Jeffrey Dunn, MD, FAAN is Professor of Clinical Neurology and Division Chief of Clinical Neuroimmunology in the Department of Neurology and Neurosciences at Stanford University. His clinical focus is the care of men and women with Multiple Sclerosis, Neuromyelitis Optica, and other conditions in which the immune system disrupts the central nervous system to cause disease. His research employs a collaborative approach to identify biomarkers of disease status and potential therapeutic targets via translational research for novel drug development. Dr. Dunn has served as Principal Investigator in more than 20 clinical trials of new and emerging treatments for MS. Dr. Dunn is dedicated to medical education, serving as the Neurology Clerkship Director for the Stanford University School of Medicine, and as Fellowship Director for the Clinical Neuroimmunology Fellowship Program that seeks to train the next generation of leaders in Multiple Sclerosis. Dr. Dunn is an elected Fellow of the American Academy of Neurology. He has been awarded the prestigious Henry J. Kaiser Family Foundation Award for Excellence in Clinical Teaching, the Arthur Bloomfield Award in recognition of excellence in the teaching of clinical medicine, and the Lysia Forno Award for teaching excellence.
- Multiple Sclerosis
- Neuromyelitis Optica
- Transverse Myelitis
Clinical Professor, Neurology & Neurological Sciences
Division Chief, Clinical Neuroimmunology, Department of Neurology & Neurological Sciences, Stanford Healthcare (2009 - Present)
Neurology Clerkship Director, Stanford University School of Medicine (2009 - Present)
Fellowship Director, Clinical Neuroimmunology Fellowship Program; Stanford University (2010 - 2016)
Vice Chair, Multiple Sclerosis Section; American Academy of Neurology (2014 - 2016)
Honors & Awards
Henry J. Kaiser Family Foundation Award for Excellence in Clinical Teaching, Stanford University School of Medicine (2013)
Top Doctors, US News & World Report (2012-2013)
AUPN Neurology national recuitment award, Association of University Professors of Neurology (2012)
Excellence in Teaching Award, Stanford University School of Medicine (2011-2012)
AUPN Neurology Recruitment Award (highest percentage in U.S.), Association of University Professors of Neurology (2011)
Arthur L. Bloomfield Award in Recognition of Excellence in the Teaching of Clinical Medicine, Stanford University School of Medicine (2011)
Excellence in Teaching Award, Stanford University School of Medicine (2010-2011)
Excellence in Teaching Award, Stanford University School of Medicine (2009-2010)
Fellow, American Academy of Neurology (2008-present)
Lysia K. Forno Award for Excellence in Teaching Neurology Residents, Stanford University Department of Neurology & Neurosciences (2008-2009)
Excellence in Neurology Clerkship Teaching Award, Stanford University Department of Neurology & Neurosciences (2008,2009,2010,2011,2012,2013,2014,2015,2016)
"America's Top Rated Physicians", Guide to Top Doctors (1998-2007, 2010-2015)
Boards, Advisory Committees, Professional Organizations
Fellow, American Academy of Neurology (2007 - Present)
Member, Association of University Professors of Neurology (2010 - Present)
Member, Consortium of MS Centers (2008 - Present)
Member, Accelerated Cure Project (2010 - Present)
Member, San Francisco Neurological Society (2009 - Present)
Board Certification: Neurology, American Board of Psychiatry and Neurology (1994)
Residency:University of Washington Medical Center (1989) WA
Medical Education:Temple University School of Medicine (1989) PA
Residency, University of Washington, Neurology (1993)
M.D., Temple University, Medicine (1989)
B.A., Haverford College, French Literature (1983)
Community and International Work
Internation Journal of MS Care
Consortium of MS Centers
Opportunities for Student Involvement
Pan Asian Committee for Treatment and Research of Multiple Sclerosis
Opportunities for Student Involvement
Current Research and Scholarly Interests
Translational research in the human application of emerging immunotherapies for neurological disease, focusing on Multiple Sclerosis, CIS, transverse myelitis and Neuromyelitis Optica (NMO). Collaborative research with Stanford and extramural scientific faculty to identify biomarkers of disease activity and treatment response in humans. Clinical trials to assess efficacy of emerging treatments for MS, CIS and NMO.
