Lyme Disease and the eyes

Topics with information and discussion about published studies related to Lyme disease and other tick-borne diseases.
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Re: Lyme Disease and the eyes

Post by RitaA » Sat 21 Jul 2012 21:04
J Clin Neurophysiol. 2012 Apr;29(2):174-80.

Pattern and motion-related visual-evoked potentials in neuroborreliosis: follow-up study.

Szanyi J, Kubová Z, Kremláček J, Langrová J, Vít F, Kuba M, Szanyi J, Plíšek S.
Department of Pathophysiology, Faculty of Medicine in Hradec Králové, Charles University, Czech Republic.

Visual-evoked potentials (VEPs) were used for objective testing of visual functions during treatment courses of Lyme neuroborreliosis (LNB) in adult patients in the Czech Republic. In 30 LNB patients with originally delayed VEP latencies, pattern-reversal (R-VEP) and motion onset (M-VEP) VEPs were repeatedly examined within 1 to 8 years. Six patients had Lyme optic neuritis (ON), five of them displayed prolonged latencies in both R-VEPs and M-VEPs, and one had only abnormal R-VEPs. The VEP recovery to normal latency values was in three of them. In the group of 24 LNB patients without ON, 14 patients displayed prolonged latencies only to motion stimuli, and 10 patients had abnormal latencies in both R-VEPs and M-VEPs. During the follow-up period, 7 patients displayed shortening to normal latencies. In 5 patients, VEPs latencies improved only partially, and in the remaining 12 patients, VEPs did not improve at all. This study provides objective evidence that in LNB, most of the patients without clinically manifesting ON display optic pathway involvement-predominantly magnocellular system/dorsal stream function changes. In patients with ON, however, mainly the parvocellular system is affected. About half of the patients without ON improved with a relatively long-time course of latency shortening.

[PubMed - in process]

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Re: Lyme Disease and the eyes

Post by RitaA » Sat 21 Jul 2012 21:44
Int Ophthalmol. 2011 Dec;31(6):493-5. Epub 2011 Dec 20.

Isolated trochlear palsy secondary to Lyme neuroborreliosis.

Bababeygy SR, Quiros PA.
Doheny Eye Institute, Department of Ophthalmology, Keck School of Medicine, University of Southern California, 1450 San Pablo Street, DVRC 311, Los Angeles, CA 90033, USA.

The objective of the study is to report the first case of isolated trochlear palsy secondary to Lyme neuroborreliosis in an adult. A 22-year-old male presented with history of flu-like illness and headache, accompanied by vertical binocular diplopia, worse on downgaze and better in upgaze and right head tilt. Physical examination revealed trochlear palsy on the left side with a compensatory head tilt to the opposite side. A subsequent workup for trochlear palsy was conducted, including hematological and cerebral spinal fluid serum studies, and magnetic resonance imaging of the brain. Immunoglobulin (Ig)M and IgG antibodies against Borrelia burgdorferi were positive in serum and cerebral spinal fluid (CSF). Symptoms of double vision completely resolved after 3 weeks of antibiotic treatment with intravenous ceftriaxone. CSF studies, in addition to clinical symptoms of vertical double vision and a positive Parks 3-step test, are a good diagnostic tool for B. burgdorferi. Resolution of symptoms was noted after a complete course of intravenous ceftriaxone.


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Re: Lyme Disease and the eyes

Post by RitaA » Fri 10 Aug 2012 9:55

Backtracking a bit to 2005 since I don't see the first two links posted on this thread (or elswhere on LNE):
J Neuroophthalmol. 2005 Jun;25(2):71-82.

Reactive Lyme serology in optic neuritis.

Sibony P, Halperin J, Coyle PK, Patel K.
Department of Ophthalmology and Neurology, State University of New York at Stony Brook, Stony Brook, NY 11794, USA.

Establishing a causal relationship between optic neuritis and Lyme disease (LD) has been hampered by technical limitations in serologic diagnosis of LD. Even so, there is a general impression that optic neuritis is a common manifestation of LD.

