What Causes Eye Tracking Problems in Adults?

Eye tracking problems in adults stem from a surprisingly wide range of causes, from traumatic brain injuries and neurodegenerative diseases to thyroid disorders, medication side effects, and even prolonged sleep loss. The eyes rely on an intricate network of brain regions, cranial nerves, and six small muscles per eye working in tight coordination. When any part of that chain is disrupted, the result can be difficulty following moving objects, trouble reading, double vision, or a vague sense that your eyes just aren’t keeping up. Because so many different systems feed into eye movement control, pinpointing the cause often requires looking well beyond the eyes themselves.

How Eye Tracking Actually Works

Your eyes produce two main types of tracking movements. Smooth pursuit keeps your gaze locked onto a moving target, like watching a bird fly across the sky. Saccades are the rapid jumps your eyes make to shift focus from one point to another, like scanning across a line of text. For decades, researchers treated these as completely separate systems, but the evidence now shows they share retinal inputs, overlap in the brain areas that control them, and frequently work together as part of a single integrated process.

1PubMed Central. Saccades and pursuit: two outcomes of a single sensorimotor process

That integration matters when things go wrong. A problem with one type of movement rarely leaves the other untouched. For instance, a group of brainstem cells called omnipause neurons were long thought to regulate only saccades, but research has shown they also influence smooth pursuit.

2PubMed. Common inhibitory mechanism for saccades and smooth-pursuit eye movements

This shared wiring explains why so many conditions produce a mix of symptoms rather than a single, neat deficit.

Traumatic Brain Injury and Concussion

Concussion is one of the most common triggers for sudden-onset eye tracking problems in otherwise healthy adults. The brain circuits that coordinate eye movements are diffuse and vulnerable to the shearing forces of head trauma, so even a “mild” concussion can throw off both smooth pursuit and saccade control. In studies of athletes after sport-related concussions, smooth pursuit eye movements were slower than in uninjured controls. To compensate, concussed individuals made larger, faster saccades, essentially using quick jumps to keep up with a target their smooth pursuit could no longer follow steadily.

3PubMed Central. Smooth Pursuit and Saccades after Sport-Related Concussion

These deficits often show up before a person even realizes something is off. You might notice difficulty reading, a sense that words are swimming on the page, or headaches after prolonged visual tasks. In many concussion patients the problems resolve within weeks or months, but a meaningful number of people develop persistent post-concussion symptoms that include chronic oculomotor dysfunction. Computer-based oculomotor rehabilitation programs designed for mild traumatic brain injury have shown success in improving both objective tracking measures and self-reported visual symptoms.

4PubMed Central. A Novel Computer Oculomotor Rehabilitation (COR) Program for Mild Traumatic Brain Injury (mTBI)

Neurodegenerative Diseases

Parkinson’s disease offers one of the clearest examples of how neurodegeneration erodes eye movement control. About three-quarters of Parkinson’s patients show some form of oculomotor impairment, making abnormal eye movements a potential clinical indicator of the disease.

5PubMed Central. Recent advances (2022–2024) in eye-tracking for Parkinson’s disease: a promising tool for diagnosing and monitoring symptoms

The problems are varied: saccades tend to undershoot their targets, voluntary eye movements are delayed, and smooth pursuit becomes choppy. Early in the disease, the most affected movements are the deliberate ones, such as looking where you intend to rather than reflexively toward a distraction. As Parkinson’s progresses, even reflexive saccades slow down and fall short of their targets.

5PubMed Central. Recent advances (2022–2024) in eye-tracking for Parkinson’s disease: a promising tool for diagnosing and monitoring symptoms

Parkinson’s is far from the only neurodegenerative condition involved. Progressive supranuclear palsy is often first suspected precisely because of eye movement abnormalities, particularly difficulty looking downward. Huntington’s disease, multiple sclerosis, and various cerebellar ataxias all produce distinct patterns of tracking disruption. The pattern of which eye movements are affected and how they fail can actually help clinicians narrow down which neurological disease is at play.

Stroke and Focal Brain Lesions

When a stroke, tumor, or hemorrhage damages a specific brain region, the resulting eye tracking problem often has a characteristic signature. Lesions in the parieto-occipital lobes, for example, produce a distinctive deficit in smooth pursuit. Patients with damage there have trouble tracking objects moving toward the side of the lesion, with the eye producing jerky “cogwheel” saccades instead of smooth motion. Pursuit of objects moving toward the opposite side is also impaired, but the effect tends to be less severe unless the damage is acute and on the non-dominant side of the brain.

