Leonard V. Messner
Leonard V. Messner

Alzheimer’s disease is a global disease of central nervous system dysfunction. Although public discourse about it tends to focus on the cognitive aspects of this terrible disease, it is reasonable to expect that global changes in brain function would have a significant impact on the functions that take up more than half the brain’s volume: vision and visual motor function.

We know, for example, that patients with Alzheimer’s disease (AD) have atrophy of the visual cortex, particularly the cuneate gyrus, or cuneus, which is where the superior retinal projections terminate.

There are also changes in ocular structures that parallel cognitive declines in AD and are increasingly being considered as biomarkers for the disease. OCT studies have shown that both the retinal nerve fiber layer and the ganglion cell complex are significantly thinner in individuals with AD. Most recently, some very interesting work done with OCT angiography identified both enlargement of the foveal avascular zone and an overall decrease in retinal vascular density in patients with AD compared to healthy controls (Yoon et al.).

It makes sense, then, that the combination of brain atrophy, changes in visual processing, and structural changes in the retina and optic nerve would begin to affect vision. It is quite common for individuals with AD, particularly in the early stages, to complain of vision abnormalities that are not clearly manifested in a routine examination. Patients may be convinced that their vision is “not quite right,” despite having no significant cataract or obvious retinal disease.

Vision or visual motor changes may be detectable with other tests, however. For example, the impairment of low-contrast acuity in patients with Alzheimer’s disease has been well established (Salobrar-Garcia et al.). Saccadic abnormalities are also quite common in AD (Noiret et al.). In a recent paper, Galetta and colleagues evaluated the performance of subjects with mild cognitive impairment (MCI) or AD compared to healthy controls on the King-Devick test, a rapid number naming test that is widely used in concussion, AD and other neurodegenerative disorders. They found that both MCI and AD patients took significantly longer to perform this test than healthy controls.

What to do about these visual changes after detecting them is another matter. There are not as yet any effective, disease-modifying treatments to offer patients with AD. With ongoing research, there is considerable hope that will change in the future.

What you can do:

  • Be empathetic. An older patient, especially one with a diagnosis of dementia or MCI, isn’t necessarily making up their symptoms.
  • Go beyond a basic exam. AD-related abnormalities may not be obvious initially. Consider testing low-contrast acuity or performing King-Devick testing or OCT examination.
  • Educate family members about how brain pathology affects visual function and visual processing. Progression of AD is devastating for family members to observe; it is not uncommon for them to blame the patient for behaviors or mistakes that are poorly understood.
  • Consider a referral to a low vision specialist. As AD progresses, it becomes more difficult to conduct an effective eye exam. There may be some role for low vision therapists who can spend more time with these challenging patients to help maximize their visual capabilities. Other pearls for eye care in AD are offered in a Primary Care Optometry News article (Nowak).

Source Link Here