Leana Doherty, MD
Clinical Associate Professor, Neurology & Neurological Sciences
Bio
Dr. Doherty is a board-certified, fellowship-trained neurologist with Stanford Health Care. She is also a clinical associate professor in the Department of Neurology & Neurological Sciences at Stanford University School of Medicine.
Dr. Doherty specializes in Guillain-Barre syndrome, myasthenia gravis, chronic inflammatory demyelinating polyneuropathy, and other neuroinflammatory, neuromuscular, and general neurologic conditions.
Her research interests include the diagnosis and management of neuromuscular disorders, and quality improvement for inpatient neurologic treatment and management. She has won numerous awards for her research, clinical, and teaching expertise in neurology.
Dr. Doherty has published in several peer-reviewed journals including Neurology, Neuromuscular Disorders, and Neurology: Neuroimmunology & Neuroinflammation. She has delivered presentations around the county and lectured before an international audience of neurology residents. Dr. Doherty serves as co-associate editor of Annals of Clinical and Translational Neurology (interACTN) and associate editor of New England Journal of Medicine (NEJM) Journal Watch Neurology. She is on the editorial board of The Neurohospitalist.
Dr. Doherty is a member of the American Academy of Neurology, American Neurological Association, Neurohospitalist Society, and Peripheral Nerve Society.
Clinical Focus
- Neurology
Honors & Awards
-
Thomas J. Preziosi Award, Johns Hopkins University School of Medicine
-
Neurology Outstanding Teacher Award – Inpatient Service, Johns Hopkins University School of Medicine
-
Jay Slotkin Award, Johns Hopkins University School of Medicine
-
Glasgow-Rubin Certificate of Commendation for Academic Achievement, American Medical Women’s Association
-
Executive Chief Resident, Johns Hopkins Neurology
-
Excellence in Patient Experience Award, University of Pittsburgh Medical Center
-
Best Clinical Teaching Award, Department of Neurology, University of Pittsburgh Medical Center (UPMC)
Professional Education
-
Board Certification: American Board of Psychiatry and Neurology, Neurology (2017)
-
Fellowship: John Hopkins University-Bayview Medical Center (2018) MD
-
Residency: Johns Hopkins Neurology Residency (2017) MD
-
Internship: Strong Mem Hosp Univ of Rochester (2014) NY
-
Medical Education: University of Rochester Medical Center (2013) NY
All Publications
- Peripheral Nerve Pathology in Paraneoplastic Neuropathy NEJM Journal Watch. 2024
- Macronutrients Associated with Slower Disease Progression in Patients with ALS NEJM Journal Watch. 2024
- Peripheral Sensory Abnormalities in ALS NEJM Journal Watch. 2024
-
Clinical Reasoning: Woman With Acute Bilateral Ophthalmoplegia.
Neurology
2023; 101 (3): 140-144
Abstract
This is a case of a 75-year-old woman who presented with severe headache, left eye ptosis, and binocular diplopia and was found to have multiple cranial neuropathies on examination. This case reviews the localization and workup of multiple cranial neuropathies and emphasizes the importance of not prematurely narrowing the differential diagnosis.
View details for DOI 10.1212/WNL.0000000000207173
View details for PubMedID 36977598
View details for PubMedCentralID PMC10382261
-
Neuroinvasive Manifestations of West Nile Virus Infection: Lumbar Polyneuropathy, Chorioretinal Lesions, Sensorineural Hearing Loss
LIPPINCOTT WILLIAMS & WILKINS. 2023
View details for DOI 10.1212/WNL.0000000000204235
View details for Web of Science ID 001053672100219
- Predicting Wheelchair Dependence in Facioscapulohumeral Muscular Dystrophy NEJM Journal Watch. 2023
- Risdiplam Shows Continued Motor Benefits for SMA After 1 Year NEJM Journal Watch. 2023
- BMI Changes in ALS and Survival NEJM Journal Watch. 2023
- Clinical Characteristics of Acute Nutritional Neuropathy NEJM Journal Watch. 2023
- Influence of Baseline Cognition on Delirium Severity NEJM Journal Watch. 2023
- The First Trial of an Antisense Oligonucleotide for Myotonic Dystrophy NEJM Journal Watch. 2023
- The Influence of Age on the Peripheral Nervous System NEJM Journal Watch. 2023
- Long-Term Efficacy of Edaravone in a European ALS Cohort NEJM Journal Watch. 2022
- Microarray Identifies Novel Autoantibodies in Small-Fiber Neuropathy NEJM Journal Watch. 2022
- Risdiplam in Spinal Muscular Atrophy Type 2 and Type 3 NEJM Journal Watch. 2022
- Low, Standard, and High Doses of IVIg for Maintenance in CIDP NEJM Journal Watch. 2022
- Discontinuation of Maintenance IVIG for CIDP NEJM Journal Watch. 2022
- Rituximab for Juvenile Myasthenia Gravis NEJM Journal Watch. 2022
- High-Dose Methylcobalamin for ALS NEJM Journal Watch. 2022
- Using Whole-Genome Sequencing for Mitochondrial Disease Diagnosis NEJM Journal Watch. 2022
- Real-World Motor Improvements in SMA from Nusinersen NEJM Journal Watch. 2022
- Elevated Plasma P-Tau181 in ALS NEJM Journal Watch. 2022
- Tofersen Fails to Slow Progression in SOD1 ALS NEJM Journal Watch. 2022
- Radiographic Subtypes of ALS NEJM Journal Watch. 2022
- Rituximab for Early-Onset Myasthenia Gravis NEJM Journal Watch. 2022
-
Inpatient Diagnosis and Management of Neuromuscular Disorders.
