OBJECTIVE: Wallerian degeneration (WD) is a well-known process after nerve injury. In this study, occurrence of remote intramedullary signal changes, consistent with WD, and its correlation with clinical and neurophysiological impairment were assessed after traumatic spinal cord injury (tSCI).
METHODS: In 35 patients with tSCI, WD was evaluated by two radiologists on T2-weighted images of serial routine MRI examinations of the cervical spine. Dorsal column (DC), lateral corticospinal tract (CS), and lateral spinothalamic tract (ST) were the analyzed anatomical regions. Impairment scoring according to the American Spinal Injury Association Impairment Scale (AIS, A-D) as well as a scoring system (0-4 points) for motor evoked potential (MEP) and sensory evoked potential (SEP) was included. Mann-Whitney U test was used to test for differences.
RESULTS: WD in the DC occurred in 71.4% (n = 25), in the CS in 57.1% (n = 20), and in 37.1% (n = 13) in the ST. With WD present, AIS grades were worse for all tracts. DC: median AIS B vs D, p < 0.001; CS: B vs D, p = 0.016; and ST: B vs D, p = 0.015. More pathological MEP scores correlated with WD in the DC (median score 0 vs 3, p < 0.001) and in the CS (0 vs 2, p = 0.032). SEP scores were lower with WD in the DC only (1 vs 2, p = 0.031).
CONCLUSIONS: WD can be detected on T2-weighted scans in the majority of cervical spinal cord injury patients and should be considered as a direct effect of the trauma. When observed, it is associated with higher degree of impairment.
CONCLUSIONS: • Wallerian degeneration is commonly seen in routine MRI after traumatic spinal cord injury. • Wallerian degeneration is visible in the anatomical regions of the dorsal column, the lateral corticospinal tract, and the lateral spinothalamic tract. • Presence of Wallerian degeneration is associated with higher degree of impairment.

Autonomous mechanisms of axon degeneration are frequently studied in vitro by mechanical axon injury of isolated sensory neurons. This has led to major advances in understanding the molecular pathways governing axon degeneration. However, this approach does not pay attention to potential glial mechanisms for the regulation of axon death. Here, I describe a straightforward protocol to seed purified rat Schwann cells on neuronal cultures in order to study the interaction between axons and these glia during axon degeneration.

Aflatoxins are mycotoxins produced by Aspergillus spp. which is a common contaminant of food items such as corn, spices, rice, nuts, and flour. Aflatoxin contamination of foods is a worldwide problem. Chronic aflatoxin exposure is found to be associated with Sciatic nerve damage. In vivo study was carried out to evaluate the toxic effect of aflatoxin B1 (AFB1) on the Sciatic nerve. Twenty-one adult male rats were included and divided equally into 3 groups (7 rats each): Group I (control group), group II (olive oil group) and group III: (AflatoxinB1 group). The rats received AFB1 (250 μg/kg B.W./day) orally by gastric tube 5 days/week for 4 weeks. Sciatic nerve specimens were prepared, and semi-thin sections were stained with Toluidine blue, examined by light microscope and photographed. Ultrathin sections (50-80 nm) from selected areas of the trimmed blocks were made, examined and photographed by transmission electron microscopy (JEOL-JSM-1011) in King Saud University Electron Microscopy Unit. The findings indicate that the administration of AFB1 to rats\' results in degeneration in the sciatic nerve in the form of Wallerian degeneration in the myelin sheath. Macrophages appear to engulf the degenerated myelin and neutrophils.

Inflammatory-like changes in the white matter (WM) are commonly observed in conditions of axonal degeneration by different etiologies. This study is a systematic comparison of the principal features of the inflammatory-like changes in the WM in different pathological conditions characterized by axonal damage/degeneration, focusing in particular on Multiple Sclerosis (MS) normal-appearing white matter (NAWM) compared to non immune-mediated disorders. The study was performed on sections of NAWM from 15 MS cases, 11 cases of non immune-mediated disorders with wallerian axonal degeneration (stroke, trauma, amyotrophic lateral sclerosis), 3 cases of viral encephalitis, 6 control cases. Common features of the inflammatory-like changes observed in all of the conditions of WM pathology were diffuse endothelial expression of VCAM-1, microglial activation with expression of M2 markers, increased expression of sphingosine receptors. Inflammation in MS NAWM was characterized, compared to non immune-mediated conditions, by higher VCAM-1 expression, higher density of perivascular lymphocytes, focal perivascular inflammation with microglial expression of M1 markers, ongoing acute axonal damage correlating with VCAM-1 expression but not with microglia activation. Inflammatory changes in MS NAWM share all the main features observed in the WM in non immune-mediated conditions with wallerian axonal degeneration (with differences to a large extent more quantitative than qualitative), but with superimposition of disease-specific perivascular inflammation and ongoing acute axonal damage.

