The key diagnostic criterion associated with localized acquired peripheral neuropathy is pain created by irritation of the involved nerve. The pathologic condition may affect the entire nerve trunk, or it may asymmetrically involve only a portion of its diameter. Sensory abnormalities tend to predominate over motor dysfunction, especially in the early phases of entrapment. Pain is usually well localized over the sensory distribution of the involved nerve and typically has the nature of a sharp or burning sensation. Dysesthesia, hypesthesia, and hyperesthesia may also be present.

Pain associated with an entrapped motor component of the nerve is typically less well defined in terms of its distribution. Motor nerve pain takes the form of a dull, aching sensation associated with the muscle and joint innervated by the involved nerve. In the advanced case, severe muscle tenderness may result in disuse atrophy, weakness, dystonia, guarding of the painful extremity, and postural abnormality. Pain caused by peripheral nerve entrapment is usually aggravated by limb motion and patient activity, and it may be severely debilitating. Rest pain is a less frequent finding, and it may mimic peripheral arterial disease without the signs of ischemia.

The actual diagnosis of localized acquired peripheral neuropathy is made after a history and physical examination. The patient may not recall a specific traumatic event to which the onset of signs and symptoms may be attributable, particularly in the presence of underlying metabolic disease. Objective evaluation centers on the sensorimotor examination (54). An altered one- and two-point static and moving touch-pressure threshold distinction over the sensory distribution of the involved nerve is an early finding (55,56 and 57). Usually, if the nerve trunk is not too deeply situated, palpation or percussion of the nerve at the suspected point of irritation can elicit pain and paresthesia. Distal tingling on percussion with or without radiation of pain and paresthesia along the sensory distribution of the nerve, or Tinel’s sign, is usually present from the early stages of localized acquired neuropathy. Valleix sign, or proximal radiation of pain and paresthesia along the neuraxis on percussion at the point of nerve injury, may also be present. Moreover, active or passive manipulation of the extremity may exacerbate symptoms. Manual muscle testing is usually not helpful unless the neuropathy is seriously advanced and muscle pain and atrophy are present. In difficult cases, nerve conduction velocity and electromyographic measurements may be helpful. Conduction velocity is decreased in most cases of nerve entrapment, whereas electromyography is of little use unless nearly complete conduction blockade is present (51). Electrodiagnostic findings should not override one’s clinical assessment, because both nerve conduction velocity and electromyography vary with the patient’s age, skin temperature, and other conditions that may lead to false-negative values. Finally, diagnostic local steroid injection, combined with a local anesthetic agent, may be used as part of the evaluation. The local anesthetic rapidly inhibits impulse conduction, whereas the glucocorticosteroid alleviates both perineural and intraneural inflammation and fibrosis when it is infiltrated around the nerve trunk. Immediate and dramatic resolution of symptoms indicates accurate localization of the nerve trunk lesion. Dramatic relief of symptoms is usually associated with a decrease in the local inflammatory process. Dramatic relief followed by recurrence of symptoms after a period of time points toward deep, diffuse scarring or a permanent anatomical structure as the cause of nerve entrapment.