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Cat scratch disease presenting as meningomyeloradiculopathy
  1. G Hmaimess1,
  2. H Kadhim1,
  3. C Saint Martin2,
  4. B Abu Serieh3,
  5. M Mousny4,
  6. G Sébire5
  1. 1Service of Paediatric Neurology, Cliniques Universitaires Saint Luc, Université Catholique de Louvain, Brussels, Belgium
  2. 2Service of Radiology, Cliniques Universitaires Saint Luc, Université Catholique de Louvain, Brussels, Belgium
  3. 3Service of Neurosurgery, Cliniques Universitaires Saint Luc, Université Catholique de Louvain, Brussels, Belgium
  4. 4Service of Orthopaedics, Cliniques Universitaires Saint Luc, Université Catholique de Louvain, Brussels, Belgium
  5. 5Child Neurology Department, CHU Fleurimont, Université de Sherbrooke, Canada
  1. Correspondence to:
    Dr H Kadhim
    Neurologie Pédiatrique (NEPE), Cliniques Universitaires Saint Luc, Avenue Hippocrate 10, Brussels, Belgium;

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We report meningomyeloradiculitis as a presenting picture in a child with cat scratch disease (CSD) and identify the need to include this infection in the differential diagnosis of meningomyeloradiculopathies. We also show the likely benefit of antibiotherapy.

Case report

An 11 year old girl presented three months prior to hospitalisation with low back pain radiating to the lower limbs with paresthesia, limping, and a progressively decreasing strength in the right lower limb. She had sphincter disturbances with frequency of micturition and dysuria. A month later, she developed a stiff spine with impairment in daily activities. Initial examination (day 0; D0) showed decreased strength in the right lower limb with thigh atrophy and reduced sensations. There was scoliosis (dextroconvexity). MRI (fig 1) revealed enlarged conus medullaris, with hyperintensity on T2. Cerebrospinal fluid (CSF; sub-occipital puncture) showed lymphocytic meningitis. Serologic immunofluorescence revealed a Bartonella henselae (BH) IgG titre of 1/1024; IgM was 1/128. Interrogation revealed cat exposure. Ofloxacin 30 mg/kg/day and rifampicin 20 mg/kg/day were given for six weeks. Recovery in general state and usual activities started a few days after treatment initiation. Improvement of scoliosis followed. All motor, sphincter, and sensory disturbances gradually recovered over one month.

Figure 1

 Sagittal MRI of the spine. T1 weighted images: (A) without, and (B) with contrast, showing meningeal enhancement of the roots and the conus medullaris.

On D60, full spine x ray, T1 and T2 weighted spinal cord MRI, and CSF normalised. BH serology showed a negative IgM, and IgG was at 1/512. At the last assessment (D90), clinical examination was normal.


CSD is a self limited infection. Neurological involvement is rare; full recovery in these cases has been reported but may take several months. In these neurological forms, antibiotics were suggested to accelerate resolution. In our patient, combined antibiotic therapy resulted in dramatic improvement, supporting such a therapeutic approach.

The spectrum of infiltrative or space occupying lesions of the central nervous system (CNS) is wide and includes infectious/parasitic conditions (such as mycobacterial infection, angiostrongylosis, and schistosomiasis), inflammatory, vascular, and metabolic diseases (“pseudotumoral” acute disseminated encephalomyelitis, sarcoidosis, Langerhans histiocytosis, GM2 gangliosidosis, and venous infarcts).1–4 CSD related CNS infective/inflammatory conditions have therefore to be added to this spectrum of infiltrative pathologies and should be carefully excluded before resorting to an invasive technique such as CNS biopsy.