Retrospective case analysis of Lyme serology in 440 patients with optic neuritis examined between 1993 and 2003 in a single neuro-ophthalmic practice at Stony Brook University Medical Center, Suffolk County, New York, a region hyper-endemic for LD.

Lyme enzyme-linked immunosorbent assay (ELISA) was positive in 28 (6.4%) patients with optic neuritis, three of whom had syphilis with cross-reactive antibodies. Among the remaining 25 ELISA-positive patients, optic neuritis could be confidently attributed to LD in only one case, a patient with papillitis. The other 24 cases had reactive Lyme serologies related to a history of LD years earlier, asymptomatic exposure, false-positive results, or non-specific humoral expansion. The ELISA in these 24 cases were weakly positive and the Western blots were negative by Centers for Disease Control criteria. There were no significant clinical differences between the 25 seropositive optic neuritis cases and 50 seronegative optic neuritis cases.

Based on these cases and a review of the literature, there is insufficient evidence for a causal link between LD and retrobulbar optic neuritis or neuroretinitis. There is sufficient evidence to establish a causal link between LD and papillitis and posterior uveitis.

Comment in

Defining the spectrum of Lyme disease: a difficult proposition. [J Neuroophthalmol. 2005] Defining the spectrum of Lyme disease: a difficult proposition.Pachner AR. J Neuroophthalmol. 2005 Jun; 25(2):67-8.

[PubMed - indexed for MEDLINE] ... ult.1.aspx
Journal of Neuro-Ophthalmology:
June 2005 - Volume 25 - Issue 2 - pp 67-68

Defining the Spectrum of Lyme Disease: A Difficult Proposition

Pachner, Andrew R MD

Department of Neurology and Neurosciences, UMDNJ-New Jersey Medical School, Newark, NJ.

Address correspondence to Andrew R. Pachner, MD, Department of Neurology and Neurosciences, UMDNJ-New Jersey Medical School, 185 S. Orange Ave, Newark, NJ 07103

Chronic infections are notoriously difficult challenges for the clinician. With respect to determining their clinical spectra, diagnosing them, treating them, or studying their epidemiology, they are daunting. HIV, tuberculosis, syphilis, malaria, and Lyme disease, to name just a few, continue to vex us and make us humbler and wiser physicians.

The study by Sibony et al in this issue of Journal of Neuro-Ophthalmology (citation here) is an effort to determine whether various forms of optic neuropathy are within the spectrum of Lyme disease. The authors used a retrospective chart review of patients within a patient database at SUNY Stony Brook School of Medicine; the school is located in an area endemic for Lyme disease.Out of 440 patients presenting with optic neuritis, the authors found that only five (1%) had compelling evidence that active Borrelia burgdorferi was responsible for, or contributed to, their visual deficit. This would indicate that in an academic center in an endemic area in the United States, extremely few patients with optic neuritis had Lyme disease as a cause, and that it is not a common cause of optic neuritis.

Why did I include the qualifier in the United States in the aforementioned sentence? Because Lyme neuroborreliosis has different clinical phenotypes for different genotypes of infecting subtypes of B. burgdorferi spirochetes. This has been an observation in the human disease (1) and its animal models (2). Thus, the conclusions drawn from the study of Sibony et al may not be readily applicable to Lyme disease in Europe, where the disease has a more aggressive neurologic presentation (3). Not surprisingly, investigators in Europe such as the Finns (4) and the Germans (5), both appropriately quoted in the study of Sibony et al, might dispute the conclusion that optic neuritis is rare in Lyme neuroborreliosis. The difference is likely because of the fact that American neuroborreliosis is caused predominantly by B. burgdorferi sensu stricto, whereas European disease is caused by B. garinii or B. afzelii, and the genetic differences between these subspecies are considerable.

