metricas
covid
Buscar en
Neurología (English Edition)
Toda la web
Inicio Neurología (English Edition) Brain Atrophy in Clinically Isolated Syndrome
Journal Information
Vol. 25. Issue 7.
Pages 430-434 (January 2010)
Share
Share
Download PDF
More article options
Vol. 25. Issue 7.
Pages 430-434 (January 2010)
Original article
Full text access
Brain Atrophy in Clinically Isolated Syndrome
Atrofia cerebral en pacientes con síndrome desmielinizante aislado
Visits
1365
J.I. Rojasa,
Corresponding author
, L. Patruccoa, C. Besadab, L. Bengoleab, E. Cristianoa
a Sección de Neuroinmunología y Enfermedades Desmielinizantes, Servicio de Neurología, Hospital Italiano, Buenos Aires, Argentina
b Sección de Neurorradiología, Servicio de Diagnóstico por Imágenes, Hospital Italiano, Buenos Aires, Argentina
This item has received
Article information
Abstract
Bibliography
Download PDF
Statistics
Abstract
Introduction

Previous reports have shown that brain atrophy appears early in the course of multiple sclerosis (MS). The aim of the present study was to evaluate whether brain atrophy already exists in clinically isolated syndrome (CIS) by comparing with a control sample.

Methods

Patients with CIS were included prospectively from June 2008 to June 2009. A control group of healthy persons, matched by age and gender with CIS, was also included during the same period of time. An automated analysis tool, SIENAX, was used to obtain total brain volume (TBV), gray matter volume (GMV) and white matter volume (WMV). Mann-Whitney U test was used to analyze the data.

Results

Twenty CIS patients and 30 healthy controls were included (8 vs. 17 females, p=0.11). Mean age for CIS was 35±6 years vs. 34.4±5 in controls (p=0.61). Mean EDSS in CIS was 1.1±0.5. Eighteen patients with CIS (90%) had abnormal baseline MRI. The TBV in CIS was 1.6μl±0.22μl×106 vs.1.65±0.15×106 in controls (p=0.005), the GMV in CIS was 0.58±0.05×106 vs. 0.67±0.03×106 in controls (p=0.001) and the WMV in CIS was 1±0.1×106 vs. 1.12±0.02×106 in controls (p=0.03).

Conclusions

This is the first study dealing with brain atrophy in a CIS sample from Latin America in which brain atrophy, mainly grey matter atrophy, was shown in early stages of the disease compared with healthy individuals.

Keywords:
Clinically isolated syndrome
Brain atrophy
SIENAX
Multiple sclerosis
Resumen
Introducción

Estudios previos demostraron que la atrofia cerebral (AC) aparece precozmente en esclerosis múltiple. Es nuestro objetivo evaluar la AC en pacientes con síndrome desmielinizante aislado (SDA) respecto a un grupo control en una población argentina.

Métodos

Se incluyó prospectivamente a pacientes con SDA durante el período junio de 2008 a junio de 2009. El grupo control estaba formado por sujetos sanos apareados por edad y sexo. Se utilizó el programa SIENAX para medir el volumen cerebral total (VCT), el volumen de sustancia gris (VSG) y de sustancia blanca (VSB) en cada grupo. Los datos se compararon con la prueba de Mann-Whitney. Se consideró significativo p<0,05.

Resultados

Se incluyó a 20 pacientes con SDA y 30 controles sanos (8 frente a 17 mujeres; p=0,11). La media de edad en SDA fue 35±6 frente a 34,4±5 años en controles (p=0.61). El EDSS de los pacientes con SDA fue 1,1±0,5; 18 pacientes (90%) con SDA tenían lesiones en la resonancia magnética cerebral. El VCT en SDA fue 1,6±0,22μl × 106 frente a 1,65±0,15 × 106 en controles (p=0,005); el VSG en SDA fue 0,58±0,05 × 106 frente a 0,67±0,03 × 106 en controles (p=0,001), y el VSB en SDA fue 1±0,1 × 106 frente a 1,12±0,02 × 106 en controles (p=0,03).

Conclusiones

Éste es el primer estudio en una población latinoamericana con SDA que demostró atrofia cerebral con predomino en la sustancia gris, respecto a un grupo control. Esta herramienta es coste-efectiva para la medición de la AC, aspecto poco estudiado en nuestro medio.

