clinical pyramidal signs may, however, reflect subclinical axonal injury in predilection sites in some patients.

Adult↗
PubMed2001

[A study on pathological changes of closed diffuse brain injury in rats with H.E., esterification-silver stain and albumin immunohistochemical stain].

OBJECTIVE: To observed the pathological changes of closed diffuse brain injury in the rats died immediately and 15 min to 5 days after the injury. METHODS: H.E. staind and esterification-silver stain were applied to investigate the closed diffuse brain injury. RESULTS: In rats died immediately after the concussive injury, a number of shrunken neurons(type I change), distended neurons(type II change) and wave-like nerve fibers were identified in the brain tissue, especially in brain-stem. At 2 h and 8 h after injury, brain edema and axonal swelling appeared clearly in the cortex and white matter, especially in brain-stem. At post-traumatic 8 h and 24 h, the axonal retraction balls began to appear. The amount of neurons undergoing type I and II changes and constraction balls increased along with the survivor time. After 4 days and 5 days, brain edema alleviated, but the retraction balls and axonal swelling still existed. With Esterifica-tion silver stain, the above changes of neurons and nerve fibers were more obvious. With ABC stain, the distribution of albumin(Al) was extended from the perio-vascular area to diffuse distribution. Al positive staining were more obvious in injuried neurons and nerve fibers. CONCLUSION: The distribution of the concussive damage in the brain are coup, contra-coup and centripental.

Albumins↗
PubMed2002

Focal application of neutralizing antibodies to soluble neurotrophic factors reduces collateral axonal branching after peripheral nerve lesion.

A major reason for the insufficient recovery of function after motor nerve injury are the numerous axonal branches which often re-innervate muscles with completely different functions. We hypothesized that a neutralization of diffusable neurotrophic factors at the lesion site in rats could reduce the branching of transected axons. Following analysis of local protein expression by immunocytochemistry and by in situ hybridization, we transected the facial nerve trunk of adult rats and inserted both ends into a silicon tube containing (i) collagen gel with neutralizing concentrations of antibodies to NGF, BDNF, bFGF, IGF-I, CNTF and GDNF; (ii) five-fold higher concentrations of the antibodies and (iii) combination of antibodies. Two months later, retrograde labelling was used to estimate the portion of motoneurons the axons of which had branched and projected into three major branches of the facial trunk. After control entubulation in collagen gel containing non-immune mouse IgG 85% of all motoneurons projecting along the zygomatic branch sprouted and sent at least one twin axon to the buccal and/or marginal-mandibular branches of the facial nerve. Neutralizing concentrations of anti-NGF, anti-BDNF and anti-IGF-I significantly reduced sprouting. The most pronounced effect was achieved after application of anti-BDNF, which reduced the portion of branched neurons to 18%. All effects after a single application of antibodies were concentration-dependent and superior to those observed after combined treatment. This first report on improved quality of reinnervation by antibody-therapy implies that, in rats, the post-transectional collateral axonal branching can be reduced without obvious harmful effects on neuronal survival and axonal elongation.

Animals↗
PubMed2004

The "dark side" of endocannabinoids: a neurotoxic role for anandamide.

Endocannabinoids, including 2-arachidonoylglycerol and anandamide (N-arachidonoylethanolamine; AEA), have neuroprotective effects in the brain through actions at CB1 receptors. However, AEA also binds to vanilloid (VR1) receptors and induces cell death in several cell lines. Here we show that anandamide causes neuronal cell death in vitro and exacerbates cell loss caused by stretch-induced axonal injury or trophic withdrawal in rat primary neuronal cultures. Administered intracerebroventricularly, AEA causes sustained cerebral edema, as reflected by diffusion-weighted magnetic resonance imaging, regional cell loss, and impairment in long-term cognitive function. These effects are mediated, in part, through VR1 as well as through calpain-dependent mechanisms, but not through CB1 receptors or caspases. Central administration of AEA also significantly upregulates genes involved in pro-inflammatory/microglial-related responses. Thus, anandamide produces neurotoxic effects both in vitro and in vivo through multiple mechanisms independent of the CB1 receptor.

