Eye Problems After a Head Injury from an Accident or Fall: Why the MRI Can Be Normal

After hitting your head in a car accident or while playing sports, you may continue to have unexplained eye problems even though your MRI was read as “normal.” This can be very distressing.

For example, symptoms like these:

• Losing your place while reading a book
• Text looks double or seems to move
• It takes a while to focus on things up close
• Your eyes tire quickly when you look at a smartphone or computer
• You have become more sensitive to glare than before

These are not “just in your head” or simple temporary fatigue.
The impact to the head may have caused real damage to the function of the eyes.
And in some cases, that damage can be confirmed objectively with certain tests.

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Why does it hurt so much when I was told “nothing is wrong”?

When patients with visual complaints after a head injury have conventional imaging (CT or MRI), they are often told that there are “no particular abnormal findings.”

Many people find this worrying. But there is a clear reason.

Reason 1: What a conventional MRI looks at

Ordinary CT and MRI scans are tests to find urgent, life-threatening large abnormalities, such as bleeding in the brain or a fractured bone¹.

With mild traumatic brain injury (mTBI) or concussion, however, the abnormalities often occur at a much finer level.

This is called diffuse axonal injury (DAI)².
Put simply, it is a state in which the nerve fibers of the brain, its “wiring,” are stretched or damaged over a wide area.

This “wiring damage” from DAI is extremely difficult to detect at the resolution of a standard MRI³.

In other words, even if you are told “the MRI is normal,” that does not mean there is no damage at all.
Rather, in mild head injury, it only shows that “there is no major bleeding or fracture, which is reassuring,” and fine “wiring” damage is normally not detected⁴.

Reason 2: Disruption of the autonomic nervous system’s “control system”

An impact to the head can also disturb the autonomic nervous system (ANS), which automatically adjusts the balance of the whole body⁵.

The autonomic nervous system controls, without our conscious effort, the ciliary muscle that focuses the eye, the pupil that adjusts the amount of light, and tear secretion.
When this “central control system” becomes oversensitive or loses its balance because of the injury, various visual symptoms can appear.

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Main eye symptoms commonly seen after a head injury

So what symptoms actually appear when there is “wiring trouble” (DAI) or autonomic dysfunction?

1. Reduced ability to “bring the eyes together” (convergence insufficiency, CI)

This is one of the most common functional problems after mild head injury⁶.
Convergence is the movement of turning both lines of sight inward when looking at something close, such as when reading.

When this control fails, the eyes tend to drift out of alignment.

Common complaints:

• “When I read a book, I lose track of where I am.”
• “Text looks double or seems to move.”
• “My eyes tire quickly when I look at a smartphone or computer.”

Convergence is not just a matter of eye muscles. It is controlled by wide areas of the brain working together.
Convergence insufficiency is thought to arise when DAI disrupts this coordination⁶.

2. Trouble with “focusing” (accommodative dysfunction, AD)

Accommodation is the function of focusing by changing the thickness of the lens, like the lens of a camera.

• Accommodative insufficiency (AI): the most common form, in which the ability to focus is reduced⁷.
• Accommodative spasm (pseudomyopia): the eye stays overly focused, and distance vision may become blurred⁸.

Common complaints:

• “Nearby text is blurry.”
• “It takes time to focus when I shift my gaze from far to near (or the reverse).”
• “I get headaches during computer work.”

Accommodative disorders and convergence insufficiency often do not occur separately; more often the whole “set of reflexes for near vision” becomes unstable⁷.

3. “Dry eye that is not dry eye” and glare

These are characteristic symptoms in which autonomic dysregulation is involved.

• Neuropathic dry eye:
  Even when tests show no abnormality in tear volume or the corneal surface, you may feel strong dryness or stinging⁹.
  Paradoxically, the irritation may also cause reflex tearing that does not stop.
  This may occur because the injury has made the sensory nerves of the cornea hypersensitive, so that they keep sending a “false signal” of dryness to the brain⁹.
• Photophobia (light sensitivity):
  This is a symptom of feeling more glare than usual. It may be partly because the “gate” (threshold) of sensory processing in the brain is broken and the senses are overloaded (the nerves are overexcited)⁵.

4. Hidden optic nerve damage (traumatic optic neuropathy, TON)

Although not frequent, damage to the optic nerve must not be missed.
In particular, indirect optic nerve injury occurring deep behind the eye may be read as “normal” on a fundus examination or MRI right after the injury¹⁰.

Even when the “wiring” of the optic nerve is damaged, it takes weeks to months before the optic disc turns pale (atrophy)¹⁰.

