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We report a patient with a relapsing form of the acute sensory neuropathy syndrome associated with IgM-K type monoclonal gammopathy of undetermined significance. He rapidly developed marked sensory ataxia without weakness following an upper respiratory tract infection at age 44. The symptoms reached their maximum in a few days, followed by subsequent gradual improvement over a few weeks. However, unsteady gait remained as a chronic deficit. Stepwise progression of his symptoms occurred over 15 years with 10 similar relapses. Sensory nerve conduction studies showed the absence of action potentials, and sural nerve biopsy revealed the marked loss of large myelinated fibers. The patient's serum had an extremely high titer of an IgM monoclonal antibody directed against gangliosides GD2, GD1b, GT1b, and GQ1b.

We performed HLA typing for class I antigens on five Japanese patients with acute polyneuropathy following Campylobacter infection, all of whom showed axonopathy causing pure motor dysfunction associated with IgG anti-GM1 antibodies. We demonstrated a statistically significant association between the disease and the HLA-B35 antigen.

We report a 26-year-old woman with Creutzfeldt-Jakob disease (CJD) who had received cadaveric dural material 33 months before the onset of neurologic symptoms. This is the fourth case in which a dural graft was the putative source of the CJD agent. All four cases had the grafting before changes in the sterilization procedure adopted in 1987 to inactivate the CJD agent.

We tried to detect HTLV-I-related sequences in Japanese patients with multiple sclerosis with a highly sensitive method that employs the polymerase chain reaction (PCR) of genomic DNA followed by Southern blot hybridization analysis. To amplify HTLV-I sequences, we used primers for LTR, pol, gag, and env coding regions. Fourteen patients with definite MS, 14 disease controls, 12 normal controls, and 3 patients with HTLV-I-associated myelopathy (HAM) were investigated. Results of particle aggregation assay for HTLV-I antibodies were negative in serum from all subjects except for the 3 HAM patients. Neither the 14 MS patients nor the 26 controls showed the presence of any highly homologous sequences to HTLV-I. We did observe faint signals for gag, pol, and env coding regions only at low stringent hybridization in some MS patients as well as some normal controls. The nucleotide sequence analysis of the faint bands was more homologous to major histocompatibility complex molecules than the HTLV-I genome.