The significance of perivascular infiltrations in multiple sclerosis

Guseo, A.; Jellinger, K. A.

doi:10.1007/bf00312463

Cited by 104 publications

(42 citation statements)

References 18 publications

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“…It is difficult therefore to understand that depletion of B cell (CD20) helps clinically since acute demyelination can evolve without B cells, and one-third of lesions in patients with MS show no cells whatsoever (Seitelberger 1960;Guseo and Jellinger 1975;Adams 1977). There is no disease-specific antibody in MS unlike other autoimmune diseases in which rituximab is effective.…”

Section: Recent Immunological Findings Implicating B Cellsmentioning

confidence: 96%

The sad plight of multiple sclerosis research (low on fact, high on fiction): critical data to support it being a neurocristopathy

Behan

Chaudhuri

2010

Inflammopharmacol

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The literature for evidence of autoimmunity in multiple sclerosis (MS) is analysed critically. In contrast to the accepted theory, the human counterpart of the animal model experimental autoimmune demyelinating disease, experimental allergic encephalomyelitis (EAE), is not MS but a different demyelinating disorder, i.e. acute disseminated encephalomyelitis and acute haemorrhagic leucoencephalitis. Extrapolation of EAE research to MS has been guided largely by faith and a blind acceptance rather than sound, scientific rationale. No specific or sensitive immunological test exists that is diagnostic of MS despite the extensive application of modern technology. Immunosuppression has failed to have any consistent effect on prognosis or disease progression. The available data on MS immunotherapy are conflicting, at times contradictory and are based on findings in animals with EAE. They show predominantly a 30% effect in relapsing/remitting MS which suggests powerful placebo effect. Critical analysis of the epidemiological data shows no association with any specific autoimmune diseases, but does suggest that geographic factors and age at development posit an early onset possibly dependent on environmental influences. Certain neurological diseases are, however, found in association with MS, namely hypertrophic peripheral neuropathy, neurofibromatosis-1, cerebral glioma, glioblastoma multiforme and certain familial forms of narcolepsy. These share a common genetic influence possibly from genes on chromosome 17 affecting cell proliferation. A significant number of these disorders are of neural crest origin, the classical example being abnormalities of the Schwann cell. These and other data allow us to propose that MS is a developmental neural crest disorder, i.e. a cristopathy, implicating glial cell dysfunction with diffuse blood-brain barrier breakdown. The data on transcription factor SOX10 mutations in animals may explain these bizarre clinical associations with MS and the phenotypic variability of such alterations (Cossais et al. 2010). Research directed to the area of neural crest associations is likely to be rewarding.

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Section: Recent Immunological Findings Implicating B Cellsmentioning

confidence: 96%

The sad plight of multiple sclerosis research (low on fact, high on fiction): critical data to support it being a neurocristopathy

Behan

Chaudhuri

2010

Inflammopharmacol

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“…The histologic features that form a clue to the diagnosis of demyelination are: presence of foamy macrophages in the absence of any associated coagulative necrosis, presence of a prominent lymphoid inflammatory infiltrate especially around blood vessels, pattern of sheets of well formed large gemistocytic astrocytes with well developed processes that are separated from each other, well defined border of the lesion with predilection for white matter/ periventricular areas. [20] Demyelinating pseudotumour should be considered in the differential diagnosis of any proliferative astroglial process presenting as a mass lesion. With experience, the morphologic features of demyelinating disease are easily recognizable in H&E sections.…”

Section: Discussionmentioning

confidence: 99%

Demyelinating disease simulating brain tumours: A histopathologic assessment of seven cases

et al. 2006

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BACKGROUND: Demyelinating diseases can present as space occupying lesions with in the brain. It is clinically and radiologically difficult to differentiate them from primary neoplasms. Histopathologically they mimic astrocytic neoplasms closely and identifying these lesions correctly has a profound impact in treatment and prognosis of these patients. AIMS AND OBJECTIVES: The objective was to determine the histopathologic features of such acute focal demyelinating disease that clinically presented as brain tumors. MATERIAL AND METHODS: Seven cases were included for the study. Detailed histopathological examination including stains for myelin and axon were performed. The histopathological keys in arriving at the right diagnoses included a well demarcated lesion that contains uniform distribution of foamy macrophages in the absence of any associated coagulative necrosis, sheets of gemistocytic astrocytes in the white matter that show well-formed processes, perivascular chronic inflammatory cell infiltration and total absence of myelin with relative preservation of axons within these areas. CONCLUSION: The degree of suspicion (clinical, radiological and histopathological) should be high to diagnose these group of lesions. The above-mentioned diagnostic keys should help in arriving at the correct histopathological diagnoses of such cases.

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“…As has previously been discussed, this disparity may be a result of differences in the technical approaches used, such as different procedures of tissue processing, cutting and staining, and cohort choice. 65,101 .…”

Section: Role Of Meningeal Inflammatory Infiltratesmentioning

confidence: 99%

Exploring the origins of grey matter damage in multiple sclerosis

et al. 2015

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Multiple sclerosis is characterized at the gross pathological level by the presence of widespread focal demyelinating lesions of the myelin-rich white matter. However, it is becoming clear that grey matter is not spared, even during the earliest phases of the disease. Furthermore, grey matter damage may have an important role both in physical and cognitive disability. Grey matter pathology involves both inflammatory and neurodegenerative mechanisms, but the relationship between the two is unclear. Histological, immunological and neuroimaging studies have provided new insight in this rapidly expanding field, and form the basis of the most recent hypotheses on the pathogenesis of grey matter damage. DOI: https://doi.org/10.1038/nrn3900Posted at the Zurich Open Repository and Archive, University of Zurich ZORA URL: https://doi.org/10.5167/uzh-111099 Accepted Version Originally published at: Calabrese, Massimiliano; Magliozzi, Roberta; Ciccarelli, Olga; Geurts, Jeroen J G; Reynolds, Richard; Martin, Roland (2015). Exploring the origins of grey matter damage in multiple sclerosis. Nature Reviews Neuroscience, 16 (3) AbstractMultiple sclerosis is characterised at the gross pathological level by the presence of widespread focal demyelinating lesions of the myelin-rich white matter. However, in recent years it has become clear that grey matter is not spared, even during the earliest phases of the disease. Furthermore, grey matter damage has been suggested to have an important role both in physical and cognitive disability. Grey matter pathology involves both inflammatory and neurodegenerative mechanisms, but the relationship between the two is unclear. This review will summarize and highlight important histological, immunological, and neuroimaging results from this rapidly expanding field and will address the most recent hypotheses on the pathogenesis of grey matter damage.

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The significance of perivascular infiltrations in multiple sclerosis

Cited by 104 publications

References 18 publications

The sad plight of multiple sclerosis research (low on fact, high on fiction): critical data to support it being a neurocristopathy

The sad plight of multiple sclerosis research (low on fact, high on fiction): critical data to support it being a neurocristopathy

Demyelinating disease simulating brain tumours: A histopathologic assessment of seven cases

Exploring the origins of grey matter damage in multiple sclerosis

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