Bio

Dr. McDonald is a fellowship-trained, board-certified neurologist and clinical assistant professor in the Department of Neurology at Stanford University School of Medicine.

She specializes in the diagnosis and treatment of multiple sclerosis and other demyelinating diseases, including neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody disease (MOGAD). Dr. McDonald also provides comprehensive care to general neurology patients.

Dr. McDonald completed her internship and adult neurology residency at the University of Utah. She has a long-standing interest in multiple sclerosis care and went on to complete a two-year clinical MS/neuroimmunology fellowship at Stanford Health Care Multiple Sclerosis Center. Dr. McDonald received the National MS Society’s Sylvia Lawry Physician Fellowship, including formalized training in conducting clinical trials. As part of her fellowship, she completed a master’s degree in epidemiology and clinical research.

Clinical Focus

  • Neurology

Academic Appointments

Professional Education

  • Board Certification: American Board of Psychiatry and Neurology, Neurology (2020)
  • Fellowship, Stanford University, Multiple Sclerosis/Neuroimmunology (2022)
  • Neurology Residency, University of Utah, Adult Neurology (2020)
  • Internship, University of Utah, Internal Medicine (2017)
  • MD, Royal College of Surgeons in Ireland School of Medicine, Graduate Entry Medicine (2016)
  • MS, Columbia University, Human Nutrition (2012)
  • BS, Cornell University, Human Development (2007)

Contact

  • Academic
    jamiecm@stanford.edu
    University - Staff Department: Adult Neurology Position: Clinical Assistant Professor
  • Clinical (Primary)  Neurology 300 Pasteur Dr Rm H3160 MC 5235 Stanford, CA 94305 (650) 723-7434 (fax)

Additional Clinical Info

Additional Info

  • Mail Code: 7972

All Publications

  • A rare neuromyelitis optica mimic: Primary CNS histiocytic sarcoma. Multiple sclerosis (Houndmills, Basingstoke, England) Rogawski, D. S., Nirschl, J. J., McDonald, J., Nie, E., Schwartz, N. U., Vogel, H., Scott, B. J., Gold, C. A., Kipp, L. B. 2022; 28 (10): 1651-1654

    Abstract

    Primary central nervous system (CNS) histiocytic sarcoma is a rare hematolymphoid malignancy with features of mature histiocytes and carries a poor prognosis. We describe a unique case in which a 50-year-old woman presented with recurrent acute brainstem syndrome, area postrema syndrome, and myelitis with corresponding magnetic resonance imaging (MRI) lesions meeting diagnostic criteria for seronegative neuromyelitis optica spectrum disorder (NMOSD). Despite initial improvement with steroids and plasma exchange, she experienced recurrent symptoms over 10months referable to new and persistently enhancing lesions. At autopsy, neuropathology revealed a diffusely infiltrative primary CNS histiocytic sarcoma. This case represents a rare clinicoradiologic mimic of NMOSD, underscoring the importance of evaluation for infiltrative diseases in cases of atypical seronegative NMOSD.

    View details for DOI 10.1177/13524585221097564

    View details for PubMedID 35876468

  • Primary central nervous system histiocytic sarcoma presenting as neuromyelitis optica Nirschl, J., Rogawski, D., McDonald, J., Nie, E., Schwartz, N., Scott, B., Gratzinger, D., Gold, C., Kipp, L., Vogel, H. OXFORD UNIV PRESS INC. 2022: 491

    View details for Web of Science ID 000798368400189

  • Dietary factors and pediatric multiple sclerosis: A case-control study MULTIPLE SCLEROSIS JOURNAL Pakpoor, J., Seminatore, B., Graves, J. S., Schreiner, T., Waldman, A. T., Lotze, T. E., Belman, A., Greenberg, B. M., Weinstock-Guttman, B., Aaen, G., Tillema, J., McDonald, J. C., Hart, J., Ness, J. M., Harris, Y., Rubin, J., Candee, M., Krupp, L., Gorman, M., Benson, L., Rodriguez, M., Chitnis, T., Mar, S., Kahn, I., Rose, J., Carmichael, S. L., Roalstad, S., Waltz, M., Casper, T., Waubant, E., US Network Pediat Multiple Scleros 2018; 24 (8): 1067–76

