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AzTrials

Progressive Multiple SclerosisNCT05811013

Effects of Transcranial Static Magnetic Field Stimulation (tSMS) in Progressive Multiple Sclerosis

A study testing Transcranial static magnetic field stimulation (tSMS) in people with Progressive Multiple Sclerosis, run by Neuromed IRCCS at 1 site in Italy.

Unknown status

Status not confirmed. The sponsor has not verified this record for over two years, so it may be out of date.

Official record
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Trial summary

In multiple sclerosis (MS) brains, inflammation induces specific abnormalities of synaptic transmission, collectively called inflammatory synaptopathy. Such synaptopathy consists in unbalanced glutamatergic and GABAergic transmission and in remarkable changes in synaptic plasticity, causing excitotoxic… Read more about this study

Who is it for?
Ages 18 to 65 years
Conditions the study is for
Progressive Multiple Sclerosis
What is being tested?
Transcranial static magnetic field stimulation (tSMS)
Type of treatment
Medical device
Could I receive a placebo?
Yes, some participants may receive a placebo
How many people
40 participants
Where
1 siteItaly
Study dates
27 May 2023to 27 May 2026
Phase
Interventional
Are there results?
None posted in the registry

Key requirements

Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.

  • Ages 18 to 65 years
  • All sexes
  • No healthy volunteers
  • Adult, Older adult

Who may be able to join

  • Ability to give written informed consent to the study
  • Age range 18-65 years
  • Diagnosis of primary of secondary progressive MS according to 2017 revised Macdonald's criteria (Thompson et al., 2017), presenting with signs of symptoms of progressive dysfunction of the corticospinal tract
  • EDSS ≤ 6,5
  • Ability to participate to the study protocol
  • No or stable (at least six months) DMT or rehabilitative treatments before study entry, and willingness not to change these therapies (including cannabinoids, SSRI, baclofen) during the study.

Who cannot join

  • Relapsing-remitting MS or progressive MS presenting with signs of symptoms other than those typical of the ascending myelopathy phenotype (i.e. progressive cerebellar or cognitive involvement)
  • Female with positive pregnancy test at baseline or having active pregnancy plans
  • Comorbidities for which synaptic plasticity may be altered (i.e., Parkinson's disease, Alzheimer's disease, stroke)
  • Contraindications to TMS
  • History or presence of any unstable medical condition such as malignancy or infection
  • Use of medications with increased risk of seizures (i.e. Fampridine, 4-Aminopyridine)
  • Concomitant use of drugs that may alter synaptic transmission and plasticity (L-dopa, antiepileptics)

Trial locations and contacts

1 site in 1 country.