6PubMed. Pursuit gaze defects in acute and chronic unilateral parieto-occipital lesions

Frontal lobe damage tends to affect the voluntary control of saccades, making it hard to suppress reflexive glances or to look deliberately away from a sudden stimulus. Cerebellar lesions, meanwhile, tend to disrupt the fine-tuning of eye movements, producing overshoot, undershoot, and oscillations. Because different brain areas handle different aspects of tracking, an experienced clinician can sometimes use eye movement testing to localize a lesion before imaging even confirms it.

Myasthenia Gravis and Neuromuscular Junction Disorders

Myasthenia gravis attacks the junction where nerves communicate with muscles, and the small, constantly active extraocular muscles are often hit first. A comprehensive review found that myasthenia gravis patients show a wide range of eye movement abnormalities, including slower saccades, longer reaction times before initiating eye movements, and fatigue-related changes in optokinetic nystagmus and pupil constriction.

7PubMed. Tracking Eye Movements for Diagnosis in Myasthenia Gravis: A Comprehensive Review

What makes myasthenia distinctive is the fatigue pattern. Your eye tracking might be fairly normal in the morning and measurably worse by evening, or it might deteriorate during sustained visual tasks. Video-based eye tracking studies confirm this: at rest, saccades in myasthenia patients are already slower with longer latencies compared to controls, and a fatigue test makes both worse.

8PubMed. Subclinical involvement of eye movements detected by video-based eye tracking in myasthenia gravis

This fatigability is a valuable diagnostic clue, since most other causes of eye tracking problems don’t fluctuate so dramatically with exertion.

Thyroid Eye Disease

Thyroid eye disease, most often linked to Graves’ disease, can swell and stiffen the muscles that move your eyes. Volumetric imaging shows that in affected patients, the extraocular muscles are substantially enlarged. The superior rectus complex averages about 2.3 times its normal volume, the inferior rectus about 2.1 times, and the other muscles between 1.6 and 1.8 times their usual size.

9PubMed Central. Extraocular Muscle Enlargement in Thyroid Eye Disease Using Volumetric Analysis

Swollen muscles don’t glide freely in the orbit, so patients often develop restricted gaze, particularly when looking upward, and double vision that worsens in certain directions. The tracking problem here is mechanical rather than neurological, but the end result for the patient feels similar: difficulty reading, driving discomfort, and visual fatigue.

Diabetes and Cranial Nerve Damage

Diabetes quietly damages small blood vessels throughout the body, and the nerves controlling eye movement are vulnerable. Diabetic oculomotor nerve palsy typically strikes suddenly: you wake up one morning with a drooping eyelid, double vision, and difficulty moving one eye inward, upward, or downward. The classic diabetic presentation tends to spare the pupil, because the nerve fibers controlling pupil constriction sit on the outside of the nerve and are spared when ischemia damages the deeper fibers.

10PubMed Central. Ptosis as the only manifestation of diabetic superior division oculomotor nerve palsy: A case report

Most diabetic cranial nerve palsies resolve on their own within two to three months as the blood supply recovers, but they tend to recur if blood sugar remains poorly controlled. Diabetes can also affect the fourth and sixth cranial nerves, each of which controls a different eye muscle. The sixth nerve palsy, which prevents the eye from turning outward, is particularly common. If you have diabetes and suddenly develop double vision or a new eyelid droop, it warrants prompt evaluation to rule out more serious causes like compression from an aneurysm.

Vestibular Disorders

Your inner ear does more than help you balance. The vestibulo-ocular reflex automatically counter-rotates your eyes when your head moves, keeping the visual world stable. When the vestibular system is damaged by conditions like vestibular neuritis, Ménière’s disease, or benign paroxysmal positional vertigo, that reflex breaks down. People with vestibular disease show slower gaze stabilization, especially during downward head movements, compared to healthy individuals.

11PubMed Central. The influence of age and vestibular disorders on gaze stabilization: a pilot study

The result is a sensation that the world bounces or slides when you walk, turn your head, or ride in a car. This isn’t strictly an “eye tracking” problem in the way a neurologist uses the term, but it feels like one to the person experiencing it. You may also notice nystagmus, an involuntary rhythmic drifting and snapping back of the eyes, particularly after quick head turns. Vestibular rehabilitation therapy can retrain these reflexes, though recovery varies widely depending on the underlying cause.

