mrhodes40 wrote: It is not making sense to me that collapsed veins are the explanation for stenosis... are you saying they are collapsed not stenosed... or that the collapse causes stenosis ...or that the stenosis makes veins collapse downstream from the stenosis itself?
1: Acta Radiol. 2008 Jun;49(5):570-9. LinksRate of ventricular enlargement in multiple sclerosis: a nine-year magnetic resonance imaging follow-up study.
Martola J, Stawiarz L, Fredrikson S, Hillert J, Bergstrom J, Flodmark O, Aspelin P, Kristoffersen Wiberg M.
Division of Radiology, Department of Clinical Science, Intervention, and Technology, Karolinska Institute, Stockholm, Sweden. firstname.lastname@example.org
BACKGROUND: In multiple sclerosis (MS), brain atrophy assessed by linear measurements of ventricular widths has been reported to be well correlated with three-dimensional (3D) measurements. Therefore, serial linear measurements with no need for advanced 3D evaluation may be proven to be robust markers of irreversible, destructive changes. PURPOSE: To evaluate the rate of supratentorial ventricular enlargement representing four decades of disease span. MATERIAL AND METHODS: 37 MS patients with disease duration at baseline ranging from 1 to 33 years were included. The mean time of the individual magnetic resonance imaging (MRI) follow-up was 9.25 years (range 7.3-10 years). Enlargement rate of the third and lateral ventricles was studied over time by applying three linear measurements on axial 5-mm T1-weighted MRI images. RESULTS: Progression of supratentorial ventricular widths during 9 years' follow-up was found. The mean annual width increase of the third ventricle was 0.20 mm (P<0.001, 95% confidence interval [CI] 0.15-0.25), for the frontal horn width 0.32 mm (P<0.001, 95% CI 0.23-0.40), and increase of the intercaudate distance was 0.26 mm (P<0.001, 95% CI 0.19-0.33). The association between these three measurements and disability status persisted at the time of follow-up. CONCLUSION: We found uniform ventricular enlargement progression during four decades of disease span, suggesting unchanging total brain atrophy progression over time.
PMID: 18568545 [PubMed - indexed for MEDLINE
[color=blue]1: Neuroimage. 2007 Nov 15;38(3):529-37. Epub 2007 Aug 16. LinksRegional brain atrophy development is related to specific aspects of clinical dysfunction in multiple sclerosis.
Jasperse B, Vrenken H, Sanz-Arigita E, de Groot V, Smith SM, Polman CH, Barkhof F.
Department of Neurology, VU University Medical Center, Boelelaan 1117, PO Box 7057, 1007 MB, Amsterdam, The Netherlands. email@example.com
Brain atrophy in multiple sclerosis (MS) is thought to reflect irreversible tissue damage leading to persistent clinical deficit. Little is known about the rate of atrophy in specific brain regions in relation to specific clinical deficits. We determined the displacement of the brain surface between two T1-weighted MRI images obtained at baseline and after a median follow-up time of 2.2 years for 79 recently diagnosed, mildly disabled MS patients. Voxel- and cluster-wise permutation-based statistics were used to identify brain regions in which atrophy development was significantly related to Expanded Disability Status Scale (EDSS), Timed Walk Test (TWT), Paced Auditory Serial Addition Test (PASAT) and 9-Hole Peg Test (HPT). Clusters were considered significant at a corrected cluster-wise p-value of 0.05. Worse EDSS change-score and worse follow-up EDSS were related to atrophy development of periventricular and brainstem regions and right-sided parietal, occipital and temporal regions. Worse PASAT at follow-up was significantly related to atrophy of the ventricles. A worse TWT change-score and worse follow-up TWT were exclusively related to atrophy around the ventricles and of the brainstem. Worse HPT change-score and worse follow-up HPT of either arm were significantly related to the atrophy of widely distributed peripheral regions, as well as atrophy of periventricular and brainstem regions. Our findings suggest that decline in ambulatory function is related to atrophy of central brain regions exclusively, whereas decline in neurologically more complex tasks for coordinated hand function is related to atrophy of both central and
and peripheral brain regions.
PMID: 17889567 [PubMed - indexed for MEDLINE
I am an otherwise healthy 65 yo woman from Hawaii.
I was dx with NPH in 2005 and had a programmable shunt implanted 2006; triad of symptoms: falling; wobbly; UI.
next 6 months symptoms resolved; however, became increasingly wobbly; gait imbalance; UI; depression 2007 to present;
2009 dx MS (RR); "numerous lesions brain, neck, spinal cord
RX: Copaxone; Provigil; Buproprion; Prozac; Folic Acid; B12
Are there others with both diagnosis?
HI doctors say I'm the only one, but it cannot be...
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