Mary A. Johnson, PhD

• University of Delaware   Newark, Delaware   B.A. with Distinction  1977   Biology & Psychology
• Johns Hopkins University   Baltimore, MD     M.A.  1980   Physiological Psychology
• Johns Hopkins University   Baltimore, MD     Ph.D. 1982   Physiological Psychology
• Wilmer Eye Institute, Johns Hopkins University School of Medicine   Post-doctoral fellowship 1982-1983  Ophthalmology

Dr. Johnson is a vision scientist, specializing in clinical applications of electrophysiology and psychophysics. She uses these techniques to study how disease affects visual function, and from these data she develops insights into the mechanisms of damage.  She is best known for her work in retinal disease caused by poor blood flow to the eye, from disorders such as diabetic retinopathy, central retinal vein and artery occlusions, and carotid artery occlusion. Dr. Johnson provided the unifying concept explaining that all patients at risk of blinding complications of from these disorders shared the same mechanism of action - that retina with just enough blood flow to keep it alive, i.e. retina with very reduced sensitivity – was responsible for generating a diffusible substance that caused new, abnormal blood vessels to grow and bleed and form connective tissue, leading to blindness. Today, a device that she helped develop to estimate retinal sensitivity loss in ischemic disorders is used around the world to identify diabetic patients that require urgent ophthalmic intervention. In another example of how understanding mechanisms of function loss aid in disease management, Dr. Johnson showed that the anti-epileptic drug vigabatrin was preferentially toxic to intraretinal neurons connected to cone photoreceptors, producing irreversible cone sensitivity loss throughout the visual field. She identified an electroretinogram (ERG) protocol that is now used as a surrogate for visual field loss in patients taking vigabatrin that cannot perform a visual field test, such as babies with infantile spasms. She also developed a new ERG protocol to reflect an inhibitory neuron in the retina, and determined that the response of that neuron is abnormal in traumatic brain injury and in an animal model of Huntington's disease, possibly explaining some of these patients' unusual visual symptoms.

Dr. Johnson applies what she has learned in her studies directly to patient care, as director of the Visual Electrodiagnostics laboratory.  This has resulted in the identification of several new or exceedingly rare disorders among patients referred for unexplained vision loss.

Dr. Johnson is internationally-recognized for her work: She was elected a fellow of the Optical Society of America for her contributions and has held a number of leadership roles in this organization.  She is also a fellow of the Association for Research in Vision and Ophthalmology. Currently, she serves on the Board of Directors of the International Society for the Clinical Electrophysiology of Vision, and is a member of the editorial board of its journal, Documenta Ophthalmologica. Her current studies include identifying occult retinal damage from traumatic brain injury, developing neuroprotective/neuroregenerative treatments in nonarteritic anterior ischemic optic neuropathy (NAION), and investigating a putative biomarker for Huntington’s disease, so that treatment trials can be run with more rigor.

traumatic brain injury, retinal ischemia, central retinal vein occlusion (CRVO), diabetic retinopathy, nonarteritic anterior ischemic optic neuropathy (NAION), vigabatrin toxicity, electroretinogram (ERG), visual evoked potential (VEP), pattern ERG (PERG)

Johnson, M.A., Choy, D.:  On the definition of age-related norms for visual function testing.  Appl. Optics 26, 1449-1454 (1987).

Johnson, M.A., Drum, B.A., Quigley, H.A., Sanchez, R.M., Dunkelberger, G.R.:  Pattern-evoked potentials and optic nerve fiber loss in monocular laser-induced glaucoma.   Invest. Ophthalmol. Vis. Sci. 30, 897-907 (1989).

Johnson, M.A., McPhee, T.J.:  Electroretinographic findings in iris neovascularization due to acute central retinal vein occlusion.  Arch. Ophthalmol.  111: 806-814 (1993).

Madreperla, S.A., Johnson, M.A., Nakatani, K.:  Electrophysiologic and electroretinographic evidence for photoreceptor dysfunction as a toxic effect of digoxin.  Arch. Ophthalmol. 112:  807-812 (1994).

Johnson, M.A., Krauss, G.L., Miller, N.R., Medura, M., Paul, S.R.:  Visual function loss from vigabatrin:  Effect of stopping the drug.  Neurology 55: 40-45 (2000).

Kim, S.Y., Johnson, M.A., McLeod, D.S., Alexander, T., Otsuji, T., Steidl, S.M., Hansen, B.C., Lutty, G.A.:  Retinopathy in monkeys with spontaneous type 2 diabetes.  Invest. Ophthalmol. Vis. Sci. 45:4543 – 4553 (2004).

Chen, CS*, Johnson, MA*, Flower, RA, Slater, BJ, Miller, NR, Bernstein, SL: A primate model of non-arteritic anterior ischemic optic neuropathy (pNAION). Invest Ophthalmol Vis Sci. 2008 Jul;49(7):2985-92. * First authors contributed equally

Johnson MA, Miller NR, Nolan T, Bernstein SL: Peripapillary Retinal Nerve Fiber Layer Swelling Predicts Peripapillary Atrophy in a Primate Model of Nonarteritic Anterior Ischemic Optic Neuropathy. Invest Ophthalmol Vis Sci. 2016 Feb 1;57(2):527-32.

Johnson MA, Jeffrey BG, Messias AMV, Robson AG: ISCEV extended protocol for the stimulus-response series for the dark-adapted full-field ERG b-wave. Doc Ophthalmol. 2019 Jun;138(3):217-227.