Brenda Banwell

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Brenda Banwell
Born1967
Winnipeg, Canada
Alma mater University of Western Ontario
Known forInternational expert in pediatric demyelinating diseases including multiple sclerosis, neuromyelitis optica and MOG antibody disease
Awards2007 Women Against Multiple Sclerosis - Woman of the Year Award, 2015 American Academy of Neurology Sydney Carter Lifetime Achievement Award in Child Neurology, 2016 The Lady Barbara Colyton Prize for Autoimmune Research, Perelman School of Medicine, University of Pennsylvania
Scientific career
FieldsNeurology, pediatrics, neuroimmunology, neuromuscular disease
InstitutionsUniversity of Toronto
University of Pennsylvania Medical School
Children's Hospital of Philadelphia

Brenda Banwell is Chief of the Division of Neurology and Co-Director of the Neuroscience Center, and Professor of Neurology at Children's Hospital of Philadelphia and holder of the Grace R. Loeb Endowed Chair in Neurosciences. She also holds the title of Professor of Pediatrics and Neurology at the Perelman School of Medicine at the University of Pennsylvania.

Contents

Banwell is the co-director of the Pediatric Multiple Sclerosis and Neuroinflammatory Disorders Clinic at the Children's Hospital of Philadelphia. She has published extensively on pediatric demyelinating diseases including multiple sclerosis, neuromyelitis optica and MOG antibody disease. Banwell is the co-director of the Canadian Pediatric Demyelinating Disease Network, [1] the chair of the International Pediatric Multiple Sclerosis Study Group, [2] and the chair of the International Medical and Scientific Board of the MS International Federation. [3] Banwell also sits on the International Advisory Committee on Clinical Trials of New Drugs in Multiple Sclerosis. [4]

Banwell is a fellow of the American Academy of Neurology, [5] and serves as vice chair of the Academic Neurology Committee. [6] She has been active in the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS), delivering the 2022 ECTRIMS lecture. [7]

Early life and education

Banwell was born in Winnipeg, Canada. [8] She did her undergraduate training at the University of Western Ontario, where she remained for her MD and her residency in pediatrics. She completed her pediatric neurology residency at the University of Toronto Hospital for Sick Children, where she was chief resident. She then went to Mayo Clinic for a two year fellowship in neuromuscular disease. [9]

Career and Research

Banwell returned to the University of Toronto Hospital for Sick Children as an assistant professor in 1999. She became a full professor at the University of Toronto in 2012. In July 2012, she took a position as full professor in neurology and pediatrics at and chief of neurology at the Children's Hospital of Philadelphia. [10]

Research in Multiple Sclerosis

Banwell initially took her position at the University of Toronto intending to focus on neuromuscular disease in children. When she inherited five patients with multiple sclerosis from a retiring physician, she reports that her focus shifted to pediatric demyelinating disease. [11]

To better study a rare disease, Banwell created the Canadian Pediatric Demyelinating Disease Network in 2004, a multi-site network including all pediatric health-care facilities in Canada. [12] This has allowed Banwell and co-investigators to better understand diagnosis, treatment, and comorbidities of pediatric demyelinating disease.

Diagnosis: Banwell has been instrumented in evaluating the use of the McDonald criteria - standardized criteria to diagnose multiple sclerosis through determination of dissemination of central nervous system demyelination in space and time - in pediatric multiple sclerosis. [13] She has been the primary pediatric neurologist involved in international work to develop updates of the McDonald criteria for adults and children in 2010 [14] and in 2017. [15]

Treatment: While many medications have become available for the treatment of multiple sclerosis over the last three decades, testing in children has been challenging due to the rarity of pediatric multiple sclerosis and ethical considerations with the use of placebo. [16] To facilitate and improve clinical trial design, Banwell created and currently chairs the International Pediatric Multiple Sclerosis Study Group. This allowed for the success of the PARADIGMS clinical trial, studying the safety and efficacy of fingolimod in a comparison with interferon beta-1a, [17] and led to approval of fingolimod by the Food and Drug Administration for pediatric multiple sclerosis, the first approval of a medication for this indication. [18]

Comorbidities: Banwell's work has shown that while children may recover physically from flares of multiple sclerosis, neuropsychological deficits may be apparent on testing, particularly in those who present at a younger age. [19] [20] This knowledge has changed how families are counseled and supported through the diagnosis of multiple sclerosis. [21]

Acute Disseminated Encephalomyelitis, Neuromyelitis Optica and MOG Antibody Disease

Because demyelinating diseases in the pediatric population can be difficult to distinguish from each other, Banwell has worked to define and provide clinical guidelines for physicians working to delineate the diseases. [22]

In 2015, Banwell was on the International Panel for NMO Diagnosis (IPND) to develop international consensus diagnostic criteria for what became termed neuromyelitis optica spectrum disorder (NMO-SD). [23] She has also worked to determine the best treatment options for pediatric NMO-SD.

