Lyme disease, caused by infection with
Borrelia burgdorferi, is the most common tick-borne disease in temperate regions of the Northern Hemisphere.
1 The Centers for Disease Control and Prevention (CDC) estimates approximately 300,000 new infections occur annually in the United States.
2 The number of cases has increased in recent decades due in part to climate change, shifting land use patterns, and the relative abundance and distribution of reservoir hosts.
3
Lyme disease often initially presents with a cutaneous lesion, erythema migrans, at the site of the bite of an infected tick, with or without other concurrent signs of infection.
4 If untreated,
B. burgdorferi may then disseminate from the site of skin inoculation to other areas of the skin, as well as the musculoskeletal, cardiac, and neurologic systems.
5 Ocular symptoms, including photophobia, conjunctivitis, and periorbital edema, have been described in up to 11% of patients in acute infections.
6 Antibiotic treatment for Lyme disease generally resolves objective signs of infection for most patients.
7 However, a subset of treated patients develops a chronic illness of persistent or recurrent symptoms following treatment.
8,9 The most prominent of these symptoms include fatigue, widespread musculoskeletal pain, and cognitive difficulties, but patients also report a range of neurologic, sleep, ocular, mood, and other symptoms.
10–12 A standardized, highly specific definition for posttreatment Lyme disease (PTLD) has been operationalized to identify these patients.
7,10,13
Testing of contrast sensitivity (CS) has been proposed as a means to aid diagnosis, identify neurologic effects, and assess treatment response among patients with PTLD.
14 CS is impaired in a variety of ocular conditions such as cataract and retinal degeneration, as well as in neurologic diseases, which commonly manifest with optic neuritis, such as multiple sclerosis (MS).
15–19 In addition to possibly reflecting ocular structural changes, CS loss may also indicate specific or nonspecific deficits in neurologic and/or cognitive function.
17,20,21
Whether CS is depressed in patients with PTLD or is associated with ocular complaints and/or objective neurologic or neurocognitive findings is not known. This study was able to test CS in a well-characterized cohort of patients with PTLD and controls who were either non-Lyme infected without a history of Lyme disease or who had recovered from acute Lyme disease. We hypothesized that patients with PTLD would have more CS impairment than controls and that this impairment would be associated with neurologic and cognitive abnormalities.