Lyme disease — caused by the Borrelia group of spirochete bacteria, most often Borrelia burgdorferi in North America, transmitted by infected Ixodes ticks — has a settled clinical core and a contested margin. The settled core: an early infection that, recognised promptly, responds to antibiotics, with a recognised list of acute and later manifestations including ophthalmologic findings. The contested margin: a population of patients who report ongoing symptoms after standard treatment, sometimes including visual complaints, where the mechanism, the right name, and the right next step are matters of active disagreement between mainstream medical bodies and patient-advocacy clinical networks.
We will not adjudicate that disagreement here. Two well-organised camps read overlapping evidence and reach different conclusions, and a person on either side deserves a description of what is documented in the peer-reviewed literature about vision and Lyme — separate from which side is right about the larger questions.
This post covers the established ocular findings in acute and later Lyme; the contested landscape around post-treatment Lyme disease syndrome (PTLDS) and chronic Lyme disease; the small amount of direct contrast-sensitivity literature in Lyme populations; and what an at-home contrast sensitivity test can and cannot do for someone with Lyme symptoms or a diagnosis.
Acute and later Lyme: the documented ocular findings
The peer-reviewed ophthalmology literature on Lyme is small relative to better-studied infections, but consistent enough that the main findings are settled. The most-cited anchor reviews come from the Helsinki group: Karma et al., 1995, American Journal of Ophthalmology reported on a 2-year diagnostic series of 236 patients screened for ocular Lyme borreliosis (Karma et al., 1995). A follow-up paper, Mikkilä et al., 2000, Ophthalmology, summarised the "expanding clinical spectrum" of ocular Lyme borreliosis across 20 patients. Both are European cohorts — the Borrelia species mix in Europe differs from the North American mix, so disease patterns are not perfectly interchangeable — but the broad categories of ophthalmologic involvement are recognised on both continents.
What those reviews and the broader literature describe:
Conjunctivitis is the most common early eye finding. It is mild, self-resolving with treatment of the underlying infection, and not specific — many viral infections look the same.
Later-stage involvement is more varied and clinically meaningful. Reported manifestations include uveitis (inflammation of the middle eye, often the most clinically significant ocular Lyme finding), keratitis, episcleritis, optic neuritis, retinal vasculitis, and rarely branch retinal vein occlusion. The Mikkilä cohort found that, of the 20 cases described, 10 had uveitis and 4 had neuro-ophthalmologic disorders — though that distribution comes from a referral population at a specialised eye clinic and is not a population prevalence.
Neuro-borreliosis — central nervous system involvement — can produce cranial nerve palsies. The most-recognised is facial nerve (cranial VII) palsy, sometimes bilateral, which can affect eyelid closure (and indirectly the cornea) but is not strictly a "vision" finding. Less commonly, abducens (cranial VI) palsy can produce horizontal double vision. Optic neuritis with visual-pathway involvement is documented in case reports but uncommon.
All of these ocular findings are rare relative to the underlying condition: most patients with Lyme do not have eye involvement, and most patients with these eye findings do not have Lyme. The differential for uveitis or optic neuritis is long, and Lyme is one entry on it. Ophthalmologists test serology for Borrelia in patients with otherwise-unexplained uveitis or retinal vasculitis in endemic regions; it is not part of a routine eye exam. Treatment follows the antibiotic protocols for the underlying disease stage.
The take-away from this section is narrow: acute Lyme has documented ocular findings, well-described, treated by treating the underlying infection. None are diagnosed by a contrast sensitivity test.
Post-treatment Lyme disease: the contested landscape
The contested part of the conversation is what happens after acute treatment. A subset of patients who had documented acute Lyme — including those treated with the IDSA-recommended antibiotic regimens — report persistent symptoms over months or years afterward: fatigue, musculoskeletal pain, cognitive complaints (often described as "brain fog"), sleep changes, mood changes, autonomic symptoms, and, in some, visual complaints. The disagreement is over what to call this, what causes it, and what to do about it.
