A previously reported patient presenting sensory‐dominant neuropathy with antiganglioside antibodies, bound preferentially to polysi‐ alogangliosides including GD1b, was autopsied. While axonal degeneration was predominant in the sural nerve, many demyelinated fibers were present in the spinal roots. Dorsal roots had undergone significant damage. These pathological findings were well correlated with the electrophysiological results showing decreased F‐wave conduction velocities and conduction blocks in motor nerves and decreased or absent sensory action potentials in sensory nerves, with distribution of GD1b in nerve tissues such as dorsal root ganglia and paranodal myelin in the ventral and dorsal roots. © 1999 John Wiley & Sons, Inc. Muscle Nerve 22: 1426–1431, 1999

A 77-year-old man presented sensory-dominant neuropathy associated with IgM M-protein reacting with various gangliosides. The M-protein bound to gangliosides with polysialosyl residue, such as GD1b, GD3, GT1b, GT3, GQ1b, and GQ1c. In addition, GD1a, GM3 and LM1, having a terminal monosialosyl epitope, were also recognized. Previously, Ilyas et al. described a similar case in which sensory symptoms were associated with IgM M-protein reacting with gangliosides containing a disialosyl group, such as GD3, GD1b, and GT1b, but not GM3 and GD1a. It is suggested that the reactivity of IgM M-protein with polysialogangliosides may be associated with the pathogenesis of sensory-dominant neuropathy.

No abstract

A patient who had experienced water intoxication despite normal renal function and normal urinary diluting ability was observed during the initiation stage of hyponatremia. Upon the excessive water intake (10 to 15 L) for several days, he developed moderate hyponatremia (121 mEq/L) and headache, an early symptom frequently seen in water intoxication. During this period, his urine was maximally dilute (50 to 60 mOsm/kg H2O), and his urinary sodium excretion increased. This report suggests that 10 to 15 L of water intake for several days can cause water intoxication in subjects with normal urinary diluting ability and that the increase in sodium excretion is prerequisite for the high urine flow rate.