Ross Hauser, MD

Temporary loss of vision in one eye can feel like a curtain, shadow, gray haze, or sudden blackout. The vision may return within seconds or minutes, but the brief duration does not make the event harmless. A new episode of monocular vision loss—vision loss affecting one eye—should be treated as an urgent medical problem until retinal ischemia, carotid artery disease, stroke, arterial dissection, giant cell arteritis, and other time-sensitive disorders have been evaluated.

At Caring Medical, we generally meet patients later in this process. Many have already undergone ophthalmologic, neurologic, cardiac, and vascular testing. Their vision symptoms may occur alongside neck pain, headaches, dizziness, pulsatile tinnitus, light sensitivity, visual blurring, or symptoms that change with head position. In this selected group, we may consider whether impaired venous drainage, altered intracranial pressure, or cervical instability could be contributing factors.

This article explains the established causes that must be addressed first, the limited research connecting internal jugular venous abnormalities with transient monocular blindness, and our clinical hypothesis about how neck structure may matter in certain patients. It is important to be clear: cervical instability is not an established general cause of temporary monocular blindness, and cervical Prolotherapy has not been proven in controlled trials to restore vision or prevent stroke.

What is transient monocular vision loss?

Transient monocular vision loss is a temporary reduction or loss of sight in one eye. The traditional term amaurosis fugax is often used when the event is believed to result from brief retinal ischemia—insufficient blood flow to the retina. However, not every transient visual disturbance is ischemic, and not every patient can reliably tell whether one or both eyes were affected.

Descriptions may include:

• A curtain or shade passing over one eye
• Vision fading to gray or black
• Patchy or partial visual-field loss
• Sudden blurring or dimming
• Recurrent episodes lasting seconds or minutes

A careful history helps distinguish monocular loss from visual aura, which commonly involves both eyes and may include shimmering, zigzag, or expanding patterns. Even so, migraine should not be assumed until urgent vascular and ocular causes have been considered. Reviews of transient vision loss emphasize that the evaluation depends on the pattern, duration, accompanying symptoms, vascular risk factors, and eye examination. (1)

In the image below the neck-eye reflexes are described.

These reflexes keep the head balanced while a person is watching moving objects or the body or head is in motion.

• The reflex vestibulo-ocular (VOR) causes eye gaze stabilization during head motion
• The reflex cervico-ocular (COR) helps the eyes to move in relation to neck rotation, (because of cervical ligament and facet joint proprioceptors – neurons that sense motion.)
• The reflex vestibulocollic (VCR) helps to stabilize head in space when the body moves.
• The reflex cervicalcollic (CCR) muscles tightened to stabilize head (because of cervical ligament and facet joint proprioceptors – neurons that sense motion.)

Potentially all these reflexes are impaired with ligament cervical instability causing symptoms of vertigo, dizziness, Nystagmus, Oscillopsia, visual disturbance and poor balance.

Temporary blindness in one eye can be a medical emergency

If vision is currently absent, newly impaired, or accompanied by weakness, numbness, facial droop, speech difficulty, severe headache, eye pain, a drooping eyelid, unequal pupils, chest pain, or loss of consciousness, emergency evaluation is appropriate. A person should not drive themselves.

Important causes include:

• Retinal or ophthalmic artery ischemia
• Carotid artery narrowing or embolism
• Carotid or vertebral artery dissection, particularly after neck trauma
• Transient ischemic attack or stroke
• Giant cell arteritis, especially in adults over age 50 with scalp tenderness, jaw pain, fever, or a new headache
• Retinal detachment, acute glaucoma, optic neuritis, or other eye disease
• Migraine or retinal migraine after other dangerous causes have been excluded
• Papilledema associated with elevated intracranial pressure

Evaluation may include a dilated eye examination, retinal imaging, measurement of intraocular pressure, neurologic assessment, vascular imaging, brain imaging, cardiac evaluation, and laboratory testing. The exact workup is individualized. The neck should not become the focus until clinicians have addressed these established and potentially dangerous explanations.

Papilledema, intracranial pressure, and brief visual dimming

Papilledema is swelling of the optic nerve head caused by elevated pressure inside the skull. It can produce brief visual obscurations—episodes of dimming, graying, or blackout—often triggered by bending, coughing, straining, or changing position. Other symptoms can include headache, pulsatile tinnitus, double vision, nausea, and visual-field loss.

Idiopathic intracranial hypertension is diagnosed when intracranial pressure is elevated without a mass lesion, hydrocephalus, or another identified cause. The condition can threaten vision and requires appropriate neuro-ophthalmologic or neurologic management. Consensus guidance emphasizes formal visual assessment, optic-nerve monitoring, appropriate imaging, and treatment directed at preserving vision and reducing pressure. (2)

Research has also documented reduced contrast sensitivity in patients with idiopathic intracranial hypertension. Contrast sensitivity is the ability to distinguish an object from its background, including subtle differences between light and dark. This may help explain why some patients describe their vision as washed out, hazy, or gray rather than completely black. (3)

Patients can learn more in our discussion of intracranial hypertension, venous outflow, and cervical spine instability. That discussion presents a proposed mechanism for a selected patient population; it should not replace standard evaluation for intracranial hypertension.