Vitamin D Supplementation in Multiple Sclerosis
Low vitamin D levels have been shown to increase a person's risk of developing multiple sclerosis (MS), and patients with MS who have lower vitamin D levels are at increased risk of having attacks. However, it is not known if giving supplemental vitamin D to those with MS reduces the risk of attacks, and some research suggests that vitamin D could even be harmful to people with MS. In this clinical trial, patients with relapsing-remitting MS will receive high-dose or low-dose oral vitamin D in addition to an approved therapy for MS, glatiramer acetate. Patients will be evaluated for two years, and the effect of high-dose vitamin D supplementation on the rate of MS attacks and on the number of new lesions and change in brain volume on MRI will be determined. Establishing this association will have major implications for the treatment of individuals with MS throughout the world.
A Study of Ocrelizumab in Comparison With Interferon Beta-1a (Rebif) in Participants With Relapsing Multiple Sclerosis
This randomized, double-blind, double-dummy, parallel-group study will evaluate the efficacy and safety of ocrelizumab in comparison with interferon beta-1a (Rebif) in participants with relapsing multiple sclerosis. Participants will be randomized to receive either ocrelizumab 600 mg or matching placebo intravenous (IV) as 300 mg infusions on Days 1 and 15 for the first dose and as a single infusion of 600 mg for all subsequent infusions every 24 weeks, with placebo injections matching interferon beta-1a SC three times per week; or interferon beta-1a 44 mcg SC injections three times per week (with placebo infusions matching ocrelizumab infusions every 24 weeks).
Stanford is currently not accepting patients for this trial. For more information, please contact Clinical Trials Office, (650) 498-7061.
An Extension Protocol for Multiple Sclerosis Patients Who Participated in Genzyme-Sponsored Studies of Alemtuzumab
This open-label, rater-blinded extension study enrolled participants who had relapsing-remitting multiple sclerosis (RRMS) and who participated in one of three prior Genzyme-sponsored studies of alemtuzumab (CAMMS223 [NCT00050778], CAMMS323 [NCT00530348] also known as CARE-MS I, or CAMMS324 [NCT00548405] also known as CARE-MS II). The purposes of this study were: 1. To examine the long term safety and efficacy of alemtuzumab treatment in participants who received alemtuzumab as their study treatment in one of the prior studies. 2. To examine the safety and efficacy of initial alemtuzumab treatment in this study for participants who received Rebif® (interferon beta-1a) as their study treatment in one of the prior studies. 3. To determine the safety and efficacy of additional "as needed" alemtuzumab treatment courses. This applied both to participants who received alemtuzumab for the first time in one of the prior studies or for the first time in this extension study.
Stanford is currently not accepting patients for this trial. For more information, please contact Jeffrey Dunn, MD, 650-736-4310.
An Intravenous Infusion Study of rHIgM22 in Patients With Multiple Sclerosis
This is a Phase I, multi-center, double-blind, randomized, placebo-controlled, dose-escalation study designed to evaluate safety, tolerability, pharmacokinetics, and immunogenicity of single intravenous (IV) administrations of rHIgM22 in patients with all clinical presentations of MS.
Stanford is currently not accepting patients for this trial. For more information, please contact Julia Buckingham, (650) 725-7545.
Clinical Study to Investigate the Long-term Safety, Tolerability, and Efficacy of Ponesimod in Patients With Relapsing-remitting Multiple Sclerosis
This study is an extension to the study AC-058B201 and will investigate the long-term safety, tolerability and efficacy of ponesimod in patients with relapsing-remitting multiple sclerosis.
Stanford is currently not accepting patients for this trial. For more information, please contact Angela Campbell, (650) 721-6188.
Comparison of Alemtuzumab and Rebif® Efficacy in Multiple Sclerosis, Study Two
The purpose of this study was to establish the efficacy and safety of two different doses of alemtuzumab (Lemtrada™) as a treatment for relapsing-remitting multiple sclerosis (MS), in comparison with subcutaneous interferon beta-1a (Rebif®). The study enrolled participants who had received an adequate trial of disease-modifying therapies but experienced at least 1 relapse during prior treatment, and who met a minimum severity of disease as measured by magnetic resonance imaging (MRI). Participants had monthly laboratory tests and comprehensive testing every 3 months.
Stanford is currently not accepting patients for this trial. For more information, please contact Maria Coburn, (650) 736 - 9551.