Common complaints:

• “Vision in just one eye seems somehow off.”
• “Colors seem faded.”
• “Part of my vision looks dark.”

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Why standard eye tests can miss it

Even with symptoms, health checkups and ordinary eye examinations tend to say “no abnormality” because conventional tests have different purposes.

• MRI/CT:
  As noted above, these are tests to look for urgent abnormalities. It is difficult for them to find fine “wiring” damage (DAI)³.
• Standard automated perimetry (SAP, Humphrey® visual field):
  This test, used for example to diagnose glaucoma, depends heavily on the patient’s attention and concentration¹¹. After a concussion, patients may have reduced concentration and unstable fixation, the ability to hold the gaze on a single point.
  As a result, “poor reliability” results are likely.
  This may not reflect lack of effort by the patient; it may be an “objective manifestation” that the injury itself makes the test difficult to perform.
• OCT (optical coherence tomography):
  This measures the “thickness” of the retina. Even when the optic nerve has been injured (TON), in the acute phase function may be lost while retinal thickness still shows no change. Thickness changes can be confirmed only in the chronic phase (several months later or beyond)¹².

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Outlook and what can be done

A finding of “no abnormality on MRI”never means “nothing can be done.”
In fact, there is a lot that can be done.

1. Objectively assess “function”

What matters is to check whether the symptoms you feel are related to a “reduction in eye function.”
Accommodative and convergence insufficiency can be quantified objectively with clinical tests such as the following.

• Amplitude of accommodation test (push-up test):
  This measures how close you can keep focusing⁷. Comparing it with the average for your age shows whether function is reduced.
• Near point of convergence (NPC) test:
  This measures the limit to which both eyes can be brought together (the point at which things start to look double).
• VOMS (Vestibular/Ocular Motor Screening):
  This evaluates the coordination between eye movements and the sense of balance and checks whether particular movements provoke symptoms.

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If these functional tests show abnormal values, it confirms that the symptoms are not a “subjective feeling” but an “objective functional deficit.”

2. “Vision therapy” as neurorehabilitation

If convergence insufficiency (CI) or accommodative insufficiency (AI) is diagnosed, vision therapy (orthoptic training), a specialized form of rehabilitation, may be considered. However, evidence of its effectiveness after head injury (mTBI) is currently limited, and, as described below, careful evaluation is needed.¹³。

This is not merely “exercise for the eye muscles.”

For example, it involves repeating convergence and accommodation tasks, such as following a pen tip with the eyes as it is brought closer (convergence), or using special lenses (flippers) to deliberately refocus between far and near.

By repeating convergence and accommodation tasks, it encourages the brain’s neuroplasticity (the ability to rebuild its wiring) and is a “neurorehabilitation” that changes brain function itself.
In fact, studies using fMRI (functional MRI) have shown that this training changes activity in the brain regions that control eye movements¹⁴.

Visual problems after a head injury greatly reduce quality of life (QOL).
If you continue to have symptoms such as difficulty reading, easily tired eyes, double vision, or strong glare even though you were told “the tests are normal,” objective visual function impairment due to DAI or autonomic dysfunction may be hidden behind them.

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A careful view of the evidence for treatment

Here we explain, from a cautious standpoint, the scientific evidence currently available on visual rehabilitation after mTBI¹³.

Many symptoms tend to improve naturally over time, so in studies without a group that received no treatment (a control group), it is difficult to evaluate the effect of rehabilitation itself.

In fact, some experts take the view that most visual rehabilitation after mTBI is currently “not proven effective.”

Evidence on diagnostic labels

Diagnostic names such as “post-trauma vision syndrome,” “visual midline shift syndrome,” and “vertical heterophoria syndrome (VHS)” are sometimes used, but the scientific evidence supporting these conditions medically is not sufficient.

Reasons given for the insufficient evidence include that the diagnosis sometimes relies only on the patient’s subjective symptoms, and that studies have reported no difference in the incidence of objective eye misalignment between healthy people and mTBI patients.

Evidence on treatments

For treatments as well, it has been pointed out that firm evidence proving their effectiveness is lacking.

