Histogenesis of demyelinating lesions in the spinal cord of guinea pigs with chronic relapsing experimental allergic encephalomyelitis☆
References (24)
- et al.
Chronic relapsing experimental allergic encephalomyelitis — Morphological sequence of myelin degradation
Brain Res.
(1979) The histology of disseminated sclerosis
Trans. roy. Soc. Edinb.
(1916)Topographic distribution of plaques in the spinal cord in multiple sclerosis
Arch. Neurol. (Chic.)
(1950)- et al.
Blood vessels and tissue space associated with the brain of the rat
Amer. J. Anat.
(1969) Die zentralen Entmarkungserkrankungen
Dtsch. Z. Nervenheilk.
(1940)- et al.
Über die konzentrische Sklerose und die physikalisch-chemischen Faktoren bei der Ausbreitung von Entmarkungsprozessen
Arch. Psychiat. Nervenkr.
(1933) - et al.
About demyelinating properties of humoral antibodies in experimental allergic encephalomyelitis
Acta neuropath. (Berl.)
(1976) Demyelination and remyelination in experimental allergic encephalomyelitis
J. Neuropath. exp. Neurol.
(1965)- et al.
Chronic relapsing EAE — Time course of neurological symptoms and pathology
Acta neuropath. (Berl.)
(1978) - et al.
Chronic relapsing experimental allergic encephalomyelitis Clinicopathological comparison with multiple sclerosis
Arch. Neurol. (Chic.)
(1979)
The neuropathology of multiple sclerosis
Die sogenannte “akute multiple Sklerose”
Jahrb. Psychiat.
Cited by (14)
Morphometric analysis of blood vessels in chronic experimental spinal cord injury: Hypervascularity and recovery of function
1991, Journal of the Neurological SciencesInflammatory cortical demyelination in early multiple sclerosis
2011, New England Journal of MedicineCitation Excerpt :These findings do not support a primary (noninflammatory) neurodegenerative process during early-stage multiple sclerosis. Differences between cortical demyelination in early multiple sclerosis and in long-standing, progressive multiple sclerosis, in which inflammatory cortical demyelination is typically not observed, may relate to efficient clearance of cortical inflammation.38,39 With respect to a potential mechanism of disease progression, we speculate that myelin-laden macrophages may leave the cortex, enter the cerebrospinal fluid (CSF), gain access to deep cervical lymph nodes to promote epitope spreading,40 and thus propagate the disease process (Fig. 5 in the Supplementary Appendix).
- ☆
This study was partly funded by the Fonds zur Förderung der wissenschaftlichen Forschung, Project No. S-25/07.