Independent Studies (5)
- Directed Reading in Neurology and Neurological Science
NENS 299 (Aut, Win, Spr, Sum)
- Early Clinical Experience in Neurology and Neurological Sciences
NENS 280 (Aut, Win, Spr, Sum)
- Graduate Research
NENS 399 (Aut, Win, Spr, Sum)
- Medical Scholars Research
NENS 370 (Aut, Win, Spr, Sum)
- Undergraduate Research
NENS 199 (Aut, Win, Spr, Sum)
- Directed Reading in Neurology and Neurological Science
Ocrelizumab versus Interferon beta 1a in Relapsing Multiple Sclerosis
New England Journal of Medicine
2017; 376 (3): 221-234
View details for DOI 10.1056/NEJMoa1601277
Alemtuzumab improves preexisting disability in active relapsing-remitting MS patients.
2016; 87 (19): 1985–92
To characterize effects of alemtuzumab treatment on measures of disability improvement in patients with relapsing-remitting multiple sclerosis (RRMS) with inadequate response (≥1 relapse) to prior therapy.Comparison of Alemtuzumab and Rebif Efficacy in Multiple Sclerosis (CARE-MS) II, a 2-year randomized, rater-blinded, active-controlled, head-to-head, phase 3 trial, compared efficacy and safety of alemtuzumab 12 mg with subcutaneous interferon-β-1a (SC IFN-β-1a) 44 μg in patients with RRMS. Prespecified and post hoc disability outcomes based on Expanded Disability Status Scale (EDSS), Multiple Sclerosis Functional Composite (MSFC), and Sloan low-contrast letter acuity (SLCLA) are reported, focusing on improvement of preexisting disability in addition to slowing of disability accumulation.Alemtuzumab-treated patients were more likely than SC IFN-β-1a-treated patients to show improvement in EDSS scores (p < 0.0001) on all 7 functional systems. Significantly more alemtuzumab patients demonstrated 6-month confirmed disability improvement. The likelihood of improved vs stable/worsening MSFC scores was greater with alemtuzumab than SC IFN-β-1a (p = 0.0300); improvement in MSFC scores with alemtuzumab was primarily driven by the upper limb coordination and dexterity domain. Alemtuzumab-treated patients had more favorable changes from baseline in SLCLA (2.5% contrast) scores (p = 0.0014) and MSFC + SLCLA composite scores (p = 0.0097) than SC IFN-β-1a-treated patients.In patients with RRMS and inadequate response to prior disease-modifying therapies, alemtuzumab provides greater benefits than SC IFN-β-1a across several disability outcomes, reflecting improvement of preexisting disabilities.This study provides Class I evidence (based on rater blinding and a balance in baseline characteristics between arms) that alemtuzumab modifies disability measures favorably compared with SC IFN-β-1a.
View details for DOI 10.1212/WNL.0000000000003319
View details for PubMedID 27733571
IFN-ß Treatment Requires B Cells for Efficacy in Neuroautoimmunity.
Journal of immunology
2015; 194 (5): 2110-2116
IFN-β remains the most widely prescribed treatment for relapsing remitting multiple sclerosis. Despite widespread use of IFN-β, the therapeutic mechanism is still partially understood. Particularly, the clinical relevance of increased B cell activity during IFN-β treatment is unclear. In this article, we show that IFN-β pushes some B cells into a transitional, regulatory population that is a critical mechanism for therapy. IFN-β treatment increases the absolute number of regulatory CD19(+)CD24(++)CD38(++) transitional B cells in peripheral blood relative to treatment-naive and Copaxone-treated patients. In addition, we found that transitional B cells from both healthy controls and IFN-β-treated MS patients are potent producers of IL-10, and that the capability of IFN-β to induce IL-10 is amplified when B cells are stimulated. Similar changes are seen in mice with experimental autoimmune encephalomyelitis. IFN-β treatment increases transitional and regulatory B cell populations, as well as IL-10 secretion in the spleen. Furthermore, we found that IFN-β increases autoantibody production, implicating humoral immune activation in B cell regulatory responses. Finally, we demonstrate that IFN-β therapy requires immune-regulatory B cells by showing that B cell-deficient mice do not benefit clinically or histopathologically from IFN-β treatment. These results have significant implications for the diagnosis and treatment of relapsing remitting multiple sclerosis.
