Pain

Pain is a frequent complaint after peripheral nerve damage, and its cause may be multifactorial.⁵ The location, quality (e.g., burning, paresthetic, crushing), exacerbating/relieving maneuvers, and any response to medication should be sought.

Both neuropathic and non-neuropathic types of pain may occur after nerve injury or entrapment. One common source of non-neuropathic pain is disuse-related swelling, joint stiffness, and shortening and fibrosis of muscles and tendons. Such pain may occur when affected limbs are immobilized or not adequately mobilized. Moreover, muscle paralysis causes alterations in joint stability and dynamics, thereby predisposing the patient to arthropathy and pain from pathologic strain (e.g., patients with sciatic or peroneal nerve injury often have lower back or hip pain secondary to their asymmetric gait). Autonomic disturbance may also cause significant pain in these patients and is a hallmark of both type I (reflex sympathetic dystrophy) and type II (causalgia) complex regional pain syndrome (CRPS).⁶ CRPS type I usually occurs after a minor injury to the extremity (e.g., sprained ankle), whereas CRPS type II occurs after significant damage to a major mixed nerve (e.g., gunshot wound). Severe burning pain, careful attempts to protect the involved extremity from movement or manipulation, and evidence of autonomic overactivity are cardinal features of CRPS. Another type of pain that may occur with nerve injury is avulsion pain (i.e., deafferentation pain), which is a result of nerve root avulsion from the spinal cord. Avulsion pain is usually manifested as a constant burning or crushing pain that is poorly responsive to any intervention short of dorsal root entry zone ablation.⁷ Regenerating nerves may also produce pain, which is often described as tingling, electric shocks, and dysesthesias along the course of the nerve. Injured nerves, especially small cutaneous branches, demonstrate a profound capacity to regenerate. When they extend into a scar or superficial area, painful neuromas may form. Patients with neuromas usually describe localized pain with a trigger point overlying an often palpable, exquisitely tender subcutaneous lesion. A diagnostic trigger point injection of lidocaine or bupivacaine near the neuroma can frequently confirm this diagnosis.

With peripheral nerve entrapment, pain is often referred adjacent to and along the distribution of the compressed nerve. For example, the description of aching discomfort in the wrist and forearm, along with nocturnal symptoms, including paresthesias in the median nerve distribution, is so characteristic that it is virtually diagnostic of carpal tunnel syndrome. Pain and tenderness may also be present at the entrapment site (e.g., near the retrocondylar groove with ulnar nerve entrapment at the elbow). When peripheral nerves that do not contain cutaneous sensory afferents are compressed, numbness and paresthesias do not occur, but frequently a deep aching pain is felt not only at the point of entrapment but also within any joints from which the entrapped nerve carries proprioceptive sensation (e.g., shoulder pain during the early stages of suprascapular entrapment). Along with pain, significant damage to a motor-sensory nerve also produces concomitant sensory abnormalities, including paresthesias, hypoesthesias, and hyperesthesias, characteristically in a well-defined region that represents the nerve’s sensory territory.⁸ Quantitative sensory testing may reveal either an increase (hyperesthesia) or a decrease (hypoesthesia) in response to varying thresholds.⁹ When there is no sensory loss or if it involves more than one peripheral nerve territory, other diagnoses must be considered, including radiculopathy, musculoskeletal injury, nonfocal neuropathies, and CRPS.

Sensory Loss

The precise distribution and alteration of sensation are sought from the patient. Patients may describe their sensory deficit in one or many ways. Any exacerbating or relieving maneuvers should be documented. Any current or past neuropathic processes should be questioned (e.g., stocking-glove diabetic neuropathy). Although patients may not notice subtle sensory loss in the torso, proximal part of limbs, or feet, even small patches of sensory loss on the face or hands are readily described. They may relate a complete loss of sensation (anesthesia) or an alteration, either decreased (hypoesthesia) or increased (hyperesthesia) sensation. Other patients may report dysesthesias or paresthesias, such as tingling, electric shock sensations, or pins and needles. Light touch or other nonpainful stimuli may be perceived as painful (allodynia). Functional consequences may include accidental burning, cutaneous injury, Charcot joints, and even frank ulcer formation. The evolution of the sensory loss is sought, particularly to ascertain whether recovery is occurring.

Motor Deficit

The location and severity of muscle weakness are key features of the history. Most patients describe their deficit in terms of general movements, their impact on activities of daily living, and changes in coordination. For example, a patient with a severe groin-level femoral nerve injury with complete denervation of the quadriceps may simply give the impression that the leg feels weak overall and has a limp. Directing questions on how the patient performs on stairs or getting up from a sitting or squatting position will lead to improved understanding of the nature of the functional deficit. Any consequences on occupational and recreational performance should also be discussed. In a similar manner, further questioning may provide insight into evolution of the deficit. For instance, patients with complete peroneal nerve injuries should be questioned about any dorsiflexion of the toes or foot while supine (i.e., with gravity eliminated), which may suggest recovery.