Animals↗
PubMed1984

Primary brain trauma in non-accidental injury.

The brains from 12 babies up to 21/2 years of age, who died after repeated non-accidental injury to the head, were subjected to detailed neuropathological examination. The nine brains from infants under 5 months showed contusional tears--slit like lesions in the white matter surrounded by astrocytes and associated with evidence of old and recent haemorrhage. The three brains from infants over 5 months showed white matter lesions similar to those seen in adults after closed head injury, including damage in the dorsolateral quadrant of the brain stem without axonal hemispheric damage, which may have been a result of whiplash injury after shaking. In addition, all the brains examined showed diffuse gliosis. This paper draws attention to contusional tears and other white matter lesions, which the authors believe are manifestations of mechanical damage produced by trauma. The long term neurological and intellectual defects observed in patients suffering non-accidental injury early in life are increasingly being recognised, although it is difficult to identify the extent to which these are due to social or neuropathological factors. We suggest that the white matter damage we describe has an important role.

Brain Injuries↗
PubMed1986

Extensive intraneuronal spread of horseradish peroxidase from a focus of vasogenic edema into remote areas of central nervous system. Observations on mouse central nervous system subjected to cortical cold injury.

A study was made of the uptake of horseradish peroxidase (HRP) into neurons from a cryogenic cortical lesion in the mouse brain associated with vasogenic edema, following intravenous administration of the tracer. Particular emphasis was placed on the axonal spread of HRP from the primary lesion to other areas of the central nervous system. The distribution of HRP was studied by light microscopy, using highly sensitive histochemical methods, 3-144 h after the onset of the injury. Extravasated HRP was taken up into nerve cell bodies in and around the primary lesion, forming different patterns of labelling: (1) granular, (2) diffuse, and (3) a combination of granular and diffuse staining. Granularity is considered to be the result of HRP accumulation in lysosomes occurring in undamaged or slightly damaged nerve cells, whereas the diffuse, non-granular pattern presumably occurs in severely damaged neurons. Nerve cell bodies containing HRP reaction product were also found in the contralateral cortex, ipsilateral thalamus, substantia nigra, amygdala and ventral tegmental area, presumably a consequence of retrograde axonal transport of the tracer from the primary injury. HRP-containing axons were present in the corpus callosum and in the pyramidal tract of the injured hemisphere all the way down to the cervical spinal cord. Labelling of axonal terminals and preterminal axons in the ipsilateral thalamus, entopeduncular nucleus, subthalamic nucleus, substantia nigra and pons indicated anterograde transport of HRP to these regions. Thus very extensive intraneuronal spread of a macromolecular edema component takes place from a primary focal brain lesion to areas located far away from but neuroanatomically connected to this injured region. The brain thus seems to be affected by focal vasogenic edema in many more ways than are recognized at present.

Animals↗
PubMed2004

Alzheimer's pathology in human temporal cortex surgically excised after severe brain injury.

