Vertical Gaze Palsy (VGP) is a neurological condition defined by the inability to voluntarily move both eyes together in the vertical direction, including looking up or looking down. This impairment is classified as a supranuclear gaze palsy, meaning the issue lies in the higher brain centers that command eye movement, rather than the muscles or nerves that directly control them. VGP is a distinct symptom of an underlying neurological dysfunction, signaling damage to a specific, small area within the brainstem. It is a manifestation of a separate, often serious, neurological disorder.
How Vertical Gaze Palsy Affects Vision
A patient with VGP loses the ability to perform rapid, voluntary eye movements, known as saccades, in the vertical plane. The most common presentation is an impaired ability to look upwards, frequently referred to as Parinaud syndrome or dorsal midbrain syndrome. This restriction makes simple tasks difficult, such as looking up at a shelf or reading signs above eye level.
Impaired downward gaze is also a significant symptom, often associated with specific neurodegenerative conditions. The inability to look down creates profound challenges for daily life, impacting activities like reading, navigating stairs, or seeing one’s feet while walking. The restriction is typically described as a slowing of eye velocity before a full limitation of the range of motion occurs.
Patients may also develop secondary visual disturbances, including light sensitivity (photophobia) or nystagmus, an involuntary, repetitive fluttering of the eye. To compensate for the inability to move their eyes, individuals often resort to moving their entire head to shift their line of sight. These visual restrictions increase the risk of falls and cause generalized difficulty with depth perception and spatial awareness.
The Brain Structures Controlling Vertical Gaze
The control center for vertical eye movements is concentrated in the midbrain, the uppermost part of the brainstem. This region contains a specialized neural network responsible for generating the commands for upward and downward movement. The entire process is managed by a supranuclear system, located above the cranial nerve nuclei that directly power the eye muscles.
Two primary structures within this midbrain area are the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) and the posterior commissure. The riMLF acts as the “vertical gaze center,” containing the burst neurons that generate the fast, precise signals for vertical saccades. Damage to this small nucleus severely impairs the initiation and speed of vertical eye movements.
The posterior commissure is an essential white matter tract located near the riMLF, acting as a relay point for signals that command upward eye movement. The fibers that control upward gaze cross through this commissure to communicate with the motor neurons that elevate the eyes. Lesions affecting the riMLF and the posterior commissure are the direct anatomical cause of VGP.
Primary Causes of Vertical Gaze Palsy
The conditions that cause Vertical Gaze Palsy directly damage or compress the delicate midbrain structures that control vertical gaze. Vascular events, such as a stroke or hemorrhage in the brainstem, are a frequent and acute cause of VGP. A lack of blood flow (infarct) to the midbrain can rapidly destroy the cells of the riMLF or interrupt the pathways of the posterior commissure.
Tumors are another significant cause, particularly those located near the pineal gland, adjacent to the dorsal midbrain. These masses can exert pressure on the posterior commissure, often leading to impaired upward gaze (Parinaud syndrome). Similarly, obstructive hydrocephalus, a buildup of cerebrospinal fluid, can increase pressure on the midbrain and cause mechanical compression.
Neurodegenerative disorders represent a major chronic cause, most notably Progressive Supranuclear Palsy (PSP). This condition is characterized by the progressive degeneration of specific brain cells, often targeting the riMLF early in the disease course. Consequently, the inability to look downward is a defining and early hallmark of PSP. Less common causes include metabolic disorders and autoimmune or inflammatory conditions.
Confirming Diagnosis and Treatment Options
Diagnosis begins with a detailed clinical examination by a neurologist or ophthalmologist, who tests the patient’s voluntary and reflexive eye movements. The clinician looks for the characteristic slowing of vertical saccades and the inability to move the eyes up or down on command. A key finding is the preservation of the vestibulo-ocular reflex (VOR), often tested with the “doll’s head maneuver,” which confirms the supranuclear nature of the palsy.
Following the clinical assessment, medical imaging is necessary to identify the exact location and nature of the lesion causing the damage. Magnetic Resonance Imaging (MRI) of the brainstem is the preferred method, as it clearly visualizes small strokes, tumors, or signs of atrophy characteristic of neurodegenerative diseases like PSP. This imaging is crucial for distinguishing between the various potential causes.
Treatment for VGP is primarily directed at managing the underlying condition responsible for the midbrain damage. If the cause is a treatable issue, such as a tumor or hydrocephalus, surgical removal or the placement of a shunt may resolve or improve the gaze limitation. For untreatable underlying causes, such as chronic stroke damage or PSP, management shifts to symptomatic support and adaptation. Physical and occupational therapy can help patients adapt their head movements and improve balance. Specialized glasses containing prisms may also be used to shift the visual field into the remaining range of eye movement.