Dr. Kipp specializes in the diagnosis and treatment of neuroimmunological disorders, particularly demyelinating conditions such as multiple sclerosis and neuromyelitis optica. He is interested in translational research connecting expert MS clinicians, world-renown immunology laboratories, and advanced neuroimaging techniques to identify biomarkers of disease and treatment response.
Clinical Assistant Professor, Neurology & Neurological Sciences
Director, MS/Clinical Neuroimmunology Fellowship Program (2016 - Present)
Honors & Awards
MS Clinical Fellowship Award, Canadian Network of Multiple Sclerosis Clinics (2014)
Boards, Advisory Committees, Professional Organizations
Fellow, Royal College of Physicians and Surgeons of Canada (2014 - Present)
Member, American Academy of Neurology (2008 - Present)
Member, National Consortium of MS Clinics (2016 - Present)
Fellowship:Stanford University Neuroimmunology and Multiple Sclerosis FellowshipCA
Fellowship:University College London Institute of Neurology (2015) United Kingdom
Residency:University of British Columbia Dept of Neurology (2014) Canada
Clinical Fellowship, Stanford University School of Medicine, CA, MS/Neuroimmunology (2016)
Board Certification: Neurology, Royal College of Physicians and Surgeons of Canada (2014)
Research Fellowship, University College London, London, UK, MS Advanced Neuroimaging (2015)
Neurology Residency, University of British Columbia, Vancouver, Canada (2014)
Medical Education:University of Western Ontario (2009) Canada
Doctor of Medicine (MD), University of Western Ontario, London, Canada (2009)
Bachelor of Science (BSc), University of Western Ontario, London, Canada (2005)
Reduced neurite density in the brain and cervical spinal cord in relapsing-remitting multiple sclerosis: A NODDI study.
Multiple sclerosis (Houndmills, Basingstoke, England)
BACKGROUND: Multiple sclerosis (MS) affects both brain and spinal cord. However, studies of the neuraxis with advanced magnetic resonance imaging (MRI) are rare because of long acquisition times. We investigated neurodegeneration in MS brain and cervical spinal cord using neurite orientation dispersion and density imaging (NODDI).OBJECTIVE: The aim of this study was to investigate possible alterations, and their clinical relevance, in neurite morphology along the brain and cervical spinal cord of relapsing-remitting MS (RRMS) patients.METHODS: In total, 28 RRMS patients and 20 healthy controls (HCs) underwent brain and spinal cord NODDI at 3T. Physical and cognitive disability was assessed. Individual maps of orientation dispersion index (ODI) and neurite density index (NDI) in brain and spinal cord were obtained. We examined differences in NODDI measures between groups and the relationships between NODDI metrics and clinical scores using linear regression models adjusted for age, sex and brain tissue volumes or cord cross-sectional area (CSA).RESULTS: Patients showed lower NDI in the brain normal-appearing white matter (WM) and spinal cord WM than HCs. In patients, a lower NDI in the spinal cord WM was associated with higher disability.CONCLUSION: Reduced neurite density occurs in the neuraxis but, especially when affecting the spinal cord, it may represent a mechanism of disability in MS.
View details for DOI 10.1177/1352458519885107
View details for PubMedID 31682198
- Coexistence of Neuromyelitis Optica and Amyotrophic Lateral Sclerosis: A Case Report NEUROHOSPITALIST 2019; 9 (1): 37–40
A case of GFAP-astroglial autoimmunity presenting with reversible parkinsonism.
Multiple sclerosis and related disorders
2019; 39: 101900
Autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy is a newly recognized autoimmune central nervous system (CNS) inflammatory disorder, presenting with an array of neurological symptoms in association with autoantibodies against GFAP, a hallmark protein expressed on astrocytes. Limited knowledge is available on the disease pathogenesis and clinical outcome. Here, we report a case of autoimmune GFAP astrocytopathy presenting with encephalomyelitis and parkinsonism. Our patient was a 66-year old male who experienced progressive somnolence, apathy, anxiety, right arm tremor, urinary retention, progressive weakness, and falls over the course of three months, followed by acute delusional psychosis. His neurologic exam on hospital admission was notable for cognitive impairment, myoclonus, rigidity, right hand action tremor, bradykinesia, shuffling gait, and dysmetria. Cerebrospinal fluid examination showed elevated protein, lymphocytic pleocytosis, and one unique oligoclonal band. Magnetic resonance imaging (MRI) revealed non-specific T2/FLAIR hyperintensities in the brain and longitudinally extensive transverse myelitis in the cervical spine. FDG-PET showed a pattern of brain uptake suspicious for limbic encephalitis. Serum and CSF paraneoplastic panel showed presence of GFAP immunoglobulin G (IgG). Treatment with corticosteroids resulted in clinical and radiographic improvement. However, the patient was treated with anti-CD20 immunotherapy due to steroid-dependence. This case exemplifies the recently described neurologic syndrome of autoimmune GFAP astrocytopathy presenting with encephalomyelitis and parkinsonism, reversed by B lymphocyte depletion.
View details for DOI 10.1016/j.msard.2019.101900
View details for PubMedID 31881522
Immunomodulatory receptors are differentially expressed in B and T cell subsets relevant to autoimmune disease.
Clinical immunology (Orlando, Fla.)
Inhibitory cell-surface receptors on lymphocytes, often called immune checkpoints, are powerful targets for cancer therapy. Despite their direct involvement in autoimmune pathology, they are currently not exploited therapeutically for autoimmune diseases. Understanding the receptors' expression patterns in health and disease is essential for targeted drug design. Here, we designed three 23-colour flow cytometry panels for peripheral-blood T cells, including 15 lineage-defining markers and 21 immunomodulatory cell-surface receptors, and a 22-marker panel for B cells. Blood samples from healthy individuals, multiple sclerosis (MS), and lupus (SLE) patients were included in the study. Several receptors show differential expression on regulatory T cells (Treg) compared to T helper (Th) 1 and Th17 cells, and functional relevance of this difference could be shown for BTLA and CD5. Unbiased multiparametric analysis revealed a subset of activated CD8+ T cells and a subset of unswitched memory B cells that are diminished in MS and SLE, respectively.
View details for DOI 10.1016/j.clim.2019.108276
View details for PubMedID 31669582
Autoimmune Hepatitis During Treatment of Multiple Sclerosis with Alemtuzumab
LIPPINCOTT WILLIAMS & WILKINS. 2018
View details for Web of Science ID 000453090804181
Patient-Reported Benefits of Extracranial Venous Therapy: British Columbia CCSVI Registry
CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES
2017; 44 (3): 246-254
Objective Chronic cerebrospinal venous insufficiency (CCSVI) has been hypothesized to be a risk factor for multiple sclerosis (MS). Venoplasty has been proposed as a treatment for CCSVI. The aim of our study was to gain a better understanding of the "real-world" safety and longitudinal effectiveness of venoplasty Methods: British Columbia residents who self-reported having had venoplasty and consented to participate in the study were interviewed and followed for up to 24 months post-therapy using standardized structured questionnaires Results: Participants reported procedure-related complications (11.5%) and complications within the first month after the procedure (17.3%). Initially, more than 40% of participants perceived that the venoplasty had had positive effects on their health conditions, such as fatigue, numbness, balance, concentration/memory and mobility. However, this improvement was not maintained over time Conclusions: Follow-up patient-reported outcomes indicated that the initial perception of the positive impact of venoplasty on the health conditions of MS patients was not sustained over time. In addition, venoplasty was not without associated morbidity.
View details for DOI 10.1017/cjn.2017.27
View details for Web of Science ID 000401287500003
View details for PubMedID 28270250