Kenneth Leung, MD, MS
Clinical Assistant Professor, Neurology & Neurological Sciences
Bio
Dr. Leung is a board-certified neurologist who practices both comprehensive neurology and neuromuscular medicine. He is a Clinical Assistant Professor in the Department of Neurology within the Stanford University School of Medicine.
Dr. Leung has a particular interest in the diagnosis and management of a broad range of disorders affecting muscle and nerves, including motor neuron disease, neuropathy, neuromuscular junction disorders, and myopathy. He also is an avid clinician educator who develops course work, is involved in education research, and teaches medical students and neurology residents/fellows. He currently serves as Director of the Neurology Clerkship for medical students and Associate Director of the Neuromuscular Medicine Fellowship within the Stanford University School of Medicine.
He earned his bachelor’s degree from the University of California, Berkeley where he was awarded the 2011 Departmental Citation Award for Excellence in Research in Immunology. In 2016 he earned his medical degree and concurrent master’s degree in applied anatomy from Case Western Reserve University School of Medicine. He then completed his internal medicine internship at Santa Clara Valley Medical Center and neurology residency at the Mount Sinai Hospital in New York. During this time, he developed a passion for neurology education and served on graduate medical education committees for curricular development, trainee well-being and resilience, and quality improvement. For his work in medical education, he was selected as a Harvard Macy Institute Scholar in 2018 and was awarded the 2020 Institute for Medical Education House Staff Excellence in Teaching Award. He was also inducted as a house staff in the Alpha Omega Alpha honor society. He then went on to complete a neuromuscular medicine fellowship at Stanford prior to joining as faculty.-
Clinical Focus
- Neuromuscular Diseases
- Neuromuscular Medicine
Honors & Awards
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Alpha Omega Alpha Honor Medical Society, AOA (2020)
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Institute for Medical Education House Staff Excellence in Teaching Award, Icahn School of Medicine at Mount Sinai (2020)
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Harvard Macy Institute Scholar for Future Academic Clinician Educators, Harvard Macy Institute (2018)
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Dean's Summer Research Award Fellowship, Case Western Reserve University School of Medicine (2013-2014)
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Departmental Citation Award for Excellence in Research in Immunology, University of California, Berkeley (2011)
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Departmental Honors in Molecular and Cell Biology, University of California, Berkeley (2011)
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Academic Honors with General Distinction, University of California, Berkeley (2011)
Boards, Advisory Committees, Professional Organizations
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Member, Teaching and Mentoring Academy, Stanford University School of Medicine (2021 - Present)
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Member, American Association of Neuromuscular and Electrodiagnostic Medicine (2021 - Present)
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Member, American Academy of Neurology (2018 - Present)
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Member, American Neurological Association (2018 - Present)
Professional Education
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Board Certification, American Board of Electrodiagnostic Medicine (2024)
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Board Certification: American Board of Psychiatry and Neurology, Neuromuscular Medicine (2022)
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Fellowship: Stanford University Dept of Neurology (2021) CA
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Board Certification, American Board of Psychiatry and Neurology, Neurology (2020)
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Fellowship, Stanford University School of Medicine, Neuromuscular Medicine (2021)
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Residency, Icahn School of Medicine at Mount Sinai, The Mount Sinai Hospital, Neurology (2020)
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Internship, Santa Clara Valley Medical Center, Internal Medicine (2017)
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MS, Case Western Reserve University School of Medicine, Applied Anatomy (2016)
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MD, Case Western Reserve University School of Medicine (2016)
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BA, University of California, Berkeley, Molecular and Cellular Biology, Immunology (2011)
All Publications
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Safety and outcomes with efgartigimod use for acetylcholine receptor-positive generalized myasthenia gravis in clinical practice.
Muscle & nerve
2023
Abstract
Multiple novel therapies have been approved for patients with myasthenia gravis. Our aim is to describe the early experience of efgartigimod use in acetylcholine receptor antibody-positive generalized myasthenia gravis (AChR+ve gMG).This multicenter retrospective study included AChR+ve gMG patients from five major neuromuscular centers who were treated with efgartigimod and had both pre- and post-efgartigimod myasthenia gravis activities of daily living (MG-ADL) scores. Information regarding MG history, concomitant treatment(s), MG-ADL and other MG-specific measures, laboratory data, and adverse events were recorded.A total of 37 patients (M:23, F:14) with a mean age of 65.56 (±14.74) y were included in this cohort. A total of 36/37 patients completed at least one cycle and 28 patients completed at least two cycles of efgartigimod. A total of 72% (26/36) of patients had a clinically meaningful reduction (≥2 point change) in MG-ADL after the completion of the first cycle of efgartigimod (mean pre-efgartigimod 8.02) (±3.09) versus post-efgartigimod 4.33 (±3.62). Twenty-five percent (9/36) achieved minimal symptom expression status after one cycle and 25% (7/28) after the second cycle. Treatment benefit was sustained after cycle 2. Three out of four patients with thymoma in this cohort had clinically significant reductions in MG-ADL scores. Immunoglobulin G (IgG) levels decreased by about 60% (n = 10). One patient had a relapse of Clostridium difficile infection resulting in the discontinuation of therapy. Four patients had mild side effects.Efgartigimod led to clinically meaningful improvement in MG-ADL in diverse AChR+ve gMG patients but treatment frequency to achieve optimal symptom control needs to be explored.
View details for DOI 10.1002/mus.27974
View details for PubMedID 37695277
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Small nerve fiber involvement in chilblain lupus erythematosus (late breaking abstract)
WILEY. 2021: 440
View details for Web of Science ID 000696233800295
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Cerebral Venous Sinus Thrombosis as a Rare Complication of Nephrotic Syndrome
WILEY. 2019: S139
View details for Web of Science ID 000488891800226
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Frequent Flyers: Retrospective Review of Repeat Stroke Codes.
LIPPINCOTT WILLIAMS & WILKINS. 2019
View details for Web of Science ID 000478733400479
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A Rare Case of Migrating Stroke-Like Lesions Masquerading as Stroke: MELAS
WILEY. 2018: S156-S157
View details for Web of Science ID 000446520900280
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Transient Isolated Downbeating Vertical Nystagmus as a Complication of Intrathecal Anesthesia
LIPPINCOTT WILLIAMS & WILKINS. 2018
View details for Web of Science ID 000453090804302
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T cell-specific inhibition of multiple apoptotic pathways blocks negative selection and causes autoimmunity.
eLife
2014; 3
Abstract
T cell self-tolerance is thought to involve peripheral tolerance and negative selection, involving apoptosis of autoreactive thymocytes. However, evidence supporting an essential role for negative selection is limited. Loss of Bim, a Bcl-2 BH3-only protein essential for thymocyte apoptosis, rarely results in autoimmunity on the C57BL/6 background. Mice with T cell-specific over-expression of Bcl-2, that blocks multiple BH3-only proteins, are also largely normal. The nuclear receptor Nur77, also implicated in negative selection, might function redundantly to promote apoptosis by associating with Bcl-2 and exposing its potentially pro-apoptotic BH3 domain. Here, we report that T cell-specific expression of a Bcl2 BH3 mutant transgene results in enhanced rescue of thymocytes from negative selection. Concomitantly, Treg development is increased. However, aged BH3 mutant mice progressively accumulate activated, autoreactive T cells, culminating in development of multi-organ autoimmunity and lethality. These data provide strong evidence that negative selection is crucial for establishing T cell tolerance.
View details for DOI 10.7554/eLife.03468
View details for PubMedID 25182415
View details for PubMedCentralID PMC4171708