The ability to track a moving object smoothly (smooth pursuit) and rapidly shift gaze between targets (saccades) is fundamental to interacting with the world. These precise eye movements allow for clear vision during activities like reading, driving, and maintaining spatial awareness. When this coordination fails, a person can experience blurred vision, difficulty concentrating, or imbalance. Eye tracking problems in adults often reflect a disruption in the complex neurological pathways that control them, stemming from conditions affecting the central nervous system, peripheral nerves, or the body’s overall balance system.
Neurological Conditions Affecting Coordination
The most common causes of adult-onset eye tracking problems originate within the Central Nervous System (CNS), specifically in brain regions that coordinate movement and vision. These disorders disrupt the signaling pathways that dictate when and how quickly the eyes should move. Damage to the cerebellum, which is responsible for fine motor control, often impairs smooth pursuit, causing the eyes to track a moving target with noticeable, jerky movements instead of a fluid motion.
A stroke in the brainstem or cerebellum can immediately compromise eye movement control by damaging the nuclei and fiber tracts that relay commands to the ocular muscles. This damage can lead to profound deficits in smooth pursuit, making it nearly impossible to follow an object. Traumatic Brain Injury (TBI), including concussions, frequently results in oculomotor dysfunction, often presenting as slower and less accurate saccades. These tracking deficits can persist long after other symptoms of TBI have resolved, indicating sustained disruption of neural integrity.
Neurodegenerative diseases also progressively undermine the brain’s ability to coordinate eye movements. In Parkinson’s disease, the degeneration of dopamine-producing neurons affects areas crucial for voluntary eye control. This often manifests as hypometric saccades, where the eye repeatedly undershoots the target, requiring several small movements to fixate. Multiple Sclerosis (MS) attacks the myelin sheath protecting nerve fibers. This autoimmune disorder can slow or block signal transmission, leading to discoordinated eye movements, such as internuclear ophthalmoplegia when brainstem tracts are affected.
Structural and Ocular Motor Nerve Damage
Eye tracking failures can also result from a breakdown in the peripheral hardware, involving the eye muscles and the three cranial nerves that supply them. The oculomotor (CN III), trochlear (CN IV), and abducens (CN VI) nerves manage the six extrinsic eye muscles. A palsy in any of these nerves causes paralysis or weakness in the muscles they innervate.
A CN VI palsy, for example, prevents the lateral rectus muscle from pulling the eye outward, resulting in an inability to look away from the nose. Cranial nerve palsies can be caused by compression (aneurysm, tumor) or microvascular damage due to conditions like diabetes. Physical trauma to the eye orbit can also injure the extraocular muscles or the nerves, leading to mechanical restriction and double vision.
Disorders affecting the connection between the nerve and the muscle, known as the neuromuscular junction, also cause tracking problems. Myasthenia Gravis (MG) is an autoimmune disorder where the body attacks receptors on the muscle fibers, leading to fatigable muscle weakness. For many people with MG, the extraocular muscles are the first or only ones affected, causing symptoms like drooping eyelids and weakened eye movements that worsen with sustained use. This results in slow saccade velocities and difficulty maintaining fixation, indicating a problem with signal delivery rather than central generation.
Systemic and Vestibular Disruptions
Impaired eye tracking can stem from issues outside the central or peripheral nervous system, particularly those involving the balance system and systemic metabolic disorders. The Vestibulo-Ocular Reflex (VOR) stabilizes gaze by moving the eyes opposite to head movement, relying on input from the inner ear. When the inner ear is inflamed or damaged, the VOR is disrupted, causing involuntary, erratic eye movements called nystagmus, which interferes with stable tracking.
Vestibular Causes
Inner ear disorders such as labyrinthitis or Ménière’s disease can cause episodic or persistent vertigo and nystagmus, reflecting a faulty balance signal. The fluctuating nature of the vestibular signal in Ménière’s disease can temporarily reduce the VOR gain, meaning the eyes cannot move fast enough to counteract head motion.
Systemic and Medication Effects
Chronic metabolic conditions like advanced diabetes can cause microvascular damage to the small blood vessels supplying the cranial nerves. This leads to peripheral neuropathy that may impair CN III, IV, or VI function, resulting in poor eye coordination. Certain prescription medications, particularly sedatives or anti-epileptic drugs, may also temporarily impair cerebellar function, leading to reduced smooth pursuit performance.
Determining the Underlying Cause
Pinpointing the cause of an adult’s eye tracking difficulty requires a structured diagnostic approach. The process begins with a detailed clinical evaluation, including a patient history focusing on the onset, duration, and specific triggers for the eye movement problems. Specialized testing is then utilized to objectively measure and quantify the movement deficits.
Videonystagmography (VNG) or Electronystagmography (ENG) are common non-invasive tests that use cameras or electrodes to record eye movements in response to visual targets and positional changes. The oculomotor portion of the VNG assesses saccades and smooth pursuit. Findings like slow saccades or the inability to smoothly follow a target often point toward a central lesion in the brain. Conversely, specific patterns of nystagmus or VOR abnormalities help localize the problem to the peripheral vestibular system in the inner ear.
If the testing suggests a central nervous system issue, such as a stroke or tumor, imaging studies like Magnetic Resonance Imaging (MRI) or Computed Tomography (CT) scans are typically ordered. These scans provide high-resolution images, allowing doctors to visualize structural damage, lesions, or compression affecting the neural pathways responsible for eye movement control.