    Abstract

    The role of diet in multiple sclerosis (MS) is largely uncharacterized, particularly as it pertains to pediatric-onset disease.To determine the association between dietary factors and MS in children.Pediatric MS patients and controls were recruited from 16 US centers (MS or clinically isolated syndrome onset before age 18, <4 years from symptom onset and at least 2 silent lesions on magnetic resonance imaging). The validated Block Kids Food Screener questionnaire was administered 2011-2016. Chi-squared test compared categorical variables, Kruskal-Wallis test compared continuous variables, and multivariable logistic regression analysis was performed.In total, 312 cases and 456 controls were included (mean ages 15.1 and 14.4 years). In unadjusted analyses, there was no difference in intake of fats, proteins, carbohydrates, sugars, fruits, or vegetables. Dietary iron was lower in cases ( p = 0.04), and cases were more likely to consume below recommended guidelines of iron (77.2% of cases vs 62.9% of controls, p < 0.001). In multivariable analysis, iron consumption below recommended guidelines was associated with MS (odds ratio = 1.80, p < 0.01).Pediatric MS cases may be less likely to consume sufficient iron compared to controls, and this warrants broader study to characterize a temporal relationship. No other significant difference in intake of most dietary factors was found.

    View details for PubMedID 28608728

    View details for PubMedCentralID PMC5711616

  • A case-control study of dietary salt intake in pediatric-onset multiple sclerosis MULTIPLE SCLEROSIS AND RELATED DISORDERS McDonald, J., Graves, J., Waldman, A., Lotze, T., Schreiner, T., Belman, A., Greenberg, B., Weinstock-Guttman, B., Aaen, G., Tillema, J., Hart, J., Lulu, S., Ness, J., Harris, Y., Rubin, J., Candee, M., Krupp, L. B., Gorman, M., Benson, L., Rodriguez, M., Chitnis, T., Mar, S., Barcellos, L. F., Laraia, B., Rose, J., Roalstad, S., Simmons, T., Casper, T., Waubant, E. 2016; 6: 87–92

    Abstract

    High salt intake may be associated with pro-inflammatory changes in the immune response, and increased clinical and MRI activity in adults with relapsing-remitting multiple sclerosis.We sought to determine if dietary salt intake is associated with pediatric-onset MS risk in a multicenter, case-control study.Pediatric-onset CIS/MS cases within four years of onset and controls less than 22 years old recruited from 14 pediatric-MS centers were studied. Dietary sodium intake was assessed using the validated Block Kids Food Screener (NutritionQuest). Sodium intake, excess sodium, and sodium terciles were compared between cases and controls. Logistic regression models were adjusted for age, gender, ethnicity, body mass index, and socioeconomic status.Among 170 cases (mean age=15.2±3.5) and 331 controls (mean age=14.0±3.7), no significant difference in unadjusted mean sodium intake was found between cases (2044mg/d) and controls (2030mg/d, p=0.99). The proportion of subjects consuming excess sodium, based on the adequate intake for age and gender, was similar between cases and controls (65% versus 69%, p=0.34). There were no increased odds of higher sodium intake among cases as compared to controls (for each 100mg/d increase in sodium, OR=1.00, 95% CI 0.98, 1.02; p=0.93, for excess sodium intake, OR=1.05, 95% CI 0.67, 1.64; p=0.84).Our results show no strong association between dietary salt intake and pediatric-onset MS risk, suggesting that salt intake may not play a prominent role in susceptibility to MS in children.

    View details for DOI 10.1016/j.msard.2016.02.011

    View details for Web of Science ID 000375044800016

    View details for PubMedID 27063630

    View details for PubMedCentralID PMC4830915

  • Association of Multiple Sclerosis Susceptibility Variants and Early Attack Location in the CNS PLOS ONE Mowry, E. M., Carey, R. F., Blasco, M. R., Pelletier, J., Duquette, P., Villoslada, P., Malikova, I., Roger, E., Kinkel, R., McDonald, J., Bacchetti, P., Waubant, E. 2013; 8 (10): e75565

    Abstract

    The anatomic location of subsequent relapses in early multiple sclerosis (MS) appears to be predicted by the first attack location. We sought to determine if genetic polymorphisms associated with MS susceptibility are associated with attack location.17 genome-wide association study-identified MS susceptibility polymorphisms were genotyped in 503 white, non-Hispanic patients seen within a year of MS onset. Their association with the CNS location of the first two MS attacks was assessed in multivariate repeated measures analyses (generalized estimating equations with robust standard errors).The IL12A polymorphism was independently associated with increased odds of attacks involving the spinal cord (OR = 1.52, 95% CI 1.11, 2.07, p = 0.009), as was the IRF8 polymorphism (OR = 2.40, 95% CI [1.04, 5.50], p = 0.040). The IL7R polymorphism was associated with reduced odds of attacks involving the brainstem/cerebellum (OR = 0.46, 95% CI 0.22, 0.97, p = 0.041), as were the TNFRSF1A and IL12A polymorphisms. The CD6 polymorphism conferred reduced odds of optic neuritis as an attack location (OR = 0.69, 95% CI [0.49, 0.97], p = 0.034). Several other genes showed trends for association with attack location.Some of the MS susceptibility genes may be associated with MS attack location. The IL12A polymorphism is of particular interest given that interferon beta therapy appears to influence IL12 levels. These findings may lead to improved understanding of MS pathogenesis and treatment.