View details for DOI 10.4049/jimmunol.1402029
View details for PubMedID 25646307
- Randomized study combining interferon and glatiramer acetate in Multiple Sclerosis Annals of Neurology 2013; 73 (3): 327-340
- Mobility Concerns in Multiple Sclerosis US Neurology 2013; 9 (1): 17-23
- Disease modifying therapies for non relapsing Multiple Sclerosis Neurol Clin Pract 2013; December (3): 515-518
Alemtuzumab for patients with relapsing multiple sclerosis after disease-modifying therapy: a randomised controlled phase 3 trial
2012; 380 (9856): 1829-1839
The anti-CD52 monoclonal antibody alemtuzumab reduces disease activity in previously untreated patients with relapsing-remitting multiple sclerosis. We aimed to assess efficacy and safety of alemtuzumab compared with interferon beta 1a in patients who have relapsed despite first-line treatment.In our 2 year, rater-masked, randomised controlled phase 3 trial, we enrolled adults aged 18-55 years with relapsing-remitting multiple sclerosis and at least one relapse on interferon beta or glatiramer. Eligible participants were randomly allocated in a 1:2:2 ratio by an interactive voice response system, stratified by site, to receive subcutaneous interferon beta 1a 44 μg, intravenous alemtuzumab 12 mg per day, or intravenous alemtuzumab 24 mg per day. Interferon beta 1a was given three-times per week and alemtuzumab was given once per day for 5 days at baseline and for 3 days at 12 months. The 24 mg per day group was discontinued to aid recruitment, but data are included for safety assessments. Coprimary endpoints were relapse rate and time to 6 month sustained accumulation of disability, comparing alemtuzumab 12 mg and interferon beta 1a in all patients who received at least one dose of study drug. This study is registered with ClinicalTrials.gov, number NCT00548405.202 (87%) of 231 patients randomly allocated interferon beta 1a and 426 (98%) of 436 patients randomly allocated alemtuzumab 12 mg were included in the primary analyses. 104 (51%) patients in the interferon beta 1a group relapsed (201 events) compared with 147 (35%) patients in the alemtuzumab group (236 events; rate ratio 0·51 [95% CI 0·39-0·65]; p<0·0001), corresponding to a 49·4% improvement with alemtuzumab. 94 (47%) patients in the interferon beta 1a group were relapse-free at 2 years compared with 278 (65%) patients in the alemtuzumab group (p<0·0001). 40 (20%) patients in the interferon beta 1a group had sustained accumulation of disability compared with 54 (13%) in the alemtuzumab group (hazard ratio 0·58 [95% CI 0·38-0·87]; p=0·008), corresponding to a 42% improvement in the alemtuzumab group. For 435 patients allocated alemtuzumab 12 mg, 393 (90%) had infusion-associated reactions, 334 (77%) had infections (compared with 134 [66%] of 202 patients in the interferon beta 1a group) that were mostly mild-moderate with none fatal, 69 (16%) had thyroid disorders, and three (1%) had immune thrombocytopenia.For patients with first-line treatment-refractory relapsing-remitting multiple sclerosis, alemtuzumab could be used to reduce relapse rates and sustained accumulation of disability. Suitable risk management strategies allow for early identification of alemtuzumab's main adverse effect of secondary autoimmunity.Genzyme (Sanofi) and Bayer Schering Pharma.
View details for DOI 10.1016/S0140-6736(12)61768-1
View details for Web of Science ID 000311435000028
View details for PubMedID 23122650
Protective effect of an elastase inhibitor in a neuromyelitis optica-like disease driven by a peptide of myelin oligodendroglial glycoprotein
MULTIPLE SCLEROSIS JOURNAL
2012; 18 (4): 398-408
The pathology of neuromyelitis optica (NMO), in contrast to multiple sclerosis, comprises granulocyte infiltrates along extensive lengths of spinal cord, as well as optic nerve. Furthermore, IFN-β treatment worsens NMO. We recently found that experimental autoimmune encephalomyelitis (EAE) induced with Th17 cells is exacerbated by IFN-β, in contrast to disease induced with Th1 where treatment attenuated symptoms.This study demonstrates the similarities between NMO and Th17 EAE and how neutrophils mediate pathology in Th17 disease.Levels of blood biomarkers in NMO were assessed by Luminex and ELISA. Effects of IFN-β on neutrophils were assessed by culture assays and immunofluorescence. EAE was induced by transfer of myelin-specific Th1 or Th17 cells and treated with Sivelestat sodium hydrate, a neutrophil elastase inhibitor.We show Th17 cytokines, granulocyte chemokines, type 1 interferon and neutrophil elastase are elevated in patients with definitive NMO. In culture, we find that IFN-β stimulates neutrophils to release neutrophil elastase. In Th17 EAE, we demonstrate neutrophilic infiltration in the optic nerve and spinal cord which was not present in Th1 EAE. Blockade of neutrophil elastase with Sivelestat had efficacy in Th17 EAE but not Th1 EAE.The similarities between Th17 EAE and NMO indicate that this model represents several aspects of NMO. Neutrophils are critical in the pathologies of both Th17-EAE and NMO, and therefore blockade of neutrophil elastase is a promising target in treating NMO.