Another issue that the authors did not address is the nagging question of whether our serological assays (enzyme-linked immunosorbent assay and Western blot) are so powerful that they will always be positive in cases of optic neuritis caused by B. burgdorferi. My answer is, possibly not! The concern is that in this chronic infection, it is conceivable that spirochetes can be cleared from the periphery but retained in immune-privileged sites such as the eye or the brain. Thus, an enzyme-linked immunosorbent assay-positive but Western blot-negative patient with optic neuritis could conceivably be infected yet have a localized process without adequate peripheral activation to become Western blot positive. A similar situation occurs in tertiary neurosyphilis, in which the CSF (cerebrospinal fluid) VDRL can be negative in a substantial percentage of cases despite a positive serum FTA-ABS.

These remarks do not detract, of course, from a very nice contribution to the literature by Sibony et al, especially in pointing out that optic nerve involvement in Lyme borreliosis in the United States is predominantly found in the child with meningitis, increased intracranial pressure, and optic disc edema. Retrobulbar neuritis remains very unlikely to be caused by Lyme disease; most likely it has another cause.


1. Steere AC, Berardi VP, Weeks KE, et al. Evaluation of the intrathecal antibody response to Borrelia burgdorferi as a diagnostic test for Lyme neuroborreliosis. J Infect Dis 1990;161:1203-9.

2. Pachner, AR, Dail D, Bai Y, et al. Genotype determines phenotype in experimental Lyme neuroborreliosis. Ann Neurol 2004;56:361-70.

3. Hansen K, Lebech AM. The clinical and epidemiological profile of Lyme neuroborreliosis in Denmark 1985-1990. A prospective study of 187 patients with Borrelia burgdorferi specific intrathecal antibody production. Brain 1992;115:399-423.

4. Karma A, Seppala I, Mikkila H, Kaakkola, et al. Diagnosis and clinical characteristics of ocular Lyme Borreliosis. Am J Ophthalmol 1995;119:127-35.

5. Preac-Mursic V, Pfister HW, Spiegel H, et al. First isolation of Borrelia burgdorferi from an iris biopsy. J Clin Neuroophalmol 1993;13:155-61.

The jury may still be out as far as Lyme optic neuritis and retrobulbar neuritis caused by Lyme disease, however these were published after 2005:
Oftalmologia. 2006;50(1):16-20.

[Lyme disease--a relatively new entity].

[Article in Romanian]
Tsirmpas MD, Tsirmpas D.
Clinica de Oftalmologie, Spitalul Clinic de Urgenta, Militar Central, Bucuresti.

PURPOSE: To bring in the attention of the medical personnel a relatively new discovered disease with serious consequences, that is often mistaken with a great multitude of miscellaneous syndromes. Also we want to highlight that it is not a rare disease taken into account its endemicity in Europe and consequently in Romania. SUMMARY: Lyme disease is a bacterial infection caused by a spirochete named "Borrelia Burgdorferi" transmitted to humans by a minuscule tick. It is a multi-systemic illness with ocular involvement as well. The disease mimics other pathologic conditions and because of this goes frequently undiagnosed and consequently untreated. Its ocular involvement may vary from a mild conjunctivitis to uveitis, optic neuritis and sometimes lead to blindness. The disease is endemic in Romania. If it is correctly diagnosed it can be successfully treated with specific antibiotics administrated orally or i.v.

[PubMed - indexed for MEDLINE]
J Neurol Neurosurg Psychiatry2007;78:1409-1410 doi:10.1136/jnnp.2006.113761



Retrobulbar optic neuritis: a complication of Lyme disease?

