Peripheral Nerve Exam & Focal Neuropathies

The peripheral nervous system is the neurology of the everyday. Carpal tunnel syndrome, ulnar neuropathy at the elbow, peroneal nerve palsy at the fibular head, meralgia paresthetica, diabetic radiculoplexus neuropathy — these are some of the most common neurological consults in general practice. They reward a clinician who knows the peripheral anatomy precisely enough to localize a lesion to a single nerve at a specific location, who can perform the few key provocative maneuvers, and who understands the patterns of length-dependent neuropathy, mononeuropathy multiplex, and the recognized hereditary and acquired neuropathies that complicate the picture.

This page covers the bedside exam of the peripheral nervous system: the major peripheral nerves and their distributions, the provocative tests for the common entrapments, and the clinical patterns of peripheral nerve disease. The point throughout is that peripheral nerve lesions are local — a single nerve at a single anatomical site — and that the bedside exam, properly performed, often makes the diagnosis without imaging or electrodiagnostics.

The Distinction Between Mononeuropathy, Polyneuropathy, and Plexopathy

Before the specifics of any nerve, the bedside question is the pattern of involvement:

  • Mononeuropathy: a single peripheral nerve is affected. The deficit is confined to that nerve’s distribution; muscles innervated by the nerve are weak, the sensory territory is impaired, and reflexes mediated by the nerve are reduced. The lesion is typically at a known anatomical pinch point.
  • Mononeuropathy multiplex: multiple peripheral nerves are affected, in separate territories, often asymmetric and painful. The pattern suggests a process targeting the vasa nervorum or multiple discrete nerves — vasculitis, diabetes, leprosy, HIV, sarcoidosis, hereditary neuropathy with liability to pressure palsies.
  • Polyneuropathy: a symmetric, length-dependent process. Symptoms begin distally (feet) and progress proximally; both sides involved equally. The vast majority of polyneuropathies fit this length-dependent pattern.
  • Plexopathy: a lesion at the brachial or lumbosacral plexus produces deficits that span multiple peripheral nerves and multiple root distributions in a single body region (arm or leg). The pattern is wider than a single nerve or single root.
  • Radiculopathy: deficits in a dermatomal pattern from a single nerve root.

Major Peripheral Nerves of the Upper Extremity

Median Nerve

The median nerve carries fibers from C5-T1 roots, providing motor supply to most of the forearm flexors, the lateral two lumbricals, and the thenar muscles (abductor pollicis brevis, opponens pollicis, superficial head of flexor pollicis brevis). Sensory supply is the palmar surface of the thumb, index, middle, and lateral half of the ring finger, and the corresponding dorsum of the distal phalanges.

The two important sites of median nerve compression:

  • Carpal tunnel (at the wrist): the most common entrapment neuropathy. Compression of the median nerve as it passes through the carpal tunnel beneath the flexor retinaculum. Sensory symptoms (numbness, tingling) in the thumb, index, middle, and lateral ring finger, often worse at night, often awakening the patient. The patient may shake the hand to relieve the symptoms (the “flick sign”). With chronic compression, thenar atrophy develops, with weakness of thumb abduction (abductor pollicis brevis). Provocative tests:
    • Tinel sign at the wrist: tapping over the median nerve at the wrist produces tingling in the median distribution.
    • Phalen test: maximal wrist flexion for thirty to sixty seconds produces symptoms.
    • Reverse Phalen: extending the wrist produces symptoms.
    • Carpal compression test: applying pressure directly over the carpal tunnel for thirty seconds produces symptoms (often the most sensitive bedside test).
  • Anterior interosseous syndrome: a pure motor branch of the median nerve that supplies the flexor pollicis longus, the lateral half of the flexor digitorum profundus (to the index and middle fingers), and the pronator quadratus. Compression in the forearm produces weakness of flexion of the distal interphalangeal joints of the index and middle fingers and of the thumb’s interphalangeal joint. The patient cannot make an “OK” sign — the thumb and index finger pinch is replaced by a clumsy circle. No sensory loss.
  • Pronator syndrome: compression in the proximal forearm, between the heads of the pronator teres. Produces median sensory and motor symptoms similar to carpal tunnel, but with forearm pain and tenderness over the pronator teres, and with involvement of the more proximal median-supplied muscles (flexor carpi radialis, palmaris longus, flexor digitorum superficialis).

