BACKGROUND: In patients with clinically isolated syndromes (CIS) suggestive of multiple sclerosis (MS), the extent of brain magnetic resonance imaging (MRI) lesion load influences the probability and time to development of clinically definite MS. Cerebral atrophy is recognised in established MS, but its time of onset and whether, in early disease, it is related to MRI lesion load or clinical outcome is less certain. OBJECTIVES: This study investigated ventricular enlargement over one year in CIS patients and explored its relation with lesion load and clinical outcome. METHODS: A semi-automated thresholding technique for measuring ventricular volume (MIDAS) was applied to MRI scans in a cohort of 55 patients with CIS, recruited consecutively and imaged within three months of the onset of symptoms and again after one year. RESULTS: Clinical MS had developed after one year in 16 of 40 patients with an abnormal baseline T2 scan and 2 of 15 with a normal scan. Significant ventricular enlargement was seen in 27 of 55 patients who fulfilled the new McDonald MRI criteria for MS using all available MRI at clinical follow up (median increase 0.3 cm(3), p=0.005) Significant increase in ventricular volume was also seen in the 18 of 55 patients who developed clinical MS over the follow up period (median increase 0.5 cm(3), p=0.006). There were significant but modest correlations between baseline lesion measures and subsequent ventricular enlargement. CONCLUSIONS: (1) Lesions and atrophy are both associated with early relapse leading to a diagnosis of clinical MS; (2) while lesions contribute to the development of atrophy, atrophy may also develop by other mechanisms. This suggests that MR measures have a complementary role in monitoring the course of MS, even from the earliest clinical stage.
BACKGROUND: In patients with clinically isolated syndromes (CIS) suggestive of multiple sclerosis (MS), the extent of brain magnetic resonance imaging (MRI) lesion load influences the probability and time to development of clinically definite MS. Cerebral atrophy is recognised in established MS, but its time of onset and whether, in early disease, it is related to MRI lesion load or clinical outcome is less certain. OBJECTIVES: This study investigated ventricular enlargement over one year in CIS patients and explored its relation with lesion load and clinical outcome. METHODS: A semi-automated thresholding technique for measuring ventricular volume (MIDAS) was applied to MRI scans in a cohort of 55 patients with CIS, recruited consecutively and imaged within three months of the onset of symptoms and again after one year. RESULTS: Clinical MS had developed after one year in 16 of 40 patients with an abnormal baseline T2 scan and 2 of 15 with a normal scan. Significant ventricular enlargement was seen in 27 of 55 patients who fulfilled the new McDonald MRI criteria for MS using all available MRI at clinical follow up (median increase 0.3 cm(3), p=0.005) Significant increase in ventricular volume was also seen in the 18 of 55 patients who developed clinical MS over the follow up period (median increase 0.5 cm(3), p=0.006). There were significant but modest correlations between baseline lesion measures and subsequent ventricular enlargement. CONCLUSIONS: (1) Lesions and atrophy are both associated with early relapse leading to a diagnosis of clinical MS; (2) while lesions contribute to the development of atrophy, atrophy may also develop by other mechanisms. This suggests that MR measures have a complementary role in monitoring the course of MS, even from the earliest clinical stage.
Authors: N A Losseff; L Wang; H M Lai; D S Yoo; M L Gawne-Cain; W I McDonald; D H Miller; A J Thompson Journal: Brain Date: 1996-12 Impact factor: 13.501
Authors: C M Poser; D W Paty; L Scheinberg; W I McDonald; F A Davis; G C Ebers; K P Johnson; W A Sibley; D H Silberberg; W W Tourtellotte Journal: Ann Neurol Date: 1983-03 Impact factor: 10.422
Authors: N A Losseff; S L Webb; J I O'Riordan; R Page; L Wang; G J Barker; P S Tofts; W I McDonald; D H Miller; A J Thompson Journal: Brain Date: 1996-06 Impact factor: 13.501
Authors: C A Davie; G J Barker; S Webb; P S Tofts; A J Thompson; A E Harding; W I McDonald; D H Miller Journal: Brain Date: 1995-12 Impact factor: 13.501
Authors: L D Jacobs; D L Cookfair; R A Rudick; R M Herndon; J R Richert; A M Salazar; J S Fischer; D E Goodkin; C V Granger; J H Simon; J J Alam; D M Bartoszak; D N Bourdette; J Braiman; C M Brownscheidle; M E Coats; S L Cohan; D S Dougherty; R P Kinkel; M K Mass; F E Munschauer; R L Priore; P M Pullicino; B J Scherokman; R H Whitham Journal: Ann Neurol Date: 1996-03 Impact factor: 10.422
Authors: Olaf Stüve; Jeffrey L Bennett; Bernhard Hemmer; Heinz Wiendl; Michael K Racke; Amit Bar-Or; Wei Hu; Robert Zivadinov; Martin S Weber; Scott S Zamvil; Maria F Pacheco; Til Menge; Hans-Peter Hartung; Bernd C Kieseier; Elliot M Frohman Journal: Drugs Date: 2008 Impact factor: 9.546
Authors: Nicola De Stefano; Laura Airas; Nikolaos Grigoriadis; Heinrich P Mattle; Jonathan O'Riordan; Celia Oreja-Guevara; Finn Sellebjerg; Bruno Stankoff; Agata Walczak; Heinz Wiendl; Bernd C Kieseier Journal: CNS Drugs Date: 2014-02 Impact factor: 5.749
Authors: Maria A Rocca; Marco Battaglini; Ralph H B Benedict; Nicola De Stefano; Jeroen J G Geurts; Roland G Henry; Mark A Horsfield; Mark Jenkinson; Elisabetta Pagani; Massimo Filippi Journal: Neurology Date: 2016-12-16 Impact factor: 9.910
Authors: Maria A Rocca; Federica Agosta; Maria P Sormani; Kryshani Fernando; Mar Tintorè; Tijmen Korteweg; Paola Tortorella; David H Miller; Alan Thompson; Alex Rovira; Xavier Montalban; Chris Polman; Frederik Barkhof; Massimo Filippi Journal: J Neurol Date: 2008-02-18 Impact factor: 4.849