T. Michael Nork, M.S., M.D.
Associate Professor
Clinical Sciences Center, Room F4/336
600 Highland Avenue
Madison, WI 53792-3284
Office : (608) 263-4823
Clinic : (608) 263-7171
| Degrees: | BS 1970, Univ. Maryland. MS 1972, Georgia. Tech BS 1974, Univ. Maryland MD 1980, Univ. Texas Medical School at San Antonio |
| Residency: | 1984, Texas Tech Univ. Health Sciences Center |
| Fellowships: | Ophthalmic Pathology 1985, Univ. Illinois Eye and Ear Infirmary Diseases and Surgery of the Retina 1986, Univ. Wisconsin |
| Research: | My research focuses on the mechanisms by which various ocular diseases affect the outer retina (especially the rods and cones) and how injury to the outer retina might, in turn, affect disease pathogenesis. For example, we have found selective blue cone loss in retinal detachment and diabetic retinopathy. We are currently investigating the possibility that the retinal cones may also be injured in glaucoma—a disease that is not traditionally associated with the outer retina. Working with other members of our Department, we have described morphologic changes in the photoreceptors in post-mortem human eyes that were donated by people who carried a diagnosis of glaucoma. Following up on this, my colleague, Dr. Robert Nickells, reasoned that the photoreceptors, if injured in glaucoma, should produce less of their specific opsin mRNA. We have been investigating this possibility with RNase protection assay and in situ hybridization with opsin-specific mRNA probes. Unlike the case in retinal detachment and diabetic retinopathy in which the blue cones are lost, it is the red and green cones that seem to be most affected in both experimental glaucoma as well as post-mortem, donated human eyes with documented primary open angle glaucoma. A third line of evidence for outer retinal effects in glaucoma comes from work in collaboration with Drs. James Ver Hoeve, Gregg Heatley and Paul Kaufman, using the multifocal electroretinogram (mERG) in human as well as experimental glaucoma. Preliminary evidence suggests that there is delay in the latency of the a-like wave, which may reflect outer retinal function. Interestingly, this effect is seen most prominently in the arcuate region of the retina, which is the area most often associated with the visual field loss seen in early and moderately advanced human glaucoma. Although the photoreceptors in glaucoma may simply be responding to ganglion cell injury, an intriguing possibility is that they may be contributing to ganglion cell death by release of (or failure to adequately re-uptake) their neurotransmitter, glutamate. To test this possibility, we first eliminated the photoreceptors by focal retinal laser photocoagulation. This was followed by the induction of experimental glaucoma. The ganglion cells were seen to survive in greater numbers over the laser spots. Even though this is consistent with the concept of anterograde injury to the ganglion cells, a non-specific effect cannot be ruled out. We are currently using immunohistochemical techniques to look for known neuroprotectants in the vicinity of the laser spots. |
| Publications: | Nork TM, Ver Hoeve JN, Poulsen GL, et al. Swelling and loss of photoreceptors in chronic human and experimental glaucomas. Arch Ophthalmol 2000;118:235-45. Nork TM, Millecchia LL, Strickland BD, Linberg JV, Chao GM. Selective loss of blue cones and rods in human retinal detachment. Arch Ophthalmol 1995;113:1066-73. Nork TM, Ver Hoeve JN, Poulsen GL, Nickells RW, Davis MD, Weber AJ, Vaegan, Sarks SH, Lemley HL, Millecchia LL. Swelling and loss of photoreceptors in primary open angle and experimental glaucomas. Arch Ophthalmol 2000;118:235-45. Nork TM, Poulsen GL, Nickells RW, Ver Hoeve JN, Cho NC, Levin LA, Lucarelli MJ. Protection of ganglion cells in experimental glaucoma by retinal laser photocoagulation. Arch Ophthalmol 2000;18:1242-50. Cho NC, Poulsen GL, Ver Hoeve JN, Nork TM. Selective loss of S-cones in human diabetic retinopathy. Arch Ophthalmol 2000;118:1393-1400 Nork TM. Acquired color vision loss and a possible mechanism of ganglion cell death in glaucoma. Trans Am Ophthalmol Soc 2000;98:31-63. |