What Is Vertical Gaze Palsy and What Causes It?

Vertical gaze palsy is the inability to move both eyes upward, downward, or both, caused by damage to specific brainstem and midbrain structures that coordinate vertical eye movement. The range of disorders behind it is wide, spanning neurodegenerative diseases, strokes, tumors, metabolic conditions, and infections.¹ Unlike a problem with the eye muscles themselves, vertical gaze palsy almost always traces back to the brain, which makes the pattern of the palsy a valuable clue for figuring out what went wrong.

How the Brain Controls Vertical Eye Movement

To understand why vertical gaze palsy happens, it helps to know that looking up or down is not just a matter of contracting eye muscles. The brain has a dedicated relay system in the upper brainstem, specifically in and around the midbrain, that generates and sustains vertical eye movements. Two small clusters of nerve cells do most of the heavy lifting. The first, called the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), is responsible for generating the quick, darting movements the eyes make when you shift your gaze, known as saccades. The second, the interstitial nucleus of Cajal (INC), is responsible for holding the eyes in place once they have moved to a new position.²

What makes these nuclei interesting is their wiring. The riMLF sends signals to eye muscles in an asymmetric way: it projects to the muscles that pull the eyes down on only one side, but projects to the muscles that pull the eyes up on both sides. This means a lesion on one side of the riMLF tends to knock out downward gaze more readily than upward gaze, because upward signals have a backup path through the opposite side. When both sides are damaged, vertical gaze in both directions can be lost entirely.² Damage to the INC, meanwhile, limits how far the eyes can range vertically and disrupts the ability to hold a steady gaze position after movement.²

The blood supply feeding these structures comes from small arteries branching off the back of the brain. One variant in particular, called the artery of Percheron, is a single vessel that supplies both sides of this region. If it becomes blocked, the damage can be bilateral and sudden, knocking out vertical gaze in one stroke.³

Why the Direction of Gaze Loss Matters

Clinicians pay close attention to whether someone has lost the ability to look up, look down, or both, because the direction often points toward the underlying cause. A study of 113 patients with supranuclear vertical gaze palsy found that the pattern varied strikingly by disease type. Among patients with vascular problems like strokes, upward gaze palsy was far more common, with 35 patients affected in their upward gaze compared to only 3 with predominantly downward gaze loss. In patients with Parkinsonian disorders, the pattern flipped: downward gaze palsy was more prevalent, affecting 28 patients, while 16 had upward gaze palsy alone.⁴

That same study found an even finer distinction. All patients who had downward gaze palsy alongside a Parkinsonian condition had atypical parkinsonism, a group of rarer, more aggressive diseases. Among patients with upward gaze palsy alone, the majority with standard Parkinson’s disease had only upward involvement, while those with atypical parkinsonism more often progressed to include downward gaze as well. The difference was statistically significant, which makes the direction of gaze loss a practical bedside tool for distinguishing ordinary Parkinson’s from its more aggressive cousins.⁴

Progressive Supranuclear Palsy

The disease most closely associated with vertical gaze palsy is progressive supranuclear palsy (PSP), a neurodegenerative condition that typically strikes later in life. PSP involves the accumulation of an abnormal form of a protein called tau in the brain, and gaze disturbance is one of its defining clinical features. In PSP, vertical saccades become slow and fall short of their target in both the upward and downward directions, though downward saccades tend to be hit harder. Patients also struggle with convergence, the ability to turn both eyes inward to focus on something close, and with adjusting their vestibular reflexes for different viewing distances.⁵

What makes PSP particularly debilitating is that the gaze problem tends to worsen over time. Early on, vertical eye movements are merely sluggish. As the disease advances, voluntary vertical gaze can be lost altogether. In some cases, the damage extends beyond the brainstem relay stations down into the motor nerve nuclei themselves, which means even reflexive eye movements, like those triggered by turning the head, stop working. Case reports describe patients reaching a stage of nearly complete eye immobility, where the eyes drift outward and no amount of head turning or stimulation can coax them to move vertically.⁶

This progression carries real consequences for everyday safety. Research on gaze control during stair climbing in PSP patients has found that deficits in the ability to look down interfere with how people place their feet on steps, raising the risk of tripping and falling.⁷ For someone who cannot look at the ground in front of them, stairs, curbs, and uneven surfaces become genuinely dangerous.

Strokes and Blood Vessel Problems

Stroke is one of the more common acute causes of vertical gaze palsy, and the culprit is almost always a blockage in one of the small arteries that feed the midbrain or thalamus. The posterior circulation of the brain, the network of vessels running along the back and underside of the brain, supplies the exact structures involved in vertical gaze control. A stroke here can produce sudden-onset vertical gaze palsy, often accompanied by drowsiness, confusion, or memory problems, depending on how much tissue is affected.