E Krim1,
D Guehl2,
P Burbaud2,
A Lagueny3

1 Service de Neurologie, Hôpital du Haut Lévêque, Pessac, France
2 Service d’explorations fonctionnelles du système nerveux, Hôpital du Haut Lévêque, Pessac, France
3 Service de Neurologie, Hôpital du Haut Lévêque, Pessac, France

Dr Elsa Krim, Service de Neurologie, Hôpital du Haut Lévêque, Avenue de Magellan, 33600 Pessac, France

Retrobulbar optic neuritis (RON) is an unusual complication of Lyme disease. The diagnosis of early Lyme disease is difficult, and the relationship between RON and Lyme disease remains controversial. None of the 14 cases of optic neuritis described in the literature in association with Lyme disease fulfilled the Halperin and Sibony criteria for active Lyme disease. We report the first case of acute Lyme disease complicated by RON established using the Halperin and Sibony criteria.

Lyme disease is a multisystem infectious disease caused by tick borne spirochetes of the Borrelia burgdorferi group. Diagnosis of this infection can be difficult and serological testing such as western blot can be useful. Cranial neuropathies are common but RON has been reported in a few isolated cases.1 A causal link between optic neuritis and Lyme disease has not been established and remains controversial. We report a case of active neuro-Lyme disease complicated by RON.

Case report
A 67-year-old man who lives in a wooded area of southwest France developed an erythema migrans 3 days after a tick bite on his right arm. He was admitted to hospital 2 weeks later with fatigue, myalgia, painful radiculopathy, facial weakness, ptosis and diplopia. Physical examination showed fever (38°C), cervical radiculoneuropathy with radicular pain and paresis in the right arm, …
Med Arh. 2008;62(2):117-8.Links

Bilateral retrobulbar optic neuritis as first signs of Lyme disease.

Todorovic L, Ibisevic M, Alajbegovic A, Suljic-Mehmedika E, Jurisic V.
Clinic for Neurology, Clinical center University of Sarajevo.

Bilateral retrobulbar optic neuritis in young adults are most often caused by demyelinate disease (MS). In all cases where MS was eliminated, we have used selected tests regarding to history, clinical findings and differential diagnosis. Diagnosis of Lyme disease is approved by diagnostic criteria proposed by Center for Control and Prevention of disease. In our case diagnosis of Lyme disease was established by history of illness, clinical findings and positive serlological tests.

PMID: 18669236
J Neurol Sci. 2010 Aug 15;295(1-2):117-9. Epub 2010 Jun 8.

Lyme optic neuritis.

Blanc F, Ballonzoli L, Marcel C, De Martino S, Jaulhac B, de Seze J.

Department of Neurology, University Hospital of Strasbourg, Strasbourg, France.


Lyme optic neuritis (ON) is a rare disease and only a few cases have been reported. We describe two cases of isolated Lyme ON, one with recurrence 9 months after the appearance of initial symptoms. Diagnosis criteria for multiple sclerosis and neuromyelitis optica were not met. The etiological diagnosis was based on European case definition criteria for neuroborreliosis. Both patients had positive serum and cerebrospinal fluid serology, a positive intrathecal anti-Borrelia antibody index, and a good outcome on ceftriaxone. Specific diagnosis of Lyme ON is important since improvement of visual acuity is possible with specific antibiotherapy, even after many months.

Copyright (c) 2010 Elsevier B.V. All rights reserved.

PMID: 20621802

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Re: Lyme Disease and the eyes

Post by Claudia » Wed 29 Aug 2012 2:29
J Fr Ophtalmol. 2012 Jan;35(1):17-22. Epub 2011 Jun 22.

Ocular Lyme disease occurring during childhood: five case reports.
[Article in French]
Sauer A, Hansmann Y, Jaulhac B, Bourcier T, Speeg-Schatz C.
Service d'Ophtalmologie, Nouvel Hôpital Civil, CHU de Strasbourg, BP 426, 67091 Strasbourg cedex, France.


Lyme borreliosis (LB) is the most common human tick-borne disease in the Northern hemisphere. The various ophthalmologic manifestations of Lyme borreliosis (LB) during childhood are discussed in this paper.

Six children with LB-associated ocular manifestations were treated between 2000 and 2010 in the ophthalmology department of Strasbourg University Hospital (an endemic area). Medical history, ocular and systemic clinical findings, determinations of antibodies related to Borrelia, as well as exclusion of other causes were the diagnosis criteria.

