Ulnar neuropathy at the elbow

Differential diagnosis
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By Mazen M Dimachkie MD and Aparajitha K Verma MD

Weakness of non-ulnar C8 muscles is the usual clue to disease involving the lower brachial plexus, C8 root, or cervical spinal cord. This finding should, in turn, prompt further examination of the cervical spine and a check for Horner syndrome. Elderly patients, particularly those with dementia, Parkinson disease, and other debilitating illnesses, may have nonspecific atrophy of the hand muscles that should not be mistaken for ulnar neuropathy. An ulnar nerve lesion at the wrist can usually be identified by more significant slowing of nerve conduction across the wrist than across the elbow, a normal dorsal ulnar cutaneous sensory potential, and by lack of denervation in the forearm. A lesion of the deep palmar branch produces a characteristic, but complicated electrodiagnostic picture. True neurogenic thoracic outlet syndrome classically produces ulnar distribution paresthesias and sensory loss accompanied by median distribution weakness and atrophy. Possible diagnoses of amyotrophic lateral sclerosis and syringomyelia can be excluded by identification of sensory nerve abnormality and the finding of denervation restricted to ulnar-innervated muscles. A polyneuropathy presenting as an ulnar nerve lesion can be recognized by identifying generalized abnormalities of nerve conduction. Several neurologic and non-neurologic conditions can produce an abnormal hand posture (pseudoulnar claw) that could be confused with an ulnar griffe (Campbell et al 1995).

Dupuytren contracture is a painless thickening characterized by fibroblastic proliferation and disorderly collagen deposition of tissue beneath the skin on the palm of the hand and fingers. Subsequently, nodules will form due to contraction of fibroblasts in the superficial palmar fascia. The possibility of a T-cell mediated autoimmune disorder as a cause of Dupuytren contracture is suggested by the demonstration of the presence of CD3-positive lymphocytes and the expression of major histocompatibility complex class II proteins along the affected areas. The flexor tendons are not intrinsically involved, but invasion of the dermis occurs, resulting in the characteristic puckering and tethering of the skin. Progressive contracture results in deformity and loss of function of the hand. This disorder is usually observed in white males older than 50 years, and, curiously, it appears to have a pronounced genetic predisposition with up to 68% of male relatives of affected patients developing the disease at some time. Although the treatment of choice is surgery, indications for the timing of surgery exist. In general, operative management should be performed on the affected MCP joint if the contracture is 30 degrees or greater. Usually, a limited fasciectomy of the pretendinous cord is sufficient to establish normal function in the corresponding joint. Techniques for this are also varied. Some favor use of a regional fasciectomy of the pretendinous cord to prevent recurrence. Since its initial description during the sixteenth century, Dupuytren disease has been exhaustively researched. However, controversy corresponding to the exact cause of the disease is ongoing. Future nonoperative therapies may include percutaneous needle fasciotomy, skeletal traction, therapy with calcium channel blockers, and treatment with gamma interferon. The last of these treatments shows the most promise. Until any of these treatments is proven to be therapeutic, surgery is still the only option for a cure.

In This Article

Historical note and nomenclature
Clinical manifestations
Pathogenesis and pathophysiology
Differential diagnosis
Diagnostic workup
Prognosis and complications
References cited