Ulnar Nerve

The ulnar nerve carries fibers from C8-T1, providing motor supply to most of the intrinsic hand muscles (the hypothenar muscles, the interossei, the medial two lumbricals, the adductor pollicis, the deep head of flexor pollicis brevis). In the forearm it supplies flexor carpi ulnaris and the medial half of the flexor digitorum profundus. Sensory supply is the little finger, medial half of the ring finger, and the medial palm and dorsum of the hand.

The two important entrapment sites:

  • Cubital tunnel (at the elbow): the most common ulnar nerve entrapment. The nerve passes behind the medial epicondyle in a shallow groove and through the cubital tunnel between the heads of the flexor carpi ulnaris. Compression produces sensory symptoms in the little finger and medial half of the ring finger, with weakness of intrinsic hand muscles and (in severe cases) atrophy. Specific findings:
    • Tinel sign at the elbow: tapping behind the medial epicondyle produces tingling in the ulnar distribution.
    • Elbow flexion test: holding the elbow in maximal flexion for one minute reproduces symptoms.
    • Wasting of the first dorsal interosseous: visible as a hollow on the dorsum of the hand between the thumb and index finger.
    • Froment sign: the patient grips a piece of paper between thumb and index finger; with ulnar weakness, the thumb’s interphalangeal joint flexes (using flexor pollicis longus, supplied by median, to substitute for the weak adductor pollicis).
    • Wartenberg sign: the little finger drifts into abduction at rest because of unopposed action of the extensor digiti minimi (supplied by radial nerve).
  • Ulnar tunnel at the wrist (Guyon canal): less common. Produces pure motor weakness if only the deep branch is affected, or sensorimotor symptoms if the superficial branch is also involved. Spares the dorsal sensory branch (which leaves the nerve proximal to the wrist), so the dorsum of the medial hand has preserved sensation — a useful localizing point.

Radial Nerve

The radial nerve carries fibers from C5-C8 (and T1), supplying the extensor muscles of the elbow, wrist, and fingers. Sensory supply is the dorsum of the hand on the radial side, including the dorsum of the thumb, index, middle, and lateral half of the ring finger (proximal phalanges).

Common sites of injury:

  • Spiral groove of the humerus: the radial nerve runs along the back of the humerus in the spiral groove, where it is vulnerable to compression. The classical injury is “Saturday night palsy” — compression during sleep with the arm draped over a chair or another object. Wrist drop results, with sensory loss on the dorsum of the hand (radial side). Triceps function is spared because the branches to triceps leave the nerve above the spiral groove.
  • Axilla (“crutch palsy”): compression of the radial nerve in the axilla produces weakness including triceps (whereas spiral groove injury spares triceps), plus wrist drop and sensory loss.
  • Posterior interosseous nerve syndrome: compression in the supinator muscle. Pure motor; weakness of finger extension at the MCP joints, often with relative preservation of wrist extension (which is partly supplied by branches leaving the nerve proximal to the supinator). The patient cannot extend the fingers at the knuckles but the wrist may still extend (drifting radially because of weak ulnar wrist extensors).
  • Radial tunnel syndrome: pain over the proximal forearm without significant weakness; controversial entity.

Brachial Plexus

The brachial plexus is formed by the ventral rami of C5-T1 and arranged into trunks (upper, middle, lower), divisions (anterior, posterior), cords (lateral, posterior, medial), and finally peripheral nerves. Lesions can be at any level. Common patterns:

  • Upper trunk (C5-C6) lesion (Erb palsy): from trauma (the classical obstetric injury, or motorcycle accident with shoulder depression). Weakness of shoulder abduction, elbow flexion, supination, and external rotation of the shoulder. The arm hangs in the “waiter’s tip” position. Sensory loss in the lateral arm and forearm.
  • Lower trunk (C8-T1) lesion (Klumpke palsy): from traction on an abducted arm. Weakness of the intrinsic hand muscles and finger flexors. Sensory loss in the medial forearm and ulnar side of the hand. T1 involvement may produce ipsilateral Horner syndrome.
  • Pancoast tumor: superior sulcus lung cancer invading the lower brachial plexus. Combines lower trunk plexopathy with ipsilateral Horner syndrome from sympathetic chain involvement.
  • Neuralgic amyotrophy (Parsonage-Turner syndrome): idiopathic, often after immunization, surgery, or infection. Sudden severe shoulder pain followed by patchy weakness in a brachial plexus distribution, often involving long thoracic nerve (serratus anterior) or suprascapular nerve. Wasting follows. Recovery is usually substantial but slow (months to years).
  • Thoracic outlet syndrome: compression of the lower trunk by a cervical rib, fibrous band, or other anatomical anomaly. Produces lower brachial plexus features. Vascular compression can coexist (subclavian artery or vein compression).