Traumatic brain injury (TBI) is a risk factor for the development of Alzheimer's disease (AD). This immunohistochemical study determined the extent of AD-related changes in temporal cortex resected from individuals treated surgically for severe TBI. Antisera generated against Abeta species (total Abeta, Abeta(1-42), and Abeta(1-40)), the C-terminal of the Abeta precursor protein (APP), apolipoprotein E (apoE), and markers of neuron structure and degeneration (tau, ubiquitin, alpha-, beta-, and gamma-synuclein) were used to examine the extent of Abeta plaque deposition and neurodegenerative changes in 18 TBI subjects (ages 18-64 years). Diffuse cortical Abeta deposits were observed in one third of subjects (aged 35-62 years) as early as 2 h after injury, with only one (35-year old) individual exhibiting "mature", dense-cored plaques. Plaque-like deposits, neurons, glia, and axonal changes were also immunostained with APP and apoE antibodies. In plaque-positive cases, the only statistically significant change in cellular immunostaining was increased neuronal APP (P = 0.013). There was no significant correlation between the distribution of Abeta plaques and markers of neuronal degeneration. Diffuse tau immunostaining was localized to neuronal cell soma, axons or glial cells in a larger subset of individuals. Tau-positive, neurofibrillary tangle (NFT)-like changes were detected in only two subjects, both of more advanced age and who were without Abeta deposits. Other neurodegenerative changes, evidenced by ubiquitin- and synuclein-immunoreactive neurons, were abundant in the majority of cases. Our results demonstrate a differential distribution and course of intra- and extra-cellular AD-like changes during the acute phase following severe TBI in humans. Abeta plaques and early evidence of neuronal degenerative changes can develop rapidly after TBI, while fully developed NFTs most likely result from more chronic disease- or injury-related processes. These observations lend further support to the hypothesis that head trauma significantly increases the risk of developing pathological and clinical symptoms of AD, and provide insight into the molecular mechanisms that initiate these pathological cascades very early during severe brain injury.

Adolescent↗
PubMed2003

Redistribution of neurofilaments and accumulation of beta-amyloid protein after brain injury by rotational acceleration of the head.

Rotational acceleration of the head, as occurs in falls, car crashes, and sport injuries, may result in diffuse brain damage, with acute and chronic neurological and psychiatric symptoms. The present study addresses the effects of rotational trauma on the neuronal cytoskeleton, which stabilizes perikaryal, dendritic and axonal shape and function. The study focuses upon the distribution of (1) the phosphorylated form of the heavy neurofilament subunit, (2) the light neurofilament subunit, and (3) beta-amyloid, a marker for brain injury. While normally restricted to axons, the phosphorylated heavy neurofilament subunits were drastically decreased in the axons after rotational trauma. Instead, they accumulated in the neuronal perikarya, normally devoid of the phosphorylated subunit. This alteration was seen, not only in the cerebral cortex, but also in the hippocampus, the cervical spinal cord, the cerebellum, the cranial nerves and the pyramidal tract. The distribution of the light subunit of neurofilaments was also altered post trauma. Only a weak beta-amyloid immunoreactivity was detected in the brains of control animals. Promptly after the trauma, a large number of beta-amyloid positive neurons appeared. Intensely co-localized immunoreactivity for the light subunit of neurofilaments and of beta-amyloid was seen 3 days after the rotational trauma axons of in the subcortical white matter and in the granule cell layer of the dentate gyrus as well as in neurons of the hypoglossal nucleus. The reported alterations in the central nervous system neurons are similar to those in the human brain after closed head injury and in chronic degenerative diseases. Regions of importance for social behavior, memory and body movement were affected.

Acceleration↗
PubMed1999

Accumulation of amyloid beta and tau and the formation of neurofilament inclusions following diffuse brain injury in the pig.

Brain trauma in humans increases the risk for developing Alzheimer disease (AD) and may induce the acute formation of AD-like plaques containing amyloid beta (A beta). To further explore the potential link between brain trauma and neurodegeneration, we conducted neuropathological studies using a pig model of diffuse brain injury. Brain injury was induced in anesthetized animals via nonimpact head rotational acceleration of 110 degrees over 20 ms in the coronal plane (n = 15 injured, n = 3 noninjured). At 1, 3, 7, and 10 days post-trauma, control and injured animals were euthanized and immunohistochemical analysis was performed on brain sections using antibodies specific for A beta, beta-amyloid precursor protein (betaPP), tau, and neurofilament (NF) proteins. In addition to diffuse axonal pathology, we detected accumulation of A beta and tau that colocalized with immunoreactive betaPP and NF in damaged axons throughout the white matter in all injured animals at 3-10 days post-trauma. In a subset of brain injured animals, diffuse A beta-containing plaque-like profiles were found in both the gray and white matter, and accumulations of tau and NF rich inclusions were observed in neuronal perikarya. These results show that this pig model of diffuse brain injury is characterized by accumulations of proteins that also form pathological aggregates in AD and related neurodegenerative diseases.