What does research say about jugular venous outflow and one-eye vision loss?

The internal jugular veins are major pathways through which venous blood leaves the brain. A small body of research has asked whether impaired jugular outflow or retrograde flow could disturb ocular venous circulation.

In a 2010 case-control study, investigators compared 31 patients with transient monocular blindness with 31 matched controls. Patients had wider retinal venules, and jugular venous reflux during a Valsalva maneuver was associated with greater retinal venule dilation. The authors proposed that jugular reflux could impede ocular venous outflow. (4)

A 2013 study examined 23 patients with transient monocular blindness who did not have carotid stenosis and 23 matched controls. Moderate or severe internal jugular vein narrowing was more frequent in the patient group at the upper and middle jugular levels. The authors proposed cerebral venous outflow impairment as one possible contributor. (5)

These studies are relevant but limited. Both were small, observational studies from a related research group. They demonstrate associations, not proof that jugular narrowing caused the visual events. They also do not establish that cervical ligament instability produced the jugular findings or that treating the neck will prevent further episodes.

How might the cervical spine enter the discussion?

The upper internal jugular vein travels through a crowded region beside the cervical spine, carotid artery, cranial nerves, and surrounding muscles. Its caliber can vary with anatomy, posture, hydration, breathing, and head position. External narrowing can occur between nearby structures, but an imaging finding of compression does not automatically mean that blood flow is clinically impaired.

At Caring Medical, we consider a cervical contribution only after urgent causes have been addressed and when the broader history supports further investigation. Findings that may justify a neck-focused assessment include:

• Significant neck pain or a history of whiplash or head-and-neck trauma
• Symptoms reproducibly worsened by rotation, extension, or prolonged forward-head posture
• Headache, pulsatile tinnitus, dizziness, visual blurring, or head pressure accompanying the visual complaint
• Suspected hypermobility or craniocervical instability
• Objective evidence of altered venous flow, intracranial pressure, or optic-nerve changes that requires correlation with specialist findings

We describe cervical spine instability as excessive or poorly controlled motion involving cervical joints and supporting ligaments. Standard static MRI can identify many important disorders but may not explain symptoms that occur only during movement. When appropriate, a comprehensive evaluation may incorporate physical examination and selected dynamic diagnostic studies. No single scan, ultrasound measurement, or postural finding proves that cervical instability is responsible for temporary vision loss.

Video: Vision problems, autonomic dysfunction, and cervical instability

In the following video, Ross Hauser, MD, explains our clinical model for how upper cervical instability could contribute to visual symptoms in a selected group of patients.

The possible pathways discussed in the video

The video describes several mechanisms that we consider when a patient has both neck dysfunction and otherwise-unexplained visual complaints:

• Altered autonomic signaling: The autonomic nervous system helps regulate pupil size and the response to light. Disturbed signaling may be associated with unusually large pupils, limited constriction, or exaggerated fluctuation in pupil diameter, sometimes called pupillary hippus.
• Difficulty with visual accommodation: Accommodation is the process through which the eye changes focus between near and distant objects. Patients may describe delayed focusing, eye strain, or intermittent blurring.
• Changes in ocular blood flow: Reduced blood flow to the retina or optic nerve can affect vision. Because true retinal ischemia is an emergency, vascular and ophthalmologic causes must be investigated before symptoms are attributed to the neck.
• Impaired venous drainage and pressure around the optic nerve: Restricted cerebral venous outflow could, in theory, contribute to pressure-related visual symptoms. This possibility must be differentiated from established causes of papilledema and intracranial hypertension.
• Disrupted coordination among the neck, vestibular system, and eyes: Altered cervical sensory input may interfere with gaze stability and contribute to dizziness, visual motion sensitivity, or difficulty focusing during head movement.

These pathways could produce different symptoms, including blurred vision, light sensitivity, difficulty focusing, visual motion sensitivity, spots, or visual dimming. They should not all be described as the same condition. In particular, temporary blindness in one eye is different from chronic blurring or photophobia and demands an urgent vascular and ophthalmologic evaluation.

The proposed vagus nerve and vasospasm mechanism

In the video, we propose that abnormal movement near C1-C2 could irritate or affect the vagus nerve and other autonomic structures, potentially contributing to abnormal vascular regulation or vasospasm. If blood flow through the ophthalmic circulation were reduced, a patient could experience dimming, grayness, blind spots, or loss of vision.

This remains a proposed mechanism. Direct clinical evidence has not established that C1-C2 instability causes ophthalmic artery vasospasm through vagus nerve irritation. The vagus nerve also does not act alone in ocular vascular regulation; sympathetic pathways, local vascular control, systemic blood pressure, and other neurologic mechanisms may be involved. We therefore do not diagnose a vagus-mediated visual disorder from symptoms or cervical imaging alone.

The video provides a useful explanation of the clinical hypothesis that guided some of our later research. It should be viewed together with the newer objective findings discussed below and with the important limitations of that research.

