Nerve Roots, Dermatomes and Reflexes

When a patient points to a stripe of numbness down the outside of the leg, or a reflex hammer meets a quiet ankle, the nervous system is telling you exactly which level of the spine to look at. Dermatomes, myotomes and reflexes link a symptom in the hand or foot to a single spinal segment. This chapter builds the map from the spinal nerve outward, then shows how to tell true root irritation from referred pain and from a nerve trapped farther down the limb.

Section 1Spinal nerve formation and the intervertebral foramen

From rootlets to rami

Each segment of the spinal cord gives off a series of small rootlets from its back and front surfaces. The rootlets on the back gather into the dorsal (posterior) root, and those on the front gather into the ventral (anterior) root. The two roots carry very different traffic. The dorsal root is purely sensory (afferent): it carries information from skin, muscle spindles, joints, ligaments and viscera into the cord. Their cell bodies sit outside the cord in a swelling on the dorsal root, the dorsal root ganglion (DRG). The ventral root is motor (efferent). It carries alpha motor axons to skeletal muscle, gamma motor axons to muscle spindles and, at T1 to L2 and S2 to S4, preganglionic autonomic fibers.

Just beyond the DRG, usually within the intervertebral foramen, the roots merge to form the spinal nerve. The spinal nerve is short, roughly a centimeter long, and it is mixed: from here outward every branch can carry both sensory and motor fibers. Almost as soon as it leaves the foramen the spinal nerve divides:

• The dorsal (posterior) ramus turns backward to supply the deep intrinsic back muscles (the erector spinae and transversospinalis groups), the skin of the back near the midline, and, through its medial branch, the zygapophyseal (facet) joints.
• The ventral (anterior) ramus is much larger. It supplies the muscles and skin of the front and sides of the trunk and all of the limbs. In the thoracic region the ventral rami stay separate as the intercostal and subcostal nerves. In the neck and the lumbosacral region they mix to form the cervical plexus (C1 to C4), brachial plexus (C5 to T1), lumbar plexus (L1 to L4) and sacral plexus (L4 to S4).
• The rami communicantes link the spinal nerve to the sympathetic chain. White rami (myelinated preganglionic fibers) exist only from T1 to L2; gray rami (unmyelinated postganglionic fibers) return to every spinal nerve so that sweat glands, blood vessels and arrector pili muscles everywhere receive sympathetic supply.
• The recurrent meningeal (sinuvertebral) nerve loops back through the foramen into the canal to supply the posterior longitudinal ligament, the outer third of the annulus fibrosus, the anterior dura and the vessels of the canal. It is a key reason the disc itself can hurt.

Thirty one pairs and the numbering rule

Humans have 31 pairs of spinal nerves: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral and 1 coccygeal. The only mismatch with the vertebrae is in the neck, which has seven vertebrae but eight nerves. The first cervical nerve leaves between the skull and the atlas, so each cervical nerve from C1 to C7 exits above the vertebra that shares its number. The C8 nerve exits between C7 and T1, and from T1 downward every nerve exits below its numbered vertebra. This rule has a direct clinical payoff. A disc between C5 and C6 sits next to the foramen through which the C6 nerve leaves, so a posterolateral C5 to C6 herniation usually produces a C6 radiculopathy. In the lumbar spine the L4 nerve leaves below the L4 pedicle, through the L4 to L5 foramen.

A second mismatch develops during growth. The vertebral column lengthens faster than the cord, so in the adult the cord ends as the conus medullaris at about the L1 to L2 disc. Below that, lumbar and sacral roots must travel downward inside the dural sac before they reach their exit foramina. This bundle of descending roots is the cauda equina ("horse's tail"). A large central herniation in the lumbar spine compresses roots, not cord, so it produces a lower motor neuron picture with saddle numbness and bladder dysfunction (the cauda equina syndrome) rather than spasticity.

The intervertebral foramen

The intervertebral foramen (IVF) is the window between two adjacent vertebrae through which the spinal nerve leaves the canal. Its borders are:

• Roof: the pedicle of the vertebra above (its inferior vertebral notch).
• Floor: the pedicle of the vertebra below (its superior vertebral notch).
• Anterior wall: the back of the two vertebral bodies and the intervertebral disc between them; in the neck, the uncovertebral joint (joint of Luschka) also forms part of this wall.
• Posterior wall: the zygapophyseal (facet) joint, with its capsule and the lateral extension of the ligamentum flavum.

