Gaze palsy is a neurological condition defined by the inability to move both eyes simultaneously in a specific direction, known as conjugate gaze. This impairment is caused by damage to the brain pathways that coordinate eye movement, not by a problem with the eye muscles themselves. Depending on the location of the damage, the ability to look left, right, up, or down may be restricted or completely lost. This condition significantly impacts daily life, making it difficult to read, track objects, or maintain spatial awareness. Because gaze palsy signals a breakdown in the central nervous system, it requires prompt medical attention.
How the Brain Controls Eye Movement
The ability to move both eyes in perfect synchrony relies on a complex, rapid communication network primarily located within the brainstem. To shift gaze horizontally, the brain must activate the muscle pulling one eye outward (lateral rectus) while simultaneously activating the muscle pulling the other eye inward (medial rectus).
For horizontal movements, the command center is the paramedian pontine reticular formation (PPRF), situated in the pons region of the brainstem. The PPRF acts as the primary “go” signal, integrating inputs from higher brain centers to initiate a quick, conjugate movement (saccade). A signal from the PPRF to look left, for instance, directly activates the nerve nucleus for the left lateral rectus muscle.
This signal must also reach the opposite eye’s medial rectus muscle to pull it inward. The connection ensuring this synchronized movement is the Medial Longitudinal Fasciculus (MLF), a heavily myelinated tract of nerve fibers running vertically through the brainstem. The MLF allows the PPRF’s signal to cross over and instruct the opposite eye’s muscle to move simultaneously.
Vertical gaze (looking up and down) is controlled by distinct centers located higher up in the midbrain. These vertical centers, specifically the rostral interstitial nucleus of the MLF, integrate commands for upward and downward movements, enabling smooth and precise visual tracking.
Types of Gaze Palsy
Gaze palsies are classified based on the direction of movement impaired and the location of the neurological damage. The most common presentation is Horizontal Gaze Palsy, involving an inability to look left, right, or both. This type is caused by a lesion in the pons, often affecting the PPRF or the adjacent abducens nerve nucleus.
When the damage is unilateral, the patient cannot move both eyes toward the side of the lesion. For example, a lesion on the right side of the pons prevents the eyes from looking right. This results in an inability to initiate quick eye movement in the affected direction.
Vertical Gaze Palsy restricts the ability to look up, down, or both, and points to damage in the midbrain. Parinaud syndrome, or dorsal midbrain syndrome, is the most common form of vertical palsy, typically restricting upward gaze. This syndrome is caused by compression or damage to the vertical gaze centers.
A third classification is Internuclear Ophthalmoplegia (INO), which results from damage to the Medial Longitudinal Fasciculus (MLF). In INO, one eye cannot turn inward (adduct) when attempting to look to the side, though the other eye moves normally outward. The outward-moving eye often exhibits nystagmus, an involuntary shaking.
Common Causes of Gaze Palsy
The neurological damage leading to gaze palsy results from an abrupt or progressive medical event affecting the brainstem or its pathways. Ischemic events, such as a stroke or transient ischemic attack (TIA), are the most frequent cause, particularly for horizontal gaze palsy. A stroke interrupts blood flow to the pons, causing the death of PPRF neurons and eliminating the command signal for lateral gaze.
Demyelinating diseases, such as Multiple Sclerosis (MS), are another leading cause, often associated with Internuclear Ophthalmoplegia (INO). In MS, the immune system attacks the myelin sheath surrounding nerve fibers; the MLF is a common target. This demyelination blocks the transmission of the coordinating signal, resulting in uncoordinated horizontal movement.
Space-occupying lesions, like tumors, cause gaze palsy by compressing brainstem structures. For instance, a pineal tumor in the midbrain can press on vertical gaze centers, leading to the upward gaze restriction seen in Parinaud syndrome. Head trauma can also cause acute onset of a palsy due to swelling or hemorrhage within the brainstem.
Less common causes include neurodegenerative disorders, such as Progressive Supranuclear Palsy (PSP), which often first manifests as impaired downward vertical gaze.
Identifying and Treating Gaze Palsy
The initial manifestation of gaze palsy is often the sudden onset of double vision (diplopia), occurring because the eyes cannot align on a single target. Patients report difficulty tracking objects or reading, and frequently adopt compensatory head movements, such as turning the head instead of their eyes, to change their visual focus. The examining physician often observes nystagmus, an involuntary, rhythmic oscillation of the eyes, which helps locate the lesion.
Diagnosis begins with a detailed neurological examination testing the patient’s ability to follow a target in all directions of gaze. Specific maneuvers, like the doll’s head maneuver, which tests reflex eye movements by passively turning the patient’s head, help differentiate a gaze palsy (a central nervous system problem) from a muscle or peripheral nerve issue. Immediate diagnostic imaging is required due to the underlying structural damage.
Magnetic Resonance Imaging (MRI) is the standard for diagnosis, providing high-resolution images of the brainstem to pinpoint the location and nature of the lesion (e.g., stroke, tumor, or MS plaque). A Computed Tomography (CT) scan is sometimes used acutely if a hemorrhage or large mass is suspected.
Treatment focuses primarily on addressing the underlying medical cause of the damage. This may involve acute stroke management with clot-busting drugs, chemotherapy or surgery for tumors, or immunosuppressive therapy for multiple sclerosis. Supportive measures manage resulting visual symptoms, including using prism glasses to fuse double images, or patching one eye to eliminate severe diplopia. Vision therapy may also be prescribed to help the patient adapt to the restricted eye movement.