Medications That Disrupt Eye Movements

Several categories of prescription drugs can interfere with eye tracking, sometimes subtly enough that neither the patient nor prescriber immediately connects the dots. Antiseizure medications are among the best-documented offenders. Drugs that block sodium channels in the brain, including phenytoin, carbamazepine, lamotrigine, oxcarbazepine, and lacosamide, can induce nystagmus. The likely mechanism involves impairment of voltage-gated sodium channels in the cerebellum’s Purkinje cells, and the nystagmus can be horizontal, vertical, or both.

12PubMed Central. Antiseizure Medication-Induced Nystagmus During Eye Closure Identified by Electroencephalography

Benzodiazepines, sedating antihistamines, lithium, and some antidepressants can also slow saccades or degrade smooth pursuit. The effect is usually dose-dependent: higher doses produce more noticeable tracking problems. If you started a new medication and notice blurred vision while reading, difficulty fixating, or the world seeming to jump when you move your eyes, it’s worth raising the issue with your prescriber. Dose adjustment or switching to an alternative drug often resolves the problem.

ADHD and Saccade Preparation

Adults with attention-deficit/hyperactivity disorder show a characteristic eye tracking pattern that’s distinct from the issues caused by structural brain damage. A meta-analysis of oculomotor studies in ADHD found disturbances across several tasks, particularly in inhibiting unwanted saccades, remembering visual target locations, and initiating saccades that go against a reflexive pull.

13PubMed. Oculomotor deficits in attention deficit hyperactivity disorder (ADHD): A systematic review and comprehensive meta-analysis

The interesting wrinkle is that once a saccade is launched, adults with ADHD execute it just as well as anyone else. The problem lies in the preparation phase: longer reaction times, more errors when asked to look away from a sudden stimulus, and more variability in when saccades begin. Neuroimaging confirms that the preparatory brain networks are less active in ADHD adults before they have to make an eye movement.

14PubMed Central. Preparatory neural networks are impaired in adults with attention-deficit/hyperactivity disorder during the antisaccade task

This means ADHD-related tracking issues are more about “when to move” than “how to move,” which has practical implications: difficulty reading is more likely related to inconsistent timing and impulsive glances than to any mechanical inability to move the eyes smoothly.

Schizophrenia and Smooth Pursuit

Impaired smooth pursuit eye movement is one of the most consistently replicated findings in schizophrenia research. When people with schizophrenia try to follow a moving target, their eyes typically lag behind it. The speed of eye movement doesn’t keep pace with the target, and the brain compensates by injecting catch-up saccades, producing a jagged, stop-and-start tracking pattern instead of the smooth following seen in healthy individuals.

15PubMed Central. Eye movement characteristics in schizophrenia: A recent update with clinical implications

The deficit is most pronounced during the steady-state tracking phase, especially when following predictable target movement, and it correlates with broader difficulties in processing visual motion.

16PubMed Central. Eye tracking dysfunction in schizophrenia: characterization and pathophysiology

What makes this finding particularly striking is that it also shows up at higher rates in first-degree relatives of people with schizophrenia who have no psychotic symptoms themselves. Research suggests eye tracking dysfunction is a sensitive biological marker for vulnerability to schizophrenia, present even when no other clinical signs are obvious.

17PubMed. Schizophrenia spectrum disorders and eye tracking dysfunction in singleton and multiplex schizophrenia families

Nutritional Deficiencies

Severe thiamine (vitamin B1) deficiency can produce Wernicke encephalopathy, a medical emergency that classically includes confusion, unsteady gait, and oculomotor dysfunction. In documented cases, patients have presented with inability to move their eyes outward (abduction palsy), followed by progressive restriction of upward and downward gaze. Brain imaging in these patients shows characteristic bright spots in deep brain structures. Crucially, thiamine replacement leads to measurable improvement in eye movement function, mental clarity, vision, and gait.

18BMJ Case Reports. Wernicke encephalopathy presenting with severe optic neuropathy and oculomotor dysfunction

Wernicke encephalopathy isn’t limited to people with alcohol use disorder, though that remains the most common association. It can occur after bariatric surgery, prolonged vomiting (including hyperemesis gravidarum), cancer chemotherapy, or any condition that severely depletes thiamine stores. The oculomotor signs are often the first abnormality a clinician notices, and they should trigger urgent thiamine supplementation before waiting for lab confirmation.

Digital Eye Strain and Convergence Insufficiency

Hours of screen use don’t directly damage your eye tracking system, but they can push an existing weakness past its breaking point. Prolonged near work places continuous demands on the convergence system (the inward rotation of both eyes toward a close target) and accommodation (focusing at near distance). If you have a latent binocular vision anomaly, sustained screen time can tip you from “managing fine” to symptomatic, with headaches, blurred vision, and difficulty maintaining focus.

