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Abstract
Cognitive impairment affects 40–60% of patients with multiple sclerosis. It may be present early in the course of the disease and has an impact on a patient’s employability, social interactions, and quality of life. In the last three decades, an increasing interest in diagnosis and management of cognitive impairment has arisen. Neuropsychological assessment and neuroimaging studies focusing on cognitive impairment are now being incorporated as primary outcomes in clinical trials. However, there are still key uncertainties concerning the underlying mechanisms of damage, neural basis, sensitivity and validity of neuropsychological tests, and efficacy of pharmacological and non-pharmacological interventions. The present article aimed to present an overview of the assessment, neural correlates, and impact of cognitive impairment in multiple sclerosis.
Highlights
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS)
These phenotypes are related to potentially different pathophysiological disease mechanisms, including acute/chronic inflammation, axonal/neuronal loss and gliosis, and variable degrees of tissue repair, as well as plasticity and clinical recovery, mainly related to each individual [7], these differences have yet to be demonstrated at the molecular level [2]
The assessment of social cognition in MS include a myriad of tests used in other neurological disorders, for example the Face and Emotion Recognition (e.g., Ekman faces [64]) for social perception, Faux Pas, or Reading the Mind in the Eyes tests for theory of the mind tasks, or compound batteries previously used in other neurological disorders such as in frontotemporal dementia (e.g., Social Emotion Assessment [65,66])
Summary
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS). MS can be clinically categorized in different phenotypes, including clinically isolated syndrome (CIS), relapsing/remitting (RRMS), primary progressive and secondary progressive MS (SPMS), and can be subclassified according to its clinical and radiological activity [8] These phenotypes are related to potentially different pathophysiological disease mechanisms, including acute/chronic inflammation, axonal/neuronal loss and gliosis, and variable degrees of tissue repair, as well as plasticity and clinical recovery, mainly related to each individual [7], these differences have yet to be demonstrated at the molecular level [2]. Clinical symptoms of MS may include motor dysfunction (pyramidal); tremor, dysmetria, or ataxia (cerebellar); diplopia or nystagmus (brainstem); numbness (sensory); urinary/bowel hesitancy, incontinence, or retention; disturbances in vision and cognitive impairment The latter functional systems can be measured with the Expanded Disability Status Scale (EDSS), which range from. The following manuscript is not a systematic review about the topic, but an overview that aims to raise awareness on the cognitive deficits in MS, including the most affected cognitive domains and related neuropsychological batteries for their assessment, their neural correlates with an emphasis on neuroimaging, and a potential therapeutic approach as well as future perspectives
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