Most ME patients report sensitivity to light. Dry eyes and “red eyes” are also common. I have tried to look into the subject, but there is not much literature on the subject. I found this from the CFIDS Association:
Visual Dysfunction in Chronic Fatigue Syndrome.
And this article Pathology of the organ of vision in chronic fatigue syndrome:
"218 patients were examined and the chronic fatigue syndrome (CFS) was diagnosed in them on the basis of clinical-and-immunologic data. 126 somatically healthy persons of the same age and sex were in the control group. Vascular pathology of the vision organ was found in 153 (70.2%) persons, and dystrophic pathology was found in 115 (52.8%) persons. A combination of vascular and dystrophic pathologies of the vision organ was diagnosed in 46 (21.1%) patients. The detection of vision pathology in the CFS patients essentially exceeded the morbidity of similar pathology in the controls. No reliable differences of refraction anomalies were found between the CFS patients and the controls."
But research is coming up. In the 2012 spring issue from ME research UK, a research project is described:
“People with ME/CFS often have problems with their vision; in fact, around three-quarters of the 2,073 consecutive patients described in the Canadian Consensus Document 2003 specifically reported sensitivity to light and dullness of vision to be significant problems.
ME Research UK and the Irish ME Trust have jointly funded a one-year pilot study that aims to determine quantitatively and objectively the main visual symptoms that people with ME/CFS experience. The study will also determine their rate of occurrence and establish whether the types and extent of visual symptoms experienced can be correlated with the severity of the condition and the specificity of other (non-visual) symptoms.”
At Phoenix Rising you can read about a patient donating a tear sample to the CFI pathogen study. This study will be testing for new and novel pathogens in various body fluids (tears, saliva, urine and rectal swab), including blood.
Then I wondered…are Epstein Barr Virus or other viruses involved in eye problems? I did a search:
Ocular disease associated with Epstein-Barr virus infection
"Epstein-Barr virus (EBV) is a ubiquitous DNA virus of the herpesvirus genus with a high prevalence rate for antibody (about 90%) in the adult population. It is the most common causative agent of infectious mononucleosis syndrome. During recent years an increasing number of ocular disease entities have been reported to be linked to EBV infection. These entities include oculoglandular syndrome, conjunctivitis, dry eye, keratitis, uveitis, choroiditis, retinitis, papillitis and ophthalmoplegia. While EBV-specific serologic tests can now document recent and past primary infection with EBV and also identify patients manifesting atypical immunologic reactions to EBV, the lack of an animal model, the absence of clear-cut response to therapy and the paucity of documentation by culture render the pathogenesis uncertain or the association questionable in many of these cases."
Epstein-Barr virus (types 1 and 2) in the tear film in Sjogren's syndrome and HIV infection
"Evidence of Epstein-Barr virus (EBV) shedding in the saliva and tear film has been sought to explain the pathogenesis of the oral and ocular features of Sjogren's syndrome. Patients with human immunodeficiency virus (HIV) infection are purported to have a higher incidence of keratoconjunctivitis sicca. Twenty patients with definite Sjogren's syndrome (primary and secondary), 19 with HIV infection, and 15 normal controls were recruited and studied. Human herpes viruses (EBV 1 and 2, CMV, HZV, and HSV-1) in tear film were detected by polymerase chain reaction of DNA extracted from Schirmer strips. HSV-1, VZV, and CMV were not detected in any tear samples. EBV-1 DNA was found in the tear film of 4 patients with Sjogren's syndrome, which was not significantly different from the control group (P = 0.18). Twelve patients with HIV infection had evidence of EBV-1 in their tears, which was significantly different from controls (P = 0.0002) and patients with Sjogren's syndrome (P = 0.014). EBV-2 was found in 3 patients with HIV and in 1 patient with secondary Sjogren's syndrome, and was always found as a co-infection with EBV-1 (P = 0.01). This represents the first report examining EBV types 1 and 2 in the tear film and also EBV in the tear film of patients with HIV. Shedding of EBV in the tear film was not related to the presence of keratoconjunctivitis sicca in Sjogren's syndrome. EBV-2 co-infection with EBV-1 has not been previously reported in the tear film. EBV infection is abnormally regulated in Sjogren's syndrome and HIV, and it is likely that the presence of EBV in the tear film is related to the patients' altered immune status."
Multiplex detection of herpesviruses in tear fluid using the "stair primers" PCR method: prospective study of 93 patients
"Human herpesviruses can infect the eye and be excreted subsequently in tears. The aim of the present study was to use a multiplex PCR to detect herpesviruses (HSV-1, -2, VZV, CMV, EBV, HHV-6) in tears from normal subjects and from patients with pathological conditions (acute herpes, zoster, papillary conjunctivitis, and dry eye). Schirmer test strips were used to collect tear fluid from 93 patients, sampling both eyes. DNA was then extracted from the 186 samples by chromatography, and viral DNA amplified using a commercialised multiplex "stair primer" method. Thirty-four samples (18.3%) contained Taq inhibitors. The multiplex test gave positive results for HSV and VZV in tear fluid from patients with acute dendritic keratitis (3 patients) and acute ocular zoster (4 patients) and was, therefore, considered effective in testing samples from patients with acute lesions. HSV-1 and HSV-2 were found in two samples from patients with metaherpetic corneal scarring. Among 28 cases of dry eye, two were positive for HHV-6, the latter being associated with EBV in one patient. HHV-6 was also found in 4 out of 54 cases of papillary conjunctivitis. This raised occurrence of HHV-6 in dry eye or papillary conjunctivitis, suggests new clinical patterns for HHV-6 latency or reactivation. Detection of EBV in 1 out of 80 healthy eyes confirms previous evidence that lacrimal glands constitute potentially a site for latent-phase EBV.”