19PubMed Central. A Review of Digital Eye Strain: Binocular Vision Anomalies, Ocular Surface Changes, and the Need for Objective Assessment

Convergence insufficiency is a specific condition where the eyes struggle to turn inward sufficiently for near tasks. Adults with convergence insufficiency have measurably slower convergence peak velocity compared to people without the condition, which may explain the eyestrain complaints that are the hallmark symptom.

20PubMed Central. Vision Therapy in Adults with Convergence Insufficiency: Clinical and Functional Magnetic Resonance Imaging Measures

This is worth knowing because convergence insufficiency is treatable with office-based vision therapy and home exercises, yet many adults assume their symptoms are just “normal” screen fatigue and never seek evaluation.

Sleep Deprivation and Temporary Impairment

Not every eye tracking problem points to an underlying disease. Sleep deprivation alone is enough to measurably degrade how well your two eyes work together. Research has shown that going without adequate sleep destabilizes both binocular coordination (keeping the two eyes aligned with each other) and gaze-target synchronization (keeping your eyes locked onto what you’re trying to look at). The horizontal component of binocular coordination is especially sensitive to sleep loss, a finding that has been explored as a potential tool for fitness-for-duty screening.

21PubMed Central. Degradation of Binocular Coordination during Sleep Deprivation

The practical implication is straightforward: if your main complaint is intermittent difficulty focusing or eyes that feel “off” during prolonged visual tasks, poor sleep should be near the top of the list of suspects before pursuing extensive neurological workup.

How Aging Affects Eye Tracking

Even without any disease, aging brings measurable changes to saccade performance. A study of 34 healthy adults aged 25 to 85 found that saccade frequency, amplitude, peak velocity, and mean velocity all decline with age during real-world tasks like walking down a hallway.

22PubMed Central. Effects of aging on eye movements in the real world

Interestingly, the same study found no significant age effect on smooth pursuit tracking of a real-world object during walking, a departure from what lab-based pursuit studies typically show. The discrepancy may reflect the fact that real-world tracking benefits from additional cues (head movement, context, prediction) that laboratory setups strip away.

This matters because a 70-year-old noticing that reading feels harder or driving at night is more stressful may be experiencing normal aging of the saccade system rather than early neurodegeneration. That said, the line between normal age-related decline and early pathology can be blurry, and any sudden or rapid worsening warrants evaluation.

How Eye Tracking Problems Are Diagnosed

Evaluation usually starts with a thorough neuro-ophthalmic examination that includes watching how your eyes move during pursuit, saccade, and convergence tasks. If the clinician suspects a vestibular component, videonystagmography (VNG) is a standard tool. Compared with the older electronystagmography approach, VNG tracings are more detailed and can capture subtle findings that might otherwise be missed.

23PubMed. Videonystagmography and Posturography

Modern video-based eye trackers are increasingly used in research settings to quantify saccade velocity, latency, and accuracy with enough precision to detect subclinical deficits. For many conditions, the pattern of abnormality on eye movement testing can suggest a diagnosis before more invasive testing is ordered. Blood work (thyroid function, blood glucose, thiamine levels), brain imaging, and nerve conduction studies round out the workup depending on the clinical picture.

Treatment Approaches

Treatment depends entirely on the underlying cause, which is why accurate diagnosis matters so much. For concussion-related oculomotor dysfunction, structured rehabilitation programs that progressively challenge the saccade and pursuit systems have proven effective, improving both objective tracking performance and subjective symptoms like headache and reading difficulty.

4PubMed Central. A Novel Computer Oculomotor Rehabilitation (COR) Program for Mild Traumatic Brain Injury (mTBI)

Follow-up data show that after such rehabilitation, visual-evoked brain responses become stronger and less variable, and measures of visual attention improve.

24PubMed. Effect of oculomotor vision rehabilitation on the visual-evoked potential and visual attention in mild traumatic brain injury

For convergence insufficiency, office-based vision therapy remains the gold standard. Prism glasses can compensate for certain alignment problems, and in cases of double vision related to retinal conditions, a combination of Bangerter foils (translucent filters placed over one lens) and Fresnel prisms can relieve symptoms by manipulating how the two eyes’ images overlap.

25PubMed Central. Management of binocular diplopia due to maculopathy with combined bangerter filter and fresnel prism

For medication-induced problems, the fix is often dose reduction or substitution. For neurodegenerative and autoimmune conditions, managing the underlying disease is the primary strategy, with optical aids and rehabilitation filling in the gaps that disease management alone cannot close.