Two cases of uveitis, two cases of abducens palsies, one case of optical neuropathy, and one case of orbital myositis associated with LB were diagnosed. Systemic findings, such as arthritis, rash, or erythema migrans were mentioned in all cases. Two children also complained of severe knee arthritis. Determination of antibodies was positive in all patients. They were all treated with antibiotics adjusted to individual circumstances and some of them (two cases of uveitis and one of optic neuropathy) also had anti-inflammatory treatment. Resolution of ocular signs, with no relapse, was observed in all patients within two to 12 weeks.

For any unexplained ocular symptom, even in children, LB should be taken into account, especially in endemic areas. Such patients should undergo serological testing. If the clinical presentation is suggestive of LB, a course of oral antibiotics should be used. All in all, permanent defects are extremely rare during the childhood period, even following long-term manifestation at an early age.

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Re: Lyme Disease and the eyes

Post by RitaA » Wed 10 Oct 2012 19:48
Curr Opin Ophthalmol. 2012 Nov;23(6):485-490.

Optic nerve involvement in Lyme disease.

Träisk F, Lindquist L.


a Department of Clinical Neuroscience and Clinic of Neuro-Ophthalmology, Karolinska Institute, St Erik Eye Hospital, Stockholm b Department of Medicine and Clinic for Infectious Diseases, Karolinska Institute, Karolinska University Hospital, Huddinge, Sweden.



The tick-borne spirochete Borrelia burgdorferi sensu lato can cause several neural manifestations from the peripheral and central neural system. There are several case reports in the literature of optic nerve involvement in association with Lyme neuroborreliosis, but clinical guidelines as to when Lyme disease should be considered in optic neuropathy is lacking.


Papilledema caused by raised intracranial pressure in Lyme meningitis seems mainly to affect children, although some adult cases have been reported. Very few cases of retrobulbar optic neuritis, papillitis, neuroretinitis and ischemic optic neuropathy have shown evidence of a strong association with Lyme neuroborreliosis.


Optic neuropathy in Lyme neuroborreliosis is rare. The cases reported in the literature are not sufficient for making a list of clinical 'red flags'. However, in adult cases, special attention seems reasonable in patients with painless visual loss, bilateral optic nerve head swelling with or without an elevated cerebrospinal fluid opening pressure. In endemic areas, any optic neuropathy may still be considered for a Lyme neuroborreliosis work-up. The use of accepted criteria for establishing the diagnosis of Lyme neuroborreliosis is emphasised.

PMID: 23047166 [PubMed - as supplied by publisher]

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Re: Lyme Disease and the eyes

Post by RitaA » Sat 13 Apr 2013 8:20

It doesn't look like the correspondence related to the following article has been posted here on LNE yet: ... 7123450207
Free Preview


Lyme Disease

Allen C. Steere, M.D.
N Engl J Med 2001; 345:115-125July 12, 2001DOI: 10.1056/NEJM200107123450207 ... 1013451816

Ocular Lyme Borreliosis

N Engl J Med 2001; 345:1350-1351November 1, 2001DOI: 10.1056/NEJM200111013451816

To the Editor:

The superb review article on Lyme disease by Steere (July 12 issue)1 omitted a manifestation associated with the disease: ocular Lyme borreliosis. Ocular Lyme borreliosis is probably underdiagnosed not only because of difficulties in the serologic diagnosis of the disease, but also because the clinical ocular features are often not recognized. Uveitis (which may be associated with photophobia, macular edema, retinal vasculitis, and decreased vision), neuroretinitis, and choroiditis with retinal detachment may develop.2 Neuro-ophthalmic manifestations include optic neuropathy and other cranial neuropathies such as abducens-nerve palsy and paresis of the seventh nerve (which may lead to neurotrophic keratopathy) and pseudotumor cerebri. Interstitial keratitis, episcleritis, and follicular conjunctivitis are possible anterior-segment manifestations. Transient worsening of symptoms after the intravenous administration of ceftriaxone as a result of a Jarisch–Herxheimer reaction has also been described.3

These manifestations are important components of the clinical spectrum of Lyme borreliosis. They occasionally develop in the early stages of the disease, but in most cases they are late manifestations. Interestingly, it was Steere and colleagues who first described proven ocular Lyme borreliosis in their 1985 report of a patient who was blinded from severe panophthalmitis and in whose vitreous Borrelia burgdorferi spirochetes were found.4

Michael Colucciello, M.D.