Amyloid beta-Peptides↗
PubMed2006

Differential RIP antigen (CNPase) expression in peripheral ensheathing glia.

The RIP monoclonal antibody is commonly used to identify oligodendrocytes. Recently, the RIP antigen was identified as 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase), a known non-compact myelin protein [Watanabe, M., Sakurai, Y., Ichinose, T., Aikawa, Y., Kotani, M., Itoh, K., 2006. Monoclonal antibody Rip specifically recognizes 2',3'-cyclic nucleotide 3'-phosphodiesterase in oligodendrocytes. J. Neurosci. Res. 84, 525-533]. In the present study we characterize normal and axotomy-induced changes in RIP immunoreactivity in peripheral glia. In myelinating Schwann cells, RIP demarcated paranodal regions of myelinated axons and clearly defined Schmidt-Lantermann incisures. Surprisingly, RIP immunoreactivity was not confined to myelinating glia. Robust RIP immunoreactivity was present in Remak bundles in mixed nerves and in sympathetic ganglia and grey rami. Following peripheral nerve injury, RIP immunoreactivity was redistributed diffusely throughout de-differentiating Schwann cell cytoplasm. In uninjured rats, low levels of RIP immunoreactivity were detectable in satellite cells surrounding dorsal root ganglion (DRG) neurons and in terminal Schwann cells at neuromuscular junctions. This pattern suggested a correlation between RIP immunoreactivity and the amount of axon-glial contact. We therefore injured the L5 spinal nerve to induce sympathetic sprouting and pericellular basket formation in the DRG, and asked whether relatively RIP-negative satellite glia, which normally contact only neuronal somata, would upregulate the RIP antigen upon contact with sprouting sympathetic axons. All perineuronal sympathetic sprouts infiltrated heavily RIP-immunoreactive satellite cell sheaths. RIP immunoreactivity was absent from placode-derived olfactory ensheathing glia, indicating that the relationship between axon-glial contact and RIP-immunoreactivity is restricted to peripheral ensheathing glia of the neural crest-derived Schwann cell lineage.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed2005

Detecting axon damage in spinal cord from a mouse model of multiple sclerosis.

In the current study, the feasibility and reproducibility of in vivo diffusion tensor imaging (DTI) of the spinal cord in normal mice are illustrated followed by its application to mice with experimental allergic encephalomyelitis (EAE) to detect and differentiate axon and myelin damage. Axial diffusivity, describing water movement along the axonal fiber tract, in all regions of spinal cord white matter from EAE-affected C57BL/6 mice was significantly decreased compared to normal mice, whereas there was no statistically significant change in radial diffusivity, describing water movement across the fiber tract. Furthermore, a direct comparison between DTI and histology from a single mouse demonstrated a decrease in axial diffusivity that was supported by widespread staining of antibody against beta-amyloid precursor protein. Regionally elevated radial diffusivity corresponded with locally diminished Luxol fast blue staining in the same tissue from the EAE mouse cord. Our findings suggest that axonal damage is more widespread than myelin damage in the spinal cord white matter of mice with EAE and that in vivo DTI may provide a sensitive and specific measure of white matter injury.

Animals↗
PubMed1991

Distribution of traumatic lesions of corpus callosum in "inner cerebral trauma".