Newer Caring Medical research on chronic eye symptoms

In 2025, our research group published a retrospective cross-sectional study of patients seeking care at an outpatient neck center for chronic eye symptoms without a known cause. The study examined symptoms such as light sensitivity, blurry vision, eye pain or pressure, visual changes, flashes, and tearing, along with measures that included cervical structure, pupillary findings, intraocular pressure, optic nerve sheath diameter, vagus nerve size, and internal jugular vein measurements. (6)

The observed findings supported further study of possible relationships among cervical structure, autonomic function, jugular outflow, intracranial pressure indicators, and chronic eye symptoms. However, the study did not specifically prove a cause of transient monocular blindness. It was performed in a highly selected clinic population, had no healthy control group, and was cross-sectional, meaning measurements were collected at one point in time. It cannot establish cause and effect or prove that treating cervical instability will correct an eye disorder.

This research is best interpreted as hypothesis-generating. It supports asking better questions and designing controlled studies. It does not justify bypassing ophthalmology, neurology, stroke assessment, or established treatment.

Cervico-ocular reflexes and visual disturbance

Not all neck-related visual complaints involve retinal blood flow. The brain coordinates visual stability using information from the eyes, inner ears, and sensory receptors in the neck. The vestibulo-ocular reflex stabilizes gaze during head movement, while the cervico-ocular reflex uses neck sensory input to help coordinate eye movement.

When cervical proprioception—the nervous system’s awareness of neck position—is disturbed, some patients may experience visual motion sensitivity, difficulty focusing while moving, dizziness, imbalance, or oscillopsia, the sensation that the environment is bouncing or moving. These symptoms differ from ischemic blindness, although patients may use overlapping language such as “blurred vision” or “my vision goes out.” Our related article explains the connection between chronic neck pain and visual symptoms.

How we evaluate a possible cervical contribution

Our first question is not simply, “Is the neck unstable?” It is, “Has the visual symptom been appropriately evaluated, and do the history, examination, and objective findings form a coherent pattern?”

An assessment may review:

1. The visual episode: one eye or both, duration, positive visual effects, pain, triggers, and recovery.
2. Emergency and specialist findings: ophthalmology, neurology, vascular imaging, laboratory results, and relevant cardiac testing.
3. Neck history: trauma, pain, hypermobility, headaches, and positional symptom changes.
4. Neurologic and musculoskeletal examination: cranial nerves, balance, coordination, cervical motion, and ligament-related findings.
5. Selected objective testing: only when clinically justified and interpreted in the context of the complete workup.

We do not regard an isolated loss of cervical lordosis, jugular narrowing on one image, or an enlarged optic nerve sheath measurement as a stand-alone diagnosis. Each finding has alternative explanations and must be correlated with the patient’s symptoms and specialist evaluation.

Prolotherapy?

Prolotherapy is an injection treatment commonly using dextrose solution at painful or injured ligament and tendon attachments. Our 2014 review proposed that capsular ligament laxity can contribute to chronic neck pain and cervical instability. (7)

For a carefully selected patient with documented ligament-related cervical instability, we may discuss Prolotherapy as one component of a broader stabilization and rehabilitation plan. The intended target is the painful or unstable musculoskeletal structure—not the eye, optic nerve, or jugular vein. Published Prolotherapy research across musculoskeletal conditions cannot be generalized automatically to temporary blindness. There are no high-quality controlled trials demonstrating that cervical Prolotherapy treats transient monocular vision loss, relieves papilledema, reverses jugular compression, or prevents stroke. Improvement reported by individual patients or in clinic-based observational work should be viewed as clinical experience, not proof of effectiveness for a visual disorder.

Any treatment plan should be individualized and may include conventional medical care, physical rehabilitation, postural and ergonomic changes, management of migraine or intracranial hypertension, and treatment of an identified vascular or ophthalmologic condition. Cervical injections are not appropriate for every patient and carry procedural risks that must be discussed during informed consent.

Summary

Temporary loss of vision in one eye is a symptom, not a diagnosis. The first priority is prompt evaluation for retinal ischemia, carotid disease, stroke, arterial dissection, giant cell arteritis, and urgent eye disorders.

In patients whose standard evaluation does not reveal a cause—and particularly when episodes occur with neck pain, trauma history, head-position sensitivity, pulsatile tinnitus, dizziness, or pressure symptoms—cervical structure and cerebral venous outflow may warrant consideration as part of a broader investigation. Small observational studies have associated jugular venous abnormalities with transient monocular blindness, and our 2025 clinic cohort identified associations among chronic eye symptoms and several cervical, autonomic, and pressure-related measurements. These findings remain preliminary and do not establish causation.

At Caring Medical, our goal is to identify the most plausible contributors without overlooking more common or dangerous diagnoses. When cervical instability is objectively supported, treatment is directed at the musculoskeletal instability. Patients should understand that using Prolotherapy specifically to treat temporary vision loss remains unproven.

Medical disclaimer

This article is for educational purposes and is not a substitute for diagnosis or treatment by a qualified clinician. Sudden or recurrent vision loss requires prompt medical evaluation. Call emergency services for active vision loss or associated stroke-like symptoms.

Published research

References

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