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Principal Cause of Cerebral Atrophy in Multiple Sclerosis Unknown.

Until now, it was thought that the lesions or plaques observed in the white matter were the cause of the damage to the brain. New data indicates that these plaques account for only 30% of the atrophy in the grey matter; other unexplained neurodegenerative mechanisms are therefore also implicated.

Multiple sclerosis is a chronic inflammatory neurodegenerative disease of the central nervous system that affects the brain and spinal cord. It is the most common chronic neurologic disease in young people and adults in Europe and affects approximately 2.5 million people throughout the world. The study, published in the journal  Archives of Neurology (66(2):173-9), was carried out by the team of Dr. Pablo Villoslada at the University of Navarre. Last December, these researchers joined Hospital Clínic, Barcelona-IDIBAPS. Until now, it was thought that the atrophy seen in the brains of patients with multiple sclerosis was caused by the plaque in the white matter. The new results show that these plaques explain only 30% of the lesions.

Until now it was assumed that multiple sclerosis predominantly affected myelin, a fat that sheaths the nerves. It was thought that the plaques that form in the myelin were directly responsible for the atrophy of the grey matter. This study was designed to determine whether the loss of volume–atrophy–in the brain’s structures was related to the presence of lesions or cuts in the nerves connected to them.

Scheme of the raising of the study published at Archives of Neurology The researchers analyzed the brains of 81 people (61 with multiple sclerosis and 20 healthy people) using magnetic resonance imaging and a morphometric method (volumetry). The study focused on the optical pathway, starting with the hypothesis that lesions in this part of the brain, and in no other, correlate with atrophy of the occipital cortex and the lateral geniculate nucleus (LGN), the main centers for processing visual information. The results indicate that the lesions in the white matter of the nerves originating in the LGN explain up to 28% of the variation in volume. Atrophy of the occipital cortex did not correspond to the presence of lesions in the optical pathway, probably because it is associated with many other pathways.

Thus, although the sclerotic plaques in the nerves contribute significantly to the atrophy of the grey matter, the remaining 72% must still be explained. The data suggest that other neurodegenerative processes are involved. Because atrophy of the grey matter is the main cause of the progressive form of the disease and its severe sequelae, it is important to gain a better understanding of the principal mechanism of the damage, apart from the classic plaques, in order to be able to apply this knowledge to treating the disease.