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Dr. Heather Moss is Associate Professor and Director of Clinical Research in the Stanford Department of Ophthalmology. She directs an innovative clinical-research program in biomarker discovery at the Spencer Center for Vision Research at Stanford and provides expert neuro-ophthalmic clinical care at the Byers Eye Institute at Stanford.Dr. Moss pursued undergraduate studies in biomedical engineering at the University of Guelph, followed by doctoral studies in medical engineering at Harvard and MIT, seeking to improve human health through application of engineering principles. Working with patients inspired her to become a physician; after earning her medical degree at Harvard, she completed residency training in Neurology and fellowship training in Neuro-ophthalmology at the University of Pennsylvania. She spent six years on the faculty of the University of Illinois at Chicago, serving as the Director of Neuro-ophthalmology and starting a neuro-ophthalmology fellowship training program, before joining the Stanford faculty in 2016.Her clinical expertise includes diagnosis and treatment of optic nerve diseases, eye movement disorders, and neurological pathology affecting visual pathways. She is a national leader in application of telemedicine to improve access to neuro-ophthalmic care. Her research lab is developing novel diagnostic approaches to neurological and neuro-ophthalmic diseases through application of innovative electrophysiology, imaging, and mathematical modeling. She has published over 80 articles in peer-reviewed journals, has authored numerous book chapters, and serves on the editorial board of four journals. She is a fellow of the American Academy of Neurology (AAN) and the North American Neuro-Ophthalmology Society (NANOS) and has been elected to leadership roles in both organizations.Outside of work Dr. Moss enjoys spending time with her two children, exploring northern California, and renovating her 100-year-old house.
Permanent visual impairment due to papilledema, an optic neuropathy characterized by optic nerve swelling, occurs in approximately half of patients with IIH. There is a significant clinical need for non-invasive biomarkers that will advance diagnosis and management of IIH. The objective of my research is to establish physiologically based markers of retinal ganglion cell(RGC) function and retinal/cerebral vasculature as markers of IIH that detect abnormalities, monitor treatment and distinguish peripheral vision outcomes. I have demonstrated that retinal vein diameter changes over the course of disease. Through collaboration with Dr. Ali Alaraj, an endovascular neurosurgeon, we have defined characteristic changes in cerebral venous blood flow and pressure in IIH patients. Through collaboration with Dr. McAnany, a psychophysics expert, we have demonstrated alterations in objective markers of optic nerve function that correlate with other measures of disease in IIH patients. These results are laying the scientific and technical foundation for the development of these markers as clinical tools and clinical trial outcome measures. Furthermore, the results are advancing scientific understanding of the pathophysiology underlying papilledema and other optic neuropathies.
Palo Alto, Ca
Perioperative visual loss (POVL) is a devastating complication, with no known treatment or prevention,most commonly due to ischemic optic neuropathy (ION), and retinal arterial occlusion (RAO), and less commonlycortical blindness. We reported in 2009 that POVL had an estimated incidence of 3-10 cases/10,000procedures in two of the highest volume surgical procedures.1 The resulting severe visual impairment costs >$27,000/y, or $675,000 during the estimated remainder of a middle-aged individual’s life from increased healthcare spending alone. Lost productivity costing > $250,000, and frequent litigation further increase costs. Theemotional toll of sudden, unexpected visual loss is immeasurable. It is imperative to understand the risk factorsfor POVL in order to develop means to prevent these blinding complications. In collaboration with the University of Illinois at Chicago and University of Illinois at Chicago we are studying risk factors and developing a predictive model for perioperative visual loss (POVL) in spinal fusion and cardiac surgery.
Clinical and post-mortem observations of pathological effects spreading beyond the motor system in some people with ALS have led to a shift from the classical characterization of ALS as a disease exclusively of motor neurons to that of a multisystem disorder. During my fellowship training in neuro-ophthalmology I led the largest characterization of clinical eye movement disorders in this population and discovered previously undocumented afferent visual dysfunction. Collaboration with Dr. Amani Fawzi at Northwestern University has indicated that retinal pathology may account for this observation. We have surveyed different tests of afferent visual function to determine which are abnormal in ALS patients and which has the best correlation with visual system pathology in ALS patients.Current efforts involve infrastructure development to improve access to ophthalmic imaging in the neurosciences clinic to facilitate studies of ophthalmic markers of neurodegenerative disease and efforts to develop pupillometry apparatus with which to study diagnostic potential in neuro-degenerative disease.
