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Case Reports
. 2014 Dec 11;6(4):5496.
doi: 10.4081/idr.2014.5496. eCollection 2014 Nov 19.

A Case of Chronic Progressive Lyme Encephalitis as a Manifestation of Late Lyme Neuroborreliosis

Free PMC article
Case Reports

A Case of Chronic Progressive Lyme Encephalitis as a Manifestation of Late Lyme Neuroborreliosis

Vivek Verma et al. Infect Dis Rep. .
Free PMC article


A 54-year-old female living in Europe presented with gait ataxia, dizziness, and bilateral hearing loss. Magnetic resonance imaging (MRI) revealed non-specific white matter changes. The patient's condition gradually deteriorated over two years without diagnosis. The patient continued to decline cognitively and neurologically with worsening ataxia and upper motor neuron signs. Repeat MRI showed worsening white matter changes. Lumbar puncture, not previously done, showed positive Lyme testing. Treatment with intravenous ceftriaxone resulted in marked neurological improvement. Four years after symptom, the patient has short-term memory deficits and chronic fatigue, but is otherwise neurologically, cognitively, and functionally intact. Follow up MRI findings remain largely unchanged. Because cases of intraparenchymal or encephalopathic neuroborreliosis in America are lacking, so are treatment options. We present a rare case and discuss our experience with antibiotic treatment. This case lends evidence to define optimal treatment of this disease, imperative for hastening neurological recovery.

Keywords: Borrelia burgdorferi; Lyme neuroborreliosis; encephalopathy.

Conflict of interest statement

Conflict of interests: the authors declare no potential conflict of interest.


Figure 1.
Figure 1.
Fluid-attenuated inversion recovery - fast spin echo sequence images of the patient’s brain on initial presentation to our hospital. Lesions are present in the periventricular areas (A), white matter (A,B), pons (C, arrow), and middle cerebellar peduncle (left>right, D).
Figure 2.
Figure 2.
Fluid-attenuated inversion recovery - conventional spin echo sequence images of the patient’s brain at two-year follow-up. Lesions persist in the periventricular areas and white matter (A,B), but show decreased signal in the pons (C) and middle cerebellar peduncle (D) relative to corresponding images in Figure 1.

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