The contents are the dural sleeve holding the roots or spinal nerve, the dorsal root ganglion, the recurrent meningeal nerve, a spinal branch of a segmental artery, communicating veins and fat. In the lumbar spine the nerve occupies a relatively small part of the foramen, often quoted as about one third to one half of its area, and it lies in the upper part, tucked under the pedicle above. The disc lies at the level of the lower part of the foramen. This is why loss of disc height, which lets the upper pedicle drop toward the lower one, squeezes the exiting root.

In the neck the foramen is shaped more like a gutter that runs forward and outward at roughly 45 degrees, and the nerve fills a larger share of it. Uncovertebral spurs project into the front of the foramen and facet joint enlargement projects into the back, so cervical foraminal stenosis is common in middle age and is the most frequent cause of cervical radiculopathy, ahead of soft disc herniation.

What changes the size of the foramen

The foramen is a dynamic space. Flexion opens it, because the pedicles separate and the ligamentum flavum is stretched thin. Extension closes it, because the facets slide together, the ligamentum flavum buckles inward and the disc bulges slightly backward. Lateral flexion and rotation toward one side narrow the foramen on that side. This is why patients with foraminal stenosis often lean forward, find walking downhill harder than uphill, and get relief from sitting, and why the Spurling test (extension, side bending and rotation toward the painful side with gentle downward pressure) can reproduce cervical radicular pain.

Disc height loss, herniation, osteophytes, facet hypertrophy, ligamentum flavum thickening and spondylolisthesis all shrink the foramen over time. Compression of the root does not by itself cause pain. A healthy nerve that is compressed tends to go numb or weak. Pain arises when the root is also inflamed. Chemical mediators released from herniated nucleus pulposus (including phospholipase A2, tumor necrosis factor alpha and other cytokines), together with venous congestion and reduced blood flow inside the root, make the DRG and root hyperexcitable.

Section 2Dermatomes and myotomes

What a dermatome is, and is not

A dermatome is the area of skin supplied by the sensory fibers of a single spinal nerve root. A myotome is the group of muscles supplied mainly by the motor fibers of a single root. Both ideas come from embryology. Each embryonic somite carries its own nerve supply as it grows, which gives neat horizontal bands in the trunk. In the limbs the pattern is stretched and twisted, because the limb buds grow out from the body wall and then rotate: the upper limb rotates laterally and the lower limb rotates medially. That is why the dermatomes of the leg spiral around the shin and why the big toe, which is on the inner side of the foot, belongs to L5 while the little toe belongs to S1.

Dermatome maps are useful, but they are approximations. Three facts keep them honest. First, adjacent dermatomes overlap. Each root sends some fibers into the territory of its neighbors, so cutting a single root rarely produces a clean band of total numbness; usually there is reduced sensation in a smaller central zone, often called the autonomous zone. Second, the maps disagree. Classic maps were built by different methods and draw several borders differently; modern evidence based maps show the most consistent zones rather than sharp lines. Third, people vary. A given person may have a prefixed or postfixed brachial plexus that shifts everything up or down by about half a segment. For these reasons, examiners test key sensory points near the center of each dermatome rather than trying to trace borders.

Key sensory points

The standard examination tests one key point per dermatome for light touch and pinprick. A few landmarks make the trunk easy: the nipple line is about T4, the xiphoid process about T6, the umbilicus T10, and the inguinal ligament T12 to L1. The cape over the top of the shoulder is C4, which lies right next to T2 on the upper chest because the C5 to T1 territories have been pulled out into the arm.

Myotomes and how to test them

Most limb muscles receive fibers from two or three roots, so a single root lesion usually causes partial weakness rather than paralysis. Still, each movement has one root that contributes most, and testing a key movement for each root gives a quick and reasonably reliable screen. Strength is graded on the Medical Research Council scale: 0 no contraction; 1 a flicker of contraction without movement; 2 movement with gravity eliminated; 3 movement against gravity but not resistance; 4 movement against some resistance; 5 normal strength. Most root weakness falls within grade 4.

