Wartenberg Migratory Sensory Neuritis: A Case Report

Abstract

Migratory sensory neuropathy, also known as Wartenberg sensory neuritis, is a rare pure sensory mononeuropathy characterized by sudden sensory loss and numbness of individual cutaneous nerves induced by stretch or trauma. Multiple sensory nerves can be affected sequentially or at the same time and are typically preceded by a painful burning sensation. Herein, we report a case of a healthy male patient who presented with the acute onset of painful sensory mononeuropathy following the excision of a non-invasive skin cancer to the foot. The patient’s symptoms developed 1 week following the operation and resolved over 3 months. Investigation revealed no primary pathology or underlying systemic disease.

Introduction

Wartenberg neuritis is a pure sensory mononeuropathy characterized by sudden sensory loss and numbness of cutaneous nerves induced by stretch or trauma. Since its original description in 1958 by Wartenberg et al, ¹ very few cases have been reported ^{2 –12} supporting it being a rare disorder. Previously described cases describe a relapsing and remitting benign condition provoked by a specific event and followed by a period of painful paresthesias. While any cutaneous nerves can be affected, it is most common in the nerves of the upper and lower extremities and is precipitating by movements including repeated lifting, ² kneeling, passive stretching or everyday activities such as pointing the foot or turning a handle. ³ If the initiating offence is stopped immediately upon the onset of pain, symptoms can be avoided, however repeated offence leads to a gradual loss in sensation of the cutaneous nerves with no effect on motor function. Recovery is gradual, with complete resolution of symptoms usually occurring in approximately 6 weeks; however, persistent sensory deficits have been reported. ³

Wartenberg neuritis remains a clinical diagnosis. The diagnostic criteria for small fiber neuropathies in general are not well defined, and to date, there is no gold standard for clinical practice and research. ¹³ At presentation, patients are typically 40 to 50 years old and are generally healthy with no systemic manifestations, however, diabetes, vascular disease, ³ and an association with AIDS have been reported in the literature. ^2,5 Depending on the time of presentation, patients might describe a spectrum of sensory disturbances, ranging from paresthesias, hypoaesthesias, numbness, sharp shooting electric pains, and complete loss of touch. Patients are usually well aware of the relationship to movement, frequently describing distinct motions that must be avoided to prevent the onset, or progression of symptoms. Some explicitly describe an association with stretch, complaining that the nerve feels too tight. ³ On physical examination, mental status, motor and cranial nerve function, and deep tendon reflexes remain normal. ² A positive Tinel’s sign may or may not be present at the site of symptoms. Partial loss of touch can be appreciated upon evaluation of pin-prick sensation.

Laboratory investigations are largely non-contributory; however, a mild elevation in immunoglobulin M level, ² non-quantifiable immunoglobin G (IgG) paraproteinemia, and a marginally elevated angiotensin-converting enzyme level ⁴ have been reported. Electrophysiological studies typically portray the sensory abnormality via an abnormal, low amplitude sensory nerve action potential. Nerve biopsies have shown Wallerian degeneration, consistent with ischemic pathology and perineural inflammatory changes with IgG deposition consistent vasculitic neuropathy. ^4,2 Some studies also point to abnormal narrowing of the perineurial tube and anchoring of the nerve fibers to their connective tissue coverings as possible mechanisms as well. ³

Herein, we report a case of Wartenberg migrant sensory neuritis following a minor surgical excision. The purpose of this description is to contribute to the clinical presentation and underlying pathophysiology of this benign and poorly understood condition.

Case Presentation

The patient is a 68-year-old, otherwise healthy gentleman who had a biopsy proven basal cell carcinoma (BCC) on the dorsal lateral aspect of his left foot. Before the definitive excision, he had no symptoms around this area that would suggest any nerve irritation.

The BCC was excised under local anesthetic with a 4-mm margin and closed as an ellipse without complication. This was a full thickness excision of the skin and did not involve any deeper dissection to the level of the dorsal sensory nerves. Post-operatively he did well; however, 1 week following the excision, he developed hypersensitivity on the dorsal-lateral aspect of the foot with a positive Tinel’s sign. The incision was well approximated with no erythema or warmth. The Tinel’s was lateral to the incision and radiated to the dorsal aspect of the 4th and 5th toes. Light touch sensation in the area was present, however, sensitive. Interestingly, the patient had previously been diagnosed with Wartenberg migrant sensory neuritis after a past excision under local anesthetic which presented similarly. Both of these episodes resolved after several weeks of conservative management without further complications.

Discussion

Wartenberg original case series described a distinct subset of sensory neuropathy which were triggered by stretch or trauma and exclusively involved cutaneous sensory nerves. Unlike previously documented cases of sensory neuropathy which resulted as a consequence of infectious, inflammatory, toxin-mediated, and systemic conditions, Wartenberg definition was unique in that it described abrupt sensory loss as a result of relatively unremarkable movements or injury.

A select number of cases of migratory sensory neuritis have since been documented, illustrating a discrete clinical entity defined by the abrupt onset of pain and sensory loss along discrete cutaneous nerve distributions following an instigating trigger. To date, only 26 cases have been reported in line with Wartenberg original definition.

While the clinical entity is well established, diagnostic criteria remain far less understood. Conflicting laboratory and histopathological data demonstrate that Wartenberg sensory neuritis strictly remains a clinical diagnosis with various hypothesized etiologies. Laboratory findings and nerve biopsy alone in the absence of typical clinical features are therefore insufficient for a diagnosis. Nerve conductions studies may support the diagnosis, however, are not essential.

The present case adds to the paucity of cases describing migratory sensory neuritis and demonstrates that clinical presentation, as apposed to histopathologic or electrodiagnostic findings, is the mainstay for diagnosing a condition whose treatment is almost exclusively conservative in nature. Consistent with previous reports, we find that a history revealing the sudden onset of pain and numbness in a discrete sensory distribution following stretch or trauma is sufficient for supporting the diagnosis of Wartenberg migratory sensory neuritis. Future work is required to further explore this poorly understood disease and perhaps expand current diagnostic criteria. As it stands, Wartenberg migratory neuritis remains purely a clinical entity.