    View details for DOI 10.1371/journal.pone.0075565

    View details for Web of Science ID 000325814200015

    View details for PubMedID 24130718

    View details for PubMedCentralID PMC3794979

  • Multiple Sclerosis Susceptibility Genes: Associations with Relapse Severity and Recovery PLOS ONE Mowry, E. M., Carey, R. F., Blasco, M. R., Pelletier, J., Duquette, P., Villoslada, P., Malikova, I., Roger, E., Kinkel, R., McDonald, J., Bacchetti, P., Waubant, E. 2013; 8 (10): e75416

    Abstract

    Patients with early multiple sclerosis (MS) have stereotyped attack severity and recovery. We sought to determine if polymorphisms in MS susceptibility genes are associated with these attack features or with the risk of a second attack.503 white subjects evaluated within a year of MS onset were included in the study. The severity of and recovery from the first two attacks were determined based on published definitions. Seventeen MS susceptibility genes were genotyped at the UCSF MS Genetics laboratory. Each polymorphism was evaluated in multivariate ordinal models, adjusted for the other polymorphisms, for its association with attack severity and recovery. We also assessed if these polymorphisms were associated with increased risk of a second attack.The MPHOSPH9 polymorphism was associated with greater attack severity (odds ratios [OR] = 1.47, 95% CI [1.11, 1.94], p = 0.008), while the RGS1 and TNFRSF1A polymorphisms tended to be associated with reduced attack severity. The CD6 polymorphism tended to be associated with increased odds of worse attack recovery (OR = 1.25, 95% CI [0.93, 1.68], p = 0.13). In those who were HLA-DRB1-negative, the EVI5 polymorphism was associated with attacks of less severity; in HLA-DRB1 positive patients, EVI5 was associated with attacks of greater severity and worse recovery. The IL7R, TNFRSF1A, and GPC5 polymorphisms tended to be associated with having a second event within a year.Some MS susceptibility polymorphisms may be associated with attack severity, recovery, or frequency. Further characterization of these genes may lead to a better understanding of MS pathogenesis and to a more individualized treatment approach.

    View details for DOI 10.1371/journal.pone.0075416

    View details for Web of Science ID 000325810900035

    View details for PubMedID 24130709

    View details for PubMedCentralID PMC3793991

  • Effect of medication and STN-DBS on postural control in subjects with Parkinson's disease PARKINSONISM & RELATED DISORDERS Nantel, J., McDonald, J. C., Bronte-Stewart, H. 2012; 18 (3): 285-289

    Abstract

    To assess the effect of disease severity, dopaminergic medication (med) and STN-DBS on postural stability in Parkinson's disease (PD).Postural sway in quiet stance, and the Unified Parkinson's Disease Rating Scale (motor) (UPDRS III) were evaluated in 129 subjects in the off-med state. A subgroup of 28 subjects was studied on-med and after STN-DBS. Postural sway was measured using center of pressure (CoP) root mean square displacement (RMS(CoP)) and mean velocity (V(CoP)) in the anterior-posterior (AP) and medial-lateral (ML) directions.All CoP parameters were larger in moderate/advanced subjects vs controls (P < 0.001) and early subjects. Only RMS(CoP)ML was larger in early subjects vs controls (P < 0.05). Med, DBS and DBS + med decreased UPDRS III compared to off-med (P < 0.001). RMS(CoP)ML and V(CoP)ML were larger on-med vs off-med and vs DBS (P < 0.001). Compared to controls and PD subjects with normal CoP sway off-med, med increased all CoP parameters (P < 0.01) but DBS returned V(CoP)ML to normal values. For 'abnormal' PD subjects, STN-DBS improved the excessive V(CoP) in ML compared to off and on-med pre-DBS (P < 0.05).Postural sway in quiet stance increased with disease severity. Only ML CoP displacement was abnormal in early stage PD, and this may be a compensatory mechanism. Medication increased ML postural sway. In 'normal' PD subjects, STN-DBS reversed medication induced postural instability. Subjects with abnormal balance in quiet stance did not benefit from medication or DBS, except for improvement in ML CoP velocity from DBS. This may serve to reduce postural instability and falling.