MOG antibody disease (MOGAD) was first described in the early 2000s as a subset of cases of neuromyelitis optica with antibodies to myelin oligocyte glycoprotein (MOG). [24] Banwell and colleagues worked to characterize pediatric MOGAD to determine methods of diagnosis, [25] treatment options, [26] and prognosis. [27]

Awards and honors

Related Research Articles

<span class="mw-page-title-main">Acute disseminated encephalomyelitis</span> Autoimmune disease

Acute disseminated encephalomyelitis (ADEM), or acute demyelinating encephalomyelitis, is a rare autoimmune disease marked by a sudden, widespread attack of inflammation in the brain and spinal cord. As well as causing the brain and spinal cord to become inflamed, ADEM also attacks the nerves of the central nervous system and damages their myelin insulation, which, as a result, destroys the white matter. The cause is often a trigger such as from viral infection or vaccinations.

<span class="mw-page-title-main">Optic neuritis</span> Inflammation of the optic nerve

Optic neuritis describes any condition that causes inflammation of the optic nerve; it may be associated with demyelinating diseases, or infectious or inflammatory processes.

<span class="mw-page-title-main">Transverse myelitis</span> Inflammation of the entire cross-section of the spinal cord

Transverse myelitis (TM) is a rare neurological condition wherein the spinal cord is inflamed. The adjective transverse implies that the spinal inflammation (myelitis) extends horizontally throughout the cross section of the spinal cord; the terms partial transverse myelitis and partial myelitis are sometimes used to specify inflammation that affects only part of the width of the spinal cord. TM is characterized by weakness and numbness of the limbs, deficits in sensation and motor skills, dysfunctional urethral and anal sphincter activities, and dysfunction of the autonomic nervous system that can lead to episodes of high blood pressure. Signs and symptoms vary according to the affected level of the spinal cord. The underlying cause of TM is unknown. The spinal cord inflammation seen in TM has been associated with various infections, immune system disorders, or damage to nerve fibers, by loss of myelin. As opposed to leukomyelitis which affects only the white matter, it affects the entire cross-section of the spinal cord. Decreased electrical conductivity in the nervous system can result.

<span class="mw-page-title-main">Multiple sclerosis</span> Disease that damages the myelin sheaths around nerves

Multiple sclerosis (MS) is an autoimmune disease in which the insulating covers of nerve cells in the brain and spinal cord are damaged. Being a demyelinating disease, MS disrupts the ability of parts of the nervous system to transmit signals, resulting in a range of signs and symptoms, including physical, mental, and sometimes psychiatric problems. Symptoms include double vision, vision loss, eye pain, muscle weakness, and loss of sensation or coordination. MS takes several forms, with new symptoms either occurring in isolated attacks or building up over time. In relapsing forms of MS, between attacks, symptoms may disappear completely, although some permanent neurological problems often remain, especially as the disease advances. In progressive forms of MS, bodily function slowly deteriorates once symptoms manifest and will steadily worsen if left untreated.

Neuromyelitis optica spectrum disorders (NMOSD) are a spectrum of autoimmune diseases characterized by acute inflammation of the optic nerve and the spinal cord (myelitis). Episodes of ON and myelitis can be simultaneous or successive. A relapsing disease course is common, especially in untreated patients.

<span class="mw-page-title-main">Myelin oligodendrocyte glycoprotein</span>

Myelin oligodendrocyte glycoprotein (MOG) is a glycoprotein believed to be important in the myelination of nerves in the central nervous system (CNS). In humans this protein is encoded by the MOG gene. It is speculated to serve as a necessary "adhesion molecule" to provide structural integrity to the myelin sheath and is known to develop late on the oligodendrocyte.

