Abstract

Multiple sclerosis (MS) is a demyelinating disorder of the central nervous system. Disease progression is variable and unpredictable, warranting the development of biomarkers of disease status. Transcranial magnetic stimulation (TMS) is a noninvasive method used to study the human motor system, which has shown potential in MS research. However, few reviews have summarized the use of TMS combined with clinical measures of MS and no work has comprehensively assessed study quality. This review explored the viability of TMS as a biomarker in studies of MS examining disease severity, cognitive impairment, motor impairment, or fatigue. Methodological quality and risk of bias were evaluated in studies meeting selection criteria. After screening 1603 records, 30 were included for review. All studies showed high risk of bias, attributed largely to issues surrounding sample size justification, experimenter blinding, and failure to account for key potential confounding variables. Central motor conduction time and motor-evoked potentials were the most commonly used TMS techniques and showed relationships with disease severity, motor impairment, and fatigue. Short-latency afferent inhibition was the only outcome related to cognitive impairment. Although there is insufficient evidence for TMS in clinical assessments of MS, this review serves as a template to inform future research.

Highlights

  • Multiple sclerosis (MS) is a neuroimmune-regulated demyelinating disease affecting the central nervous system (CNS) [1, 2]

  • The above outcomes suggest that further research is required to assert the viability of Transcranial magnetic stimulation (TMS) as a clinical marker of MS disease status

  • Due in part to a relative paucity of biological markers for MS disease status, some authors have promoted the use of TMS in clinical assessments of MS

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Summary

Introduction

Multiple sclerosis (MS) is a neuroimmune-regulated demyelinating disease affecting the central nervous system (CNS) [1, 2]. The exact etiology of MS is not fully understood, disease pathophysiology is characterized by a process of blood-brain barrier damage, inflammation involving macrophages and microglia, demyelination of gray and white matter, loss of oligodendrocytes, reactive gliosis in parenchymal tissue, axonal degeneration and transection, and cortical atrophy [2]. This process is thought to be incited by environmental triggers in a genetically susceptible individual, albeit both the suspected environmental factors and candidate genes are numerous [1, 2]. The above evidence emphasizes the urgent need to establish viable biological markers (“biomarkers”) of disease status in MS [2, 24]

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