Displaying One Session
TC07.01 - Assessment and Monitoring of Cognitive Function in MS (ID 607)
Abstract
Abstract
The hallmarks of cognitive impairment (CI) in MS are slowed cognitive processing and deficient learning, as originally described by Charcot nearly 150 years ago. This session undertakes the question of what specific tools should be applied in clinical routine care of MS patients, and how often they should be applied? Cognitive assessment is becoming a mainstay of routine care in MS clinics, as a result of initiatives such as the Brief International Cognitive Assessment for MS (BICAMS) and the MS Outcomes Assessment Consortium (MSOAC). Computerized Assessment Neuropsychological Devices (CNADs) are more common and were recently reviewed by a Cognition Work Group from the National MS Society (NMSS). In this lecture, we will cover recent research on CI that presents as progressive decline, and, acute disease activity. Using the Symbol Digit Modalities Test (SDMT), slowed cognitive processing has been documented in clinical relapses, and in isolation, presumably an isolated transient decline in cognition. The authors will review recommendations of a recent National MS Society (NMSS) consensus opinion paper, and discuss ways to apply conventional and computer-assisted methods to address various triggers for neuropsychological evaluation, including cognitive relapse, treatment monitoring, negative work events, and psychiatric exacerbation.
TC07.02 - MRI Predictors of Cognitive Impairment (ID 608)
Abstract
Abstract
Several magnetic resonance imaging (MRI) studies have been performed to characterize the pathological abnormalities associated with cognitive impairment (CI), using both morphological and functional analyses.For a better understanding of the role of the different mechanisms involved in CI, it could be worth to study specific cognitive domains separately and to focus on early stages when all mechanisms could be more easily disentangled. Indeed, when considering the two more frequent cognitive processes impaired at the early stage of the disease, Information processing speed (IPS) and memory, different mechanisms could be discussed. At this early stage of the disease, the role of focal lesions, network disruption or gray matter (GM) vulnerability has been suggested. IPS depend on the integrity of large-scale cortical integrative processes, which involve long-distance white matter projections which can be impaired due to diffuse demyelinating injury in patients (focal lesions) and the axonal pathology related to these lesions. In early RRMS the correlation of CI with lesion load is no longer significant when diffuse white matter pathology (normal appearing white matter magnetization transfer ratio or DTI metrics) are taken into account suggesting that disconnection play an important role in CI, mainly in IPS deficits. The involvement of several key brain regions has been shown, contributing to these deficits, such as the thalamus, the cerebellum and default mode network. Episodic memory impairment is associated with deep GM injury in the limbic system, in particular the hippocampi and the basal ganglia. The growing role, along the disease course, of GM pathology spreading initially in regions with more vulnerability in deep GM and the cortex and leading to progressive brain atrophy could explain the deterioration of memory or other domains like executive functions.
Functional MRI studies gave evidence of brain reorganization at these early stages suggesting the presence of compensatory mechanisms. The evolution of structure-function relationships during the early stages of MS and their role in cognitive performance have been studied recently. Alteration of structural-functional coupling could contribute to network collapse associated with a decline in cognitive status.
TC07.03 - Treatment of Cognitive Deficits in MS Patients (ID 609)
Abstract
Abstract
Title
Treatment of cognitive deficits in MS
Background
Despite the high prevalence of cognitive impairment in Multiple Sclerosis (MS) and its tremendous effects on working ability and quality of life, evidence-based and effective treatment strategies are still an unmet need and solutions urgently requested.
Objectives
To provide an overview on the efficacy of pharmacological and non-pharmacological approaches in managing cognitive deficits in MS.
Methods
This part of the teaching course will review and critically discuss whether pharmacological and non-pharmacological treatment options have the potential to treat cognitive impairment in MS.
Results
Overall, patients receiving immunotherapy show better cognitive performance than patients under placebo. Since head-to-head studies are missing no clear statement about superiority can be given. Non-pharmacological treatment strategies (e.g. exercise, cognitive training, cognitive behavioral approaches, meditation) have the potential to support cognitive reserve and self-efficacy which in turn helps to manage cognitive impairment.
Conclusions
Immunotherapies are able to stabilize cognitive performance over time or even to improve cognitive status by targeting on inflammation. From all data available it can be assumed that the earlier we treat, the better the cognitive outcome in the long run.
Non-pharmacological treatment strategies offer the opportunity to improve patients’ self-efficacy and cognitive performance, do not have considerable side-effects, are cost-efficient and therefore highly recommendable in treating MS patients with cognitive problems.