Axonal transection in the lesions of multiple sclerosis.

@article{Trapp1998AxonalTI,
  title={Axonal transection in the lesions of multiple sclerosis.},
  author={Bruce D. Trapp and John W. Peterson and Richard M. Ransohoff and Richard A. Rudick and Sverre J. M{\"o}rk and Lars B{\"o}},
  journal={The New England journal of medicine},
  year={1998},
  volume={338 5},
  pages={
          278-85
        }
}
  • B. Trapp, J. Peterson, L. Bö
  • Published 29 January 1998
  • Medicine, Biology, Psychology
  • The New England journal of medicine
BACKGROUND Multiple sclerosis is an inflammatory demyelinating disease of the central nervous system and is the most common cause of neurologic disability in young adults. Despite antiinflammatory or immunosuppressive therapy, most patients have progressive neurologic deterioration that may reflect axonal loss. We conducted pathological studies of brain tissues to define the changes in axons in patients with multiple sclerosis. METHODS Brain tissue was obtained at autopsy from 11 patients… 

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...

References

SHOWING 1-10 OF 46 REFERENCES

Axonal damage in acute multiple sclerosis lesions.

TLDR
The results show the expression of amyloid precursor protein in damaged axons within acute multiple sclerosis lesions, and in the active borders of less acute lesions, which may have implications for the design and timing of therapeutic intervention.

Chemical pathology of acute demyelinating lesions and its correlation with disability

TLDR
The results suggest that neuronal dysfunction may be a proximate mechanism of disability even in inflammatory disorders primarily affecting myelin and oligodendroglial cells.

Axonal dystrophy as a consequence of long-term demyelination.

  • C. RaineA. Cross
  • Biology
    Laboratory investigation; a journal of technical methods and pathology
  • 1989
TLDR
It is hypothesized that the disease process in experimental allergic encephalomyelitis may be more dynamic than previously described and that prolonged interruption in normal axon-glial relationships in chronically demyelination (sometimes remyelinated) gliotic lesions might lead to a block in axoplasmic transport and a disruption of the axonal cytoskeleton.

Progressive cerebral atrophy in multiple sclerosis. A serial MRI study.

TLDR
This study demonstrates that progressive cerebral atrophy can be detected in individual patients with multiple sclerosis, correlates with worsening disability and gives additional information to that obtained with conventional MRI.

Assessment of lesion pathology in multiple sclerosis using quantitative MRI morphometry and magnetic resonance spectroscopy.

TLDR
The results emphasize a limitation of using T2-weighted MRI lesion volume alone and suggest that combined analysis of MR-based chemical and imaging data might allow improved non-invasive assessment of lesion pathology in order to better understand its relationship to clinical features of multiple sclerosis.

Imaging of axonal damage in multiple sclerosis: Spatial distribution of magnetic resonance imaging lesions

We performed magnetic resonance imaging and magnetic resonance spectroscopic imaging on 28 patients with multiple sclerosis stratified for disability and clinical course (relapsing with at least

Identification of lymphotoxin and tumor necrosis factor in multiple sclerosis lesions.

TLDR
Results indicate that LT and TNF may be involved in the immunopathogenesis of MS, and can be detected in both inflammatory cells and cells endogenous to the CNS.

Persistent functional deficit in multiple sclerosis and autosomal dominant cerebellar ataxia is associated with axon loss.

TLDR
The hypothesis that axonal loss is important in the development of persistent clinical disability in multiple sclerosis is supported.

Continual Breakdown and Regeneration of Myelin in Progressive Multiple Sclerosis Plaques a

TLDR
It is concluded that the two processes of sometimes massive remyelination and active demyelinated frequently coexist in "fatty" subacute plaques filled with lipid-containing macrophages, and that myelin breakdown at the edges of progressive lesions includes destruction of Remyelinating internodes.

Spinal cord atrophy and disability in multiple sclerosis. A new reproducible and sensitive MRI method with potential to monitor disease progression.

TLDR
Given its reproducibility, the magnitude of the change detected and the strong correlation with disability, this new technique should prove to be a sensitive measure of progressive neurological deterioration and could be readily incorporated into imaging protocols aimed at monitoring therapy.