Diego Centonze, MD, PhD contact

+39 0865 929170

centonze@uniroma2.it

Italy1 site, 1 recruiting

  • IRCCS Neuromed

    Pozzilli, Isernia, 86077

    Diego Centonze, MD, PhD, +39 0865 929170, centonze@uniroma2.it

    Recruiting

Other trials in Italy

About this study

In multiple sclerosis (MS) brains, inflammation induces specific abnormalities of synaptic transmission, collectively called inflammatory synaptopathy. Such synaptopathy consists in unbalanced glutamatergic and GABAergic transmission and in remarkable changes in synaptic plasticity, causing excitotoxic neurodegeneration and impairing the clinical compensation of the ongoing brain damage, thereby exacerbating the clinical manifestation of the disease. In progressive MS (PMS), synaptopathy is characterized by pathological potentatiation of glutamate-mediated synaptic up-scaling (Centonze et al., 2008; Rossi et al., 2013) and loss of long-term synaptic potentiation [LTP (Weiss et al., 2014)], both caused by proinflammatory molecules (released by microglia, astroglia, and infiltrating T and B lymphocytes) (Malenka et al., 2004; Di Filippo et al., 2017; Stampanoni Bassi et al., 2019). The combination of increased up-scaling and decreased LTP has a significant impact on the clinical manifestations of PMS, often presenting with signs and symptoms indicating length-dependent degeneration of neurons of the corticospinal tract. Altered LTP expression impairs brain ability to compensate ongoing neuronal loss (Stampanoni Bassi et al., 2020), and pathological TNF-mediated up-scaling may directly promote excitotoxic damage and neurodegeneration (Rossi et al., 2014). In addition, up-scaling and LTP are mutually exclusive at a given synapse through a mechanism of synaptic occlusion (i.e., pre-existing up-scaling saturates and prevents subsequent LTP expression), further promoting neurodegeneration by preventing the pro-survival effect of LTP, the induction of which activates intracellular anti-apoptotic pathways (Bartlett \& Wang, 2013). It follows that a neuromodulation approach that can chronically (over several months) dampen up-scaling expression in the primary motor cortex (M1) of PMS patients could be beneficial by preventing excitotoxic neurodegenerative damage triggered by up-scaling itself (Centonze et al. 2008, Rossi et al. 2014), and also by promoting LTP induction and LTP-dependent functional compensation of deficits, thereby reducing the speed of the neurodegeneration process through increased LTP-dependent neuronal survival and preservation of dendritic spines (Ksiazek-Winiarek et al., 2015). Our study aims to test whether transcranial static magnetic field stimulation (tSMS) could represent such a therapeutic approach, as recently proposed in patients with amyotrophic lateral sclerosis (ALS) (Di Lazzaro et al, 2021). Forty (40) ambulatory patients with PMS, presenting with the ascending myelopathy phenotype of the disease, will be recruited at the MS Center of the Unit of Neurology of the IRCCS Neuromed in Pozzilli (IS). In this randomized, sham-controlled, double-blind, within-subjects, cross-over study (allocation ratio 1:1), we will test the ability of repeated sessions of tSMS applied bilaterally over the M1 to safely reduce disability progression in patients with PMS. Patients will be randomly assigned to either real or sham tSMS. Each patient will participate in two experimental phases (real or sham stimulation). Each patient will self-administer tSMS over right and left M1, two session per day, 60 minutes each. The order will be randomly established and counterbalanced across participants. Both investigators and participants will be blinded to stimulation parameters. In the "real stimulation" phase, tSMS will be applied for 120 minutes each day, at home, for 12 consecutive months. In the "sham stimulation" phase, sham tSMS will be delivered with non-magnetic metal cylinders, with the same size, weight and appearance of the magnets. Clinical evaluations, including the Multiple Sclerosis Functional Composite measure (MSFC) will be performed before, during and after each experimental phase ("real" and "sham"). In addition, blood levels of neurofilaments, excitability and plasticity of M1, and MRI measures of cortical thickness will be measured before, during and after each stimulation phase.

Being tested
Transcranial static magnetic field stimulation (tSMS), Sham Transcranial static magnetic field stimulation (tSMS)
Keywords
Progressive Multiple Sclerosis, transcranial Static Magnetic Field Stimulation, disability progression, cortical hyperexcitability, cortical plasticity
Medical subject headings
Multiple Sclerosis, Chronic Progressive

What participants receive

What participants receive. In a randomised study each person is assigned to one group by chance.

  • Transcranial static magnetic field stimulation (tSMS)Device

    Patients will be randomly assigned to either real or sham tSMS. Real or sham tSMS will be performed daily without any interruption during each session of 60 min. Each patient will be instructed to self-administer tSMS, two sessions per day (AM and PM, 6-10 hours apart), sequentially for 60 minutes each, for 6 +6 months. Patients will choose whether to undergo stimulation at home or in the hospital on an outpatient setting. Real tSMS will be delivered with two cylindrical neodymium magnets (grade N45) of 45 mm diameter and 30 mm of thickness, with a weight of 360 g (MAG45r; Neurek SL, Toledo, Spain), applied with south polarity, each pointing toward the motor cortex. To discharge the weight of the helmet from the head during the sessions, patients will be instructed to rest the back of head and helmet on an inclined surface in a comfortable position. They will be also instructed to rest, minimizing movement, and not to watch audiovisuals during the stimulation sessions.