<span class="mw-page-title-main">Uhthoff's phenomenon</span> Worsening of neurologic symptoms in multiple sclerosis caused by heat

Uhthoff's phenomenon is the worsening of neurologic symptoms in multiple sclerosis (MS) and other demyelinating diseases when the body is overheated. This may occur due to hot weather, exercise, fever, saunas, hot tubs, hot baths, and hot food and drink. Increased temperature slows nerve conduction, but the exact mechanism remains unknown. With an increased body temperature, nerve impulses are either blocked or slowed in a damaged nerve. Once the body temperature is normalized, signs and symptoms typically reverse.

<span class="mw-page-title-main">Lesional demyelinations of the central nervous system</span>

Multiple sclerosis and other demyelinating diseases of the central nervous system (CNS) produce lesions and glial scars or scleroses. They present different shapes and histological findings according to the underlying condition that produces them.

Inflammatory demyelinating diseases (IDDs), sometimes called Idiopathic (IIDDs) due to the unknown etiology of some of them, are a heterogenous group of demyelinating diseases - conditions that cause damage to myelin, the protective sheath of nerve fibers - that occur against the background of an acute or chronic inflammatory process. IDDs share characteristics with and are often grouped together under Multiple Sclerosis. They are sometimes considered different diseases from Multiple Sclerosis, but considered by others to form a spectrum differing only in terms of chronicity, severity, and clinical course.

<span class="mw-page-title-main">Balo concentric sclerosis</span> Medical condition

Baló's concentric sclerosis is a disease in which the white matter of the brain appears damaged in concentric layers, leaving the axis cylinder intact. It was described by József Mátyás Baló who initially named it "leuko-encephalitis periaxialis concentrica" from the previous definition, and it is currently considered one of the borderline forms of multiple sclerosis.

<span class="mw-page-title-main">Marburg acute multiple sclerosis</span> Medical condition

Marburg acute multiple sclerosis, also known as Marburg multiple sclerosis or acute fulminant multiple sclerosis, is considered one of the multiple sclerosis borderline diseases, which is a collection of diseases classified by some as MS variants and by others as different diseases. Other diseases in this group are neuromyelitis optica (NMO), Balo concentric sclerosis, and Schilder's disease. The graver course is one form of malignant multiple sclerosis, with patients reaching a significant level of disability in less than five years from their first symptoms, often in a matter of months.

Research in multiple sclerosis may find new pathways to interact with the disease, improve function, curtail attacks, or limit the progression of the underlying disease. Many treatments already in clinical trials involve drugs that are used in other diseases or medications that have not been designed specifically for multiple sclerosis. There are also trials involving the combination of drugs that are already in use for multiple sclerosis. Finally, there are also many basic investigations that try to understand the disease better and in the future may help to find new treatments.

A clinically isolated syndrome (CIS) is a clinical situation of an individual's first neurological episode, caused by inflammation or demyelination of nerve tissue. An episode may be monofocal, in which symptoms present at a single site in the central nervous system, or multifocal, in which multiple sites exhibit symptoms. CIS with enough paraclinical evidence can be considered as a clinical stage of multiple sclerosis (MS). It can also be retrospectively diagnosed as a kind of MS when more evidence is available.

<span class="mw-page-title-main">Tumefactive multiple sclerosis</span> Medical condition

Tumefactive multiple sclerosis is a condition in which the central nervous system of a person has multiple demyelinating lesions with atypical characteristics for those of standard multiple sclerosis (MS). It is called tumefactive as the lesions are "tumor-like" and they mimic tumors clinically, radiologically and sometimes pathologically.

Diffuse myelinoclastic sclerosis, sometimes referred to as Schilder's disease, is a very infrequent neurodegenerative disease that presents clinically as pseudotumoural demyelinating lesions, making its diagnosis difficult. It usually begins in childhood, affecting children between 5 and 14 years old, but cases in adults are also possible.

Malignant multiple sclerosis is used to describe MS patients who reach significant level of disability in a short period of time. Malignant MS cases are not common, less than 5% of patients with MS experience this type of progression.

<span class="mw-page-title-main">Diagnosis of multiple sclerosis</span>

Current standards for diagnosing multiple sclerosis (MS) are based on the 2018 revision of McDonald criteria. They rely on MRI detection of demyelinating lesions in the CNS, which are distributed in space (DIS) and in time (DIT). It is also a requirement that any possible known disease that produces demyelinating lesions is ruled out before applying McDonald's criteria.

