Saccades are the rapid, simultaneous movements of both eyes used to shift gaze quickly between two points of interest. These movements are ballistic, meaning they are exceptionally fast and cannot be altered once initiated. Their purpose is to position the fovea—the area of highest visual acuity—onto the intended target. Saccades are important for reading and general visual exploration. When these movements fail to execute correctly, the resulting abnormalities can severely impair visual processing and indicate underlying neurological issues.
Understanding Normal Saccades
Normal saccades are defined by specific dynamic properties, which include their high peak velocity, short duration, and remarkable accuracy. The velocity of these movements is exceptionally high, with a typical 10-degree saccade reaching a peak velocity of around 167 to 196 degrees per second. This speed is directly related to the amplitude of the movement, a relationship known as the main sequence.
These rapid movements are generated by a complex neural circuit involving the brainstem and higher brain centers. Specifically, the speed and amplitude of horizontal saccades are controlled by the saccade burst generator located in the paramedian pontine reticular formation (PPRF) in the brainstem. The PPRF receives input from the frontal eye fields in the cortex, the superior colliculus in the midbrain, and the cerebellum. The cerebellum acts as a calibrator, constantly monitoring and adjusting the movements to ensure they land accurately on the target.
Classifying Deviations in Saccadic Movements
Abnormal saccades are classified based on deviations from normal velocity, timing, and accuracy.
Slow saccades are a primary type of abnormality, characterized by the eye movement taking longer to complete and failing to reach the expected peak velocity for its amplitude. Slow saccades are frequently seen in disorders affecting the brainstem, which houses the neural machinery responsible for generating the movement’s force.
A second type of deviation is saccadic dysmetria, which relates to the precision of the movement. This occurs when the eye fails to land precisely on the target, requiring an immediate corrective movement. If the eye movement falls short of the target, it is hypometric (undershoot dysmetria). Conversely, if the eye travels past the intended target, it is hypermetric (overshoot dysmetria).
Saccadic intrusions and oscillations disrupt steady fixation. These are irregular, involuntary, fast eye movements that momentarily pull the eye off the target. Examples include square wave jerks, where a small saccade moves the eye away and a corrective saccade returns it after a brief pause. Another example is ocular flutter, which involves back-to-back horizontal saccades without any pause between them, causing the eyes to rapidly oscillate.
Underlying Conditions Leading to Saccadic Dysfunction
Saccadic abnormalities indicate damage within the central nervous system, often affecting the neural pathways that control eye movement. Damage to the cerebellum, the brain’s control center for coordination and motor learning, is strongly associated with saccadic dysmetria. Since the cerebellum fine-tunes the amplitude of the eye movement, lesions in this area result in characteristic undershooting or overshooting of the target.
Disorders primarily affecting the brainstem often manifest as slow saccades, particularly in the vertical plane. The brainstem contains the burst neurons required for the high-velocity pulse of the saccade, and their degradation directly reduces the speed of the movement. Certain neurodegenerative disorders, such as Progressive Supranuclear Palsy (PSP), are known for causing a significant slowing of vertical saccades due to damage in midbrain areas.
Saccadic dysfunction is seen in many neurodegenerative disorders, including Multiple Sclerosis and Parkinsonian syndromes. Huntington’s disease is associated with markedly slowed horizontal saccades. Certain hereditary ataxias, like Spinocerebellar Ataxia type 2, also present with profoundly slowed saccadic velocities. Beyond structural disease, some medications, such as anti-epileptics or heavy sedatives, can temporarily impair the brain’s control signals, leading to transient dysmetria or slowing.
Assessment and Management Strategies
The assessment of abnormal saccades begins with clinical observation, where a clinician asks a patient to quickly shift their gaze between two targets. For a precise diagnosis, specialized equipment is used to objectively measure the movement’s characteristics. Videonystagmography (VNG) is a standard diagnostic tool that uses infrared cameras to track and record eye movements with high precision.
VNG testing provides quantitative data on three main parameters: latency, velocity, and accuracy. Latency measures the time required to start the movement, velocity reflects the integrity of the brainstem burst neurons, and accuracy assesses cerebellar function. By analyzing this data, a doctor can differentiate between a problem in the cerebellum, which affects accuracy, and a problem in the brainstem, which affects speed.
Management of saccadic dysfunction focuses on treating the underlying cause, such as managing the progression of a neurodegenerative disease or adjusting the dosage of a causative medication. While a cure for the underlying neurological condition may not exist, specific vision therapies can be employed to help manage the resulting symptoms. These therapies often involve targeted exercises to improve the coordination and efficiency of the eye movements, aiming to enhance reading ability and visual stability.