  • Sham Transcranial static magnetic field stimulation (tSMS)Device

    Real or sham tSMS will be performed daily without any interruption during each session of 60 min. Each patient will be instructed to self-administer tSMS, two sessions per day (AM and PM, 6-10 hours apart), sequentially for 60 minutes each, for 6 +6 months. Sham tSMS will be delivered with non-magnetic metal cylinders, with the same size, weight and appearance of the magnets (MAG45s; Neurek SL, Toledo, Spain).

Study groups in NCT05811013
Study groupRoleWhat they receive
Transcranial static magnetic field stimulation (tSMS)ExperimentalTranscranial static magnetic field stimulation (tSMS) will be performed daily without any interruption during each session of 60 min. Each patient will be instructed to self-administer tSMS, two sessions per day (AM and PM, 6-10 hours apart), sequentially for 60 minutes each, for 6 +6 months.
Receives: Device: Transcranial static magnetic field stimulation (tSMS)
Sham tSMSSham comparatorSham Transcranial static magnetic field stimulation (tSMS) Sham tSMS will be delivered with non-magnetic metal cylinders, with the same size, weight and appearance of the magnets (MAG45s; Neurek SL, Toledo, Spain). Real and sham magnets will be held with an ergonomic helmet (MAGmv1.0; Neurek SL, Toledo, Spain).
Receives: Device: Sham Transcranial static magnetic field stimulation (tSMS)

What is being measured

The primary outcome is the main question the study is designed to answer.

  1. Functional assessment, that "change" is being assessed.

    The primary aim the project is to evaluate the effect of tSMS in ambulatory patients with PMS with ascending myelopathy phenotype (from now on, simply called PMS) on clinical severity, assessed through the three components of the Multiple Sclerosis Functional Composite (MSFC).

    Measured: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

Secondary outcomes (18)

  1. Neurological Assessment, that "change" is being assessed.

    Clinical severity will be assessed through the Expanded Disability Status Scale (EDSS).

    Measured: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

  2. Neuropsychological and psychometric evaluation

    Verbal episodic long-term memory will be evaluated with the Selective Reminding Test as LongTerm Storage (SeRT-LTS).

    Measured: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

  3. Neuropsychological and psychometric evaluation

    Verbal episodic long-term memory will be evaluated with the Consistent Long Term Retreival (SeRT-CLTR).

    Measured: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

  4. Neuropsychological and psychometric evaluation

    Verbal episodic long-term memory will be evaluated with the Delayed Recall (SeRT-DR).

    Measured: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

  5. Neuropsychological and psychometric evaluation

    Visuos patial episodic long-term memory will be evaluated with the Delayed Recall of Rey's Complex Figure (RCF- DR).

    Measured: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

  6. Neuropsychological and psychometric evaluation

    Executive functions and attention will be evaluated with Word List Generation (WLG).

    Measured: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

  7. Neuropsychological and psychometric evaluation

    Executive functions and attention will be evaluated with Symbol Digit Modalities Test (SDMT).

    Measured: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

  8. Neuropsychological and psychometric evaluation

    Executive functions and attention will be evaluated with Paced Auditory Serial Addition Test (PASAT).

    Measured: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

  9. Neuropsychological and psychometric evaluation

    Executive functions and attention will be evaluated with Stroop Test interference both in terms of errors (ST-E)

    Measured: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

  10. Neuropsychological and psychometric evaluation

    Executive functions and attention will be evaluated with response time (ST-RT)

    Measured: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

  11. Neuropsychological and psychometric evaluation

    Executive functions and attention will be evaluated with Brief Visuospatial Memory Test (BVMT)

    Measured: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

  12. Neuropsychological and psychometric evaluation

    Praxis ability will be evaluated with the Copy of Rey's Complex.

    Measured: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

  13. Neuropsychological and psychometric evaluation

    Anxiety will be assessed by State-Trait Anxiety Inventory form Y (STAI-Y)

    Measured: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

  14. Neuropsychological and psychometric evaluation

    Depression will be assessed with the Beck Depression Inventory-Second Edition (BDI-II).