View details for DOI 10.1177/1352458512440060
View details for Web of Science ID 000302289900006
View details for PubMedID 22343184
- Protective Effect of elastase inhibitor in a neuromyelitis optica-like disease driven by a peptide of myelin olidodendrocyte glycoprotein Multiple Sclerosis 2012; 18 (4): 398-408
- Alemtuzumab for patients with relapsing Multiple Sclerosis after disease modifying therapy: a randomized controlled Phase 3 trial. Lancet 2012; Nov 24 (380): 1829-1839
Dalfampridine: a brief review of its mechanism of action and efficacy as a treatment to improve walking in patients with multiple sclerosis
CURRENT MEDICAL RESEARCH AND OPINION
2011; 27 (7): 1415-1423
Multiple sclerosis (MS) can cause progressive walking impairment that contributes to disability, loss of independence, and reduced quality of life. Dalfampridine (4-aminopyridine), a voltage-dependent potassium channel blocker, has been shown to improve walking in patients with MS, as demonstrated by an increase in walking speed.To summarize knowledge about the mechanism of action of dalfampridine in the context of clinical evidence of walking improvement in MS patients.Although this was not a systematic review, which is the primary limitation of this study, searches of PubMed were performed using relevant search terms to identify studies that examined the mechanism of action related to MS and its effects in patients with MS in clinical trials.Voltage-gated potassium channels represent a family of related proteins that span cell membranes, open and close in response to changes in the transmembrane potential, and help regulate ionic potassium currents. Action potential conduction deficits in demyelinated axons result in part from the exposure after demyelination of the paranodal and internodal potassium channels that are distributed in the axonal membrane. This exposure leads to abnormal currents across the axonal membrane that can slow action potential conduction, result in conduction failure, or affect the axon's capacity for repetitive discharge. While dalfampridine is a broad-spectrum blocker of voltage-dependent potassium channels at millimolar concentrations, studies have shown improvement in action potential conduction in demyelinated axons at concentrations as low as 1 μM, and therapeutic plasma concentrations (associated with improved walking) are in the range of 0.25 µM. However, no specific potassium channel subtype has yet been characterized with significant sensitivity to dalfampridine in this range, and the effects of the drug at this low concentration appear to be quite selective. Improved conduction translates into clinical benefit as measured by objectively and subjectively assessed walking relative to placebo. Such improvements were observed in approximately one third of patients treated with an extended-release formulation of dalfampridine in clinical trials. These patients who responded to dalfampridine had an average increase in walking speed of approximately 25%, and greater improvements than nonresponders on a self-reported subjective measure of walking.The extended-release formulation of dalfampridine has been shown in clinical trials to improve walking speed in approximately one third of MS patients with ambulatory impairment. The putative mechanism of action of dalfampridine is restoration of action potential conduction via blockade of an as yet uncharacterized subset of potassium channels in demyelinated axons.
View details for DOI 10.1185/03007995.2011.583229
View details for Web of Science ID 000291662300014
View details for PubMedID 21595605
- Dalfampridine: A brief review of its Mechanism of Action and Efficacy as a treatment to improve walking in patients with Multiple Sclerosis Current Research Medical Opinion 2011; 27 (7): 1415-1423
Impact of mobility impairment on the burden of caregiving in individuals with multiple sclerosis
EXPERT REVIEW OF PHARMACOECONOMICS & OUTCOMES RESEARCH
2010; 10 (4): 433-440
Multiple sclerosis (MS) is a chronic, immune-mediated neurologic disease that typically strikes young adults during their most productive years, and is associated with a wide range of functional deficits and progressive disability. Loss of mobility is among the most disabling effects of MS, adversely affecting multiple outcomes, including independence, employment and quality of life. Relative to other common diseases, MS is associated with a disproportionately high socioeconomic burden. Informal and unpaid caregivers, such as family and friends, play a vital, sustained and often difficult role in supporting the ability of MS patients to live and function at home. However, there are few data characterizing caregiver burden in MS. This review was conducted to examine the need and impact of caregiving for patients with MS, focusing on the contribution of mobility impairment to loss of patient independence.