The mainstream position — articulated most clearly in the Infectious Diseases Society of America (IDSA), American Academy of Neurology (AAN), and American College of Rheumatology (ACR) joint 2020 guidelines (Lantos et al., 2020) — recognises post-treatment Lyme disease syndrome (PTLDS) as a real entity affecting a small subset of patients treated for documented Lyme. The guidelines, building on earlier reviews (e.g., Marques, 2008), hold that the mechanism is not active ongoing infection but likely some combination of post-infectious immune and neurological sequelae, and that extended or repeat courses of antibiotics have not been shown to improve outcomes in randomised trials. The most-cited evidence is Klempner and colleagues, 2001, New England Journal of Medicine, two parallel randomised placebo-controlled trials of 90 days of antibiotics in patients with persistent symptoms after Lyme; the trials found no benefit over placebo (Klempner et al., 2001). Two later NIH-funded trials reached compatible conclusions. The IDSA position is that PTLDS exists, is real, deserves clinical attention focused on symptom management and rehabilitation, but is not a sign that the original infection persists.
The patient-advocacy position — articulated through the International Lyme and Associated Diseases Society (ILADS) and a clinical network often described in patient communities as "Lyme-literate" clinicians (sometimes abbreviated LLMD for Lyme-literate medical doctor) — uses the term chronic Lyme disease to describe a broader clinical syndrome that, in this framework, includes some patients without a clear-cut history of acute Lyme. Proponents hold that the syndrome is associated with measurable physiological abnormalities, that standard serology misses a subset of infected patients, and that some patients respond to extended antibiotic regimens the IDSA guidelines do not recommend. ILADS publishes its own clinical guidelines and references its own cohort data. The IDSA and the ILADS positions are not the same; both are advocated by physicians; the disagreement is well-documented and has been litigated repeatedly in the medical and policy press.
Where the disagreement actually lives is over (a) whether persistent symptoms reflect active ongoing infection that standard testing fails to detect, (b) whether extended antibiotic therapy is the right treatment for that subset, and (c) what other entities (co-infections, post-infectious immune dysregulation, separately-acquired chronic illness) might explain the same symptom picture. Both camps have published; the published evidence does not, at the time of this post, resolve to a single answer that both camps accept. The IDSA/AAN/ACR guideline and the ILADS clinical guideline are both worth reading directly if they bear on your decisions.
A parallel contested landscape — the Shoemaker / CIRS framework, which names Lyme alongside mold as a biotoxin source — is covered in a separate post on mold, CIRS, and contrast sensitivity. The contested-science notes here apply to Lyme specifically; we do not conflate the two debates.
What's measured about contrast sensitivity in Lyme populations
The peer-reviewed literature on contrast sensitivity specifically in Lyme or post-Lyme cohorts is sparse compared to better-studied conditions like multiple sclerosis, glaucoma, or post-concussion vision changes. There are case reports describing reduced contrast sensitivity in patients with documented neuro-borreliosis where there is optic nerve involvement, and PTLDS cohort symptom inventories that include "blurred vision" or "visual disturbance" — Aucott and colleagues' work on the Johns Hopkins SLICE cohort is one anchor (Aucott, Crowder & Kortte, 2013). But specific contrast-sensitivity-function (CSF) measurements in well-defined post-Lyme cohorts, against age-matched controls, with the sample size to support population-level claims, are not a substantial published body of work as of this post's date.
Why contrast sensitivity might plausibly be relevant — at the mechanism level — is that several neuroinflammatory conditions with documented CNS involvement do affect mid-frequency contrast sensitivity. Multiple sclerosis is the cleanest example (see our contrast sensitivity in MS post); post-concussion vision changes are another (see the post-concussion post). Neuro-borreliosis, where it involves CNS structures relevant to vision, could plausibly produce a similar pattern; PTLDS, if the symptoms reflect a post-infectious neuroinflammatory process — one of the hypothesised mechanisms within the mainstream framework — could also plausibly produce a CSF signature.
Plausible is not established. The mechanism would not be a surprise if it turned up, but the studies that would establish it are not where the published literature is dense. A careful clinician would say "a reduced CSF result in a patient with Lyme history is consistent with, but not specific to, that history." Neither side would say "the test diagnoses anything specifically."
The Pelli-Robson chart (Pelli, Robson & Wilkins, 1988) is the most-cited clinical instrument; the Functional Acuity Contrast Test (FACT) is the one most commonly cited in patient-advocacy-protocol literature, with known methodology concerns we have written about elsewhere (see Pelli-Robson vs FACT vs qCSF).
What an online contrast sensitivity test can do
If you have a Lyme diagnosis or persistent symptoms after a tick bite, an at-home CSF test can do a few specific things:
Provide a baseline. A well-calibrated CSF curve on your own device, taken once, gives you a fixed reference point in a way that nothing else cheap and at-home does. If symptoms change over weeks or months, you have something to compare against.
