The American Psychiatric Association (APA) has updated its Privacy Policy and Terms of Use, including with new information specifically addressed to individuals in the European Economic Area. As described in the Privacy Policy and Terms of Use, this website utilizes cookies, including for the purpose of offering an optimal online experience and services tailored to your preferences.

Please read the entire Privacy Policy and Terms of Use. By closing this message, browsing this website, continuing the navigation, or otherwise continuing to use the APA's websites, you confirm that you understand and accept the terms of the Privacy Policy and Terms of Use, including the utilization of cookies.

×
LetterFull Access

Acute Disseminated Encephalomyelitis

Published Online:https://doi.org/10.1176/jnp.10.3.366

SIR: Drs. Patel and Friedman presented a cogent and informative discussion of the neuropsychiatric features of acute disseminated encephalomyelitis.1 The section on differential diagnosis, however, mistakenly included syphilis and Lyme disease under the category of viral encephalitides. Both syphilis and Lyme disease are in fact caused by bacteria—in particular, spirochetes.

Further, although acute and convalescent titers can be very helpful in monitoring the course of syphilis, the serologic or CSF test results in Lyme disease are less reliable.2 This is of critical importance among patients with Lyme-induced encephalomyelitis. Some patients may have a positive CSF polymerase chain reaction assay for Borrelia burgdorferi (the agent of Lyme disease) or positive immune complex dissociation studies but have an otherwise normal-appearing CSF and equivocal or nonreactive serum.3 Although serologic and CSF titer monitoring is routinely done in the European strains of Lyme encephalomyelitis to monitor progress in the treatment of the disease, the CSF of patients with neurologic Lyme disease in North American strains is less often abnormal initially and therefore less helpful for serial monitoring.3,4

In endemic areas or in patients with a clinical history suggestive of neuropsychiatric Lyme disease, we urge physicians therefore to consider Lyme disease as a treatable cause of persistent encephalomyelitis even in cases where the CSF or serologic results are negative or equivocal.5

References

1. Patel SP, Friedman RS: Neuropsychiatric features of acute disseminated encephalomyelitis: a review. J Neuropsychiatry Clin Neurosci 1997; 9:534–540LinkGoogle Scholar

2. Burlington DB: FDA Public Health Advisory: Assays for antibodies to Borrelia burgdorferi: limitations, use, and interpretation for supporting a clinical diagnosis of Lyme disease. Department of Health and Human Services, US Public Health Service, Food and Drug Administration, July 7, 1997Google Scholar

3. Coyle PK, Schutzer SE, Deng Z, et al: Detection of Borrelia burgdorferi–specific antigen in antibody-negative cerebrospinal fluid in neurologic Lyme disease. Neurology 1995; 45:2010–2015Crossref, MedlineGoogle Scholar

4. Liegner KB, Duray PH, Agricola MD: Lyme disease and the clinical spectrum of antibiotic-responsive chronic meningoencephalomyelitides. Abstract #D627. VII International Congress on Lyme Borreliosis, San Francisco, CA, 1996 Google Scholar

5. Fallon BA, Nields JA: Lyme disease: a neuropsychiatric illness. Am J Psychiatry 1994; 151:1571–1583Crossref, MedlineGoogle Scholar