Wartenberg's migratory sensory neuropathy (also known as Wartenberg's migrant sensory neuritis) (WMSN) is a rare condition identified by Robert Wartenberg in 1958 which is easy to confuse with the early stages of multiple sclerosis or Guillain–Barré syndrome. However this is a benign relapsing and remitting condition in which pain and subsequent loss of sensation in the distribution of individual cutaneous nerves is induced by movement of the limbs inducing stretch. The movements may be very small, and the periods of pain, dysaesthesia, and numbness can vary from almost instantaneous to chronic. In some cases, reports discount WMSN as a diagnosis where there is less prominent pain. Wartenberg’s sensory neuritis is a distinct, exclusively sensory, neuropathy, marked by pain preceding numbness in affected nerves. An episode of stretching preceding pain is not necessary for the diagnosis. Wartenberg’s sensory neuritis often retains its spotty, exclusively sensory characteristics after long term follow-up.
Only a few case studies have ever been reported, and even of Wartenberg's own patients only 2 of the 9 conform strictly to his own description of the clinical characteristics; however there are a couple of surprising case clusters of this condition in both the Thames Valley and San Francisco. The limited number of published clinical studies seems to suggest that it is a rare disorder. Most studies included few patients and were retrospective.
Positive Tinel's sign is often present. Any cutaneous sensory nerve can be involved with patients usually showing a slow start, building up to sensations in many parts of the body. At times, the focal nerve lesions can be painful. Most symptoms resolve but permanent sensory loss can persist. Electrodiagnostic studies demonstrate axon loss in the distribution of the involved cutaneous nerves [1]. Patients sometimes described a sensation of electric discharge when elongating nerve trunks. In half of the cases the attacks of dysesthesia or of sensory loss followed one another within less than one year. The deficits were fully reversible in a third of the cases studied by Rev Neurol (Paris) after a mean total evolution of 4 to 8 years.