@article{pmid41990479,

title = {Increased PET C-PBR28 binding in multiple sclerosis normal-appearing white matter correlates with MRI measures of myelin loss},

author = {Irene M Vavasour and Nasim Vafai and Philippe Beauchemin and Elham Shahinfard and Cornelia Laule and Anthony Traboulsee and Vesna Sossi and Shannon H Kolind and Robert L Carruthers},

doi = {10.1016/j.msard.2026.107189},

issn = {2211-0356},

year  = {2026},

date = {2026-04-01},

journal = {Mult Scler Relat Disord},

volume = {110},

pages = {107189},

abstract = {INTRODUCTION: The Positron Emission Tomography (PET) tracer C-PBR28 binds to the Translocator Protein (TSPO), a marker of activated microglia. Advanced Magnetic Resonance (MR) techniques are sensitive to different tissue properties such as myelin (myelin water fraction, MWF; magnetisation transfer ratio, MTR; radial diffusivity, RD; choline, tCho), axons (axial diffusivity, AD; n-acetylaspartate, tNAA) and gliosis (myo-inositol, mI).nnOBJECTIVE: To compare C-PBR28 binding across MS subtypes and investigate the correlation between C-PBR28 binding and advanced MR measures in normal-appearing white matter (NAWM) and lesions.nnMETHODS: Twelve people living with MS (7 relapsing-remitting MS (RRMS) and 5 progressive MS (PMS)) and 6 healthy controls (HC) were scanned with PET and MRI. A 70-minute C-PBR28 PET session was used to determine the non-displaceable binding potential (BP). Advanced 3T MR included myelin water imaging, diffusion tensor imaging and spectroscopy. Mean measurements were extracted from lesion and NAWM masks.nnRESULTS: Within NAWM, C-PBR28 binding was different between groups (BP HC=0.70, RRMS=0.72, PMS=0.79; p = 0.03) and lesions exhibited lower BP (NAWM=0.75, lesion=0.63; p = 0.0002). Lesions also had lower MWF (NAWM=0.13, lesion=0.08) and MTR (NAWM=41.5, lesion=33.5), and higher AD (NAWM=1.05, lesion=1.41) and RD (NAWM=0.50, lesion=0.83) than NAWM (all p < 0.0001). In NAWM, correlations were found between PBR-BP and MWF (R=-0.71, p = 0.001) and MTR (R=-0.68, p = 0.003).nnCONCLUSIONS: Increased inflammation and gliosis indicated by elevated C-PBR28 binding in NAWM are associated with demyelination (decreased MWF and MTR), especially in PMS. The ability to measure and monitor diffuse inflammation could help evaluate therapies designed to target whole brain immune activity and more specifically microglia.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38343112,

title = {Hypogammaglobulinemia and Infection Risk in an Ocrelizumab-treated Multiple Sclerosis Cohort},

author = {Steven Nobile and Philippe Beauchemin},

doi = {10.1017/cjn.2024.21},

issn = {0317-1671},

year  = {2024},

date = {2024-02-01},

journal = {Can J Neurol Sci},

pages = {1--8},

abstract = {BACKGROUND: Ocrelizumab is an effective anti-CD20 therapy approved for Relapsing Remitting (RRMS) and Primary Progressive Multiple Sclerosis (PPMS). In clinical trials, a proportion of patients developed hypogammaglobulinemia which could contribute to infection risk. This study aimed to identify hypogammaglobulinemia and its risk factors and evaluate potentially associated serious infection risk in a real-world cohort of patients.nnMETHODS: All MS patients treated with ocrelizumab in a Quebec City MS clinic from January 2017 to August 2021 were included and detailed patient characteristics were collected by chart review. Levels of immunoglobulins (IgM, IgA and IgG) were assessed prior to each treatment. Serious infection was defined as an infection requiring hospitalization or emergency room treatment. Association between hypogammaglobulinemia and serious infection was analyzed.nnRESULTS: A total of 266 patients (average follow-up 2.05 years) were included (87% RRMS). After 6 infusions, 32.8%, 3.5% and 4.2% of patients had at least one IgM, IgA and IgG hypogammaglobulinemia event respectively. Aside from pre-treatment hypogammaglobulinemia, there were no variables associated with on-treatment hypogammaglobulinemia. There was a total of 21 serious infections (3.36 and 12.33 per 100-person-years in RRMS and PPMS). Developing hypogammaglobulinemia during treatment was not associated with serious infection. A regression analysis did not show associations between serious infection and key disease characteristics.nnCONCLUSION: Similar to ocrelizumab extension studies, our cohort demonstrated a significant rate of hypogammaglobulinemia over time, mostly with IgM. No association was found between hypogammaglobulinemia and serious infection.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid37066757,

title = {Virtual Management of Multiple Sclerosis: Providing Access or Just Phoning it in?},

author = {Paul S Giacomini and Jiwon Oh and Sarah A Morrow and Philippe Beauchemin and Fraser Clift and Virginia Devonshire and Penelope Smyth},

doi = {10.1017/cjn.2023.41},

issn = {0317-1671},

year  = {2024},

date = {2024-01-01},

journal = {Can J Neurol Sci},

volume = {51},

number = {1},

pages = {113--116},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid37320939,

title = {Clinical course, imaging, and pathological features of 45 adult and pediatric cases of myelin oligodendrocyte glycoprotein antibody-associated disease},

