Vertical nystagmus is an involuntary, repetitive movement of the eyes in an up-and-down direction. Unlike the more common horizontal nystagmus (side to side), vertical nystagmus is considered a red flag for a problem in the brain or brainstem rather than the inner ear. It can be present all the time or triggered by certain head positions, and it typically points to dysfunction in the neural pathways that control vertical eye movements.
Upbeat vs. Downbeat Types
Vertical nystagmus comes in two main forms, named for the direction of the fast-beating phase. In upbeat nystagmus, the eyes drift downward and then snap back upward. In downbeat nystagmus, the eyes drift upward and snap back down. When either type is visible while you’re simply looking straight ahead, it carries more clinical significance than nystagmus that only appears when your eyes move to an extreme position.
Downbeat nystagmus is the more commonly studied form and is strongly associated with problems at the base of the skull where the brain meets the spinal cord. Upbeat nystagmus tends to arise from lesions scattered throughout the brainstem, most often in the medulla (the lowest part of the brainstem). In a study of 15 patients with upbeat nystagmus, medullary lesions were the most frequent cause, found in eight of those patients.
What It Feels Like
Many people with vertical nystagmus experience oscillopsia, a visual illusion where the world appears to bounce, shake, or oscillate vertically. This can make reading difficult and interfere with balance and walking. Some people describe feeling as though the ground is moving beneath them or that text on a page jumps up and down. The sensation can be constant or come in episodes, depending on the underlying cause. In episodic cases, people may have stretches of normal vision between flare-ups that last minutes to hours.
Common Causes
Because vertical eye movements are controlled by structures deep in the brainstem and cerebellum, the list of possible causes is long and almost always points to something affecting the central nervous system.
Structural Problems
One of the best-known causes of downbeat nystagmus is a Chiari malformation, a condition where part of the brain extends into the spinal canal. Roughly 4 to 7 percent of people with type I Chiari malformation develop downbeat nystagmus. Other structural causes include tumors near the base of the skull, hydrocephalus (fluid buildup in the brain), and head trauma.
Degenerative and Autoimmune Conditions
Cerebellar degeneration, whether inherited or sporadic, is a major cause. Specific genetic conditions like spinocerebellar ataxia type 6 and episodic ataxia type 2 are well-documented triggers. Multiple sclerosis and other demyelinating diseases can damage the brainstem pathways that stabilize vertical gaze. Autoimmune conditions including celiac disease, Hashimoto’s encephalopathy, and various antibody-mediated brain inflammations have all been linked to downbeat nystagmus.
Nutritional Deficiencies
Thiamine (vitamin B1) deficiency causes Wernicke encephalopathy, a life-threatening but reversible brain condition frequently seen in chronic alcohol use and severe malnutrition. Nystagmus is one of the earliest signs of thiamine deficiency, and both upbeat and downbeat forms have been reported. In some cases, upbeat nystagmus that appears early on later converts to permanent downbeat nystagmus. Vitamin B12 and magnesium deficiencies can also contribute.
Medications and Toxins
Lithium, commonly prescribed for bipolar disorder, can cause downbeat nystagmus through brainstem toxicity. Notably, this side effect doesn’t always correspond to blood levels of the drug. In one documented case, a patient developed downbeat nystagmus with lithium levels only slightly above the therapeutic range. Anticonvulsants and some sedatives can also provoke vertical nystagmus.
Stroke and Vascular Events
Strokes affecting the brainstem or cerebellum can produce vertical nystagmus suddenly. Both medial and lateral medullary strokes (affecting different zones of the lower brainstem) have been identified as causes of upbeat nystagmus. Vertebrobasilar insufficiency, where blood flow to the back of the brain is compromised, is another vascular trigger.
Why It’s Considered a Red Flag
In clinical vestibular assessment, vertical nystagmus is one of several findings that strongly suggest a central (brain-based) rather than peripheral (inner ear-based) cause of dizziness. Other red flags that often accompany it include nystagmus that changes direction when you look in different directions, and misalignment of the eyes vertically (called skew deviation). When a patient has acute vertigo, clinicians use a bedside exam called HINTS, which checks for these patterns, to determine whether brain imaging is needed. Vertical nystagmus that persists without suppression when you focus on an object is particularly concerning.
This distinction matters because inner ear causes of dizziness, while unpleasant, are rarely dangerous. Central causes like stroke or tumor can be life-threatening and require urgent evaluation.
How It’s Diagnosed
The first step is usually a clinical eye movement exam where a provider watches your eyes in different gaze positions and head positions. Infrared goggles that block your ability to focus on a fixed point can make subtle nystagmus more visible, since visual fixation naturally suppresses some types of eye movement.
A more formal test called videonystagmography (VNG) uses infrared cameras mounted in goggles to record your eye movements precisely. During the test, you’ll be asked to follow visual targets, move your head and body into various positions, and undergo caloric testing, where warm and cool air or water is delivered to each ear to stimulate the balance organs. The way your eyes respond helps pinpoint whether the problem is in the inner ear or the brain. For vertical nystagmus specifically, the positional testing component is especially informative.
Because vertical nystagmus almost always signals a central cause, brain imaging with MRI is typically the next step. This can reveal structural abnormalities, strokes, demyelinating lesions, or tumors. Blood work may follow to check for vitamin deficiencies, autoimmune markers, or drug levels.
Treatment Approaches
Treatment depends entirely on the underlying cause. When vertical nystagmus stems from a correctable problem, addressing that problem often resolves or reduces the eye movements.
Thiamine deficiency is one of the most dramatically treatable causes. Nystagmus improves within hours of thiamine supplementation in about two-thirds of patients with Wernicke encephalopathy. Most remaining patients see improvement over the following weeks, though a small number have persistent nystagmus long-term. When lithium is the culprit, discontinuing or reducing the medication typically allows the nystagmus to resolve.
For cases where the underlying condition can’t be fully reversed, such as cerebellar degeneration, medications can help reduce the intensity of the eye movements and the resulting oscillopsia. Gabapentin and memantine are the two most commonly studied options. Gabapentin is typically started at lower doses and gradually increased, with doses for nystagmus ranging from 900 to 2400 mg per day in clinical use. Patients who don’t respond to gabapentin may be switched to memantine, gradually increased up to 20 mg per day. These medications don’t cure the underlying condition but can meaningfully reduce how much the world appears to bounce.
Surgical intervention is sometimes appropriate for structural causes. Chiari malformation, for example, can be treated with decompression surgery, which may relieve the downbeat nystagmus if the cerebellar pathways haven’t been permanently damaged.