Chronic Inflammatory Demyelinating Polyradiculoneuropathy Associated With Multiple Sclerosis

Sharma, Khema R.; Saadia, Daniela; Facca, Alicia; Bhatia, Rita; Ayyar, D. R.; Sheremata, William A.

doi:10.1097/cnd.0b013e31816f18e3

Cited by 28 publications

(21 citation statements)

References 49 publications

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“…Other neuropathies have also been found in association with MS (Lassmann et al 1981;Tachi et al 1985;Mills and Murray 1986;Poser 1987;Acar et al 2004;Kwon et al 2008;Sharma et al 2008).…”

Section: Hypertrophic Peripheral Neuropathiesmentioning

confidence: 93%

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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“…Other neuropathies have also been found in association with MS (Lassmann et al 1981;Tachi et al 1985;Mills and Murray 1986;Poser 1987;Acar et al 2004;Kwon et al 2008;Sharma et al 2008).…”

Section: Hypertrophic Peripheral Neuropathiesmentioning

confidence: 93%

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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“…There is strong evidence that the chronic L-dopa therapy exerts a pulsed non-physiological stimulation of the dopamine receptors, resulting in the upregulation of the glutamatergic NMDA receptors in the striatum. 1,10 As a consequence, the glutamatergic transmission from the striatum to specific cortical areas, such as the supplementary motor area and the dorsolateral prefrontal cortex, 11,12 becomes overactive in PD, leading to the abnormal motor patterns of LIDs and motor fluctuations.…”

Section: Nmda Antagonist Memantine Improves Levodopa-induced Dyskinesmentioning

confidence: 99%

TremAn: A tool for measuring tremor frequency from video sequences

et al. 2010

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“…There is strong evidence that the chronic L-dopa therapy exerts a pulsed nonphysiological stimulation of the dopamine receptors, resulting in the upregulation of the glutamatergic NMDA receptors in the striatum. 1,10 As a consequence, the glutamatergic transmission from the striatum to specific cortical areas, such as the supplementary motor area and the dorsolateral prefrontal cortex, 11,12 becomes overactive in PD, leading to the abnormal motor patterns of LIDs and motor fluctuations.…”

Section: Mortality In Parkinson's Diseasementioning

confidence: 99%

Psychogenic movement disorder after a venlafaxine‐induced dystonia

2010

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Chronic Inflammatory Demyelinating Polyradiculoneuropathy Associated With Multiple Sclerosis

Abstract: When patients with MS develop CIDP, manifestations of central and peripheral disease involvement seem to respond to intravenous immunoglobulin. These cases suggest that there may be common antigenic targets in central and peripheral nervous system in this subset of patients.

Cited by 28 publications

References 49 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

TremAn: A tool for measuring tremor frequency from video sequences

Psychogenic movement disorder after a venlafaxine‐induced dystonia

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