    View details for DOI 10.1016/j.parkreldis.2011.11.005

    View details for Web of Science ID 000301813200015

    View details for PubMedID 22130147

  • Common viruses associated with lower pediatric multiple sclerosis risk NEUROLOGY Waubant, E., Mowry, E. M., Krupp, L., Chitnis, T., Yeh, E. A., Kuntz, N., Ness, J., Chabas, D., Strober, J., McDonald, J., Belman, A., Milazzo, M., Gorman, M., Weinstock-Guttman, B., Rodriguez, M., Oksenberg, J. R., JAMES, J. A. 2011; 76 (23): 1989-1995

    Abstract

    Because common viruses are encountered during childhood, pediatric multiple sclerosis (MS) offers a unique opportunity to investigate the influence of these viruses on disease susceptibility and the interactions between seroprevalence and select HLA genotypes. We studied seroprevalence for Epstein-Barr virus (EBV), cytomegalovirus (CMV), and herpes simplex virus (HSV) type 1 and HLA-DRB1*1501/1503 status as predictors of pediatric MS.This was a retrospective analysis of prospectively collected demographic, clinical, and biologic data in subjects up to 18 years of age with early MS, control subjects seen at the same regional referral pediatric MS clinics, and additional healthy pediatric control subjects.Patients with early pediatric MS (n=189) and pediatric control subjects (n=66) were tested. Epstein-Barr nuclear antigen-1 seropositivity was associated with an increased odds of MS (odds ratio [OR] 3.78, 95% confidence interval [CI] 1.52-9.38, p=0.004) in analyses adjusted for age, sex, race, ethnicity, and HLA-DRB1*1501/1503 status. In multivariate analyses including EBV status, a remote infection with CMV (OR 0.27, 95% CI 0.11-0.67, p=0.004) was associated with a lower risk of developing MS. Although a remote infection with HSV-1 was not associated with an increased odds of MS, a strong interaction was found between HSV-1 status and HLA-DRB1 in predicting MS (p<0.001). HSV-1 was associated with an increased risk of MS in those without a DRB1*15 allele (OR 4.11, 95% CI 1.17-14.37, p=0.03), whereas the effect was reversed in those who were DRB1*15-positive (OR 0.07, 95% CI 0.02-0.32, p=0.001).These findings suggest that some infections with common viruses may in fact lower MS susceptibility. If this is confirmed, the pathways for risk modification remain to be elucidated.

    View details for DOI 10.1212/WNL.0b013e31821e552a

    View details for Web of Science ID 000291343500011

    View details for PubMedID 21646624

    View details for PubMedCentralID PMC3109881

  • Vitamin D Status Is Associated with Relapse Rate in Pediatric-Onset Multiple Sclerosis ANNALS OF NEUROLOGY Mowry, E. M., Krupp, L. B., Milazzo, M., Chabas, D., Strober, J. B., Belman, A. L., McDonald, J. C., Oksenberg, J. R., Bacchetti, P., Waubant, E. 2010; 67 (5): 618-624

    Abstract

    We sought to determine if vitamin D status, a risk factor for multiple sclerosis, is associated with the rate of subsequent clinical relapses in pediatric-onset multiple sclerosis.This is a retrospective study of patients with pediatric-onset multiple sclerosis or clinically isolated syndrome who were consecutively recruited into a prospective cohort at their clinical visit at the pediatric multiple sclerosis center of University of California, San Francisco or State University of New York at Stony Brook. Of 171 eligible patients, 134 (78%) with multiple sclerosis/clinically isolated syndrome were included in the cohort; a further 24 were excluded from this analysis due to lack of available serum (n = 7) or lack of follow-up (n = 17). Serum 25-hydroxyvitamin D(3) levels were measured and were adjusted to reflect a deseasonalized value. The adjusted serum 25-hydroxyvitamin D(3) level was the primary predictor in a multivariate negative binomial regression model in which the main outcome measure was the number of subsequent relapses.Among the 110 subjects, the mean unadjusted 25-hydroxyvitamin D(3) level was 22 +/- 9 ng/ml. After adjustment for age, gender, race, ethnicity, disease duration, disease-modifying therapy, and length of follow-up, every 10 ng/ml increase in the adjusted 25-hydroxyvitamin D(3) level was associated with a 34% decrease in the rate of subsequent relapses (incidence rate ratio, 0.66; 95% confidence interval, 0.46-0.95; p = 0.024).Lower serum 25-hydroxyvitamin D(3) levels are associated with a substantially increased subsequent relapse rate in pediatric-onset multiple sclerosis or clinically isolated syndrome, providing rationale for a randomized controlled trial of vitamin D supplementation.

    View details for DOI 10.1002/ana.21972

    View details for Web of Science ID 000277190000008

    View details for PubMedID 20437559