Radiosurgery by Gamma Knife (GK) is an effective treatment for brain arteriovenous malformations (AVM). The aim of the present study was to evaluate late, radiation-induced changes detectable by MRI after AVM radiosurgery in patients treated minimally 10 years prior, with AVM obliteration proven by angiography.
Thirty-five patients with 37 AVMs were included. AVMs were irradiated 16.6 ± 3.5 years prior with AVM obliteration proven 13 ± 4 years prior. All patients underwent recent MRI examinations, including application of gadolinium-based contrast.
In one case, post-irradiative cystic formation with mass effect and signs of hemorrhage requiring surgery was found. Post-gadolinium enhancement at the site of obliterated nidi was apparent in 28 of 37 cases (76 %). In all cases except one, the mean volume of enhancement at the time of review was clearly lower than the volume of the originally irradiated AVM (88 ± 20 %; median 92 %); in one case the extent was 142 % greater than the irradiated AVM. When we compared enhancing and non-enhancing nidi, we found that enhancing nidi were significantly larger than non-enhancing nidi at the time of radiosurgery (4.39 ± 3.35 cc vs. 0.89 ± 0.79 cc, p = 0.004). Enhancement was not influenced by total radiation dose, patient age at the time of irradiation, duration since radiosurgery, or the number of irradiations. Wallerian degeneration was found in nine of 37 cases (24 %); in six cases the optical tracts were affected and visual field defects were proven. In five of nine cases (55.6 %) with Wallerian degeneration previous hemorrhage was present. Dual vascular pathology was found in eight of 35 patients (23 %).
GK radiosurgery for AVM is a safe treatment method although delayed complications may occur. Post-gadolinium enhancement of obliterated nidi may indicate an active post-irradiative process.

BACKGROUND: The aim of this study was to evaluate the white matter integrity in brains of patients with systemic lupus erythematosus (SLE) using a voxel-based analyses of diffusion tensor imaging (DTI) data.
METHODS: Fifty-seven patients with SLE were compared to 36 control patients who were matched by gender, age, education, and Mini Mental State Examination score. DTI was performed along 30 noncollinear directions in a 1.5 Tesla scanner. For tract-based spatial statistics (TBSS), a white matter skeleton was created, and a permutation-based inference with 5000 permutations and a threshold of p < 0.05 was used to identify abnormalities in fractional anisotropy (FA). The mean (MD), radial (RD), and axial diffusivities (AD) were also projected onto the mean FA skeleton.
RESULTS: We found a significant decrease of global FA in SLE patients compared to controls. The areas of reduced FA included the right superior corona radiata, the right superior longitudinal fasciculus, the body of the corpus callosum, the right inferior fronto-occipital fasciculus, the right thalamic radiation, and the right uncinate fasciculus. Patients with SLE also had increased AD and RD in several areas. Substantial overlap of areas with increased AD and RD occurred and were spatially much more extensive than the areas of reduced FA.
CONCLUSIONS: Significant increases of AD values were concordant to those of RD and MD and more extensive than FA changes. Analyzing all diffusivity parameters, using TBSS, can detect more white matter microstructural changes in patients with SLE than analyzing FA alone.

