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.

Certain motor findings are so classic that they are almost diagnostic. For example, consider a patient with an upper (with or without middle trunk) brachial plexus injury (i.e., Erb’s palsy). The typical waiter’s tip posture is apparent, with the shoulder internally rotated and held tight against the body (the deltoid and supraspinator muscles are nonfunctional), the elbow extended (the biceps and other elbow flexors are paralyzed), the forearm pronated with the hand facing backward (supination is weak), and the palm up. Another example is a humeral-level radial nerve injury that produces a typical wristdrop and fingerdrop when the patient holds the arms outstretched in front of the body. Ulnar clawhand (hyperextension of the metacarpophalangeal joints with passive flexion of the proximal and distal interphalangeal joints secondary to a tenodesis effect) with concurrent first dorsal interosseous atrophy is another example in which a finding on inspection can quickly lead to the correct diagnosis, which is subsequently confirmed with an adequate neuromuscular examination.

Orthopedic Assessment

Orthopedic assessment remains an important, albeit often forgotten part of the neuromuscular examination. After initial inspection of the patient, the affected limb and joints should be palpated and tested for both passive and active range of motion. Mechanical joint pain or stiffness during movement should be noted and may alert the clinician to a non-neurological cause of or contribution to the patient’s inability to move (e.g., fracture pseudarthrosis, joint dislocation). Long bones should be palpated and provocative joint testing may be performed. Examples include the empty can test for rotator cuff injury and Patrick’s test for hip joint abnormalities. In the empty can test, patients hold their arms at 90 degrees in front of them, internally rotated as though emptying two cans; shoulder pain during resisted pressure downward indicates joint or rotator cuff pathology. For the Patrick test, the hip and knee are flexed and the ankle is placed on the contralateral knee. The ipsilateral knee is gently pushed downward. Ipsilateral hip pain occurs in the presence of hip disease (e.g., trochanteric bursitis) but not radiculopathy. In most patients, plain radiographs of the affected joints should be performed during the initial diagnostic evaluation to exclude osseous injuries (e.g., clavicular pseudarthrosis compressing the brachial plexus), congenital bony abnormalities (e.g., supracondylar spur in patients with median nerve palsies), or degenerative bone spurs (e.g., causing compression of the ulnar nerve in the retrocondylar groove). When a significant musculoskeletal abnormality is suspected, referral to an orthopedic colleague may be advisable.

Motor Examination

Motor testing is perhaps the most objective and reproducible aspect of the neuromuscular examination. Adhering to the principles outlined earlier, the examiner compares the involved and the normal extremity with respect to bulk, tone, and strength. As indicated, each individual muscle is tested. Strength is rated with the British Medical Research Council system (Table 231-1) or the Louisiana State University Health Sciences Center system.³ The scope of this chapter does not allow detailed analysis of the key steps in testing each and every muscle, which may be reviewed elsewhere.^1–4

TABLE 231-1 Motor Function Grading Scale of the British Medical Research Council

It is important to thoroughly test all muscles when the diagnosis remains uncertain. However, as the lesion becomes better localized, a more focused motor examination can be used to isolate the lesion to a single nerve or even to a segment of a nerve. This is accomplished by testing sequential muscles innervated by the nerve in question, as well as by confirming normal findings in a nearby nerve. Complicated injuries to the brachial plexus and lumbosacral plexus often require a comprehensive strength assessment of all regional muscles to provide the best localization.

When testing a muscle, it is important to both inspect movement and palpate the muscle being examined. This allows detection of even trace contractions that may not even result in movement. Paretic muscles need to be tested both without and with the aid of gravity. To eliminate gravity, special maneuvers may need to be undertaken. For example, having the patient supine while testing for lateral abduction of the shoulder will eliminate gravity when testing the supraspinatus and deltoid muscles. Similarly, supine patients can rest their arm on the chest wall and then be asked to flex the hand toward their head, thus allowing the elbow flexors to contract with the effects of gravity minimized. Variable strength over a reduced range of motion is common when patients have partially recovered. This should be accurately documented.

Muscle atrophy is often usually obvious during visual inspection of the patient. The muscles and compartments affected should be noted. When possible, accurate assessment of muscle bulk with a tape measure should be performed. In doing so, one should first mark the extremity from a fixed bony landmark so that comparable areas are being examined on the affected and unaffected limb during serial examinations.