Major Peripheral Nerves of the Lower Extremity

Common Peroneal (Fibular) Nerve

The common peroneal nerve wraps around the fibular head, where it is superficial and vulnerable. Compression here is the most common lower-extremity entrapment neuropathy. Causes include prolonged leg crossing, prolonged squatting, casts, prolonged bed rest, weight loss with loss of subcutaneous fat over the fibular head, and direct trauma.

The deficit:

  • Weakness of dorsiflexion (tibialis anterior, supplied by deep peroneal branch).
  • Weakness of eversion (peroneus longus and brevis, supplied by superficial peroneal branch).
  • Foot drop, with the patient unable to dorsiflex the foot during the swing phase of gait, producing a steppage gait.
  • Sensory loss on the lateral leg and dorsum of the foot.
  • Preserved inversion (supplied by tibial nerve via tibialis posterior) — this distinguishes peroneal palsy from L5 radiculopathy, which weakens both eversion and inversion.

Tinel sign at the fibular head reproduces the symptoms in some patients.

Tibial Nerve

The tibial nerve supplies the calf muscles (gastrocnemius, soleus, tibialis posterior, flexor digitorum longus, flexor hallucis longus) and the intrinsic foot muscles. Sensory supply is the sole of the foot. Tibial nerve entrapment is uncommon; tarsal tunnel syndrome (tibial nerve compression behind the medial malleolus) produces pain and sensory symptoms in the sole of the foot, often without prominent weakness.

Sural Nerve

Pure sensory; supplies the lateral foot and lateral lower leg. Often biopsied in the workup of peripheral neuropathy because of its accessibility and the relatively mild functional consequence.

Femoral Nerve

The femoral nerve carries fibers from L2-L4 roots. Supplies the iliopsoas, sartorius, quadriceps, and pectineus. Sensory supply (via saphenous branch) is the medial leg. Lesions produce weakness of hip flexion and knee extension, with absent knee jerk and sensory loss on the medial leg. Common causes: diabetic amyotrophy, retroperitoneal hematoma (anticoagulation), surgical injury, prolonged lithotomy position, hip surgery.

Lateral Femoral Cutaneous Nerve (Meralgia Paresthetica)

Pure sensory; passes beneath the inguinal ligament near the anterior superior iliac spine, where it is vulnerable to compression. Produces numbness, burning, and paresthesia of the anterolateral thigh. Common in obesity, in pregnancy, with tight belts, and after pelvic surgery. The compression is at the inguinal ligament, and Tinel sign in this region is often positive.

Sciatic Nerve

The sciatic nerve carries fibers from L4-S3 roots, dividing in the popliteal fossa into the tibial and common peroneal nerves. Lesions of the sciatic nerve produce a combined deficit of tibial and peroneal functions, with weakness throughout the leg (with relative sparing of hip flexion and knee extension, which are supplied by femoral nerve) and sensory loss over the lateral and posterior leg and most of the foot. Causes: hip surgery, hip fracture, intramuscular injections in the buttock, piriformis syndrome, sciatic nerve tumor.

Lumbosacral Plexus

The lumbosacral plexus is formed by L1-S4 ventral rami. Plexopathies are less common than brachial plexopathies but produce similar broad patterns of weakness and sensory loss spanning multiple peripheral nerves. Causes include diabetic lumbosacral radiculoplexus neuropathy (Bruns-Garland syndrome, with severe pain and proximal weakness), retroperitoneal mass, radiation, and obstetric injury.

Patterns of Polyneuropathy

Distal Symmetric Polyneuropathy

The classical length-dependent pattern. Symptoms begin in the toes and progress to involve the feet, ankles, and lower legs. Hand symptoms appear when leg involvement reaches the knees. The pattern is symmetric. Most adult polyneuropathies follow this template.