This study deals with the topographic distribution of traumatic lesions in the corpus callosum within the pattern of "inner cerebral trauma". Material for neuropathological investigations consisted of 49 brains of patients who suffered closed head injury of the acceleration type with linear translation of acceleration acting along the longer axis of the head. As a control, 5 brains were investigated in which the direction of linear translation was latero-lateral. The patients were divided into 4 groups according to reconstruction of the traumatic event and ascertaining of the direction of the linear translation of acceleration: (1) Medial blow (antero-posterior and postero-anterior), (2) Semioblique left blow (frontal left-occipital right and occipital right-frontal left), (3) Semioblique right blow (frontal right-occipital left and occipital left-frontal right), (4) Vertex-base direction. Fornix and septum pellucidum, as anatomically adjacent structures were also investigated. The results showed that the lesions in the corpus callosum were related to the pattern of "inner cerebral trauma" (ICT) (Grcević 1982), and the biomechanical conditions originally proposed by Lindenberg. These investigations, carried out on a representative material of 54 brains and by subserial histological analysis of the entire corpus callosum, produced a new evidence for our previous preliminary observations about the correlation of the shape and distribution of the periaxial lesions of the pattern of "inner cerebral trauma" and direction of the linear translation of accelerating forces. Our present investigations showed a striking congruence between the pattern of lesions within the corpus callosum in such type of cerebral trauma and the course of linear translation of acceleration. Furthermore, this study proved the importance of topographic interpretation of lesions in the corpus callosum in vivo i.e. by the CT and MRI examinations, because they may serve as a significant information for reconstruction of the biomechanical conditions of the injury which can be of importance for early therapeutical strategy and forensic interpretations of the accident. By using silver impregnation-techniques for histopathological study of the corpus callosum, we could confirm our previously expressed concept on "focalized" and not "diffuse" axonal injures in ICT (Grcević 1988). In this study corpus callosum served as a representative anatomical structure for axonal studies showing that axonal lesions strictly follow the pattern of tissue lesions with definite focal principle.

Acceleration↗
PubMed1985

[Pure shearing injury--clinical signs and symptoms, diagnosis, prognosis and review of the literature].

In some of the brains of head injury, shearing of axons and vessels caused by direct impact is seen widely in the white matter. This type of injury is designated by neuropathologists as shear injury or diffuse damage of impact type. Macroscopic lesions adjacent to the superior cerebeller peduncle and lesions of the corpus callosum are commonly seen in the brains with severe shearing injuries and the former is detected by CT scan as a high density at the quadrigeminal cistern, and this indicates occurrence of a severe shearing injury. Among 600 patients with head injuries, we managed 23 cases with pure shearing injury. These cases are classified into three groups according to the duration of coma. In the fulminant type (7 cases) the patients had severe brainstem signs including impairment of vital signs and died immediately after the injury. In the severe type (8 cases) the patients were decerebrated with normal pupillary response on admission and were severely disabled (i.e. tremor, truncal ataxia, dementia). In the moderate type (8 cases), the patients had only disturbance of consciousness for a long period, and recovered almost to the pre-injury state. Follow-up CT scan showed enlargement of the ventricles and sulci.

Adolescent↗
PubMedDate not supplied

Chemoattraction of sensory neuron growth cones by diffusible concentration gradients of acetylcholine.

Axon guidance cues are critical for the development and repair of both the central and peripheral nervous systems. These cues serve to help select the pathways taken by axon growth cones, by attracting or repulsing them. During development and following injury to the adult peripheral nervous system, neurons must extend processes, often over long distances, through a variety of cellular environments composed of innervated and uninnervated cells, to find, recognize, and synapse on their appropriate targets. The responsibility for recognizing and responding to the extensive number of cues that are encountered as axons elongate falls on the growth cones at the tip of the elongating axons. Cajal (1928) proposed that denervated target cells release diffusible factors that assist in orienting the direction of out-growth of peripheral axons. However, it is only relatively recently that experiments to identify the molecules responsible for serving this function, and the molecular mechanisms by which they function, have begun to bear fruit. Gradients of both substrate-bound and diffusible factors have now been shown to play critical roles in directing axon outgrowth. The present experiments were aimed at determining whether the neurotransmitter acetylcholine (ACh) can act as a chemoattractant for adult sensory neuron growth cones.

