(PDF 202 KB)
Helen Coates* was having trouble seeing at night. The 57-year-old told us that this problem had become progressively worse over the previous nine months. Indeed, it got bad enough that when it was dark, she needed either a flashlight or somebody to help her get back to a well-lit area. At that point, her family members persuaded Ms. Coates to get her eyes checked.
Ms. Coates’ medical history included idiopathic polyneuropathy, which was previously confirmed by electromyography, and macrocytic anemia of unknown origin, which was diagnosed a year before we saw her. She had no history of hypertension, diabetes mellitus, malabsorption disorders, irritable bowel syndrome, hepatitis or gastric bypass surgery.
Initially, when her macrocytic anemia was diagnosed, the workup found normal vitamin B12, folic acid and liver enzyme levels. In addition, a bone marrow biopsy conducted at the same time found normal cells with no megaloblastic changes and no myelodysplasia.
We Get a Look
While Ms. Coates told us that she drank a minimal amount of alcohol, she admitted to having poor eating habits, which included far too much junk food and very little meat or vegetables.
The review of systems was significant for anxiety but was otherwise normal. Her family history was significant for a maternal aunt with night blindness.
Ms. Coates’ vision was 20/50 in both eyes. Her IOP by applanation was 12 mmHg in both eyes and her ocular motility was full. Her pupils reacted 3+ with no afferent pupillary defect, her visual fields showed diffuse loss in both eyes (Figs. 1 and 2) and the Amsler grid testing was normal bilaterally. Her color vision by Ishihara plates was 2/15 in both eyes.
Ms. Coates’ slit-lamp exam was normal with no evidence of conjunctival or corneal xerosis, corneal ulceration or keratomalacia. The dilated funduscopic exam showed that she had a vitreous floater in the right eye, and both discs were atrophic temporally with 0.8 cupping. Her macula, vasculature and peripheral retina were normal in both eyes with no signs of retinitis pigmentosa (Figs. 3 to 6).
Retinitis pigmentosa is the most common cause of night blindness. Patients with this genetic condition have progressive nyctalopia; eventually, daytime vision also may be affected.
Vitamin A deficiency is another common cause of night blindness, particularly in developing countries. Foods rich in vitamin A include those of animal origin, such as fish oils, liver and dairy products; in addition, vitamin A precursors can be found in some foods of plant origin, such as carrots, broccoli, oranges, bananas and spinach. Liver disease, various malabsorption syndromes and gastric bypass surgery impacting vitamin A metabolism also can cause nyctalopia.1
With regard to the optic nerve and retina, nyctalopia can be a symptom of glaucoma, X-linked congenital stationary night blindness, gyrate atrophy, Laurence-Moon syndrome, Oguchi disease, optic atrophy, peripheral chorioretinitis, siderosis retinae, cancer-associated retinopathy or hypoxia. Finally, uncorrected myopia may also lead a patient to describe symptoms similar to nyctalopia.