The artery of Percheron deserves special mention. This vessel is a normal anatomical variant, not something that develops abnormally, but it is unusual in that a single artery feeds both sides of the paramedian thalamus and upper midbrain. When it occludes, the resulting infarction is bilateral, which can wipe out vertical gaze in both directions at once.³ The artery itself is so tiny that it often escapes detection on standard imaging, and its true prevalence in the population is uncertain.

Not every stroke-related vertical gaze palsy involves the midbrain directly. MRI studies have demonstrated that infarctions confined to the thalamus, without any visible midbrain damage, can still produce vertical gaze paralysis. Three patients with vertical gaze palsies were found to have thalamic infarcts on MRI, with no evidence of midbrain involvement on repeated scans over several weeks.⁸ This challenges the traditional assumption that vertical gaze palsy always points to midbrain damage and shows that the thalamus plays a role in the vertical gaze circuitry that is sometimes underappreciated.

Tumors and Hydrocephalus

When a mass or buildup of fluid presses on the top of the midbrain, the result is a clinical picture called Parinaud syndrome, also known as dorsal midbrain syndrome. The hallmark is vertical gaze palsy, specifically a loss of upward gaze, but it comes with a characteristic cluster of accompanying signs. A 25-year review of 40 consecutive adult cases found that all 40 patients had vertical gaze palsy. About 88 percent had convergence-retraction nystagmus, a distinctive jerking of the eyes inward and backward when they try to look up. About 65 percent showed light-near dissociation, where the pupils respond to focusing on a near object but not to light. Only 65 percent of patients had the classical triad of all three signs together, which means relying on the full triad to make the diagnosis would miss a substantial fraction of cases.⁹

The causes of Parinaud syndrome reflect what can compress the dorsal midbrain. Pineal region tumors are a classic culprit, but hydrocephalus, where fluid builds up and expands the brain’s ventricles, can produce the same compression. Hydrocephalus caused by narrowing of the aqueduct, the small channel through which cerebrospinal fluid drains from one ventricle to another, is particularly well-positioned to push against this part of the midbrain.¹⁰ In these cases, treating the hydrocephalus, usually by diverting the fluid with a shunt or opening the blockage surgically, can sometimes reverse the gaze palsy.

Metabolic and Infectious Causes

Vertical gaze palsy shows up in a handful of metabolic and infectious diseases that might not seem related to the eyes at first glance. Niemann-Pick disease type C (NPC) is a rare inherited disorder of lipid metabolism that causes toxic lipid storage in cells throughout the body, including in the brain. Vertical gaze palsy is one of its most consistent neurological features, present in roughly 65 percent of patients, with downward gaze typically affected before upward gaze.¹¹¹² Because NPC can present at any age, from infancy to adulthood, unexplained vertical gaze palsy in a young person sometimes triggers the diagnostic workup that uncovers the disease.

On the infectious side, Whipple’s disease, caused by the bacterium Tropheryma whipplei, is an uncommon but treatable infection that can invade the central nervous system. A systematic review of movement disorders in Whipple’s disease found that supranuclear gaze palsy was the single most common oculomotor abnormality, appearing in 58 percent of affected patients.¹³ Whipple’s disease matters because it is one of the few causes of vertical gaze palsy that is curable with antibiotics if caught in time.

The full list of conditions that can produce vertical gaze palsy extends well beyond these examples. Wilson’s disease, a copper metabolism disorder, prion diseases like Creutzfeldt-Jakob disease, certain autoimmune conditions, and even intoxication with particular drugs or substances have all been documented as causes.¹ The sheer breadth of the differential diagnosis is part of what makes vertical gaze palsy both a useful clinical sign and a diagnostic puzzle.

How Doctors Identify the Underlying Cause

The clinical exam is the starting point. A neurologist will ask you to look up, look down, and follow a target through various positions to map out exactly which vertical movements are impaired. They will check whether the eyes can be driven vertically by turning or tilting the head, since preservation of these reflexive movements suggests the problem is “supranuclear,” meaning it is above the level of the nerves that directly control the eye muscles. If reflexive movements are also gone, the damage may have reached the nerve nuclei themselves or the nerves running to the muscles.

Imaging, particularly MRI, is essential for pinpointing the location and cause of the damage. Standard MRI sequences sometimes miss small midbrain or thalamic strokes, especially in the first hours. Diffusion-weighted imaging (DWI), a type of MRI that highlights areas of acute ischemia with high sensitivity, has proven valuable in these situations. In patients presenting with vertical gaze palsy from midbrain strokes, DWI correctly identified the ischemic area in all patients tested, while conventional MRI sequences missed the relevant lesion in several of them.¹⁴ For anyone showing up to the emergency department with sudden vertical gaze palsy, getting the right kind of MRI quickly can mean the difference between catching a treatable stroke and sending someone home with a missed diagnosis.