Palabras Claves:
Síndromes desmielinizantes aislados
Atrofia cerebral
SIENAX
Esclerosis múltiple
Full text is only aviable in PDF
References
[1.]
M. Tintore, et al.
Baseline MRI predicts future attacks and disability in clinically isolated syndromes.
[2.]
B. Ferguson, et al.
Axonal damage in acute multiple sclerosis lesions.
Brain, 120 (1997), pp. 393-399
[3.]
B.D. Trapp, et al.
Axonal transection in the lesions of multiple sclerosis.
N Engl J Med, 338 (1998), pp. 278-285
[4.]
D.L. Arnold, et al.
Proton magnetic resonance spectroscopy of human brain in vivo in the evaluation of multiple sclerosis: assessment of the load of disease.
Magn Reson Med, 14 (1990), pp. 154-159
[5.]
N. De Stefano, et al.
Chemical pathology of acute demyelinating lesions and its correlation with disability.
Ann Neurol, 38 (1995), pp. 901-909
[6.]
P.A. Narayana, et al.
Serial proton magnetic resonance spectroscopic imaging, contrast-enhanced magnetic resonance imaging, and quantitative lesion volumetry in multiple sclerosis.
Ann Neurol, 43 (1998), pp. 56-71
[7.]
R.A. Rudick, et al.
Use of the brain parenchymal fraction to measure whole brain atrophy in relapsing-remitting MS. Multiple Sclerosis Collaborative Research Group.
Neurology, 53 (1999), pp. 1698-1704
[8.]
D. Horakova, et al.
Gray matter atrophy and disability progression in patients with early relapsing-remitting multiple sclerosis: a 5-year longitudinal study.
J Neurol Sci, 282 (2009), pp. 112-119
[9.]
C.M. Dalton, et al.
Early development of multiple sclerosis is associated with progressive grey matter atrophy in patients presenting with clinically isolated syndromes.
Brain, 127 (2004), pp. 1101-1107
[10.]
S.M. Smith, et al.
Accurate, robust, and automated longitudinal and cross-sectional brain change analysis.
Neuroimage, 17 (2002), pp. 479-489
[11.]
Y. Zhang, M. Brady, S. Smith.
Segmentation of brain MR images through a hidden Markov random field model and the expectation-maximization algorithm.
IEEE Trans Med Imaging, 20 (2001), pp. 45-57
[12.]
N. De Stefano, et al.
Evidence of early cortical atrophy in MS: relevance to white matter changes and disability.
Neurology, 60 (2003), pp. 1157-1162
[13.]
J.H. Simon.
Brain atrophy in multiple sclerosis: what we know and would like to know.
Mult Scler, 12 (2006), pp. 679-687
[14.]
D. Kidd, et al.
Cortical lesions in multiple sclerosis.
Brain, 122 (1999), pp. 17-26
[15.]
J.W. Peterson, et al.
Transected neurites, apoptotic neurons, and reduced inflammation in cortical multiple sclerosis lesions.
Ann Neurol, 50 (2001), pp. 389-400
[16.]
N. Evangelou, et al.
Size-selective neuronal changes in the anterior optic pathways suggest a differential susceptibility to injury in multiple sclerosis.
Brain, 124 (2001), pp. 1813-1820
[17.]
M. Filippi, et al.
Evidence for widespread axonal damage at the earliest clinical stage of multiple sclerosis.
Brain, 126 (2003), pp. 433-437
[18.]
C. Enzinger, et al.
Accelerated evolution of brain atrophy and “black holes” in MS patients with APOE-epsilon 4.
Ann Neurol, 55 (2004), pp. 563-569
[19.]
J.H. Simon.
From enhancing lesions to brain atrophy in relapsing MS.
J Neuroimmunol, 98 (1999), pp. 7-15
[20.]
A.J. Coles, et al.
Monoclonal antibody treatment exposes three mechanisms underlying the clinical course of multiple sclerosis.
Ann Neurol, 46 (1999), pp. 296-304
Copyright © 2010. Sociedad Española de Neurología
Article options
es en pt

¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?

Você é um profissional de saúde habilitado a prescrever ou dispensar medicamentos