Seminars in neurology
2021; 41 (5): 493-510
Abstract
Although many neuromuscular conditions are evaluated on an outpatient basis owing to their chronic or progressive nature, more urgent evaluation and management is often required for the inpatient presenting with acute to subacute focal or generalized numbness or weakness. This review focuses on clinical pattern recognition and basic anatomic localization principles to aid in the identification of common, as well as some less frequently encountered, neuromuscular disorders in hospitalized patients. The characteristic clinical and diagnostic features, associated complications, and recommended treatments of key neuromuscular conditions with acute and subacute manifestations are discussed. These conditions can be life-threatening in some cases, such as in Guillain-Barré syndrome, owing to associated oropharyngeal weakness, respiratory failure, or marked dysautonomia. Prompt recognition of the clinical and pathologic features is therefore necessary to reduce associated morbidity and mortality.
View details for DOI 10.1055/s-0041-1733794
View details for PubMedID 34619777
- Neuropathy with Neurofascin-155 Immunoglobulins: Clinical Profile and Prognosis NEJM Journal Watch. 2021
- An Oral Combination of Sodium Phenylbutyrate– Taurursodiol in ALS NEJM Journal Watch. 2021
- Home Grip Strength Testing for Patients with CIDP NEJM Journal Watch. 2021
- Predicting Wheelchair Dependence in Facioscapulohumeral Muscular Dystrophy NEJM Journal Watch. 2021
- POEMS Syndrome: Clinical Features and Outcomes in a U.K. Cohort NEJM Journal Watch. 2020
-
Stopping oral steroid-sparing agents at initiation of rituximab in myasthenia gravis.
Neuromuscular disorders : NMD
2019; 29 (7): 554-561
Abstract
Rituximab is a chimeric monoclonal antibody that binds CD20 and causes the depletion of B-cell subsets. Although initially designed to treat lymphoma, it has found wide use in the management of various autoimmune conditions, including myasthenia gravis (MG), an autoimmune disorder of the neuromuscular junction. Treated myasthenia patients are often on an oral steroid-sparing agent. To determine the safety of stopping oral steroid-sparing agents at the initiation of rituximab therapy and its effectiveness we reviewed the records of 27 MG patients with rituximab, including 13 with anti-MuSK+ MG, 10 with anti-AChR+ MG, and 4 double seronegative MG patients. All patients that were on an oral steroid-sparing agent (21 of 27) were able to stop it, and they did not require re-introduction of the medication. Also, the daily prednisone dosage was significantly decreased in 20/24 patients across all three serotype groups. MGFA post intervention status analysis also showed 15/27 of all patients achieved minimal manifestation status or remission across all groups. Antibody titers decreased dramatically and promptly in anti-MuSK+ MG patients. Our data suggests that stopping oral steroid-sparing agents at initiation of rituximab therapy is safe. Also, our data indicates that rituximab is highly effective in the management of seropositive MG patients.