In certain circumstances, a history from collateral sources is extremely helpful. An obvious scenario is a baby with a plexus injury, in which case information provided by the parents is particularly helpful. Much of this information will simply reflect their day-to-day observations of the baby’s behavior and play activity. Pertinent information related to spontaneous range of movement and the relative strength of various muscle groups should be elicited. Another source of historical information is the patient’s physiotherapist. In addition to providing supervised range-of-movement activities, the therapist will often perform serial examination and documentation of the patient’s strength and movement of various muscle groups. Such a record gives an excellent profile of the evolution of the patient’s condition. The patient’s spouse, coach, supervisor, or relative may also be questioned, as indicated.

Risk Factors

Nerve entrapment may occur as a result of repetitive strain, which is often due to occupational or recreational activities. Therefore, a complete history of any repetitive strain at work or play should be sought. A few examples include carpal tunnel syndrome in jackhammer users, suprascapular nerve entrapment in baseball pitchers/volleyball players, supinator syndrome (i.e., posterior interosseous palsy) in carpenters, peroneal nerve palsy in strawberry pickers (long periods of squatting), and ulnar nerve entrapment or injury at Guyon’s canal in cyclists; the list is extensive. An improvement in symptoms after cessation of the purported cause, with or without bracing, may help confirm the causal relationship.

Numerous medical conditions, some rare, others common, may predispose patients to both spontaneous and occupational nerve entrapment. Occasionally, the initial manifestation of a systemic disease may be a focal nerve palsy, perhaps mimicking nerve entrapment (e.g., lead toxicity causing a focal wristdrop, inflammatory neuritis producing an anterior interosseous nerve palsy, and Lyme disease causing a seventh cranial nerve deficit). Alternatively, some diseases or conditions predispose patients to true nerve entrapment, including diabetes mellitus, pregnancy, renal failure and dialysis, amyloidosis, rheumatoid arthritis, hypothyroidism, acromegaly, hereditary predisposition to pressure palsy, vasculitides, and lipid storage diseases. Other focal pathologic processes that cause nerve entrapment include arthritis, tenosynovitis, osteophytes, previous or acute fractures, ganglion/synovial cysts, aneurysms, and compartment syndrome.

General

The neuromuscular examination remains the cornerstone when evaluating patients for focal peripheral nerve lesions. Full exposure of the affected limb, as well as the contralateral normal limb for use as a reference, is recommended. The examination should be performed in a consistent and reproducible fashion so that findings are not overlooked. Starting from the proximal aspect of the limb, one systematically works distally. When it becomes apparent that a single peripheral nerve is affected, confirmation of normal findings in adjacent motor and sensory nerves is important. With proximal upper extremity nerve palsies, one should always assess the parascapular and shoulder girdle muscles before proceeding more distally to the arm and hand. Once again, it cannot be overemphasized that one should compare the affected with the normal side so that the examination may be sensitive enough to identify subtle palsies in otherwise strong patients. In the lower extremity, the aforementioned principles entail examining both the anterior and posterior aspects of the patient up to and including the gluteal region and hip joint. In assessing muscle strength, an attempt is made to discriminate gross limb movement from specific muscle action because the latter provides more precise localization of lesions. For example, lateral abduction of the shoulder within the first 30 degrees is produced mostly by the supraspinatus, the next 60 degrees is produced by the deltoid (up to about 90 degrees of abduction), and lateral abduction above 90 degrees is then completed by medial rotation of the scapula. If aware of each of these muscle actions, clinicians can direct their examination and attention to assessing the strength and contributions from each of the individual muscles in turn. One must keep in mind, however, that these (and other) cutoff points are variable, with transitions between muscles often being gradual and dynamic. Finally, one needs to be aware of substitutive movements that the patient learns and adapts to overcome deficits. An inexperienced clinician can confuse such adaptations for recovery of muscle function when in fact none has taken place. For example, a patient with a complete deltoid palsy may be able to laterally abduct the shoulder to 90 degrees by using a combination of strong supraspinatus contraction and rotation of the scapula (contraction of the pectoralis and coracobrachialis may also play a role). Careful visualization of shoulder mechanics from above and behind, with concurrent palpation of the deltoid, allows the examiner to make an accurate assessment. Repetitive movement causing fatigue may also make the deficit more evident.

Inspection

The examination always begins with visual assessment of the affected limb or body region in comparison to the normal side. Muscular atrophy, traumatic and surgical scars, swelling, hair loss, perspiration patterns, erythema, and abnormal joint and limb positions are all noted (Fig. 231-1). The muscle atrophy may be profound or subtle, and the examiner must often take a step back and review the gestalt of the patient’s body symmetry. Autonomic nervous system abnormalities may include swelling, hair loss or gain, variability in sweating and vasodilation, and Horner’s syndrome. Previous scars and past operations should be questioned, especially those that may be related to the nerve in question. Protection and favoring of the injured limb are also obvious during inspection and may indicate severe neuropathic pain or CRPS. Baseline photographs may be useful for long-term follow-up and assessment of treatment efficacy.

FIGURE 231-1 Some classic abnormalities on neuromuscular examination. A, Left axillary palsy with deltoid atrophy (arrowhead). B, Right humeral-level radial nerve palsy causing wristdrop and fingerdrop (arrowhead). C, Right sciatic palsy with atrophy of the leg muscles and a flail right foot (arrowhead). Autonomic abnormalities, including erythema, alopecia, and swelling, are present in the right leg.