Literature DB >> 12821527

Evolution of T1 black holes in patients with multiple sclerosis imaged monthly for 4 years.

Francesca Bagnato1, Neal Jeffries, Nancy D Richert, Roger D Stone, Joan M Ohayon, Henry F McFarland, Joseph A Frank.   

Abstract

T1 black holes (BHs) on MRIs may represent either areas of oedema or axonal loss in patients with multiple sclerosis. BHs begin as contrast enhancing lesions (CELs) and evolve differently from patient to patient, and within the same patient over time. We analysed BHs formation over a 4-year period. Forty-eight monthly MRIs of nine non-treated multiple sclerosis patients were evaluated for numbers of CELs and BHs. A BH was defined as a hypointense lesion on a T1 pre-contrast image that coincided with a region of high signal intensity on the T2-weighted images. A BH was considered as acute (ABH) when it occurred coincidently with the presence of enhancement and as persisting (PBH) when present after the cessation of enhancement. The present study aimed to analyse: (i) the incidence of CELs and new PBHs, and the accumulation of PBHs; (ii) the relationship between the quantity of the CELs in a given month and the likelihood of accumulating PBHs in the subsequent month; and (iii) the relationship between the duration of CELs and PBHs. Pitman's correlation test evaluated the effect of time on either the increase of CELs and new PBHs or the accumulation of PBHs, while a multiple logistic regression analysis evaluated the relationship between progression of time and CELs, and the increase of PBHs in a multivariate model. The relationship between the enhancing lesions duration and the PBHs duration, or the time to revert back to an isointense lesion was analysed using Kaplan-Meier survival models. PBHs accumulated (P < 0.001) in all patients, but the formation of new PBHs increased in four patients (P < or = 0.007) in conjunction with an increase in either the quantity of CELs (P < 0.001, for two patients) or the proportion of CELs turning into PBHs (P < or = 0.02, for two patients). Logistic regression analysis showed that neither progression of time nor the number of CELs in a given month were able to predict the probability of increasing the number of PBHs in the subsequent month in any patient. Out of 397 ABHs, 55.7% evolved to a PBH. The duration of PBHs correlated with the duration of enhancement. PBHs preceded by CELs observable on a single MRI persisted for a shorter time (P < 0.002) than those preceded by CELs visible on > or =2 monthly MRIs. The formation of a new PBH was found to be related to CELs activity; however, duration of PBHs is most likely a consequence of the duration of the enhancement.

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Year:  2003        PMID: 12821527     DOI: 10.1093/brain/awg182

Source DB:  PubMed          Journal:  Brain        ISSN: 0006-8950            Impact factor:   13.501


  56 in total

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2.  In vivo detection of cortical plaques by MR imaging in patients with multiple sclerosis.

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4.  Characterizing contrast-enhancing and re-enhancing lesions in multiple sclerosis.

Authors:  Z Campbell; D Sahm; K Donohue; J Jamison; M Davis; C Pellicano; S Auh; J Ohayon; J A Frank; N Richert; F Bagnato
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Review 5.  Current and new directions in MRI in multiple sclerosis.

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Journal:  Continuum (Minneap Minn)       Date:  2013-08

Review 6.  MRI in multiple sclerosis: what's inside the toolbox?

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Review 8.  Neuroimaging in multiple sclerosis: neurotherapeutic implications.

Authors:  Nancy L Sicotte
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9.  MR imaging intensity modeling of damage and repair in multiple sclerosis: relationship of short-term lesion recovery to progression and disability.

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10.  Lack of mitochondrial DNA deletions in lesions of multiple sclerosis.

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Journal:  Neuromolecular Med       Date:  2008       Impact factor: 3.843

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