Nystagmus, also known as ocular ataxia, is a term that refers to uncontrollable eye movement- usually a repetitive cycle of slow movement in a specific direction followed by a quick adjustment back to center. The root of this movement lies in a normal reflex that we use every day: the vestibulo-ocular reflex. This reflex controls how our sense of balance and head movement (our ‘vestibular’ sense) directs the movement of our eyes (the ‘ocular’ component refers to the eye muscles).
For example, if we look at something like the space bar on our keyboard and move our head slowly back and forth, our eyes are usually able to remain fixed on the space bar without much conscious effort. This is occurring because of constant communication between our inner ear and our eye muscles as our head is moving in space.
To get slightly more technical about how this works, we have special sensory organs called “semicircular canals” in the inner ear which serve as a biological gyroscope. As you turn your head in a given direction, fluid in these canals shifts in relation to your movement. The shifting of this fluid activates specialized neurons that in turn activate other neurons to get the information of how you are turning from the ear, to the cerebellum, to the muscles that control the eye. However, there are circumstances where this line of communication may become overwhelmed or disrupted. This disruption causes our eyes to move even though our heads are still. When this happens, we get nystagmus.
For example, here is a video of someone experiencing the vestibulo-ocular reflex while spinning in a chair and nystagmus after spinning in a chair. In this instance, nystagmus happens when the person stops spinning in the chair because the fluid in the inner ear continues moving for a short time even though the head has stopped.
Ataxia, the loss of coordinated movement, is caused by degeneration of the cerebellum. One of the main roles of the cerebellum is as an integration center for how we use incoming sensory information (touch, sight, balance, etc.) to direct how we move in space. Thus, we see that as ataxia worsens, complex voluntary movements like walking become harder to control. This can also disrupt how reflexes using balance and head movement, like the vestibulo-ocular reflex, work. As one’s head moves, the information on how the head is moving initially goes to a specific area of the cerebellum which then tells the eye muscles how to move.
When the cerebellar Purkinje cells of that area stop working properly, this channel of communication becomes overactive. The eye muscles begin to move sporadically as though the head was moving or swivelling even though it is staying still. This is an important symptom to address in patients with ataxia. Nystagmus disrupts sight and is tied to secondary symptoms such as dizziness and nausea. This combination of symptoms severely impedes a person’s independence and reduces their quality of life.
If you would like to learn more about nystagmus, take a look at these resources by Johns Hopkins and the American Academy of Ophthalmology.
Snapshot written by Carrie Sheeler and edited by Dr. Siddharth Nath.