MOG antibody disease (MOGAD) or MOG antibody-associated encephalomyelitis (MOG-EM) is an inflammatory demyelinating disease of the central nervous system. Serum anti-myelin oligodendrocyte glycoprotein antibodies are present in up to half of patients with an acquired demyelinating syndrome and have been described in association with a range of phenotypic presentations, including acute disseminated encephalomyelitis, optic neuritis, transverse myelitis, and neuromyelitis optica.

Anti-neurofascin demyelinating diseases refers to health conditions engendered by auto-antibodies against neurofascins, which can produce both central and peripheral demyelination. Some cases of combined central and peripheral demyelination (CCPD) could be produced by them.

Anti-AQP4 diseases, are a group of diseases characterized by auto-antibodies against aquaporin 4.

References

  1. ↑ "Canadian Pediatric Demyelinating Disease Network". Maelstrom.
  2. ↑ "INTERNATIONAL PEDIATRIC MULTIPLE SCLEROSIS STUDY GROUP (IPMSSG) FOR MEDICAL PROFESSIONALS". International Pediatric Multiple Sclerosis Study Group. 31 October 2014. Retrieved 30 December 2023.
  3. ↑ "International Medical and Scientific Board". MS International Federation. Retrieved 30 December 2023.
  4. ↑ "Dr. Brenda Banwell". MS Canada.
  5. ↑ "The American Academy of Neurology for Pediatric Neurologists". SAGE Neuroscience and Neurology.
  6. ↑ "Academic Neurology Committee". American Academy of Neurology.
  7. ↑ Banwell, Brenda. "European Committee for Treatment and Research in Multiple Sclerosis". Multiple Sclerosis Journal. 29 (7). doi:10.1177/13524585231171047. S2CID   258968920.
  8. ↑ Ashwal, Stephen (2021). Child Neurology: Its Origins, Founders, Growth and Evolution. New York: Elsevier Science. p. 609. ISBN   978-0128216354.
  9. ↑ "02/09/2018 Brenda Louise Banwell, MD Address" (PDF). eCTRIMS 2021. Retrieved 30 December 2023.
  10. ↑ "Medical Advisory Board: Brenda L. Banwell, MD". MS Cure Fund. Retrieved 30 December 2023.
  11. ↑ "Dr. Brenda Banwell". Main Line Today. 26 Sep 2014. Retrieved 30 December 2023.
  12. ↑ "MS Scientific Research Foundation funded study boosts efforts in pediatric MS research, implications for understanding adult-onset MS". MS Canada. 21 September 2023. Retrieved 30 December 2023.
  13. ↑ Hahn, CD; Shroff, MM; Blaser, SI; Banwell, BL (Mar 2004). "MRI criteria for multiple sclerosis: Evaluation in a pediatric cohort". Neurology. 62 (5): 806–808. doi:10.1212/01.wnl.0000113723.36715.a6. PMID   15007138. S2CID   793225.
  14. ↑ Polman, CH; Reingold, SC; Banwell, B; Waubant, E; Weinshenker, B; Wolinsky, JS (Feb 2011). "Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria". Annals of Neurology. 69 (2): 292–302. doi:10.1002/ana.22366. PMC   3084507 . PMID   21387374.
  15. ↑ Thompson, AJ; Banwell, BL; Barkhof, F; Carroll, G; Coetzee, T; Comi, G (21 Dec 2017). "Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria". The Lancet. 17 (2): 162–173. doi:10.1016/S1474-4422(17)30470-2. PMID   29275977. S2CID   206164600.
  16. ↑ Waubant, E; Banwell, B; Wassmer, E; Sormani, M; Amato, M; Hintzen, R; Krupp, L; Rostasy, K; Tenembaum, S; Chitnis, T (May 28, 2019). "Clinical trials of disease-modifying agents in pediatric MS". Neurology. 92 (22): e2538–e2549. doi: 10.1212/WNL.0000000000007572 . PMC   6556085 . PMID   31043474.
