Spastic paraparesis caused by cerebrovascular neuroborreliosis in a 13-year-old boy

Neurological manifestations of borreliosis are more common in children than in adults. However, childhood neuroborreliosis with cerebrovascular symptoms has rarely been reported.

We saw a 13-year-old boy who developed difficulties in walking and standing 4 years prior to his first presentation at our clinic. On admission, he showed a spastic paraparesis with a gawky gait. Lumbar puncture was performed and revealed lymphocytic pleocytosis (17×10⁶/l), increased protein (1,13g/l), decreased glucose (0,32g/l), and an intrathecal production of IgG antibodies against Borrelia burgdorferi (antibody index CSF/serum 11,3). Diagnosis of chronic neuroborreliosis was confirmed by Western blot. A cranial MRI showed a symmetric high signal intensity in both pyramids at the level of the medulla oblongata. Treatment with intravenous ceftriaxone (56mg/kg) for 21 days did not substantially improve the clinical condition.

3 months later lumbar puncture was repeated. Lymphocytic pleocytosis (7×10⁶/l) and protein (0,48g/l) had decreased, while glucose was still low (0,36g/l). IgG antibodies and a Western blot for B. burgorferi were still positive (antibody index CSF/serum 26,7, possibly due to persistent intrathecal antibody production), and MRI showed an identical lesion.

Early-stage neuroborreliosis is known to cause vasculitis with widespread cerebral lesions, among other places in the pyramids (Romi, Eur Neurol 2004). To our knowledge this is the first case report of chronic neuroborreliosis with cranial MRI showing high signal intensitiy in the pyramids causing spastic paraparesis in a child.

With persistent spastic paraparesis 10 months after treatment, a residual syndrome cannot be ruled out. Effectiveness of a second course of antibiotic treatment has been shown in one case (Wilke, Arch Dis Child 2000), and will be started in this patient.