A Case of Disseminated Sclerosis and Glioma of the Brain in the Same Patient

Munch-Petersen, C. J.

doi:10.1111/j.1600-0447.1949.tb07342.x

Cited by 14 publications

(4 citation statements)

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“…A compelling series of reports of malignant astrocytomas associated with MS have been published (Scherer 1938;Munch-Peterson 1949;Zimmerman and Netsky 1950;Russell and Rubinstein 1977;Matthews 1962;Brihaye et al 1963;Barnard and Jellinek 1967;Aubert et al 1968;Boyazis et al 1968;Mathews and Moosy 1972;Reagan and Frieman 1973;Currie and Urich 1974;Lynch 1974;Kalimo et al 1979;Lahl 1980;Ho and Wolfe 1981;Malmgren et al 1984;Vieregge et al 1984;Nahser et al 1986;Barnard and Geddes 1987;Oldendorf and Cornford 1997;Shankar et al 1989;Perilongo et al 1999;Costa et al 2000). Other tumours reported in association with MS have included ependymomas, meningiomas, oligodendrogliomas, and odd non-gliomatous tumours, but these are very rare and likely to be pure coincidental occurrences.…”

Section: Gliomamentioning

confidence: 95%

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: Gliomamentioning

confidence: 95%

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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“…While glioma and MS co-occurring is extremely uncommon, reports of such cases have been documented dating back to 1949 ( 49 ), which raises the possibility of underlying mechanisms between glioma and MS, perhaps resulting from the environment or heredity. However, whether there exists a causal association and the effect direction remains unknown.…”

Section: Discussionmentioning

confidence: 99%

Association between glioma and neurodegenerative diseases risk: a two-sample bi-directional Mendelian randomization analysis

Liu,

Chen,

Gao

et al. 2024

Front. Neurol.

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BackgroundEarlier observational studies have demonstrated a correlation between glioma and the risk of neurodegenerative diseases (NDs), but the causality and direction of their associations remain unclear. The objective of this study was to ascertain the causal link between glioma and NDs using Mendelian randomization (MR) methodology.MethodsGenome-wide association study (GWAS) data were used in a two-sample bi-directional MR analysis. From the largest meta-analysis GWAS, encompassing 18,169 controls and 12,488 cases, summary statistics data on gliomas was extracted. Summarized statistics for NDs, including Alzheimer’s disease (AD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS) and Parkinson’s disease (PD) were obtained from the GWAS of European ancestry. Inverse variance weighted (IVW) method was elected as the core MR approach with weighted median (WM) method and MR-Egger method as complementary methods. In addition, sensitivity analyses were performed. A Bonferroni correction was used to correct the results.ResultsGenetically predicted glioma had been related to decreased risk of AD. Specifically, for all glioma (IVW: OR = 0.93, 95% CI = 0.90–0.96, p = 4.88 × 10−6) and glioblastoma (GBM) (IVW: OR = 0.93, 95% CI = 0.91–0.95, p = 5.11 × 10−9). We also found that genetically predicted all glioma has a suggestive causative association with MS (IVW: OR = 0.90, 95% CI = 0.81–1.00, p = 0.045). There was no evidence of causal association between glioma and ALS or PD. According to the results of reverse MR analysis, no discernible causal connection of NDs was found on glioma. Sensitivity analyses validated the robustness of the above associations.ConclusionWe report evidence in support of potential causal associations of different glioma subtypes with AD and MS. More studies are required to uncover the underlying mechanisms of these findings.

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“…The concurrence of cerebral glioma and multiple sclerosis has been documented in seven previously reported cases (Scherer, 1938;Munch-Petersen, 1949;Zimmerman and Netsky, 1950;Brihaye, Perier, and Stenuit, 1963;Russell and Rubinstein, 1971) and suggested in one other (Herndon, Rubenstein, Freeman, and Mathieson, 1970). In the following report, the eighth case of these two conditions occurring in a patiept is recorded.…”

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confidence: 82%