    Measured: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

  15. Neurophysiological assessment

    Transcranial magnetic stimulation will be delivered with Magstim 2002 magnetic stimulators or with a Magstim Rapid2 stimulator (The Magstim Company, Whitland, Dyfed, UK). The stimulators will be connected to a figure-of-eight coil (external wing diameter 70 mm) placed tangentially over the scalp with the handle pointing back and away from the midline at about 45°, in the optimal position for eliciting motor evoked potentials (MEPs) in the first dorsal interosseous (FDI) muscle of the dominant hand. Electromyographic signals will be recorded with surface electrodes placed on the target muscle, sampled at 5 KHz with a CED 1401 A/D laboratory interface (Cambridge Electronic Design, Cambridge, UK), and amplified and filtered (bandpass 20 Hz to 2 kHz) with a Digitimer D360 amplifier (Digitimer Ltd, Welwyn Garden City, Hertfordshire, UK), then recorded by a computer with Signal software (Cambridge Electronic Design). Motor thresholds will be calculated at rest (RMT) as the lowest stimul

    Measured: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

  16. blood neurofilament light chain (NFL) levels

    Measures of NfL will be prospectively performed in the laboratory of Dr. Roberto Furlan (IRCCS San Raffaele, Milan). As a specific marker of neuroaxonal degeneration, increasing serum levels of NfL are seen in patients with a higher degree of disability independently of ongoing relapses (Bjornevik et al., 2020). Together with the medium and heavy subunits, NfL represents one of the scaffolding proteins of the neuronal cytoskeleton and is released in the extracellular space following axonal damage (Teunissen CE, Khalil M. 2012). The levels of serum sNfL, are a sensitive biomarker of ongoing neuroaxonal degeneration and represent a sensitive and clinically meaningful blood biomarker to monitor tissue damage and the effects of therapies in MS (Di Santo et al., 2017).

    Measured: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

  17. Magnetic Resonance Imaging (MRI)

    Cortical thickness and T2 lesion load will be analyzed by using the 3T MR scanner (GE Signa HDxt, GE Healthcare, Milwaukee, Wisconsin). Will be used a 3D Spoiled Gradient Recalled (SPGR) T1-weighted sequence (178 contiguous sagittal slices, voxel size 1×1×1 mm, TR 7 ms, TE 2.856 ms, Inversion Time 450 ms) and a 3D FLAIR sequence (208 contiguous sagittal 1.6 mm slices, voxel size, 0.8 × 0.8 × 0.8 mm, TR 6000 ms, TE 139.45 ms; Inversion Time 1827 ms). White matter lesions will be segmented from FLAIR and T1 images by using the lesion growth algorithm as implemented in version 2.0.15 of the lesion segmentation tool (www.statistical-modelling.de/lst.html) for SPM12 (https://www.fl.ion.ucl.ac.uk/spm). Furthermore, the computational anatomy toolbox (CAT12, version 916, https://dbm.neuro.uni-jena.de/cat/) as implemented in SPM12 will be used to extract individual cortical thickness values from lesion-filled MR images. Finally, T2 lesion load will be computed from 3D T1 and 3d FLAIR images by

    Measured: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

  18. Patients' adherence to tSMS, potential side effects and adverse events

    The number of completed stimulation sessions will be recorded daily by each patient and/or the caregiver during the periods of self-administered tSMS treatment. Patients will fill a diary in which they will be instructed to record the following data:

    likert scale on sleep quality, presence of headache, treatment compliance. Potential side effects and adverse events will be reported by patients to the referring physician. If necessary, further clinical evaluations will be scheduled.

    At each timepoint, compliance will be assessed according to the following criteria:

    • "fully compliant" if he/she has performed at least 80% of the planned sessions of stimulation,
    • "moderately compliant" if he/she has performed between 50% and 80% of the treatment sessions,
    • "poor -compliant" if he/she has performed <50% of the treatment sessions. Caregivers will be instructed to monitor and favor treatment adherence.

    Measured: 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)

Timeline

From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.

  1. First posted13 Apr 2023
  2. Study start27 May 2023
  3. Primary completion27 May 2025 (estimated)
  4. Study completion27 May 2026 (estimated)

Resources

More details

For doctors and researchers: how the study is designed, who runs it, and its registry IDs.

