On the spectrum of leprosy neuropathies: multifocal inflammatory neuropathy heralding leprosy relapse.

We report a 52 year-old woman with a past history of lepromatous leprosy (14 years prior to our first evaluation) who presented with progressive weakness and severe arm/leg pain. CSF analysis revealed elevated protein level with normal cell count. Skin and sural nerve biopsy showed no bacilli. Immunomodulatory treatment led to major improvement on clinical, CSF and electrodiagnostic grounds, but after one year of treatment, skin test revealed leprosy relapse. To our knowledge, this is the first report of a multifocal inflammatory neuropathy heralding leprosy relapse. Extended neurological work-up may be important in unexplained neuropathy progression after leprosy treatment.

Detection of antibodies against phenolic glycolipid-1 (PGL-1), 35-kDa and 30-40-kDa components of Mycobacterium leprae in the cerebrospinal fluid of of leprosy patients.

The involvement of the central nervous system (CNS) in lepromatous leprosy (LL) patients was investigated; 33 patients were examined clinically in detail and upper motor neuron involvement was observed in eight and lower motor neuron in three of these patients. Anti-Mycobacterium leprae antibodies could be detected in the CSF by PGL-1 enzyme-linked immunosorbent assay (ELISA) and monoclonal antibody (MAb) based competitive assays against defined epitopes on the 35-kDa protein and 30-40-kDa polysaccharide (lipoarabinomannan) antigens with MAbs MLO4 and ML34, respectively. Antibodies against PGL-1 and 35-kDa protein were observed in more subjects than antibodies against the 30-40-kDa antigen. Some correlation was observed between the upper motor neuron signs and antibody positivity for 35-kDa and PGL-1 antigens in the CSF of these patients.