Always compare sides. For the large leg muscles manual testing is insensitive, so add functional tests: ten single leg heel raises for S1, walking on the heels for L4 and L5, and a single leg sit to stand or step up for L3 and L4.

Putting sensation and strength together

A root lesion is suggested when changes in sensation, strength and reflexes all point to the same level, on one side, and match the pattern of pain. A peripheral nerve lesion produces a different pattern: sensory loss with sharp, characteristic borders that cut across dermatomes, and weakness confined to muscles of one nerve even if those muscles come from different roots. For example, weakness of thumb abduction with numbness of the thumb, index and middle fingers but normal wrist extension and a normal brachioradialis reflex points to the median nerve at the wrist, not to C6.

Test both light touch (large fibers, dorsal columns) and pinprick (small fibers, spinothalamic tract). Patients often describe paresthesia (tingling or pins and needles, a positive symptom) before hypoesthesia (reduced feeling, a negative sign), and some develop dysesthesia (unpleasant, burning sensations) or allodynia (pain from a normally harmless touch).

Section 3Deep tendon and pathological reflexes

The stretch reflex arc

The deep tendon reflex, more accurately called the muscle stretch reflex, is the simplest reflex in the body and one of the most informative tests in the neurological examination. Tapping a tendon does not stimulate the tendon itself. It produces a quick, small stretch of the muscle, and that stretch is detected by muscle spindles.

Muscle spindles are small encapsulated sensory organs that lie in parallel with ordinary (extrafusal) muscle fibers. Their specialized intrafusal fibers are wrapped by sensory endings that give rise to large, fast type Ia afferent fibers that fire vigorously when the muscle is stretched quickly. The Ia fiber enters the cord through the dorsal root, its cell body in the dorsal root ganglion, and synapses directly on alpha motor neurons in the ventral horn that supply the same muscle. Because there is only one synapse between sensory input and motor output, the reflex is called monosynaptic. The alpha motor neuron fires, the muscle contracts and the limb jerks.

At the same time, branches of the Ia fiber excite a Ia inhibitory interneuron that suppresses motor neurons to the antagonist muscle. When the quadriceps is reflexly contracting, the hamstrings are told to relax. This is reciprocal inhibition. A separate receptor, the Golgi tendon organ, lies in series with the muscle at the musculotendinous junction and signals tension through type Ib fibers, which inhibit the same muscle (autogenic inhibition). Spindle sensitivity is set by gamma motor neurons, which contract the ends of the intrafusal fibers and keep the spindle taut. Descending pathways adjust this setting constantly, so reflexes change with anxiety, attention and injury to the brain or cord.

The reflexes you test and their levels

Each commonly tested reflex is carried by one or two root levels through one peripheral nerve. A reduced or absent reflex can therefore point to a root, provided the change is on one side and fits the sensory and motor findings.

Grading and reinforcement

Reflexes are graded on a five point scale: 0 absent; 1+ present but diminished (trace); 2+ normal; 3+ brisker than average, possibly with spread to neighboring muscles; 4+ very brisk, often with sustained clonus. The grade itself matters less than asymmetry and context. Many healthy people have 1+ or 3+ reflexes everywhere; an absent ankle reflex on one side only, in a patient with pain down the back of that leg, is meaningful. Ankle reflexes often fade in people over about 60, so a bilaterally absent ankle jerk in an older adult may be normal aging or a peripheral neuropathy rather than a root problem.

When a reflex seems absent, use reinforcement before calling it 0. The Jendrassik maneuver asks the patient to hook the fingers of both hands together and pull apart just as you tap a lower limb reflex; clenching the teeth or making a fist reinforces upper limb reflexes. A reflex that appears only with reinforcement is graded 1+.

Upper versus lower motor neuron signs

The upper motor neurons are the neurons of the motor cortex and brainstem whose axons descend in the corticospinal and other tracts. The lower motor neurons are the alpha motor neurons of the ventral horn and cranial nerve nuclei, along with their axons in roots and peripheral nerves. Injury at each level produces a recognizable cluster of signs, and telling them apart is one of the most important skills in spine examination, because a patient with neck pain and an upper motor neuron picture may have cord compression rather than a simple root problem.

