Wedge-shaped medullary lesions in multiple sclerosis

Qiu, Wei; Raven, Sonja; Wu, Jing-Shan; Carroll, William M.; Mastaglia, Frank; Kermode, Allan G.

doi:10.1016/j.jns.2009.12.017

Cited by 4 publications

(4 citation statements)

References 13 publications

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“…A delay of this magnitude might derive from macro-or microcirculatory abnormalities, at least in a subgroup of patients. Our results are consistent with those of many studies that showed a decrease in cerebral perfusion in normal-appearing white matter and vascular changes associated with MS (2)(3)(4)(5).…”

Section: Neuroradiology: Cerebral Circulation Time In Multiple Sclerosissupporting

confidence: 93%

“…A subset of patients with a pattern of demyelination that has not been observed in models of acute or chronic encephalomyelitis but that closely mimics the tissue alterations seen in the early stages of white matter ischemia has been observed (2). Moreover, studies based on histopathologic techniques and on magnetic resonance (MR) imaging also demonstrate hypoxia-like tissue injury (2)(3)(4) or thrombosis of small veins (5). With dynamic susceptibility contrast MR imaging, cerebral mean transit time values were found to be significantly prolonged in patients with MS (3).…”

Section: Methodsmentioning

confidence: 99%

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Multiple Sclerosis: Cerebral Circulation Time

Mancini

Morra²,

Donato³

et al. 2012

Radiology

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These results suggest that contrast-enhanced US with CCT assessment may have a role in the evaluation of cerebral blood flow in patients with MS and that a vascular impairment could be associated with MS. The finding of a prolonged CCT at contrast-enhanced US does not result from outflow impairment. Further studies are required to verify these observations and to clarify if CCT and CCSVI have any physiologic and clinical relevance in MS.

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Section: Neuroradiology: Cerebral Circulation Time In Multiple Sclerosissupporting

confidence: 93%

Section: Methodsmentioning

confidence: 99%

Multiple Sclerosis: Cerebral Circulation Time

Mancini

Morra²,

Donato³

et al. 2012

Radiology

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show abstract

“…1,2 The close relationship of plaques to deep venous structures has long been observed 3,4 and is demonstrable on MR imaging. 5,6 A body of controversial literature suggesting an alternative etiology has arisen in the past 5 years stating that the insult triggering demyelination is secondary to impaired cerebrospinal venous return. This evokes venous hypertension, blood-brain barrier breakdown, hemosiderin deposition, and a secondary immunemediated response with resultant demyelinating plaque.…”

mentioning

confidence: 99%

Mystery of Chronic Cerebrospinal Venous Insufficiency: Identical Venographic and Ultrasound Findings in Patients with MS and Controls

McAuliffe

Kermode

2013

AJNR Am J Neuroradiol

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BACKGROUND AND PURPOSE:Stenosis of the internal jugular, azygos, and other veins detected by using intracranial and neck Doppler and B-mode sonography and confirmed by venography has been reported in MS with a high degree of sensitivity. This article reports the results of sonographic findings in patients with MS and controls, looking for evidence of the controversial entity chronic cerebrospinal venous insufficiency. Furthermore, the venographic appearance in controls is documented.

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“…In this issue of the Journal of the Neurological Sciences, Qiu et al [8] describe four patients with a diagnosis of clinically definite MS (relapsing remitting in two patients and secondary progressive in the other two) and a long disease duration (range = 10-29 years), who showed unusual wedge-shaped lesions in the paramedian ventral portion of the medulla oblongata. Unfortunately, this study is retrospective and does not provide an estimate of the prevalence of such a finding in the general MS population.…”

mentioning

confidence: 99%