Acetylcholine↗
PubMed1987

White matter damage following acute head injury.

The study of a series of brains from patients who had a severe head injury and died within 72 h without a lucid interval showed that there was a step-wise progression in the development of retraction balls. At 2 h after injury sinusoidal enlargement of the axons was evident. This progressed over 16 h when the lesions appeared as retraction balls which were fully developed at 72 h. There was a similar increase of staining with an immunoperoxidase method for glial fibrillary acid protein (GFAP) initially around blood vessels spreading diffusely into the white matter. The number of reactive astrocytes also increased. In a control case where the corpus callosum was torn at post-mortem there were sinusoidally distended and torn axons in the absence of GFAP staining. It is proposed that there are three components to a head injury. First, mechanical injury as seen in the control case; second, the development of retraction balls which are an active process probably representing damaged axons which cannot undergo repair where the sinusoidal swellings develop into retraction balls and third, an astrocytic reaction. The sinusoidal change, when present on its own, may not be separable from post-mortem trauma. However, when it is associated with an astrocytic response it should be correlated with coma in the same way as retraction balls.

Axons↗
PubMed2006

The fate of axons subjected to traumatic ultrastructural (neurofilament) compaction: an electron-microscopic study.

By means of a new head-injury apparatus, a 0.75-mm-deep depression was produced momentarily at a predetermined site of the rat calvaria. This immediately evoked ultrastructural (neurofilament) compaction in many myelinated axon segments in layers IV and V of the neocortex under the impact site. The affected axon segments run quasi-parallel to the brain surface in a diffuse distribution among normal axons. Other kinds of damage to the brain tissue were insignificant; the conditions were therefore favorable for investigation of the fate of the compacted axons. Quantitative analysis of the findings on groups of ten rats that were sacrificed either immediately after the head injury or following a 1 day or a 1 week survival period showed that around 50% of the compacted axons recovered in 1 day, and a further less than 10% did so in 1 week. Electron microscopy revealed that the non-recovering compacted axons underwent a sequence of degenerative morphological changes including homogenization, fragmentation and resorption of the fragments. However, the myelin sheaths around these degenerating axons remained apparently unchanged even in the long-surviving rats, and hardly any phagocytotic cells were encountered. On the other hand, many such myelin sheaths contained axolemma-bound, normal-looking axoplasm besides the above morphological signs of axon-degeneration. It is concluded that the non-recovering compacted axons undergo an uncommon (non-Wallerian) kind of degeneration, which is mostly reversible.

Animals↗
PubMed1982

Uptake of macromolecules into neurons from a focal vasogenic cerebral edema and subsequent axonal spread to other brain regions. A preliminary study in the mouse with horseradish peroxidase as a tracer.

Intravenously (i.v.) injected horseradish peroxidase (HRP) which has leaked out of the vessels in a cryogenic cortical injury of adult mice is taken up into a large number of neurons resulting in two different forms of labeling. Diffuse neuronal labeling of the type previously reported in many conditions with vasogenic brain edema occurred particularly within the primary lesion. The other and more frequent type, here called granular neuronal labeling, was present in a wide zone immediately outside the injury. Such neurons contained HRP in numerous cytoplasmic granules and had the same characteristics as normal neurons accumulating HRP after retrograde axonal transport. By using highly sensitive histochemical methods for demonstration of HRP we could also follow bundles of labeled axons out from the primary lesion. Some of them passed the corpus callosum to the fronto-parietal cortex of the contralateral hemisphere. With this report we would like to put emphasize on certain phenomena occurring in neurons which previously have not been particularly recognized in studies on vasogenic brain edema. It can be assumed that in a focal brain lesion components from the edematous fluid and other "would substances" can be taken up into nerve cell processes and then be intracellularly transported in different directions. In this way, nerve cell populations located in other brain areas and even in the contralateral hemisphere may be influenced by components from the primary injury.

Animals↗