The pulvinar sign on magnetic resonance imaging in variant Creutzfeldt-Jakob disease

Zeidler, Martin; Sellar, Robin; Collie, Donald A.; Knight, Richard; Stewart, G.; Macleod, Margaret-Ann; Ironside, James W.; Cousens, Simon; Colchester, Alan C. F.; Hadley, Donald M.; Will, Robert

doi:10.1016/s0140-6736(00)02140-1

Cited by 313 publications

(158 citation statements)

References 25 publications

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“…From BSE and vCJD transmissions in nonhuman primates, a number of conclusions can be drawn that are of major importance for human health: (i) human-adapted BSE appears to be a variant of the BSE agent that is more virulent for humans than cattle BSE and is efficiently transmitted by the peripheral route; (ii) the detection of vCJD in unusually young patients is probably not because of a lack of diagnosis of cases in older patients, thus raising the question of the source of human contamination with BSE early in life; and (iii) iatrogenic transmissions from patients with vCJD would be readily recognized by using the same diagnostic criteria as those applied to vCJD [clinical and pathological criteria (27) comprising neuronal loss and gliosis in the thalamus correlated with high MRI signal (28,29)], whether such contaminations had occurred by the central or i.v. route.…”

Section: Discussionmentioning

confidence: 99%

Adaptation of the bovine spongiform encephalopathy agent to primates and comparison with Creutzfeldt– Jakob disease: Implications for human health

Lasmézas

Fournier²,

Nouvel³

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

158

117

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There is substantial scientific evidence to support the notion that bovine spongiform encephalopathy (BSE) has contaminated human beings, causing variant Creutzfeldt-Jakob disease (vCJD). This disease has raised concerns about the possibility of an iatrogenic secondary transmission to humans, because the biological properties of the primate-adapted BSE agent are unknown. We show that (i) BSE can be transmitted from primate to primate by intravenous route in 25 months, and (ii) an iatrogenic transmission of vCJD to humans could be readily recognized pathologically, whether it occurs by the central or peripheral route. Strain typing in mice demonstrates that the BSE agent adapts to macaques in the same way as it does to humans and confirms that the BSE agent is responsible for vCJD not only in the United Kingdom but also in France. The agent responsible for French iatrogenic growth hormone-linked CJD taken as a control is very different from vCJD but is similar to that found in one case of sporadic CJD and one sheep scrapie isolate. These data will be key in identifying the origin of human cases of prion disease, including accidental vCJD transmission, and could provide bases for vCJD risk assessment.

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Section: Discussionmentioning

confidence: 99%

Adaptation of the bovine spongiform encephalopathy agent to primates and comparison with Creutzfeldt– Jakob disease: Implications for human health

Lasmézas

Fournier²,

Nouvel³

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

158

117

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“…Although the 263K strain of scrapie is very fast acting, it was remarkable to find significant differences as early as we did. Abnormalities on MR images have previously been reported for prion diseases in both humans [12,14,[20][21][22] and rodents [18,19,23], with variable results. In the case of the human studies, all MRI scans were carried out during the symptomatic stage of disease.…”

Section: Discussionmentioning

confidence: 99%

Pre-Clinical Changes Observed by Magnetic Resonance Imaging in a Hamster Model of Transmissible Spongiform Encephalopathy: a Potential Biomarker of Prion Infection

Baydack¹,

McKenzie²,

Robertson³

2011

J Mol Biomark Diagn

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The objective of the study was to develop a model for the diagnosis of prion diseases in live animals, using magnetic resonance imaging (MRI). Hamsters experimentally infected with the 263K strain of scrapie were imaged periodically during the course of prion infection. Changes in the brain, particularly the hippocampus, were observed during the first quarter of the incubation period. These changes included an increase in T 2 relaxation time and apparent diffusion coefficient (ADC), indicative of an increase in the water content of tissues. These changes were apparent well before the appearance of clinical symptoms, and did not correlate with the typical histological changes characteristic of prion disease, (vacuolation, accumulation of PrP protein, gliosis) suggesting that the changes are caused by a progressive accumulation of fluid. This oedema may be a novel early marker of prion disease, and could play a role in pathogenesis.

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“…DWI was positive for the pulvinar sign in the two cases in which this sequence was available. In another case-control study using neuropathologically confirmed cases, the pulvinar sign had a sensitivity of 78% and a specificity of 100% (63). The vCJD epidemic occurred when DWI was not widely used and therefore, there is limited experience regarding the use of this sequence in this condition.…”

Section: Variant Cjdmentioning

confidence: 99%

Imaging of prion diseases

Létourneau-Guillon

Wada²,

Kucharczyk

2012

Magnetic Resonance Imaging

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Prion diseases are caused by self‐replicating proteins that induce lethal neurodegenerative disorders. In the last decade, the understanding of the different clinical, pathological, and neuroimaging phenotypes of this group of disorders has evolved paralleling the advances in prion molecular biology. From an imaging standpoint, the implementation of diffusion‐weighted imaging in routine practice has markedly facilitated the detection of prion diseases, especially Creutzfeldt‐Jakob. Less frequent prion‐related disorders, including genetic diseases, may also benefit from progresses in the field of quantitative diffusion‐weighted imaging, MR spectroscopy or molecular imaging. Herein, we present a review of the neuroimaging features of the prion disorders known to affect humans emphasizing the important contribution of MRI in the diagnosis of this group of disorders. J. Magn. Reson. Imaging 2012;35:998‐1012. © 2012 Wiley Periodicals, Inc.

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The pulvinar sign on magnetic resonance imaging in variant Creutzfeldt-Jakob disease

Cited by 313 publications

References 25 publications

Adaptation of the bovine spongiform encephalopathy agent to primates and comparison with Creutzfeldt– Jakob disease: Implications for human health

Adaptation of the bovine spongiform encephalopathy agent to primates and comparison with Creutzfeldt– Jakob disease: Implications for human health

Pre-Clinical Changes Observed by Magnetic Resonance Imaging in a Hamster Model of Transmissible Spongiform Encephalopathy: a Potential Biomarker of Prion Infection

Imaging of prion diseases

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