Transcranial Magnetic Stimulation (TMS) in Multiple Sclerosis

Transcranial Magnetic Stimulation (TMS) in Multiple Sclerosis

Publication date: Aug 20, 2019

Background: Transcranial Magnetic Stimulation (TMS) is a technique based on the principles of electromagnetic induction. It applies pulses of magnetic radiation that penetrate the brain tissue, and it is a non-invasive, painless and practically innocuous procedure. Previous studies advocate the therapeutic capacity of TMS in several neurodegenerative and psychiatric processes, both in animal models and in human studies. Its uses in Parkinson’s disease, Alzheimer’s disease and in Huntington’s chorea have shown improvement in the symptomatology and in the molecular profile, and even in the cellular density of the brain. Consequently, the extrapolation of these TMS results in the aforementioned neurodegenerative disease to other entities with etiopathogenic and clinical analogy would raise the relevance and feasibility of its use in multiple sclerosis (MS). The overall objective will be to demonstrate the effectiveness of the TMS in terms of safety and clinical improvement, as well as to observe the molecular changes in relation to the treatment. Methods and design: Phase I clinical trial, unicentric, controlled, randomised, single blind. A total of 90 patients diagnosed with relapsing-remitting multiple sclerosis (RRMS) who meet all the inclusion criteria and do not present any of the exclusion criteria that are established and from which clinically evaluable results can be obtained. The patients included will be assigned under the 1:1:1 randomization formula, constituting three groups for the present study: 30 patients treated with natalizumab + white (placebo) + 30 patients treated with natalizumab + TMS (1 Hertz) + 30 patients treated with natalizumab + TMS (5 Hertz). Discussion: Results of this study will inform on the efficiency of the TMS for the treatment of MS. The expected results are that TMS is a useful therapeutic resource to improve clinical status (main parameters) and neurochemical profile (surrogate parameters); both types of parameters will be checked.

Concepts Keywords
Action Potentials Accordance protocol
Acute Phase Reactants Procedures protocol
Adverse Event Neuroprotective progression disease
Albumin RRMS inflammatory forms
Alemtuzumab Contraction
ALT Chorea
Alzheimer Radiation
AST Medicine
Attenuation Clinical medicine
BDNF Organ systems
Biochemical Multiple sclerosis
Biochemistry Autoimmune diseases
Bioinformatic Electrotherapy
Biomarkers Medical devices
Blood Neurotechnology
Bone Transcranial magnetic stimulation
Brain Natalizumab
CEIC Evoked potential
Chorea Radiation
Clinical Trial Proteomics
Cognitive Procedures protocol
Confidentiality Accordance protocol
Contralateral
Craniocaudal
Depression
Differential
Dorsal
Dorsal Interosseous
Dorsal Interosseous Muscle
Electric Current
Electromagnetic Induction
Electromyograph
Electromyographic
EMG
Evoked Potentials
Evolution
External Validity
Extrapolation
Fatigue
Formula
Glucose
Glutathione
Glutathione Disulfide
Good Clinical Practice
GSSG
Helsinki
Hospital
Huntington
Hz
ICH
Informed Consent
Interrupt
Intravenous
LDH
Leukocytes
Mcl
Monoclonal Antibody
Motor Cortex
Motor Evoked Potentials
Multiple Sclerosis
Muscle
Muscle Fibres
Muscular Contraction
Natalizumab
Neurodegenerative
Neuroprotective
Neurotrophic Factors
Neutrophils
NGF
NMR
Nuclear Magnetic Resonance
Organic Law
Oxidative Damage
Oxidative Stress
PAMC
Parkinson
PEM
Perpendicular
Pharmacological
Placebo
Plasma
Platelet
Platelets
Primary Motor Cortex
Proteomic
Proteomics
Protocol
Radiation
Randomization
Relapse
REST
Serum
Single Blind
Spanish
Test
Transaminases
Transcranial Magnetic Stimulation
Vertex
Wales
Whitland
WMA

Semantics

Type Source Name
gene UNIPROT NR4A2
gene UNIPROT SLC17A5
gene UNIPROT CLEC4D
drug DRUGBANK Natalizumab
disease DOID relapsing-remitting multiple sclerosis
disease MESH relapsing-remitting multiple sclerosis
disease DOID neurodegenerative disease
disease MESH neurodegenerative disease
disease DOID Multiple Sclerosis
disease MESH Multiple Sclerosis
drug DRUGBANK Tilmicosin
gene UNIPROT ALG3
disease MESH Sclerosis

Similar

Original Article

Leave a Comment

Your email address will not be published. Required fields are marked *