And then I wondered…are TLRs involved in eye problems? Purinergic signalling? Vasoactive peptides? (all subjects mentioned in previous posts) The answer is:
Toll-like receptors in ocular surface diseases: overview and new findings
“On the ocular surface, the early response against noxious stimuli is provided by innate immunity, which represents a non-specific surveillance system and promotes adaptive immune responses. The evidence discussed in the present review highlights the emerging roles of TLRs in regulating innate immune responses during ocular surface infectious and non-infectious inflammatory conditions. In addition, increasing evidence shows that TLRs play an important role in the pathogenic mechanisms of autoimmune and allergic ocular diseases, modulating the adaptive immune responses.”
Expression of toll-like receptor (TLR) 4 contributes to corneal inflammation in experimental dry eye disease
"Purpose. To investigate the corneal expression of toll-like receptor (TLR) 4 and determine its contribution to the immunopathogenesis of dry eye disease (DED).Methods. Seven to 8 week old female C57BL/6 mice were housed in a controlled environment chamber and administered scopolamine to induce experimental DED. Mice received intravenous TLR4 inhibitor (Eritoran) to block systemic TLR4-mediated activity. The expression of TLR4 by the corneal epithelium and stroma was evaluated using real-time polymerase chain reaction and flow cytometry. Corneal fluorescein staining (CFS) was performed to evaluate clinical disease severity. The corneal expression of proinflammatory cytokines (IL-1?, IL-6, TNF, and CCL2), corneal infiltration of CD11b+ antigen-presenting cells, and lymph node frequency of mature MHC-IIhi CD11b+ cells were assessed.Results. The epithelial cells of normal corneas expressed TLR4 intracellularly; however, DED significantly increased the cell surface expression of TLR4. Similarly, flow cytometric analysis of stromal cells revealed a significant increase in the expression of TLR4 proteins by DED-induced corneas as compared to normal corneas. DED increased the mRNA expression of TLR4 in corneal stromal cells, but not epithelial cells. TLR4 inhibition decreased the severity of CFS and significantly reduced the mRNA expression of IL-1?, IL-6, and TNF. Furthermore, TLR4 inhibition significantly reduced the corneal infiltration of CD11b+ cells and the lymph node frequency of MHC-IIhi CD11b+ cells.Conclusions. These results suggest that DED increases the corneal expression of TLR4 and that TLR4 participates in the inflammatory response to ocular surface desiccating stress."
The role of purinergic receptors in retinal function and disease
"Extracellular ATP acts as a neurotransmitter in the central and peripheral nervous systems. In this review, the role of purinergic receptors in neuronal signaling and bi-directional glial-neuronal communication in the retina will be considered. There is growing evidence that a range of P2X and P2Y receptors are expressed on most classes of retinal neurons and that activation of P2 receptors modulates retinal function. Furthermore, neuronal control of glial function is achieved through neuronal release of ATP and activation of P2Y receptors expressed by Müller cells. Altered purinergic signaling in Müller cells has been implicated in gliotic changes in the diseased retina and furthermore, elevations in extracellular ATP may lead to apoptosis of retinal neurons."
Professor Don Staines who has written about a role for autoimmunity and vasoactive neuropeptides in ME, has written this about ophthalmology:
Vasoactive neuropeptides in clinical ophthalmology: An association with autoimmune retinopathy?
“The mammalian eye is protected against pathogens and inflammation in a relatively immune-privileged environment. Stringent mechanisms are activated that regulate external injury, infection, and autoimmunity. The eye contains a variety of cells expressing vasoactive neuropeptides (VNs), and their receptors, located in the sclera, cornea, iris, ciliary body, ciliary process, and the retina. VNs are important activators of adenylate cyclase, deriving cyclic adenosine monophosphate (cAMP) from adenosine triphosphate (ATP). Impairment of VN function would arguably impede cAMP production and impede utilization of ATP. Thus VN autoimmunity may be an etiological factor in retinopathy involving perturbations of purinergic signaling. A sound blood supply is necessary for the existence and functional properties of the retina. This paper postulates that impairments in the endothelial barriers and the blood-retinal barrier, as well as certain inflammatory responses, may arise from disruption to VN function. Phosphodiesterase inhibitors and purinergic modulators may have a role in the treatment of postulated VN autoimmune retinopathy.”
Is it all somehow connected: pathogens, TLRs, mimicry, autoimmunity, purinergic signalling, vasoactive peptides…?