An appreciation of hand function and deficits after upper extremity nerve injuries is especially important⁸ (Fig. 231-2). For example, a patient with an anterior interosseous nerve palsy fails to make an “O” when the tip of the thumb and index finger are brought in apposition. Instead, the pulp of the distal ends of the fingers touch because the flexor pollicis longus and flexor digitorum profundus to the index finger are weak. The previously mentioned ulnar clawhand occurs when the patient is asked to actively open the hand and is a hallmark of ulnar nerve injury. Conversely, median nerve injury produces a “Benedictine hand” in which the first two or three digits fail to properly flex when the patient is instructed to make a fist. Finally, a simian hand occurs when there is clawing of all the digits as a result of injury to both the median and ulnar nerves (or medial cord/lower trunk).

FIGURE 231-2 Nerve palsies affecting the hand. A, Anterior interosseous nerve palsy with an inability to appose the tips of the thumb and index finger (arrowheads). B, This patient has a left-sided ulnar clawhand. Atrophy of the adductor pollicis is also evident (arrow). C, This patient has a complete median nerve palsy preventing him from fully flexing his thumb and index finger (i.e., a Benedictine sign) when he attempts to make a tight fist. D, A left-sided simian hand is present as a result of a lower trunk injury affecting both the median and ulnar nerves.

Even classic neurological findings, such as those mentioned earlier, still require careful examination to localize the lesion. Consider unilateral footdrop. An upper motoneuron lesion affecting the pyramidal tract, a cord lesion affecting the L5 motoneuron pool, a spinal lesion interfering with L5 outflow, and peripheral lesions affecting the L5 nerve root, lumbosacral trunk, peroneal division of the sciatic nerve, and the peroneal nerve itself may all result in footdrop. Careful examination of the limb for increased reflexes and tone will help distinguish upper from lower motoneuron pathology. Further examination of L5-innervated muscles, such as the gluteus medius and posterior tibialis (ankle inversion), will help distinguish radicular and more proximal lumbosacral plexus lesions from distal sciatic or peroneal palsy. Furthermore, assessment of the short head of the biceps femoris (innervated by the peroneal division of the sciatic nerve above the knee) may help distinguish a peroneal division lesion from the more typical peroneal nerve entrapment at the fibular head. The exercises just discussed demonstrate that with an understanding of anatomy and a systematic examination technique, the clinician can often localize the lesion with the use of straightforward clinical findings.

Sensibility Testing

The sensory examination includes testing for light touch, pinprick, two-point discrimination, vibration sense, temperature sense, and proprioception.^10,11 A common feature of a complete peripheral nerve injury is the loss of all modalities of sensation in the distribution of the nerve. With incomplete or partial injuries, however, some modalities may be affected more so than others. Nerve entrapment syndromes are an example in which modalities of discriminative touch, which reflect receptor density, may be affected more than others. Thus, in these patients the loss of moving two-point discrimination may occur before the loss of other sensory modalities.¹²

To obtain a rapid estimation of the region of sensory loss, patients are instructed close their eyes and point to areas that are stimulated with a blunt object such as a dull pen tip. This simple technique allows the clinician to map the area of poor or absent sensation. Having the patient compare simultaneous stimulation (either in the contralateral limb or in a normal region of the affected limb) can allow a more subtle loss of sensation to be discerned. Attempts to validate a simultaneous sensory testing paradigm with a 10-point analog scale have been reported.¹¹ A more thorough sensory examination can be done with the most rudimentary instruments, such as a safety pin, cotton wool, a 128-Hz tuning fork (for both vibration and temperature sense), and either paper clips, blunt-tipped calipers, or a commercially calibrated device for two-point discrimination.

The exact distribution of sensory loss is important to document. A glove or stocking distribution of sensory loss would be compatible with a systemic, nonfocal neuropathy. Patterns of sensory loss may help discriminate between radiculopathies and focal peripheral neuropathies, with the latter characteristically having a more demarcated pattern of sensory loss limited to a single peripheral nerve territory (e.g., the splitting of sensory loss in the ring finger with an ulnar nerve lesion).

An important sensibility testing principle for peripheral nerve injuries is to examine autonomous zones of cutaneous innervation where there is the least likelihood of overlap from adjacent nerves. The standard autonomous zone for the ulnar nerve is the volar aspect beyond the distal interphalangeal joint of the fifth digit, and for the median nerve, it is the volar aspect beyond the distal interphalangeal joint of the index finger. One should understand that although the anatomic snuffbox is considered the autonomous sensory distribution of the radial nerve, there might be overlap from other cutaneous nerves such as the lateral antebrachial cutaneous nerve. Indeed, after a radial nerve injury, the patient may not even have loss of sensation because of this redundancy. Hence, as a general rule, one should not use the lack of sensory abnormality as proof of a complete peripheral nerve injury being absent. For example, patients with complete axillary nerve palsies often initially have a zone of numbness along the lateral aspect of the upper part of the arm. Over time, however, the numbness either decreases or completely resolves despite a lack of motor reinnervation to the deltoid muscle (i.e., an ongoing, severe axillary nerve palsy).