We performed voxel-guided morphometry (VGM) investigating the mechanisms of brain atrophy in multiple sclerosis (MS) related to focal lesions. VGM maps detect regional brain changes when comparing 2 time points on high resolution T1-weighted (T1w) magnetic resonace imaging (MRI). Two T1w MR datasets from 92 relapsing-remitting MS patients obtained 12 months apart were analysed with VGM. New lesions and volume changes of focal MS lesions as well as in the surrounding tissue were identified by visual inspection on colour coded VGM maps. Lesions were dichotomized in active and inactive lesions. Active lesions, defined by either new lesions (NL) (volume increase > 5% in VGM), chronic enlarging lesions (CEL) (pre-existent T1w lesions with volume increase > 5%), or chronic shrinking lesions (CSL) (pre-existent T1w lesions with volume reduction > 5%) in VGM, were accompanied by tissue shrinkage in surrounding and/or functionally related regions. Volume loss within the corpus callosum was highly correlated with the number of lesions in its close proximity. Volume loss in the lateral geniculate nucleus was correlated with lesions along the optic radiation. VGM analysis provides strong evidence that all active lesion types (NL, CEL, and CSL) contribute to brain volume reduction in the vicinity of lesions and/or in anatomically and functionally related areas of the brain.

OBJECTIVE: Cerebral hemiatrophy (CHA) is a congenital or acquired loss of volume in one hemisphere of the brain. The MR findings of the affected hemisphere have been a subject of many studies, however, the contralateral hemisphere has not been investigated. There is, in fact, an integrity between two hemispheres of the brain through transverse connection fibers. The aim of this study is to investigate the changes in the contralateral hemisphere in CHA.
METHODS: Apparent diffusion coefficient (ADC) values were measured in deep gray and white matter areas in the normal-appearing contralateral hemisphere in 23 patients with CHA, in order to get in vivo information about a possible Wallerian degeneration or microstructural changes. Results were compared with the control group.
RESULTS: Normal ADC values were encountered in the contralateral hemisphere in all (100%) CHA patients. The difference between the ADC values of gray and white matter in CHA patients and the control group was not statistically significant.
CONCLUSIONS: Normal ADC values in the contralateral hemisphere in CHA patients suggests a compensatory mechanism restricting Wallerian degeneration or diffusion alteration.

OBJECTIVE: To investigate the feasibility of T2W-SPACE technique in early detection of WD, the signal evolutions of degenerated corticospinal tract (CST) on T2W-SPACE, and their underlying pathological changes.
METHODS: The WD model of the CST was established in 23 cats through excision of cortical origins of the tract. Eight cats were scanned with the T2W-SPACE technique at 8 sequential time points, i.e. 0 (before modeling), 2, 4, 6, 8, 10, 20 and 30 days after modeling, and then they were pathologically examined. The remaining 15 cats (3 per group) also underwent pathological examination at 2, 4, 6, 10 and 20 days after modeling, respectively. The ratios of T2 signal intensity (rT2s) between the affected and unaffected sides of CST were analyzed.
RESULTS: During the first 4 days, SPACE could not detect any significant changes of the affected CST, although axonal degeneration was pathologically observed at the second day. From 6 to 10 days, the rT2s decreased monotonously, which is corresponded to histological findings of myelin degeneration and phagocyte proliferation. From 10 to 20 days, rT2s kept relatively stable at a low level and started to recover after that; the pathological changes of this period was characterized by marked phagocytizing activities.
CONCLUSIONS: SPACE technique can detect Wallerian degeneration at an early stage, and the signal evolution is consistent with the pathological processes.

BACKGROUND: Neuronal loss following damage is often greater than expected from the severity of injury to the nerve itself. The visual pathways, which comprise a well-defined system, and optic neuritis (ON), which is usually a discrete event, make a fine model to study this phenomenon.
OBJECTIVE: Understand the effect of focal optic nerve demyelination on neighboring white matter.
METHODS: Diffusion tensor imaging and probabilistic tractography were used to identify and characterize the optic tracts and radiations of 17 ON and matched controls. Data were correlated with retinal nerve fiber layer (RNFL) thickness.
RESULTS: Patients\' optic tracts exhibited reduced axial diffusivity, which correlated with RNFL thickness values. Patients\' optic radiations demonstrated intact axial diffusivity but reduced fractional anisotropy and elevated radial diffusivity, which could be explained by intra-bundle lesions. No correlations were found between diffusivity measurements in patients\' optic tracts and radiations; or between RNFL thickness and optic radiations\' diffusivity.
CONCLUSIONS: Following ON, chronic axonal loss develops distally in the optic tracts, demonstrating Wallerian degeneration. Degeneration did not proceed to the optic radiations, opposing anterograde trans-neuronal changes. DTI in ON provides fine in-vivo human model for studying histological abnormalities in normal appearing white matter, localized in close proximity to damaged bundle.