View details for DOI 10.1016/j.nmd.2019.06.002
View details for PubMedID 31296355
- Refining Diagnostic Criteria for Small Fiber Neuropathy NEJM Journal Watch. 2019
- Oromucosal Cannabinoids for Spasticity in Motor Neuron Disease NEJM Journal Watch. 2019
- Limb and Bulbar Skeletal Muscle MRI Characteristics in SBMA and ALS NEJM Journal Watch. 2019
-
Frequency of polyneuropathy and amyloid detectable in skin biopsy in wild type transthyretin cardiomyopathy
WILEY. 2018: 393
View details for Web of Science ID 000452787700355
- Revised Classification for Idiopathic Inflammatory Myopathies NEJM Journal Watch. 2018
-
Anti-DPPX encephalitis: prominent nystagmus reflected by extraocular muscle FDG-PET avidity.
Neurology(R) neuroimmunology & neuroinflammation
2017; 4 (4): e361
View details for DOI 10.1212/NXI.0000000000000361
View details for PubMedID 28626782
View details for PubMedCentralID PMC5459789
-
Frameshift mutation in p53 regulator RPL26 is associated with multiple physical abnormalities and a specific pre-ribosomal RNA processing defect in diamond-blackfan anemia
HUMAN MUTATION
2012; 33 (7): 1037-1044
Abstract
Diamond-Blackfan anemia (DBA) is an inherited form of pure red cell aplasia that usually presents in infancy or early childhood and is associated with congenital malformations in ∼30-50% of patients. DBA has been associated with mutations in nine ribosomal protein (RP) genes in about 53% of patients. We completed a large-scale screen of 79 RP genes by sequencing 16 RP genes (RPL3, RPL7, RPL8, RPL10, RPL14, RPL17, RPL19, RPL23A, RPL26, RPL27, RPL35, RPL36A, RPL39, RPS4X, RPS4Y1, and RPS21) in 96 DBA probands. We identified a de novo two-nucleotide deletion in RPL26 in one proband associated with multiple severe physical abnormalities. This mutation gives rise to a remarkable ribosome biogenesis defect that affects maturation of both the small and the large subunits. We also found a deletion in RPL19 and missense mutations in RPL3 and RPL23A, which may be variants of unknown significance. Together with RPL5, RPL11, and RPS7, RPL26 is the fourth RP regulating p53 activity that is linked to DBA.
View details for DOI 10.1002/humu.22081
View details for Web of Science ID 000304815100005
View details for PubMedID 22431104
View details for PubMedCentralID PMC3370062
-
Ribosomal Protein Genes RPS10 and RPS26 Are Commonly Mutated in Diamond-Blackfan Anemia
AMERICAN JOURNAL OF HUMAN GENETICS
2010; 86 (2): 222-228
Abstract
Diamond-Blackfan anemia (DBA), an inherited bone marrow failure syndrome characterized by anemia that usually presents before the first birthday or in early childhood, is associated with birth defects and an increased risk of cancer. Although anemia is the most prominent feature of DBA, the disease is also characterized by growth retardation and congenital malformations, in particular craniofacial, upper limb, heart, and urinary system defects that are present in approximately 30%-50% of patients. DBA has been associated with mutations in seven ribosomal protein (RP) genes, RPS19, RPS24, RPS17, RPL35A, RPL5, RPL11, and RPS7, in about 43% of patients. To continue our large-scale screen of RP genes in a DBA population, we sequenced 35 ribosomal protein genes, RPL15, RPL24, RPL29, RPL32, RPL34, RPL9, RPL37, RPS14, RPS23, RPL10A, RPS10, RPS12, RPS18, RPL30, RPS20, RPL12, RPL7A, RPS6, RPL27A, RPLP2, RPS25, RPS3, RPL41, RPL6, RPLP0, RPS26, RPL21, RPL36AL, RPS29, RPL4, RPLP1, RPL13, RPS15A, RPS2, and RPL38, in our DBA patient cohort of 117 probands. We identified three distinct mutations of RPS10 in five probands and nine distinct mutations of RPS26 in 12 probands. Pre-rRNA analysis in lymphoblastoid cells from patients bearing mutations in RPS10 and RPS26 showed elevated levels of 18S-E pre-rRNA. This accumulation is consistent with the phenotype observed in HeLa cells after knockdown of RPS10 or RPS26 expression with siRNAs, which indicates that mutations in the RPS10 and RPS26 genes in DBA patients affect the function of the proteins in rRNA processing.
View details for DOI 10.1016/j.ajhg.2009.12.015
View details for Web of Science ID 000274637200011
View details for PubMedID 20116044
View details for PubMedCentralID PMC2820177
-
Ribosomal Protein Genes S10 and S26 Are Commonly Mutated in Diamond-Blackfan Anemia
AMER SOC HEMATOLOGY. 2009: 78
View details for Web of Science ID 000272725800176