Retinal thinning may be a window on Parkinson's.
The findings may have implications for tracking disease progression in Parkinson's disease patients and also hold promise for early diagnosis in older adults during routine eye examinations, said Dr. Mohammedyusuf E. Hajee, an ophthalmologist and fellow in neurology at SUNY Downstate. "It takes literally seconds to do. It's noninvasive," he said of the examination of the retina with optical coherence tomography (OCT).
The principal investigator on the study was Dr. Ivan Bodis-Wollner, a professor of neurology and of ophthalmology at SUNY Downstate and the director for the Center for Parkinson Disease and Related Disorders, who specializes in optical findings in neurodegenerative diseases.
The investigators compared 45 eyes of 24 Parkinson's disease patients and 31 eyes of age-matched control patients after comprehensive ophthalmologic examinations and high-resolution Optovue RTVue Fourier-Domain OCT. The mean age of the Parkinson's disease patients was 64.0 years and 63.5 for the control subjects.
The patients were relatively early in their disease course, with an average disease duration of 2.9 years. Slightly more than half were on stable pharmacologic therapy regimens, and the remaining patients were de novo, having not yet begun with dopaminergic therapy. Patients and control subjects with any posterior pole pathology (macular degeneration, glaucoma, ischemic optic neurology, or other optic neuropathies) were excluded.
The investigators were interested in detecting any differences in specific layers of the inner retina (the nerve-fiber layer, the ganglion-cell layer, and the inner-plexiform layer) and the outer retina (starting from the inner nuclear layer up to and including the retinal pigment epithelium), and upon OCT examination, they found a correlation between Parkinson's disease and thickness of the superior and inferior inner and outer retinal layers, said Dr. Hajee.
The inner retinal layer was 103.5 mcm plus or minus 24.3 mcm for healthy subjects, compared with 88.79 mcm plus or minus 11.3 mcm for patients with Parkinson's disease. The mean inferior inner retinal layer was 104 mcm plus or minus 23.5 mcm for healthy subjects, compared with 89.83 mcm plus or minus 11.1 mcm for Parkinson's disease patients. The differences were highly significant in both regions.
Previous research has found substantially lower levels of dopamine in the retinas of humans and animals with Parkinson's disease--evidence of visual manifestations of the neurodegenerative disease.
The possibility of an early, easily accessible biomarker is "exciting," said Dr. Hajee, particularly now that it is known that more than 65% of dopaminergic neurons are lost in Parkinson's disease patients before motor symptoms are detected.
The finding of thin inner retinal layers is not pathognomonic for Parkinson's disease, because it may also be seen in patients with multiple sclerosis, Alzheimer's disease, and primary open-angle glaucoma, explained Dr. Hajee in an interview at the meeting.
However, there are differences. In glaucoma, the pattern of retinal thinning is nonspecific and fails to correlate with the visual defect.
In Alzheimer's disease, retinal thinning seems to be primarily in the superior quadrant.
It remains to be seen whether the precise retinal thinning patterns in Parkinson's disease would provide high specificity as a diagnostic biomarker. "However, if you had a few cardinal signs, this might be an excellent way to clinch the diagnosis," said Dr. Hajee, who highlighted several key lessons from the study.
One is that ophthalmologists should consider Parkinson's disease in the differential diagnosis in the context of this finding. In addition, the findings rule out increased intraocular pressure as an explanation for retinal thinning in Parkinson's disease patients.
The widespread availability of OCT technology provides incentives to further explore the feasibility of using retinal thinning patterns to advance clinical tracking of Parkinson's disease, either as a screening tool or for monitoring therapy and disease progression, he said.
The study was supported by the National Parkinson Foundation and New York State's Empire Clinical Research Investigator Program. No industry funding was used.
BY BETSY BATES
Los Angeles Bureau
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|Title Annotation:||Clinical Rounds|
|Publication:||Family Practice News|
|Article Type:||Clinical report|
|Date:||Dec 1, 2008|
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