Study design
Study type
Interventional
Phase
Phase N/A
Primary purpose
Treatment
Allocation
Randomised
Intervention model
Crossover
Model description
We will conduct a randomized, sham-controlled, double-blind, within-subjects, cross-over study (allocation ratio 1:1) to test the ability of repeated sessions of tSMS to safely reduce disability progression in patients with PMS.
Masking
Triple blind
Who is masked
Participant, Care provider, Outcomes assessor
Enrolment
40 participants (estimated)
IDs, dates and publications
ClinicalTrials.gov ID
NCT05811013
Sponsor's protocol ID
tSMS-MS
Status last verified
Oct 2024
First submitted
16 Mar 2023
Last updated
16 Oct 2024
Results posted
No
Data monitoring committee
No
FDA-regulated drug
No
FDA-regulated device
No

Publications

  • Bartlett TE, Wang YT. The intersections of NMDAR-dependent synaptic plasticity and cell survival. Neuropharmacology. 2013 Nov;74:59-68. doi: 10.1016/j.neuropharm.2013.01.012. Epub 2013 Jan 25.

    PubMed 23357336

  • Bjornevik K, Munger KL, Cortese M, Barro C, Healy BC, Niebuhr DW, Scher AI, Kuhle J, Ascherio A. Serum Neurofilament Light Chain Levels in Patients With Presymptomatic Multiple Sclerosis. JAMA Neurol. 2020 Jan 1;77(1):58-64. doi: 10.1001/jamaneurol.2019.3238.

    PubMed 31515562

  • Bliss TV, Lomo T. Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path. J Physiol. 1973 Jul;232(2):331-56. doi: 10.1113/jphysiol.1973.sp010273.

    PubMed 4727084

  • Centonze D, Rossi S, Tortiglione A, Picconi B, Prosperetti C, De Chiara V, Bernardi G, Calabresi P. Synaptic plasticity during recovery from permanent occlusion of the middle cerebral artery. Neurobiol Dis. 2007 Jul;27(1):44-53. doi: 10.1016/j.nbd.2007.03.012. Epub 2007 Apr 5.

    PubMed 17490888

  • Di Filippo M, Mancini A, Bellingacci L, Gaetani L, Mazzocchetti P, Zelante T, La Barbera L, De Luca A, Tantucci M, Tozzi A, Durante V, Sciaccaluga M, Megaro A, Chiasserini D, Salvadori N, Lisetti V, Portaccio E, Costa C, Sarchielli P, Amato MP, Parnetti L, Viscomi MT, Romani L, Calabresi P. Interleukin-17 affects synaptic plasticity and cognition in an experimental model of multiple sclerosis. Cell Rep. 2021 Dec 7;37(10):110094. doi: 10.1016/j.celrep.2021.110094.

    PubMed 34879272

  • Di Lazzaro V, Profice P, Pilato F, Capone F, Ranieri F, Pasqualetti P, Colosimo C, Pravata E, Cianfoni A, Dileone M. Motor cortex plasticity predicts recovery in acute stroke. Cereb Cortex. 2010 Jul;20(7):1523-8. doi: 10.1093/cercor/bhp216. Epub 2009 Oct 5.

    PubMed 19805417

  • Di Lazzaro V, Musumeci G, Boscarino M, De Liso A, Motolese F, Di Pino G, Capone F, Ranieri F. Transcranial static magnetic field stimulation can modify disease progression in amyotrophic lateral sclerosis. Brain Stimul. 2021 Jan-Feb;14(1):51-54. doi: 10.1016/j.brs.2020.11.003. Epub 2020 Nov 10. No abstract available.

    PubMed 33186779

  • Disanto G, Barro C, Benkert P, Naegelin Y, Schadelin S, Giardiello A, Zecca C, Blennow K, Zetterberg H, Leppert D, Kappos L, Gobbi C, Kuhle J; Swiss Multiple Sclerosis Cohort Study Group. Serum Neurofilament light: A biomarker of neuronal damage in multiple sclerosis. Ann Neurol. 2017 Jun;81(6):857-870. doi: 10.1002/ana.24954.