  17. ↑ Chitnis, T; Arnold, DL; Banwell, BL; Brück, W; Ghezzi, A; Wolinsky, J (September 13, 2018). "Trial of Fingolimod versus Interferon Beta-1a in Pediatric Multiple Sclerosis". The New England Journal of Medicine. 379 (11): 1017–1027. doi:10.1056/NEJMoa1800149. PMID   30207920.
  18. ↑ "FDA expands approval of Gilenya to treat multiple sclerosis in pediatric patients". FDA News Release. U.S. Food and Drug Administration. 11 May 2018. Retrieved 30 December 2023.
  19. ↑ Banwell, B; Anderson, PE (Mar 2005). "The cognitive burden of multiple sclerosis in children". Neurology. 64 (5): 891–4. doi:10.1212/01.WNL.0000152896.35341.51. PMID   15753431. S2CID   6532050.
  20. ↑ Ness, JM; Chabas, D; Sadovnick, AD; Pohl, D; Banwell, B; Weinstock-Guttman, B; International Pediatric MS Study Group (Apr 2007). "Clinical features of children and adolescents with multiple sclerosis". Neurology. 68 (16_suppl_2): S37-45. doi:10.1212/01.wnl.0000259447.77476.a9. PMID   17438237. S2CID   23680547.
  21. ↑ Akbar, Nadine; Till, Christine; Banwell, Brenda (2018). "Pediatric multiple sclerosis and cognition". In J. DeLuca; B. M. Sandroff (eds.). Cognition and behavior in multiple sclerosis. pp. 223–244. doi:10.1037/0000097-012. ISBN   978-1-4338-2932-1.
  22. ↑ Dale, RC; Brilot, F; Banwell, B (2009). "Pediatric central nervous system inflammatory demyelination: acute disseminated encephalomyelitis, clinically isolated syndromes, neuromyelitis optica, and multiple sclerosis". Curr Opin Neurol. 22 (3): 233–240. doi:10.1097/wco.0b013e32832b4c47. PMID   19434783. S2CID   36302147.
  23. ↑ Wingerchuk, DM; Banwell, B; Bennett, JL; Cabre, P; Carroll, W; Chitnis, T (2015). "International consensus diagnostic criteria for neuromyelitis optica spectrum disorders". Neurology. 85 (2): 177–189. doi: 10.1212/WNL.0000000000001729 . PMC   4515040 . PMID   26092914.
  24. ↑ Haase, CG; Schmidt, S (2001). "Detection of brain-specific autoantibodies to myelin oligodendrocyte glycoprotein, S100beta and myelin basic protein in patients with Devic's neuromyelitis optica". Neuroscience Letters. 307 (2): 131–133. doi:10.1016/s0304-3940(01)01949-8. PMID   11427318. S2CID   21184790.
  25. ↑ Waters, P; Fadda, G; Woodhall, M; O'Mahony, J; Brown, RA; Castro, DA; Banwell, Brenda; Bar-Or, Amit; Canadian Pediatric Demyelinating Disease Network (Jan 2020). "Serial Anti-Myelin Oligodendrocyte Glycoprotein Antibody Analyses and Outcomes in Children With Demyelinating Syndromes". JAMA Neurol. 77 (1): 82–93. doi:10.1001/jamaneurol.2019.2940. PMC   6763982 . PMID   31545352.
  26. ↑ Hacohen, Y; Banwell, B (2019). "Treatment Approaches for MOG-Ab-Associated Demyelination in Children". Curr Treat Options Neurol. 21 (1): 2. doi: 10.1007/s11940-019-0541-x . PMC   6342853 . PMID   30671648.
  27. ↑ Tenembaum, S; Yeh, E; Guthy-Jackson Foundation International Clinical Consortium (GJCF-ICC) (Jun 2020). "Pediatric NMOSD: A Review and Position Statement on Approach to Work-Up and Diagnosis". Front Pediatr. 8: 339. doi: 10.3389/fped.2020.00339 . PMC   7330096 . PMID   32671002.
  28. ↑ "Brenda Banwell". Children's Hospital of Philadelphia. 24 August 2014.
  29. ↑ Banwell, Brenda (2016). "Pediatric multiple sclerosis The 2015 Sydney Carter Award Lecture". Neurology. 87 (8): 822–826. doi:10.1212/WNL.0000000000003014. PMID   27550891.
  30. ↑ "Penn Medicine Awards of Excellence: 2016 Recipients". Perelman School of Medicine. Retrieved 31 December 2023.
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