Pathological reflexes

Some reflexes are normally absent in adults and appear only when descending control is damaged. They are called pathological reflexes, and their presence is a red flag for disease of the brain or spinal cord.

• Babinski sign (extensor plantar response). Stroke the lateral sole firmly from heel toward the little toe and across the ball of the foot. The normal adult response is flexion of the toes. Extension of the big toe, often with fanning of the other toes, indicates a corticospinal tract lesion. The response is normal in infants up to about one to two years, before the corticospinal tract has fully myelinated.
• Hoffmann sign. Hold the patient's middle finger and flick its nail downward. Flexion of the thumb and index finger is a positive sign. It suggests upper motor neuron involvement above the lower cervical segments, most often cervical myelopathy, although a few healthy people with generally brisk reflexes have a mild bilateral Hoffmann response.
• Clonus. A rapid, forceful dorsiflexion of the ankle that is then held produces rhythmic beats of plantar flexion. A few beats that die away can be normal; sustained clonus (more than about four or five beats, or continuing as long as the stretch is held) indicates an upper motor neuron lesion.

Among the superficial reflexes, the abdominal reflexes (T8 to T12) are lost with upper motor neuron lesions, and the anal wink and bulbocavernosus reflexes test S2 to S4, the segments that control the bladder, bowel and sexual function, and they are checked when cauda equina syndrome or conus damage is suspected.

Section 4Radiculopathy versus referred pain

Four words that are often confused

Leg and arm pain from the spine is described loosely even by clinicians, but each of these terms has a different mechanism, prognosis and meaning for referral.

• Radicular pain is pain that arises from irritation of a spinal nerve root or dorsal root ganglion, usually by a combination of mechanical compression and inflammation. It is felt in the limb, travels in a narrow band, and is often described as shooting, electric, lancinating or burning. In the lower limb it commonly passes below the knee and into the foot.
• Radiculopathy is a loss of function in a root: conduction is blocked, so the examiner finds numbness, weakness or a reduced reflex in that root's distribution. Radiculopathy is defined by objective neurological signs, not by pain. A patient can have radicular pain without radiculopathy, radiculopathy without much pain (painless foot drop), or both together.
• Somatic referred pain is pain felt in a region away from its source, where the source is a musculoskeletal structure of the spine such as the disc, a facet joint, the sacroiliac joint, ligaments or muscles. It is deep, dull, aching and hard to localize, it tends to stay in the buttock and thigh (usually above the knee), and it is not accompanied by neurological deficit.
• Visceral referred pain is pain felt in the body wall or limb whose source is an internal organ, such as the heart, gallbladder, kidney, pancreas or aorta.

"Sciatica" is a lay term that does not say whether leg pain is radicular or referred, so replace it with a precise term after the examination.

Why referral happens

Referred pain is explained by convergence. Sensory neurons from deep spinal structures, viscera and skin all synapse in the dorsal horn, and many second order neurons there receive input from more than one source. The brain has learned, over a lifetime, that activity in a given dorsal horn neuron usually comes from the skin and muscle it serves most often. When the same neuron is activated by input from a disc or an organ, the brain projects the sensation onto that familiar territory. This is called the convergence projection theory. Classic experiments injecting salt solution into the interspinous ligaments of volunteers produced aching, segmental limb pain with no root involved, and later studies showed that facets, discs and sacroiliac joints refer pain into the buttock, groin and thigh with large overlap.

Visceral referral follows the segment that supplied the organ's embryonic origin. Pain from the heart is referred to the chest, left arm and jaw (upper thoracic segments); pain from the diaphragm, through the phrenic nerve (C3 to C5), is referred to the tip of the shoulder; gallbladder disease refers to the right upper abdomen and below the right scapula; the kidneys and ureters refer to the flank and groin; the pancreas and a leaking abdominal aortic aneurysm can refer straight through to the mid back. Consider visceral causes when back pain is unchanged by movement or comes with systemic symptoms.

Which root, from which disc?