The rarity of many neuro-ophthalmic diseases is a barrier to effective clinical outcomes research. This barrier can be overcome through collaborations between investigators and institutions to increase sample size, and through application of advanced statistical techniques to clinical trial data sets to maximize data analysis efficiency. I am actively involved in the NIH sponsored Neuro-ophthalmology Research Disease Investigator Consortium. Current active treatment trials are studying nonarteritic anterior ischemic optic neuropathy, idiopathic intracranial hypertension, and Lebers hereditary optic neuropathy.
Palo Alto, CA
Permanent vision loss caused by papilledema, the swelling of the optic nerve heads due to elevation in intracranial pressure (ICP), occurs in 50% of people with idiopathic intracranial hypertension (IIH) as well as individuals with high ICP from other neurological and neurosurgical diseases. One reason that blindness results from IIH, which is a treatable disease, is lack of timely, accurate clinical markers with which to identify those who are at risk of losing vision. <br/><br/>My research program seeks to identify and develop such markers through studies of papilledema physiology in humans affected by IIH. My current studies focus on humans with IIH because this accurately captures both the disease of interest and the target population. The conceptual frameworks that underlie my research program are drawn from my doctoral level engineering training. Using a mechanical (structural) framework I am evaluating the effect of changing intra-cerebral and intra-optic nerve forces from ICP and papilledema on the shape of the optic nerve and retinal blood vessels. Using an electrical (functional) framework I am evaluating patterns of visual pathway dysfunction in papilledema using non-invasive techniques of electrophysiology, pupillary light response and psychophysics. Markers based on both of these frameworks have the potential to capture the dynamics of pathophysiological changes associated with evolving and resolving papilledema with less delay than currently used clinical markers. <br/><br/>My aim is to develop non-invasive structural and functional markers of papilledema physiology that predict visual outcomes in IIH and guide tailored intervention that will improve visual outcomes and prevent blindness. The short-term objective of my research program is to evaluate candidate markers with regards to differences between untreated IIH, treated IIH and normal patients, changes over time in IIH patients receiving treatment, and differences between IIH patients with and without vision loss. The long-term objective of my research program is to elucidate markers of papilledema physiology that can be studied non-invasively and to ascertain their ability to predict future visual function in IIH and guide clinical management. <br/><br/>Other areas of active research include study of peri-operative vision loss and visual pathway based diagnosis of neuro-degenerative diseases. I am actively involved in clinical trials through the Neuro-Ophthalmology Research Disease Investigator Consortium (NORDIC).
Surgical Idiopathic Intracranial Hypertension Treatment Trial
Randomized trial of adults (≥18 years old) with idiopathic intracranial hypertension and
moderate to severe visual loss without substantial recent treatment who are randomly assigned
to (1) medical therapy, (2) medical therapy plus ONSF, or (3) medical therapy plus VPS. The
primary outcome is visual field mean deviation change at first of Month 6 (26 weeks) or time
of treatment failure of the eligible eye(s), followed by a continuation study to assess time
to treatment failure. The determination of eligible eye(s) is based on meeting the
eligibility criteria at baseline.
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Efficacy & Safety of RPh201 Treatment in Patients With Previous Nonarteritic Anterior Ischemic Optic Neuropathy (NAION)
This study is designed as a double-masked, randomized, placebo-controlled, clinical study to
evaluate the efficacy and safety of subcutaneous (SC) administration of RPh201 in
participants with previous NAION. All participants enrolled in Cohort A of the study will
have a documented history of NAION for at least 12 months and at most, five years prior to
enrollment. Participants enrolled in Cohort B of the study will have a documented history of
NAION for at least 6 months and at most, three years prior to enrollment.
Stanford is currently not accepting patients for this trial.
For more information, please contact Mariana Nunez, 650-497-7846.
Phase 2/3, Randomized, Double-Masked, Sham-Controlled Trial of QPI-1007 in Subjects With Acute Nonarteritic Anterior Ischemic Optic Neuropathy (NAION)
This study will determine the effect of QPI-1007 on visual function in subjects with
recent-onset NAION and assess the safety and tolerability of intravitreal injections of
QPI-1007 in this population. This study will also evaluate the structural changes in the
retina following administration of QPI-1007.