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.[1] 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.[2]
Only a few case studies have ever been reported,[3] and even of Wartenbergs 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.[4]
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While the actual cause of this polyneuropathy remains unknown, most research now puts this as an immune-mediated, chronic, asymmetric polyneuropathy.[5][6] Stress may also be a contributory factor.
This condition also causes demyelination caused by an error in the actual enzyme that creates immunoglobulin (needs citation or evidence?)
Positive Tinel's sign is often present.[7] Any cutaneous sensory nerve can be involved with patients usually showing a slow start, building up to sensations in many parts of the body.[8] 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.[7]
Mean onset age, 35 years with a range of 4th and 5th decades.[9]
Pure sensory mononeuritis multiplex
Course: Episodic; Recurrent Some sensory loss improves, Other is permanent
Sensory loss: Discrete areas: Involvement of individual cutaneous nerves Sudden onset Distribution: Legs; Arms; Trunk; Face
Pain: In areas of sensory loss Painful dysesthesias: Induced by limb stretch or movement
Electrodiagnostic: Multifocal axon loss Pathology: Biopsy of affected nerve Perineurial scarring Chronic inflammation Axonal loss & regeneration: Differential fascicular involvement Endoneurial edema Immunoglobulin deposition
Due to the unknown cause of this condition, treatment seems to be symptomatic and individual to the patient. Steroid treatments such as prednisone don't seem to work[6] but there is anecdotal evidence for the use of amitriptyline, and either pregabalin or gabapentin[10] along with a variety of painkillers. This is often treated similarly to diabetic neuropathic pain, but diabetes is not necessarily present.
Some sufferers have responded well to the drug lyrica, which is a common name for the pregabalin referred to above, but others report side effects.
WMSN is not to be confused with Wartenberg's syndrome - a radial sensory nerve entrapment causing significant pain in the lower 1/3 of the forearm.[11]