About 90 to 95 percent of symptomatic lumbar disc herniations occur at L4 to L5 or L5 to S1, the two levels that carry the most load and motion. Where the herniation sits around the circumference of the disc decides which root it meets. Clinicians describe positions from the midline outward: central, subarticular (also called paracentral or lateral recess), foraminal and extraforaminal (far lateral). The most common is posterolateral (subarticular), where the posterior longitudinal ligament is thinner.

• A subarticular herniation at L4 to L5 compresses the traversing L5 root. At L5 to S1 it compresses S1.
• A foraminal or far lateral herniation at L4 to L5 compresses the exiting L4 root, often its DRG, and tends to be very painful.
• A large central herniation can compress several roots of the cauda equina at once, on both sides, which is the setting for cauda equina syndrome.

Root syndromes worth memorizing

Real patients often show only part of each classic pattern. In the neck, C7 is the most commonly involved root, followed by C6. In the low back, L5 and S1 together account for the large majority of radiculopathies.

Provocation and neurodynamic tests

Nerve roots must slide and stretch as the limbs and spine move. An inflamed or tethered root becomes sensitive to tension, and several tests take advantage of this. The straight leg raise (SLR) lifts the straight leg of a supine patient; reproduction of the patient's familiar leg pain below the knee between about 30 and 70 degrees of hip flexion is a positive test for irritation of the L5 or S1 roots. Pain only in the back, or only a stretch in the hamstrings, is not a positive result. Adding ankle dorsiflexion or neck flexion and seeing the leg pain increase strengthens the finding. The SLR is sensitive (often quoted around 0.9 for disc herniation in surgical populations) but not specific, so a negative SLR helps rule out herniation while a positive one does not confirm it. The crossed SLR, in which raising the opposite leg reproduces the symptomatic leg pain, is the reverse: insensitive but quite specific, and it suggests a large, often central or axillary herniation.

The slump test builds tension in sequence (seated slump, neck flexion, knee extension, ankle dorsiflexion) and then releases neck flexion; if the leg symptoms ease when only the neck is lifted, the response is neural rather than muscular. The prone knee bend (femoral nerve tension test) tensions the L2 to L4 roots. In the neck, the Spurling test (extension, side bending and rotation toward the symptomatic side with gentle axial pressure) narrows the foramen and is specific but only moderately sensitive for cervical radiculopathy. The upper limb tension test is sensitive but not specific, and relief when the hand rests on top of the head (the shoulder abduction relief sign) supports a root source. Combining tests helps: when several of the Spurling test, upper limb tension test, relief with neck distraction and reduced rotation toward the painful side are positive together, the likelihood of cervical radiculopathy rises sharply.

Natural history, investigation and red flags

The outlook for radicular pain from a disc herniation is generally good. Most patients improve substantially within 6 to 12 weeks, and repeat imaging shows that many herniations shrink or disappear on their own, with the largest, extruded and sequestered fragments the most likely to regress because they are exposed to the immune system and resorbed. Guidelines therefore recommend a period of conservative care for most patients without serious deficits. Imaging with MRI is reserved for red flags, progressive deficits, or symptoms that persist beyond about six weeks and when the result would change management such as an injection or surgery. MRI findings must match the examination, because herniations are common in people without pain.

Electrodiagnostic testing (nerve conduction studies and needle electromyography) assesses function rather than structure. Because a root lesion is proximal to the dorsal root ganglion, the cell bodies and their peripheral axons remain intact, so sensory nerve action potentials in the numb area are typically normal in radiculopathy. In a plexus or peripheral nerve lesion, which damages axons beyond the ganglion, they are reduced. Needle EMG may show denervation in one myotome, including the paraspinals, after about two to three weeks.

Some nerve root presentations are emergencies. Cauda equina syndrome presents with some combination of saddle (perineal) numbness, new urinary retention or incontinence, fecal incontinence, sexual dysfunction and bilateral leg pain or weakness; it requires same day emergency imaging and surgical assessment, because outcome depends on how quickly the compression is relieved. Progressive or severe motor weakness (for example a new foot drop), signs of myelopathy, and radicular pain with fever, a history of cancer or unexplained weight loss also call for urgent referral.

Section 5Peripheral nerve entrapments

How a nerve is injured by pressure

Once a spinal nerve leaves the foramen and its fibers sort themselves into peripheral nerves, it still has to pass through tight places: fibro osseous tunnels, gaps between muscles, and points where it crosses a bony edge. At these sites chronic compression and repeated stretch can produce an entrapment neuropathy.

