Abstract

The diagnosis of acute Lyme neuroborreliosis (LNB) is usually not difficult. Patients who present in summer or fall with the triad of a painful radiculoneuropathy, cranial neuropathy (particularly facial neuropathy), and meningitis, preceded by a skin rash compatible with erythema migrans or a flu-like illness after exposure in an endemic area have LNB until proven otherwise and should be promptly treated with antibiotics.1,2 However, the diagnosis of acute LNB can be problematic when patients present with only one component of the triad, particularly in the absence of preceding skin involvement. In such patients laboratory testing is needed to confirm the diagnosis. Most patients have an elevated serum Lyme titer, and nearly all have a CSF mononuclear pleocytosis with elevated protein but normal glucose (even in the absence of meningeal signs). However, the diagnostic sine qua non of LNB is demonstration of intrathecal Borrelia infection by CSF culture, intrathecal concentration of B burgdorferi antibody, or by PCR. Unfortunately, CSF culture is only rarely positive (and very rarely even attempted), the CSF/serum antibody index is sometimes normal, and PCR …

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