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feed themselves Autonomic failure was another feature in a few, and one of ours became deaf Extensive examinations for an occult cancer, paraproteinemia, Sjogren disease, Refsum disease, auto immune diseases, and all potential causes of an ataxic neuropathy, proved to be frustratingly negative Of course, it is possible that some patients had an as yet undiscovered tumor Yet other instances have had all the features of a truncal-limb sensory neuropathy, with little or no ataxia and only muted re exes; these have had a more benign course but still no cause was found (why most of our patients have been male physicians, as reported by Romero, is entirely unclear) Illa and colleagues, in a review of 17 patients with idiopathic sensory ataxic neuropathy found antibodies against the ganglioside GD1 in only one case, and concluded that the majority were not due to an immunologic mechanism The motor nerve conduction studies have been normal or slightly impaired, while the sensory potentials were eventually lost (but they may at rst be normal) A puzzling feature in two patients has been an unexpected preservation of many sensory nerve potentials even after a year of illness In these cases the process presumably lay in the dorsal roots rather than in the ganglia In a few instances the MRI has shown a change in the posterior columns of the spinal cord, presumably secondary to root disease The spinal uid has generally contained a slightly elevated protein concentration with few or no cells, up to 18 /mm3 in our cases Pathologic examination of the sensory ganglia in a few cases has exposed an in ammatory process identical to that of Sjogren disease Our attempts at treatment using plasma exchanges, IVIG, corticosteroids, and immunosuppressive agents have been mostly unsuccessful Idiopathic Autonomic Neuropathy Under this term is collected a group of dysautonomias that on extensive evaluation cannot be attributed to diabetes or amyloidosis A fair number, almost half in the series of Suarez and colleagues, are acute in onset and conform to the pure pandysautonomia condition described by Young and colleagues and discussed earlier as a variant of GBS The others, however, pursue a subacute or chronic course and about one quarter of these has an associated serum antibody that is directed against the acetylcholine receptor of sensory ganglia (Klein et al) Orthostatic hypotension is the leading feature and in those with the previously mentioned antibody, pupillary changes and dif culty with accommodation, dry mouth and dry eyes, and gastrointestinal paresis were the most common ndings according to Sandroni and colleagues Perhaps another subgroup is in some way related to Sjogren syndrome since sicca symptoms are prominent but these later features could just as well be a component of the autonomic failure and the appropriate antibodies have been found only rarely There is not enough information to determine if all these cases are accounted for by one process or to judge the effects of various immune treatments Migrant Sensory Neuritis (Wartenberg Syndrome) The de ning feature of this syndrome is a searing and pulling sensation involving a small cutaneous area of a limb evoked by extending or stretching the limb, as happens when reaching for an object with the extended arm and hand, or when kneeling, or pointing with the foot The pain is momentary but leaves in its wake a patch of numbness Cutaneous sensory nerves must be involved in some way and are irritated during such a maneuver Often the area involved is proximal to the most terminal sensory distribution of the nerve, encompassing, for example, a patch on the lateral side of.

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