Track change over time on the same setup. Re-taking on the same device, in similar lighting, at similar times of day, gives you a sequence. The trend is far more informative than any single absolute number.
Provide one piece of data to bring to your physician — whether that physician is an infectious-disease specialist working from the IDSA framework, an LLMD working from the ILADS framework, a neurologist looking at post-infectious sequelae, or your primary care doctor coordinating. We are not telling you which framework to choose; we are saying that if you bring data, it is more useful as a trend than as a snapshot.
Track alongside a symptom inventory. A few lines per session — date, fatigue, cognitive load, pain level, sleep quality, screen-time hours, the CSF result — turns the curve into something interpretable.
What an online CSF test does not do is the diagnostic work. It does not say "you have Lyme" or "you do not have Lyme." It does not distinguish between acute and post-treatment stages, between IDSA-framework PTLDS and ILADS-framework chronic Lyme, or between Lyme-associated vision changes and any of the other causes of reduced contrast sensitivity.
What it cannot tell you
Note. A contrast sensitivity test is a screening and tracking measurement, not a diagnosis.
A CSF test does not diagnose Lyme disease — the diagnosis of Lyme is a clinical determination based on history, exposure, characteristic findings (erythema migrans rash, neurologic or cardiac or arthritic manifestations), and supportive serology, made by a clinician.
A CSF test does not distinguish between active acute Lyme, treated Lyme, post-treatment Lyme disease syndrome (PTLDS) as the IDSA framework defines it, chronic Lyme disease as the ILADS framework defines it, or any of the conditions in their respective differentials.
A reduced CSF result is consistent with many things. Cataract, glaucoma (early), multiple sclerosis, optic neuritis, diabetic retinopathy, post-concussion vision changes, uncorrected refractive error, dry eye, fatigue, certain medications, and normal aging can all reduce contrast sensitivity, including in the mid-frequency band sometimes singled out in patient-advocacy literature on biotoxin-related illness. A reduction is consistent with a Lyme-related visual pattern; it is not specific to it.
A single reading is a snapshot. Test-retest variation is real even with clinical-grade instruments — the Pelli-Robson chart has a test-retest repeatability of about ±0.15 log units, and the smallest clinically meaningful change is generally taken to be about ±0.30 log units (Pelli, Robson & Wilkins, 1988). A consumer-screen test, however carefully calibrated, is noisier than that.
A normal result does not rule out Lyme, PTLDS, or chronic Lyme. Many of the symptoms that patients in either framework describe (fatigue, cognitive complaints, joint pain, autonomic symptoms) are not what a contrast sensitivity test measures.
The framing we would ask you to hold: this is one piece of objective data you can collect at home, repeat at intervals, and bring to the people who can actually examine you. It is not a substitute for that examination; it is one input that the examination otherwise would not have access to.
Practical next steps
The practical part depends on where you are in the timeline.
If you have a known tick bite and current symptoms (rash, fever, joint pain, fatigue, facial droop, double vision): see a clinician promptly. Acute Lyme is well-treated with the standard antibiotic regimens recognised in the IDSA/AAN/ACR guidelines, and earlier treatment correlates with better outcomes. A CSF test is not the right tool for an acute infectious presentation.
If you have a Lyme diagnosis and are in or recently finished treatment: standard-of-care follow-up with the prescribing clinician comes first. A baseline CSF reading taken when symptoms have stabilised can serve as a reference point for later comparison; it is not a treatment monitoring tool.
If you have persistent symptoms after treatment — fatigue, cognitive complaints, joint pain, sometimes visual complaints — you are in the contested territory. Both an evidence-based infectious-disease specialist working from the IDSA framework and an LLMD working from the ILADS framework will see patients in your situation. We make no clinical recommendation about which to consult; that is your decision, made with the information you trust. A longitudinal CSF record is evidence either kind of clinician can read. Bring the curve, not just a single number; bring the symptom journal alongside it.
If you do not have a Lyme diagnosis but are wondering — because of a known exposure, a symptom constellation, or a community discussion — a CSF test cannot answer that question. Diagnosis goes through history, exposure, clinical findings, and serology. Talk to your clinician about whether serology is appropriate for your situation.
In all cases, an eye exam is worth keeping in the picture independently. Many of the things on the CSF-affecting-causes list (refractive error, dry eye, early cataract) are routine ophthalmologic findings worth ruling out before any vision change is attributed to a less-common cause.