View details for DOI 10.1586/ERP.10.34
View details for Web of Science ID 000297009800017
View details for PubMedID 20482233
Daclizumab in active relapsing multiple sclerosis (CHOICE study): a phase 2, randomised, double-blind, placebo-controlled, add-on trial with interferon beta
2010; 9 (4): 381-390
Daclizumab, a humanised monoclonal antibody, reduced multiple sclerosis disease activity in previous non-randomised studies. We aimed to assess whether daclizumab reduces disease activity in patients with active relapsing multiple sclerosis who are receiving interferon beta treatment.We did a phase 2, randomised, double-blind, placebo-controlled study at 51 centres in the USA, Canada, Germany, Italy, and Spain. Patients with active relapsing multiple sclerosis who were taking interferon beta were randomly assigned to receive add-on subcutaneous daclizumab 2 mg/kg every 2 weeks (interferon beta and high-dose daclizumab group), daclizumab 1 mg/kg every 4 weeks (interferon beta and low-dose daclizumab group), or interferon beta and placebo for 24 weeks. The randomisation scheme was generated by Facet Biotech. All patients and assessors were masked to treatment with the exception of Facet Biotech bioanalysts who prepared data for the data safety monitoring board or generated pharmacokinetic or pharmacodynamic data, a drug accountability auditor, and the site pharmacist. The primary endpoint was total number of new or enlarged gadolinium contrast-enhancing lesions measured on brain MRI scans every 4 weeks between weeks 8 and 24. Effects of daclizumab on prespecified subsets of lymphocytes and quantitative T-cell proliferative response were assessed in an exploratory pharmacodynamic substudy. Analysis was by intention to treat. This trial is registered with ClinicalTrials.gov, number NCT00109161.From May, 2005, to March, 2006, 288 patients were assessed for eligibility, and 230 were randomly assigned to receive interferon beta and high-dose daclizumab (n=75), interferon beta and low-dose daclizumab (n=78), or interferon beta and placebo (n=77). The adjusted mean number of new or enlarged gadolinium contrast-enhancing lesions was 4.75 in the interferon beta and placebo group compared with 1.32 in the interferon beta and high-dose daclizumab group (difference 72%, 95% CI 34% to 88%; p=0.004) and 3.58 in the interferon beta and low-dose daclizumab group (25%, -76% to 68%; p=0.51). In the pharmacodynamic substudy, daclizumab was not associated with significant changes in absolute numbers of T cells, B cells, or natural killer cells, or T-cell proliferative response compared with interferon beta alone. The number of CD56(bright) natural killer cells was seven to eight times higher in both daclizumab groups than in the interferon beta and placebo group (interferon beta and low-dose daclizumab group p=0.002; interferon beta and high-dose daclizumab group p<0.0001). Common adverse events were equally distributed across groups.Add-on daclizumab treatment reduced the number of new or enlarged gadolinium contrast-enhancing lesions compared with interferon beta alone and might reduce multiple sclerosis disease activity to a greater extent than interferon beta alone.Facet Biotech and Biogen Idec.
View details for DOI 10.1016/S1474-4422(10)70033-8
View details for Web of Science ID 000276142000016
View details for PubMedID 20163990
- The impact of mobility impairment on the burden of caregiving in individuals with multiple sclerosis Expert Rev. Pharmacoeconomics Outcomes Res. 2010; 10 (4): 433-440
Cytomegalovirus Infection with MRI Signal Abnormalities Affecting the Optic Nerves, Optic Chiasm, and Optic Tracts
JOURNAL OF NEURO-OPHTHALMOLOGY
2009; 29 (3): 223-226
A 49-year-old woman who had been immunosuppressed after a renal transplant developed bilateral severe visual loss. Visual acuities were finger counting and hand movements in the two eyes. Both optic nerves were pale. There were no other ophthalmic abnormalities. Brain MRI disclosed marked signal abnormalities involving the optic nerves, optic chiasm, and optic tracts. Cerebrospinal fluid polymerase chain reaction (PCR) was positive for cytomegalovirus. Treatment did not restore vision. Such extensive clinical and imaging involvement of the anterior visual pathway, which has been previously reported with other herpes viruses, illustrates the propensity for this family of viruses to track along axons.
View details for Web of Science ID 000270048700011
View details for PubMedID 19726946
- CMV Optic Neuritis with Extensive Tracking along the Visual Pathway J Neuro-Ophthalmology 2009; 29 (3): 223-226
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- Tovaxin for Early Relapsing Multiple Sclerosis Phase 2b Placebo Controlled Trial of Autologous T cell vaccination in patients with CIS or RRMS Multiple Sclerosis 2008; 14: S5-S27
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