South Jersey Eye Physicians, Moorestown, NJ 08057
Author/Editor Response

The author replies:

To the Editor: In my original review article on Lyme disease,1 which was published in the Journal 12 years ago, I listed the known clinical manifestations of the infection. With regard to ocular manifestations, the list included reports of conjunctivitis, iritis, choroiditis, retinal hemorrhage or detachment, keratitis, and panophthalmitis. Because of space limitations, I was not able to reiterate this list in the current review.2 Instead, in the section on clinical manifestations and pathogenesis, I presented only the more common clinical manifestations of the infection and reviewed new information about the immunopathogenesis of each of these manifestations, including insights gained from animal models of the infection.

Although I was not able to include information on eye abnormalities or other uncommon manifestations of Lyme disease in my current review, in the section on neurologic involvement I did mention optic neuropathy in children with Lyme disease, citing a recent article.3 This manifestation may result from inflammation of the optic nerve, increased intracranial pressure, or both and may lead to permanent bilateral blindness, a complication that had not yet been reported 12 years ago.

In the current review,2 I stated, “The clinical manifestations of Lyme disease remain basically as they were presented in the Journal 12 years ago.” My hope was that readers who were interested in reviewing the list of clinical manifestations of the infection would refer to the original article.

Allen C. Steere, M.D.

Tufts University School of Medicine, Boston, MA 02111

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Re: Lyme Disease and the eyes

Post by panda » Sun 26 May 2013 23:06

Ann Acad Med Singapore. 2012 Apr;41(4):178-9.
Lyme neuroretinitis in Singapore: a diagnostic dilemma.
Lam JS, Sanjay S.
Neuroretinitis secondary to Lyme disease is a rare
occurrence worldwide,4 and none has been reported in
Singapore as yet. In our patient, although Western blot test
was negative for Lyme Ig G, treatment with intravenous
antibiotics was reported with a subjective improvement in
visual acuity of the patient, with gradual resolution of the
macular oedema. This case report primarily suggests that,
in the absence of all other infectious, systemic diseases or
uveitis entities, Lyme disease still remains a possible cause
in this patient. [no abstract] ... N4p178.pdf [free full text]

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Re: Lyme Disease and the eyes

Post by RitaA » Mon 14 Oct 2013 22:44

Lyme borreliosis

Ocular inflammation as a manifestation of Lyme borreliosis

BMJ 2012; 345 doi: (Published 16 July 2012)
Cite this as: BMJ 2012;345:e4721

Jael M Howlett, specialist trainee year 1, ophthalmology1, Adam P Booth, consultant ophthamologist1

Author Affiliations

1Royal Eye Infirmary, Plymouth PL4 6P, UK

Lyme disease has several important ophthalmic manifestations that are important to highlight.1 Self limiting follicular conjunctivitis is probably the most common early ocular manifestation and occurs within the …
Here’s the full letter (free of charge): ... 1.full.pdf
BMJ 2012;345:e4721 doi: 10.1136/bmj.e4721 (Published 16 July 2012)



Ocular inflammation as a manifestation of Lyme borreliosis

Jael M Howlett specialist trainee year 1, ophthalmology,
Adam P Booth consultant ophthamologist
Royal Eye Infirmary, Plymouth PL4 6P, UK