Take the test
Take the test now. Three minutes for the quick mode, around seven for the full curve. Calibration happens at the start so the numbers are comparable across sessions on the same device.
Save the result. Re-take if symptoms persist, and bring the trend to whichever clinician you work with. The curve is one piece of data that joins the rest of the picture rather than replacing any of it.
References
- Karma, A., Seppälä, I., Mikkilä, H., Kaakkola, S., Viljanen, M., & Tarkkanen, A. (1995). Diagnosis and clinical characteristics of ocular Lyme borreliosis. American Journal of Ophthalmology, 119(2), 127–135. Two-year diagnostic series at Helsinki University Central Hospital, screening 236 patients with prolonged external ocular inflammation, uveitis, retinitis, optic neuritis, or unexplained neuro-ophthalmic symptoms for Borrelia serology. Anchor reference for the documented ocular Lyme findings described above.
- Mikkilä, H. O., Seppälä, I. J. T., Viljanen, M. K., Peltomaa, M. P., & Karma, A. (2000). The expanding clinical spectrum of ocular Lyme borreliosis. Ophthalmology, 107(3), 581–587. Follow-up to Karma et al. (1995) summarising the broader clinical spectrum of ocular Lyme across 20 patients, including uveitis, neuro-ophthalmologic disorders, external inflammation, and rarer findings.
- Lantos, P. M., Rumbaugh, J., Bockenstedt, L. K., Falck-Ytter, Y. T., Aguero-Rosenfeld, M. E., Auwaerter, P. G., et al. (2020). Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA), American Academy of Neurology (AAN), and American College of Rheumatology (ACR): 2020 Guidelines for the Prevention, Diagnosis and Treatment of Lyme Disease. Clinical Infectious Diseases, 72(1), e1–e48. The current mainstream consensus document; the most-cited primary source for the IDSA/AAN/ACR framing of acute Lyme, neuro-borreliosis, and PTLDS. A primary source worth reading directly rather than filtered through a blog post.
- Klempner, M. S., Hu, L. T., Evans, J., Schmid, C. H., Johnson, G. M., Trevino, R. P., et al. (2001). Two controlled trials of antibiotic treatment in patients with persistent symptoms and a history of Lyme disease. New England Journal of Medicine, 345(2), 85–92. The landmark randomised, placebo-controlled re-treatment trials of 90 days of antibiotics in patients with persistent symptoms after Lyme; the most-cited evidence in the mainstream position that extended antibiotic regimens do not improve outcomes in PTLDS. Cited here to document the evidence base of the IDSA framework — not as an endorsement of either side of the larger disagreement.
- Marques, A. (2008). Chronic Lyme disease: a review. Infectious Disease Clinics of North America, 22(2), 341–360. NIH-authored review of the chronic-Lyme-versus-PTLDS terminology and evidence, summarising the mainstream position on persistent post-treatment symptoms and the case for symptom management rather than continued antibiotics. Useful as a single-document overview of the mainstream position with the references that support it.
- Aucott, J. N., Crowder, L. A., & Kortte, K. B. (2013). Development of a foundation for a case definition of post-treatment Lyme disease syndrome. International Journal of Infectious Diseases, 17(6), e443–e449. Operationalised PTLDS case definition applied to the Johns Hopkins SLICE cohort (74 patients with confirmed erythema migrans plus 14 controls), tracking patient-reported symptoms and SF-36 functional impact at 6 months post-treatment. Useful as an entry point to the prospective-cohort PTLDS symptom-inventory literature.
- Pelli, D. G., Robson, J. G., & Wilkins, A. J. (1988). The design of a new letter chart for measuring contrast sensitivity. Clinical Vision Sciences, 2, 187–199. The Pelli-Robson chart paper. Source for the ±0.15 log test-retest repeatability and ±0.30 log clinically-meaningful-change figures cited in the disclaimer.
A note on what we did not cite
The ILADS clinical guideline document, and the patient-advocacy clinical literature on chronic Lyme disease more broadly, sits outside the references above. That is not because the literature does not exist — it does — but because selectively quoting from it without the methodological framing that a fair evaluation would require risks misrepresenting either side. The ILADS guidelines are publicly available through the ILADS organisation directly, and we recommend reading them as primary source if the framework bears on your decisions. Where this post can be improved with additional verified references from either camp's primary literature, it will be.