Mononeuropathy Multiplex

Discrete, often asymmetric mononeuropathies in different distributions, occurring sequentially or simultaneously. Pain is often prominent. Causes: vasculitis (polyarteritis nodosa, granulomatosis with polyangiitis, rheumatoid arthritis), diabetes (multiple diabetic mononeuropathies), leprosy, HIV, sarcoidosis. Recognition is important because the underlying disease is typically treatable.

Demyelinating Neuropathies

Demyelinating polyneuropathies have several distinctive features: prominent motor involvement (often more than sensory), early loss of reflexes, sometimes preserved distal sensation while proximal sensation is impaired. The classical demyelinating neuropathies are Guillain-Barré syndrome (acute), chronic inflammatory demyelinating polyneuropathy (CIDP), multifocal motor neuropathy, hereditary demyelinating neuropathies (CMT type 1, hereditary neuropathy with liability to pressure palsies).

Axonal Neuropathies

The majority of acquired polyneuropathies — diabetic, toxic, hereditary axonal forms, paraneoplastic. Symptoms reflect axonal loss: distal sensory and motor deficits with reflexes lost in the affected distribution, and atrophy in chronic disease.

Hereditary Neuropathies

Charcot-Marie-Tooth disease is the most common inherited neuropathy. Several types:

  • CMT1 (demyelinating): autosomal dominant, most often CMT1A from PMP22 duplication. Begins in childhood or adolescence with distal lower extremity weakness, sensory loss, and pes cavus. Slowly progressive over decades. Markedly slowed nerve conduction velocities on testing.
  • CMT2 (axonal): similar clinical picture but with normal or only mildly reduced nerve conduction velocities and reduced amplitudes.
  • CMTX (X-linked): caused by mutations in GJB1. Males more severely affected.
  • Hereditary neuropathy with liability to pressure palsies (HNPP): recurrent mononeuropathies at typical entrapment sites, often after minor trauma. PMP22 deletion.

The combination of distal symmetric weakness with pes cavus and hammer toes, a positive family history (or affected parent with subtle findings), and a slowly progressive course over decades is the picture of inherited neuropathy. Genetic testing is now widely available.

🔍 Did You Know?

The Tinel sign — tapping over a nerve and producing tingling in its distribution — was originally described by Jules Tinel as a test for nerve regeneration after injury, not as a test for compression. The reasoning was that a regenerating nerve, having immature, hypersensitive axon endings, would produce tingling at the site of regrowth, which advances about one millimeter per day. The application of Tinel sign to entrapment neuropathies came later. The original use is still occasionally helpful: in monitoring recovery of a transected and repaired nerve, the advancing Tinel sign documents the progress of regeneration along the nerve.

Pitfalls and Pearls

  • The bedside exam often makes the diagnosis in entrapment neuropathy without imaging or EMG. Specific motor and sensory pattern + positive provocative test = diagnosis.
  • L5 radiculopathy vs peroneal palsy: both cause foot drop, but L5 spares the gluteus medius (test hip abduction), while peroneal palsy does not affect inversion (tibialis posterior) which L5 does.
  • The dorsum of the medial hand has preserved sensation in Guyon canal ulnar lesions, distinguishing them from cubital tunnel lesions where the dorsal sensory branch is involved.
  • Anterior interosseous syndrome is pure motor. An inability to make the “OK” sign with no sensory loss in the forearm or hand is the key finding.
  • Pancoast tumor presents with the combination of lower trunk brachial plexopathy and Horner syndrome. Image the lung apex in any patient with this combination.
  • Neuralgic amyotrophy is often missed for weeks. Severe shoulder pain followed by patchy plexus-distribution weakness in a previously well patient is the picture; recovery is slow but usually substantial.
  • Mononeuropathy multiplex is vasculitis until proven otherwise. Painful asymmetric multiple mononeuropathies warrant urgent rheumatologic and immunologic workup.
  • Pes cavus and hammer toes signal chronic distal neuropathy. CMT is the most common cause. Examine the parents and siblings for subtle findings.
  • Always check for diabetes in any unexplained polyneuropathy. Fasting glucose, HbA1c, and often a glucose tolerance test. Pre-diabetes can cause neuropathy.
  • B12 deficiency causes neuropathy without anemia in many patients. A normal CBC does not rule it out.

References

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  2. Stewart JD. Focal Peripheral Neuropathies. 4th ed. JBJ Publishing; 2010.
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