Beyond imaging, the clinical context shapes the workup. If the onset was sudden, the focus is on stroke. If the onset was gradual, neurodegenerative disease or a slowly growing tumor becomes more likely. If the patient is young, metabolic conditions like NPC or Wilson’s disease enter the picture. Blood tests, lumbar puncture, and genetic testing may all be part of the evaluation depending on the clinical suspicion.

Living with Impaired Vertical Gaze

The practical consequences of vertical gaze palsy depend on which direction is lost. Loss of downward gaze tends to be more functionally disabling than loss of upward gaze, because so much of daily life requires looking down: reading, eating, navigating stairs, seeing your feet on the sidewalk. People with downward gaze palsy often describe difficulty with meals, since they cannot see their plate, and a persistent sense of insecurity when walking because they cannot scan the ground for obstacles. Research has confirmed this intuition, showing that impaired downward gaze alters foot placement during stair climbing and increases the risk of falls.⁷

Loss of upward gaze, while less disabling in everyday tasks, still causes problems. Reaching for objects on high shelves, reading overhead signs, and making eye contact with someone taller all become difficult. Driving can be affected in either direction, since checking mirrors, scanning intersections, and reading traffic signals involve vertical eye movements that most people never think about consciously.

Management depends entirely on the underlying cause. When vertical gaze palsy results from a treatable condition like hydrocephalus, relieving the pressure can restore eye movement. When it results from an infection like Whipple’s disease, antibiotics can halt and sometimes reverse the damage. For neurodegenerative causes like PSP, there is currently no treatment that reverses the gaze palsy itself. Rehabilitation efforts in those cases focus on compensatory strategies: using head movements to substitute for eye movements, modifying the home environment to reduce fall hazards, and adjusting reading materials and screens to sit at eye level rather than below it. Optical devices such as prism glasses have been explored for patients with downgaze problems, aiming to shift the visual field downward without requiring eye movement, though their practical utility varies from person to person.

When Upward Gaze Loss Is Normal

One detail that sometimes causes unnecessary alarm: a mild reduction in upward gaze is common with aging and does not necessarily indicate disease. As people get older, the range of upward eye movement naturally shrinks somewhat. This age-related limitation is usually symmetric, gradual, and not accompanied by the other neurological signs that mark pathological vertical gaze palsy, such as slowed saccades, abnormal pupil responses, or convergence problems. The threshold for concern is when the limitation is pronounced, asymmetric, accompanied by other symptoms, or develops suddenly rather than over decades. A neurologist evaluating vertical gaze palsy will factor in a patient’s age when deciding whether the finding is pathological. If you are in your seventies and notice that looking straight up at the ceiling is harder than it used to be, that may simply be aging. If you are forty and suddenly cannot look down at your phone, that warrants prompt evaluation.

1
PubMed Central. Supranuclear Vertical Gaze Palsy in Movement Disorders
2
PubMed. A hypothetical scheme for the brainstem control of vertical gaze
3
PubMed Central. Artery of Percheron infarction presented with isolated downgaze paralysis
4
PubMed Central. Patterns and causes of supranuclear vertical gaze palsy – A retrospective, single-institutional study in 113 patients
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PubMed Central. The disturbance of gaze in progressive supranuclear palsy – implications for pathogenesis
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PubMed Central. Exodeviated ophthalmoplegia in a patient with progressive supranuclear palsy
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Physical Therapy. Gaze Control and Foot Kinematics During Stair Climbing – Characteristics Leading to Fall Risk in Progressive Supranuclear Palsy
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PubMed. Vertical gaze palsies from medial thalamic infarctions without midbrain involvement
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PubMed. Parinaud syndrome – a 25-year (1991-2016) review of 40 consecutive adult cases
10
PubMed. Hydrocephalus due to aqueductal stenosis presenting with acute bilateral ptosis
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PubMed. Vertical supranuclear gaze palsy in Niemann-Pick type C disease
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PubMed Central. Niemann-Pick type C – contemporary diagnosis and treatment of a classical disorder
13
PubMed Central. Movement Disorders and Oculomotor Abnormalities in Whipple’s Disease – An Updated Systematic Review
14
Cerebrovascular Diseases. Midbrain Ischemia Presenting as Vertical Gaze Palsy – Value of Diffusion-Weighted Magnetic Resonance Imaging