Lyme disease has several important ophthalmic manifestations that are important to highlight.1 Self limiting follicular
conjunctivitis is probably the most common early ocular manifestation and occurs within the first few weeks of infection in around 10% of patients. Periorbital oedema has also been reported in the early stage.2 3 Other ocular manifestations include anterior, intermediate, and posterior uveitis; keratitis; and episcleritis.3

Among all cases of uveitis, Lyme disease was the underlying cause in 4.3% of patients, and all patients with Lyme uveitis had posterior ocular manifestations, such as vitritis, retinal vasculitis, or neuroretinitis.4

Photophobia and severe periodic ocular pain can be characteristic symptoms of Lyme borreliosis.3 Doctors should be aware that patients presenting with eye pain, redness, photophobia, or reduced visual acuity could have ocular
manifestations of Lyme disease.

Competing interests: None declared.

1 Duncan CJA, Carle G, Seaton A. Tick bite and early Lyme borreliosis. BMJ
2012;344:e3124. (14 May.)
2 Weinberg RS. Ocular involvement in Lyme disease. Current insight. American Academy
of Ophthalmology, 2008.
3 Mikkila HO, Ilkka JT, Seppala I, Viljanen MK, Peltomaa MP, Karma A. The expanding
clinical spectrum of ocular Lyme borreliosis. Ophthalmology 2000;107:581-7.
4 Mikkila H, Seppala I, Leirisalo-Repo M, Immonen I, Karma A. The etiology of uveitis: the
role of infections with special reference to Lyme borreliosis. Acta Ophthalmol Scand
Cite this as: BMJ 2012;345:e4721

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Re: Lyme Disease and the eyes

Post by RitaA » Mon 14 Oct 2013 23:06
Eur J Ophthalmol. 2001 Apr-Jun;11(2):203-6.

Optic nerve lesion following neuroborreliosis: a case report.

Burkhard C, Gleichmann M, Wilhelm H.


Ahaus Eye Hospital, Germany.



Neuroborreliosis may cause various neuro-ophthalmological complications. We describe a case with a bilateral optic neuropathy.


A 58-year-old female developed facial paresis six weeks after an insect bite. One week later she developed bilateral optic disc swelling with haemorrhages and nerve fibre bundle defects in the lower visual field of the left eye. In CSF and serum, raised IgM and IgG titres to Borrelia burgdorferi were found. Systemic antibiotic treatment led to improvement of the vision and facial paresis, but not all visual field defects resolved, probably due to ischemic lesions of the optic disc.


In optic nerve lesions due to neuroborreliosis it is difficult to distinguish between inflammatory and ischemic lesions. This patient demonstrated features of an ischemic optic nerve lesion.

[PubMed - indexed for MEDLINE]
p.s. On a personal note, I also have visual field defects -- initially diagnosed as normal-tension glaucoma. My ophthalmologist now believes my optic nerve damage is the result of a delayed diagnosis and treatment for neuroborreliosis.

Edited to add:

The following is written by, and for, eye care professionals, however it does explain the importance of distinguishing between various types of optic neuropathy: ... id/108438/

Optic Neuropathies: Glaucomatous vs. Non-glaucomatous

While these conditions have overlapping clinical features, distinguishing one from the other is vital to chart the appropriate treatment and follow-up plan.

By Julie K. Hutchinson, O.D., Andrew S. Gurwood, O.D., and Marc D. Myers, O.D.



Differentiating non-glaucomatous optic nerve disorders from glaucomatous disease can save significant time and money that would have been spent managing a condition that is neither there nor developing. It can also save many lives. In cases where optic disc changes evolve secondary to non-glaucomatous processes, pathophysiological mechanisms may be budding, producing consequences that are systemic with the potential to impact other organ systems or mortality.

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Re: Lyme Disease and the eyes

Post by RitaA » Tue 15 Oct 2013 3:08
Eye (Lond). 2011 Nov;25(11):1524-5. doi: 10.1038/eye.2011.214. Epub 2011 Aug 19.

Abnormal corneal nerves in a patient with Lyme disease.