• Training for convergence insufficiency (CI) and accommodation:
  Effectiveness in mTBI patients has not been sufficiently proven. One small study was judged by a Cochrane review (an international research evaluation body) to be “very low-certainty evidence.”
• Saccade (jumping eye movement) and pursuit (following eye movement) training: The evidence on these eye movement trainings has been concluded to be “lacking/poor.”
• Prism glasses (yoked prisms, monocular vertical prisms):
  No scientific evidence supporting their effect has been confirmed so far. Problems have also been pointed out in study methods, such as circular reasoning (the diagnosis rests on subjective improvement with prisms) and the lack of control groups.
• Tinted lenses (light filters):
  While they may be expected to ease light-sensitive symptoms, more scientific evidence is needed. Some also point out that using the lenses may impede long-term light adaptation.

As described, many points remain scientifically unresolved in the diagnosis and treatment of visual disorders after mTBI.

Going forward, more rigorous scientific studies that minimize bias as far as possible and set up appropriate control groups are needed.

References

1. National Library of Medicine (NIH). (2018). Advanced Neuroimaging of Mild Traumatic Brain Injury. https://www.ncbi.nlm.nih.gov/books/NBK326714/
2. D’souza MM, Trivedi R, Singh K, et al. Traumatic brain injury and the post-concussion syndrome: A diffusion tensor tractography study. Indian J Radiol Imaging. 2015;25(4):404-414. https://pubmed.ncbi.nlm.nih.gov/26751097/
3. Shenton ME, Hamoda HM, Schneiderman JS, et al. A review of magnetic resonance imaging and diffusion tensor imaging findings in mild traumatic brain injury. Brain Imaging Behav. 2012;6(2):137-192. https://pubmed.ncbi.nlm.nih.gov/22438191/
4. Wilde EA, McCauley SR, Hunter JV, et al. Diffusion tensor imaging of acute mild traumatic brain injury in adolescents. Neurology. 2008;70(12):948-955. https://pubmed.ncbi.nlm.nih.gov/18347317/
5. Mitschang D, Sydorenko V, Kühlwein D, et al. Quantitative pupillometry as a sensitive biomarker for detecting subtle neurological impairment in mild traumatic brain injury – a pilot study. Neurol Sci. 2025;46(10):5243-5251. https://pubmed.ncbi.nlm.nih.gov/40797039/
6. Rockswold SB, Burton PC, Chang A, et al. Functional Magnetic Resonance Imaging and Oculomotor Dysfunction in Mild Traumatic Brain Injury. J Neurotrauma. 2019;36(7):1099-1105.
   https://pubmed.ncbi.nlm.nih.gov/30014758/
7. Almutairi NM. Visual Dysfunctions in Mild Traumatic Brain Injury: A Focus on Accommodative System Impairments. Life (Basel). 2025;15(5):744. https://pmc.ncbi.nlm.nih.gov/articles/PMC12113616/
8. Chan RV, Trobe JD. Spasm of accommodation associated with closed head trauma. J Neuroophthalmol. 2002;22(1):15-17. https://pubmed.ncbi.nlm.nih.gov/11937900/
9. Rosenthal P, Borsook D. The corneal pain system. Part I: the missing piece of the dry eye puzzle. Ocul Surf. 2012;10(1):2-14. https://pubmed.ncbi.nlm.nih.gov/22330055/
10. Ellis MJ, Ritchie L, Cordingley D, Essig M, Mansouri B. Traumatic Optic Neuropathy: A Potentially Unrecognized Diagnosis after Sports-Related Concussion. Curr Sports Med Rep. 2016;15(1):27-32. https://pubmed.ncbi.nlm.nih.gov/26745167/
11. Sharma P, Sample PA, Zangwill LM, Schuman JS. Diagnostic tools for glaucoma detection and management. Surv Ophthalmol. 2008;53 Suppl1(SUPPL1):S17-S32. https://pmc.ncbi.nlm.nih.gov/articles/PMC2643302/
12. Chan JW, Hills NK, Bakall B, Fernandez B. Indirect Traumatic Optic Neuropathy in Mild Chronic Traumatic Brain Injury. Invest Ophthalmol Vis Sci. 2019;60(6):2005-2011. https://pubmed.ncbi.nlm.nih.gov/31067321/
13. Subramanian PS, Barton JJS, Ranalli P, Smith C, Francis CE, Frishberg B. Consensus Statement on Visual Rehabilitation in Mild Traumatic Brain Injury. Neurol Clin Pract. 2022;12(6):422-428. https://pubmed.ncbi.nlm.nih.gov/36540149/
14. Sangoi A, Hajebrahimi F, Gohel S, et al. Functional activity changes after vergence and accommodative rehabilitation of concussion-related convergence insufficiency: CONCUSS clinical trial fMRI results. Front Neurosci. 2025;19:1703781. https://pubmed.ncbi.nlm.nih.gov/41195283/