author = {Hayet Boudjani and Giulia Fadda and Gabrielle Dufort and Jack Antel and Paul Giacomini and Myriam Levesque-Roy and Maryam Oskoui and Pierre Duquette and Alexandre Prat and Marc Girard and Rose-Marie Rebillard and Inge Meijer and Elana Pinchefsky and Cam-Tu Emilie Nguyen and Elsa Rossignol and Jacinthe Rouleau and Oliver Blanchard and Nicole Khairallah and Philippe Beauchemin and Anne-Marie Trudelle and Emmanuelle Lapointe and Alexander Saveriano and Catherine Larochelle},

doi = {10.1016/j.msard.2023.104787},

issn = {2211-0356},

year  = {2023},

date = {2023-08-01},

journal = {Mult Scler Relat Disord},

volume = {76},

pages = {104787},

abstract = {BACKGROUND: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a recently described neuroinflammatory demyelinating disease.nnOBJECTIVE: To better understand the clinical spectrum, risk factors and outcomes in MOGAD.nnMETHODS: Retrospective cohort study including all subjects harboring anti-MOG antibodies identified in major academic hospitals across the province of Quebec.nnRESULTS: We identified 45 MOGAD cases. The minimal estimated point-prevalence was 0.52/100 000 in Quebec. Median age at presentation was 32 years (range 1-71) with equal sex ratio. Most frequent ethnic groups were Caucasians and Asians. The most frequent clinical manifestations at onset were optic neuritis (ON), affecting 56% of adults, and acute disseminated encephalomyelitis (ADEM), affecting 33% of children. First MRI was abnormal in 84% of cases. Most CSF samples showed pleocytosis without oligoclonal bands. Two brain biopsies revealed lipid-laden macrophages and reactive astrocytes. Despite steroids, only 38% had fully recovered at 4 weeks after onset. Half of pediatric and two thirds of adult-onset MOGAD subjects experienced relapses. At last follow-up, 69% showed residual deficits, which were moderate to severe in 17% of adults.nnCONCLUSION: MOGAD has heterogeneous disease course, and it is not a benign disease for a substantial proportion of adults. Best disease-modifying therapies remain to be determined.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35760506,

title = {Autoimmune storm following alemtuzumab},

author = {Chelsea Chan and Philippe Beauchemin and Ana-Luiza Sayao and Mollie Carruthers},

doi = {10.1136/bcr-2021-248037},

issn = {1757-790X},

year  = {2022},

date = {2022-06-01},

journal = {BMJ Case Rep},

volume = {15},

number = {6},

abstract = {Alemtuzumab has been associated with the emergence of secondary autoimmune diseases. We report a case of a patient with relapsing-remitting multiple sclerosis who developed a refractory immune thrombocytopaenia associated with vasculitis, myelofibrosis and later Guillain-Barré syndrome following alemtuzumab. The medical community should be aware of unusual and unexpected adverse events that may be associated with alemtuzumab, especially when occurring simultaneously in the same patient.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid33998416,

title = {Videoconferencing and Multiple Sclerosis Management: Stopgap or Stay Tuned?},

author = {Paul S Giacomini and Jiwon Oh and Sarah A Morrow and Philippe Beauchemin and Fraser Clift and Virginia Devonshire},

doi = {10.1017/cjn.2021.113},

issn = {0317-1671},

year  = {2022},

date = {2022-05-01},

journal = {Can J Neurol Sci},

volume = {49},

number = {3},

pages = {402--405},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35572514,

title = {SARS-CoV-2 and Multiple Sclerosis: Potential for Disease Exacerbation},

author = {Madison MacDougall and Jad El-Hajj Sleiman and Philippe Beauchemin and Manu Rangachari},

doi = {10.3389/fimmu.2022.871276},

issn = {1664-3224},

year  = {2022},

date = {2022-01-01},

journal = {Front Immunol},

volume = {13},

pages = {871276},

abstract = {While the respiratory tract is the primary route of entry for SARS-CoV-2, evidence shows that the virus also impacts the central nervous system. Intriguingly, case reports have documented SARS-CoV-2 patients presenting with demyelinating lesions in the brain, spinal cord, and optic nerve, suggesting possible implications in neuroimmune disorders such as multiple sclerosis (MS) and other related neuroimmune disorders. However, the cellular mechanisms underpinning these observations remain poorly defined. The goal of this paper was to review the literature to date regarding possible links between SARS-CoV-2 infection and neuroimmune demyelinating diseases such as MS and its related disorders, with the aim of positing a hypothesis for disease exacerbation. The literature suggests that SARS-CoV, SARS-CoV-2, and orthologous murine coronaviruses invade the CNS  the olfactory bulb, spreading to connected structures  retrograde transport. We hypothesize that a glial inflammatory response may contribute to damaged oligodendrocytes and blood brain barrier (BBB) breakdown, allowing a second route for CNS invasion and lymphocyte infiltration. Potential for molecular mimicry and the stimulation of autoreactive T cells against myelin is also described. It is imperative that further studies on SARS-CoV-2 neuroinvasion address the adverse effects of the virus on myelin and exacerbation of MS symptoms, as nearly 3 million people suffer from MS worldwide.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid33750481,

title = {Acephalgic Intracranial Hypotension: Subdural Haematoma Resolution After Blood Patch},

author = {Mohamed Reda Bensaidane and Philippe Beauchemin},

doi = {10.1017/cjn.2021.43},

issn = {0317-1671},

year  = {2022},

date = {2022-01-01},

journal = {Can J Neurol Sci},

volume = {49},

number = {1},

pages = {151--153},

keywords = {},

pubstate = {published},

tppubtype = {article}

}