Ricaud X, Rozenbaum JP, Landowski S, Baudouin C, Labbé A.

PMID: 21852805 [PubMed - indexed for MEDLINE] PMCID: PMC3213668 Free PMC Article
The full, free article is here:
Abnormal corneal nerves in a patient with Lyme disease

Eye (Lond). 2011 November; 25(11): 1524–1525.
Published online 2011 August 19. doi: 10.1038/eye.2011.214
PMCID: PMC3213668

X Ricaud,1 J-P Rozenbaum,2 S Landowski,3 C Baudouin,1,4,5,6,7 and A Labbé1,4,5,6,7,*

1 Department of Ophthalmology, Quinze-Vingts National Ophthalmology Hospital, Paris and Ambroise Paré Hospital, AP-HP, University of Versailles Saint-Quentin en Yvelines, Versailles, France
2 Ophthalmology Clinic, Sartrouville, France
3 Department of Acute Medicine, Raymond-Poincaré Hospital, AP-HP, Garches and University of Versailles Saint-Quentin en Yvelines, Versailles, France
4 INSERM, U968, Paris, France
5 UPMC University Paris 06, UMR S 968, Institut de la Vision, Paris, France
6 CNRS, UMR 7210, Paris, France
7 Center of Clinical Investigations 503, Quinze-Vingts National Ophthalmology Hospital, Paris, France


Lyme disease is a multiorgan disease caused by a spirochete, Borrelia burgdorferi. Although numerous ophthalmologic manifestations have been described following Lyme disease,1, 2 this case describes a new feature: a bilateral corneal neuropathy.

Case report

A 69-year-old woman was referred for a suspicion of corneal dystrophy in both eyes that appeared during the last 6 months. Her past medical history was relevant for a tick bite complicated by Lyme disease 2 years ago. Despite oral antibiotic treatment (clarithromycin), she still suffered from peripheral neuropathy in the lower extremities.

She presented with complaints of decrease vision bilaterally. Best corrected visual acuity was 20/25 in both eyes. Slit-lamp examination revealed irregularly enlarged corneal stromal nerves in both eyes (Figure 1). These abnormalities did not reach the central cornea and were predominantly observed in the mid-peripheral area of the right eye. Except this finding, corneal examination was normal in both eyes. No sign of inflammation of the anterior segment was observed. Examination of the posterior segment of both eyes was normal. The slight decrease in visual acuity was explained by a mild bilateral cataract. Using the Cochet–Bonnet aesthesiometer, a marked hypoesthesia was observed in the central cornea of the right eye (3.5 mm), whereas the corneal sensitivity was subnormal in the left eye (5.5 mm). Except the corneas, the sensitivity in the area innervated by the trigeminal nerves was not altered. In vivo confocal microscopy (HRT3, Heidelberg Engineering, Heidelberg, Germany) revealed enlarged stromal nerves with tortuous and abnormal branching in both eyes. Some nerve fibers showed a hyper-reflective peri-nerve infiltration (Figure 2).


Cranial nerve involvements are well documented in early disseminated Lyme disease,3 but in the presented case, only the corneal nerves of both eyes showed alterations that were observed 2 years after the infection. In our patient, the association of distal paresthesia, suggesting axonal polyneuropathy and corneal nerves alterations, strongly supported the responsibility of Lyme disease. The mechanisms responsible for peripheral nerve damage in Lyme disease remain unclear. Nevertheless, peripheral sensory symptoms are frequent and could appear months and years after the onset of infection even with an adapted treatment.3, 4 Eye examination is not systematically performed in Lyme disease, the absence of symptoms may explain why this corneal neuropathy remained unobserved. Larger studies evaluating corneal nerves morphology and functionality in Lyme disease are now needed to confirm this finding.


The authors declare no conflict of interest.


Mora P, Carta A. Ocular manifestations of Lyme borreliosis in Europe. Int J Med Sci. 2009;6:124–125. [PMC free article][PubMed]
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