    PubMed 28512753

  • Kos D, Kerckhofs E, Carrea I, Verza R, Ramos M, Jansa J. Evaluation of the Modified Fatigue Impact Scale in four different European countries. Mult Scler. 2005 Feb;11(1):76-80. doi: 10.1191/1352458505ms1117oa.

    PubMed 15732270

  • Krupp LB, LaRocca NG, Muir-Nash J, Steinberg AD. The fatigue severity scale. Application to patients with multiple sclerosis and systemic lupus erythematosus. Arch Neurol. 1989 Oct;46(10):1121-3. doi: 10.1001/archneur.1989.00520460115022.

    PubMed 2803071

  • Ksiazek-Winiarek DJ, Szpakowski P, Glabinski A. Neural Plasticity in Multiple Sclerosis: The Functional and Molecular Background. Neural Plast. 2015;2015:307175. doi: 10.1155/2015/307175. Epub 2015 Jul 2.

    PubMed 26229689

  • Lu Y, Christian K, Lu B. BDNF: a key regulator for protein synthesis-dependent LTP and long-term memory? Neurobiol Learn Mem. 2008 Mar;89(3):312-23. doi: 10.1016/j.nlm.2007.08.018. Epub 2007 Oct 17.

    PubMed 17942328

  • Malenka RC, Bear MF. LTP and LTD: an embarrassment of riches. Neuron. 2004 Sep 30;44(1):5-21. doi: 10.1016/j.neuron.2004.09.012.

    PubMed 15450156

  • Mori F, Kusayanagi H, Nicoletti CG, Weiss S, Marciani MG, Centonze D. Cortical plasticity predicts recovery from relapse in multiple sclerosis. Mult Scler. 2014 Apr;20(4):451-7. doi: 10.1177/1352458513512541. Epub 2013 Nov 21.

    PubMed 24263385

  • Mori F, Rossi S, Piccinin S, Motta C, Mango D, Kusayanagi H, Bergami A, Studer V, Nicoletti CG, Buttari F, Barbieri F, Mercuri NB, Martino G, Furlan R, Nistico R, Centonze D. Synaptic plasticity and PDGF signaling defects underlie clinical progression in multiple sclerosis. J Neurosci. 2013 Dec 4;33(49):19112-9. doi: 10.1523/JNEUROSCI.2536-13.2013.

    PubMed 24305808

Questions about this trial

What is this clinical trial studying?

A study testing Transcranial static magnetic field stimulation (tSMS) in people with Progressive Multiple Sclerosis, run by Neuromed IRCCS at 1 site in Italy.

The full registered description is in the About this study section and the official record.

Who may be eligible to take part?

The sponsor lists 6 inclusion and 7 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.

Is this clinical trial currently recruiting?

The record says: status not confirmed, as of the sponsor's last update on 16 Oct 2024. Status can change between updates, so confirm with the study contact before making plans.

Where is the study taking place?

The record lists 1 site in Italy. Whether a site is taking part right now should be confirmed with that site. See every site.

What are the possible benefits and risks?

They depend on the study and the treatment, and no study can promise a benefit. Some participants in this study may receive a placebo. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.

Are results available for this study?

Results are not available in the source record.

How can a doctor refer a patient or contact the research team?

Contact Diego Centonze, MD, PhD (+39 0865 929170, centonze@uniroma2.it), or a site near the patient. AzTrials does not enrol participants or take referrals.

What does the primary outcome measure?

Functional assessment, that "change" is being assessed. (time frame: BASELINE EVALUATION 1-30 DAYS BEFORE REAL OR SHAM tSMS T0; 6 MONTHS OF STIMULATION (SESSION 1, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 1, T12); 6 MONTHS OF STIMULATION (SESSION 2, T6); 1-30 DAYS AFTER THE END OF STIMULATION (SESSION 2, T12)). It is what the study was designed to measure, not a finding.

Where can I read the original study information?

On the ClinicalTrials.gov record for NCT05811013, which also lists 25 linked publications.

Does a listing mean the treatment is approved or proven to work?

No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.

How often is this information updated?

AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 16 Oct 2024.

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