Reversible cerebral hypoperfusion in Lyme encephalopathy

Abstract

Lyme encephalopathy (LE) presents with subtle neuropsychiatric symptoms months to years after onset of infection with Borrelia burgdorferi. Brain magnetic resonance images are usually normal. We asked whether quantitative single photon emission computed tomography (SPECT) is a useful method to diagnose LE, to measure the response to antibiotic therapy, and to determine its neuroanatomic basis. In 13 patients with objective evidence of LE, SPECT demonstrated reduced cerebral perfusion (mean perfusion defect index [PDI] = 255), particularly in frontal subcortical and cortical regions. Six months after treatment with 1 month of intravenous ceftriaxone, perfusion significantly improved in all 13 patients (mean PDI = 188). In nine patients with neuropsychiatric symptoms following Lyme disease, but without objective abnormalities (e.g., possible LE), perfusion was similar to that of the treated LE group (mean PDI = 198); six possible LE patients (67%) had already received ceftriaxone prior to our evaluation. Perfusion was significantly lower in patients with LE and possible LE than in 26 normal subjects (mean PDI = 136), but 4 normal subjects (15%) had low perfusion in the LE range. We conclude that LE patients have hypoperfusion of frontal subcortical and cortical structures that is partially reversed after ceftriaxone therapy. However, SPECT cannot be used alone to diagnose LE or determine the presence of active CNS infection.

Successful Treatment of Lyme Encephalopathy with Intravenous Ceftriaxone

“…The protocol was approved by the Human Investigations Committee at New England Medical Center. As in previous studies [3,12,13], a patient with Lyme encephalopathy was characterized as having (1) previous classical manifestations of Lyme disease, (2) current neuropsychiatric symptoms, and (3) evidence of past or present B. burgdorferi infection in CSF, demonstrated by intrathecal antibody production or spirochetal DNA; or a positive IgG antibody response to B. burgdorferi, detected by ELISA and Western blotting, and verbal or visual memory impairment, as demonstrated by a score at least 2 SDs below the mean of normal control subjects. Patients were excluded if they had (1) a preexisting condition associated with cognitive impairment or (2) a history of alcohol or other drug abuse or (3) if, at any time, they had received a 1-month course of iv ceftriaxone for treatment of Lyme disease.…”

Normal pressure hydrocephalus or neuroborreliosis?

“…Moreover, certain immunmediators were found to interfere with axonal conduction and synaptic transmission [12], and might cause global cognitive dysfunction. It is also feasible that infiltration of arterial vessel walls by Borrelia burgdorferi may cause hypoperfusion -in particular of frontal lobes -disturbing cortical functions [15].…”

Lyme Neuroborreliosis: Manifestations of a Rapidly Emerging Zoonosis

“…46 The distribution of involvement including the callososeptal interface fuels speculation as to a secondary autoimmune mechanism with imaging features mimicking primary demyelinating disease (Fig 7). 40,46,48,[57][58][59][60][61][62][63][64][65] Similar mechanisms of molecular mimicry and antigen-specific T-cell response have been recognized in both multiple sclerosis (MS) and chronic LNB. 66 Yet, T-cell lines demonstrate only weak cross-reactivity between myelin basic protein and B burgdorferi.…”

“…48,[68][69][70][71][72][73][74][75] Single-photon emission CT may provide indi- rect manifestations of LNB antibiotic-reversible frontal hypoperfusion. 65,76,77 Spinal Cord LNB Spinal cord involvement by B burgdorferi is very rare. As a function of geography, LNB would be a rare differential consideration in the evaluation of transverse myelitis.…”

“…These include the amyloid deposition of Alzheimer disease, MS, autism, and neuropsychiatric illness. 65,95,[97][98][99][100][101][102][103][104][105][106] The diagnosis of chronic LNB is predicated on characteristic symptoms, specific serum antibodies, CSF pleocytosis, and intrathecal Lyme antibody production. The utility of brain MR imaging in confirming diagnostic suspicion of chronic LNB is very limited, due to the overlap with age-related basal ganglionic and subcortical white matter lesions and persistence subsequent to successful treatment of LNB.…”