Pathophysiology of cognitive impairment in multiple sclerosis

Research output: Contribution to journalArticle

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Abstract

Abstract Only in the last decade has significant progress been reached in understanding the pathophysiology of cognitive impairment in multiple sclerosis (MS). Edema, inflammation, demyelination and axonal loss may have different consequences on nerve fiber conduction, causing temporal disorganization or disruption of the inputs travelling along the intrahemispheric and interhemispheric connections among associative areas as well as between cortical and subcortical structures involved in mental functions. Neuropsychological, electrophysiological, metabolic and magnetic resonance imaging (MRI) studies have provided converging evidence that the most common type of cognitive dysfunction observed in MS patients, the so-called subcortical dementia, is an almost invariable complication of the advanced phases of the disease. In these phases, large amounts of brain white matter may be affected by microscopic and macroscopic lesions characterized by pronounced axonal loss. However, the acute occurence of transitory and isolated selective cognitive deficits or reversible dementia has been observed in a few patients. In these cases a pathogenetic role of the inflammatory process in cognitive changes is to be considered. In fact, antineural antibodies, proinflammatory cytokines and other neurotoxic substances may induce or regulate several critical cellular and electrophysiologic functions. Understan-ding how the cellular and humoral responses may be differently associated with acute or chronic disease evolution and with macroscopic and microscopic brain changes is essential for the formulation of a unifying pathogenetic model of cognitive impairment in MS.

Original languageEnglish
JournalItalian Journal of Neurological Sciences
Volume19
Issue number6 SUPPL.
Publication statusPublished - 1998

Fingerprint

Multiple Sclerosis
Dementia
Neural Conduction
Brain
Demyelinating Diseases
Acute Disease
Nerve Fibers
Edema
Chronic Disease
Magnetic Resonance Imaging
Cytokines
Inflammation
Antibodies
Cognitive Dysfunction
White Matter

Keywords

  • Cognitive dysfunction
  • Multiple sclerosis
  • Pet, event-related potentials © springer-verlag 1998

ASJC Scopus subject areas

  • Dermatology
  • Clinical Neurology
  • Psychiatry and Mental health
  • Neuroscience(all)

Cite this

Pathophysiology of cognitive impairment in multiple sclerosis. / Comi, G.; Martinelli, V.

In: Italian Journal of Neurological Sciences, Vol. 19, No. 6 SUPPL., 1998.

Research output: Contribution to journalArticle

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AB - Abstract Only in the last decade has significant progress been reached in understanding the pathophysiology of cognitive impairment in multiple sclerosis (MS). Edema, inflammation, demyelination and axonal loss may have different consequences on nerve fiber conduction, causing temporal disorganization or disruption of the inputs travelling along the intrahemispheric and interhemispheric connections among associative areas as well as between cortical and subcortical structures involved in mental functions. Neuropsychological, electrophysiological, metabolic and magnetic resonance imaging (MRI) studies have provided converging evidence that the most common type of cognitive dysfunction observed in MS patients, the so-called subcortical dementia, is an almost invariable complication of the advanced phases of the disease. In these phases, large amounts of brain white matter may be affected by microscopic and macroscopic lesions characterized by pronounced axonal loss. However, the acute occurence of transitory and isolated selective cognitive deficits or reversible dementia has been observed in a few patients. In these cases a pathogenetic role of the inflammatory process in cognitive changes is to be considered. In fact, antineural antibodies, proinflammatory cytokines and other neurotoxic substances may induce or regulate several critical cellular and electrophysiologic functions. Understan-ding how the cellular and humoral responses may be differently associated with acute or chronic disease evolution and with macroscopic and microscopic brain changes is essential for the formulation of a unifying pathogenetic model of cognitive impairment in MS.

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