Sensory loss may be graded from 5 (normal or nearly normal sensation) to 0 (insensate), and such grading is used to provide a baseline for follow-up sensory examinations (Table 231-2). As with motor function, grading of sensation is important for documenting subsequent improvement or worsening, as well as to provide a standard for comparison of treatment outcomes.

TABLE 231-2 Sensibility Grading Scale

Autonomic Testing

Most sympathetic abnormalities secondary to peripheral nerve injury are assessed during the initial visual inspection of the limb. Vasomotor, sudomotor, and dystrophic changes are documented in comparison to a normal, control limb. Sweating on the volar surface of the hand may be evaluated by focusing on the skin with an ophthalmoscope. Small beads of sweat should be present with normal sympathetic function. Alternatively, a heavy metal spoon can be passed along the skin; if it passes easily, sweating is probably absent. Both allodynia (pain from nonpainful stimulation) and hyperalgesia (painful stimulus appearing more painful than expected) should be evaluated with light touch, pinprick, and a cold tuning fork. The temperature of the affected limb should be compared with that of the normal limb, either subjectively or with a surface thermometer. When indicated (e.g., brachial plexus injury), a pupillary examination in dim light (to exclude Horner’s syndrome) should be performed.

A deceivingly simple bedside test may be performed on either the hands or feet to confirm an autonomic dysfunction. With absent sympathetics in the affected limb, wrinkling of the skin does not occur after soaking the hand or foot. To perform this test, both hands are placed in warm water (about 40°C) for 20 minutes. After removal of the hands, any wrinkling present is identified. Our current understanding of the pathophysiology behind this curious finding is poor. A lack of wrinkling (a positive test indicating nerve injury) is due either to relative vasodilation in the sympathetically denervated hand causing increased skin turgor or poor patency of sweat tubules causing a reduction in normal tubular flow during immersion.

Other Clinical Tests

Myotatic (tendon) reflexes are sensitive indicators of peripheral nerve pathology. For example, it is not uncommon to find loss or diminution of the ankle reflex in patients with buttock or mid–thigh-level sciatic nerve injuries who have complete peroneal division involvement clinically but no other objective abnormality (except the absent ankle reflex) with respect to the posterior tibial division. Furthermore, once lost, myotatic reflexes often do not return, even after the return of sensation and muscle strength.

An injured nerve often exhibits overlying mechanical hypersensitivity. Evoking a shock-like electrical sensation or paresthesias along the nerve’s distribution by percussing over the injured segment is called a Hoffman-Tinel sign.¹³ This sign is frequently found over the nerve in an area of entrapment and can remain present for a long period, sometimes indefinitely. When a Hoffman-Tinel sign is found to be advancing along the anatomic distribution of the nerve, particularly if it does so at the expected rate of nerve regeneration, approximately 1 mm/day or 1 inch/mo, this provides evidence of ongoing regeneration. Even though an advancing Hoffman-Tinel sign may be a positive indicator of regeneration, it is associated with subsequent muscle reinnervation and functional recovery in only approximately half of patients. In contrast, the lack of an advancing Hoffman-Tinel sign may be a strong negative finding suggesting complete neural interruption or poor regeneration.³

Additional provocative maneuvers may be used to instigate transient symptoms (usually paresthesias) from nerve entrapment. For instance, a Phalen test (passive flexion of the wrist for 1 minute causing paresthesias in the median nerve distribution) helps confirm the diagnosis of carpal tunnel syndrome.¹⁴ Conversely, many tests for thoracic outlet syndrome, such as the modified Adson, Roos, and others, have not been validated and have questionable significance.¹⁵

In patients with nerve sheath tumors, a careful history plus physical examination of the skin for stigmata of neurofibromatosis is important.¹⁶ With regard to the lesion itself, if it is palpable, mobility of the tumor with respect to the underlying nerve is sought. Specifically, nerve sheath tumors are generally mobile in a side-to-side manner but not along the nerve trajectory. Tapping on the tumor causes a positive Hoffman-Tinel sign, which helps confirm its parent nerve of origin. In fact, it remains good clinical practice to palpate the complete length of any peripheral nerve affected by entrapment or idiopathic palsy to exclude a nerve sheath tumor. Imaging is required for the evaluation of any mass lesions affecting a peripheral nerve.