LE was originally used to describe mild confessional state—most commonly fatigue, sleep disturbance, memory loss, and depression—in patients with active systemic Lyme disease, particularly active arthritis. However, its meaning has become more general and is often used to describe patients with similar deficits but without laboratory confirmation of active Lyme infection. This has made the diagnosis of some disorders that have been attributed to Lyme disease highly controversial. In cases in which the patient has had the characteristic clinical picture, a positive serology to B. burgdorferi, and abnormal CSF, the symptoms are likely due to active infection. Moreover, there is evidence, from MRI and SPECT studies, that the infection preferentially affects white matter areas of the brain, although the mechanism is not known. Neuropsychological testing in these patients typically shows mild, but statistically significant, deficits on memory testing. After adequate antimicrobial therapy, most patients show significant improvements in their cognitive functioning and return to normal. In the one quantitative SPECT study, demonstrating a reduction of cerebral perfusion in patients with LE, there was also a partial reduction of hypoperfusion with antibiotic therapy.

The controversy regarding the diagnosis of LE stems from patients who report encephalopathic symptoms without clear evidence of an active Lyme infection, namely those with post-Lyme disease syndrome. Although some clinicians still attribute this to a subacute B. burgdorferi infection and recommend extended antimicrobial therapy, others question whether these symptoms are caused by active brain infection. Some neuropsychological investigations have shown these patients to perform more poorly than healthy normals, whereas others have not. Neuropsychological deficits in post-Lyme syndrome patients seem to be independent of a history of psychopathology but are correlated with concurrent fatigue. Lyme patients with independent evidence of CNS infection perform significantly worse on neuro-psychological testing than post-Lyme disease syndrome patients. For patients without clear evidence of active Lyme disease, there is little efficacy to additional antimicrobial therapy. This has led some researchers to conclude that LE is probably overly diagnosed, and the lack ofresponse to antibiotic therapy is the result of misdiagnosis. In addition to latent infection, other explanations for post-Lyme disease include the psychological consequences of chronic illness, residual deficits from past infection, and possibly an immune response. It has also been suggested that a fibromyal-gia syndrome may be triggered by infection to B. burgdorferi after the infection is successfully treated since both disorders can result in similar cognitive complaints.

Patients with LE typically report memory problems independent of their performance on objective testing. The perception of cognitive difficulties may be common to a variety of physiological and psychological disorders. In chronic Lyme disease, patients with objective evidence of CNS infection, such as abnormal CSF, probably have a neurological basis to their reported cognitive decline. Other chronic Lyme patients are likely experiencing the stress and affective symptoms common to many chronic illnesses and similarly the perception of cognitive dysfunction.

Lastly, it is important to note that relative to the incidence of Lyme disease, the prevalence of chronic LE is quite low. Population studies have shown that only a small percentage of previously infected patients have neurological abnormalities, including objective evidence of memory impairment. Patients with residual deficits typically have had a longer duration of untreated disease prior to eventual treatment. Similarly, studies of children indicate that the chronic neurological deficits are rare when Lyme disease is adequately treated. Taken together, it is reasonable to conclude that the prognosis for returning to normal neurocognitive functioning after being infected with Lyme disease is good with adequate treatment.

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Suggested Reading

Adams, W. V., Rose, C. D., Eppes, S. C., and Klein, J. D. (1994). Cognitive effects of Lyme disease in children. Pediatrics 94,185189.

Halperin, J. J., Pass, H. L., Anand, A. K., Luft, B. J., Volkman, D. J., and Dattwyler, R. J. (1988). Nervous system abnormalities in Lyme disease. Ann. N. Y. Acad. Sci. 539, 24-34.

Kaplan, R. F., Jones-Woodward, L., Workman, K., Steere, A. C., Logigian, E., and Meadows, M.-E. (1999). Neuropsychological deficits in Lyme disease patients with and without other evidence of nervous system pathology. Appl. Neuropsychol. 8, 3-11.

Krupp, L. B., Masur, D., Schwartz, J., Coyle, P. K., Langenbach, L. J., Fernquist, S. K., Jandorf, L., and Halperin, J. J. (1991). Cognitive functioning in late Lyme borreliosis. Arch. Neurol. 48, 1125-1129.

Logigian, E. L., Kaplan, R. F., and Steere, A. C. (1990). Chronic neurologic manifestations of Lyme disease. N. Engl. J. Med. 323, 1438-1444.

Shadick, N. A., Phillips, C. B., Sanga, O., Logigian, E. L., Kaplan, R. F., Wright, E. A., Fossel, A. H., Fossel, K., Berardi, V., Lew, R. A., and Liang, M. H. (1999). Musculoskeletal and neurologic outcomes in patients with previously treated Lyme disease. Ann. Intern. Med. 131, 919-926.

Steere, A. C., Taylor, E., McHugh, G. L., and Logigian, E. L. (1993). The overdiagnosis of Lyme disease. J. Am. Med. Assoc. 269, 1812-1816.

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