Nerves are sensitive to pressure because of their blood supply. Each nerve has its own small vessels (the vasa nervorum) running in the epineurium and perineurium. Experimental work shows that pressures of only about 20 to 30 mmHg slow venous outflow from the nerve, and that somewhat higher pressures impair axonal transport and then arterial inflow. Venous congestion causes intraneural edema, and with time the connective tissue thickens and the myelin thins. Early symptoms are intermittent and positional (tingling at night, or when the wrist or elbow is bent for a long time), reflecting reversible ischemia. Later symptoms are constant, with numbness and then weakness and wasting, reflecting demyelination and finally axon loss.

These stages map onto the classic grades of nerve injury: neurapraxia (myelin damage with a local conduction block and full recovery in days to weeks), axonotmesis (axons divided inside intact sheaths, with regrowth of about 1 mm per day) and neurotmesis (the whole nerve divided, needing surgical repair).

Carpal tunnel syndrome

Carpal tunnel syndrome, compression of the median nerve at the wrist, is the most common entrapment neuropathy, affecting several percent of adults, more often women. The carpal tunnel is formed by the concave arch of the carpal bones as its floor and walls and the transverse carpal ligament (flexor retinaculum) as its roof. The ligament attaches to the scaphoid tubercle and trapezium on the radial side and to the pisiform and hook of the hamate on the ulnar side. Through this unyielding tunnel pass the median nerve and nine tendons: four of flexor digitorum superficialis, four of flexor digitorum profundus and the flexor pollicis longus. Anything that adds volume inside the tunnel, such as tenosynovial thickening, pregnancy, hypothyroidism, rheumatoid arthritis or diabetes, raises the pressure on the nerve. Wrist flexion and extension both raise tunnel pressure, which is why symptoms are worse at night when people sleep with curled wrists and why prolonged gripping and vibration are risk factors.

Patients report numbness, tingling and burning in the thumb, index, middle and radial half of the ring finger, often waking them at night and relieved by shaking the hand (the "flick sign"). Two anatomical details separate carpal tunnel syndrome from a C6 or C7 radiculopathy. First, the palmar cutaneous branch of the median nerve leaves above the wrist and passes over the ligament, so sensation over the thenar eminence is normal in carpal tunnel syndrome but may be reduced in a root lesion. Second, carpal tunnel syndrome weakens only the median nerve muscles of the hand (abductor pollicis brevis, opponens pollicis and the lateral two lumbricals), causing thenar wasting in advanced cases, while reflexes, wrist extension and elbow strength stay normal.

Provocative tests include Phalen's test (holding the wrists fully flexed for about a minute), Tinel's sign (tapping over the nerve at the wrist produces tingling into the fingers) and the carpal compression test (direct thumb pressure over the tunnel for about 30 seconds). Each has only moderate accuracy; nerve conduction studies showing slowed median conduction across the wrist help when the diagnosis is uncertain. Treatment begins with a neutral night splint and activity changes; corticosteroid injection gives short to medium term relief; and surgical release is definitive for severe or persistent cases. Nerve gliding exercises and manual therapy are also used, and one randomized trial reported results similar to surgery at one year, but the evidence overall is limited and of mixed quality.

Other upper limb entrapments

The ulnar nerve is the second most commonly entrapped nerve, usually at the elbow in the cubital tunnel, where it runs behind the medial epicondyle under a fibrous band between the two heads of flexor carpi ulnaris. Elbow flexion both stretches the nerve and narrows the tunnel, so leaning on the elbow, sleeping with the arms bent and holding a phone to the ear provoke symptoms. Numbness affects the little finger, the ulnar half of the ring finger and the ulnar side of the back of the hand. Weak interossei and adductor pollicis produce a weak pinch with compensatory thumb flexion (Froment sign) and, in severe cases, clawing of the ring and little fingers. At the wrist, the ulnar nerve can be compressed in Guyon canal, between the pisiform and the hook of the hamate, as in long distance cyclists; this spares the dorsal hand sensation.

The radial nerve can be compressed in the spiral groove of the humerus (for example after sleeping with an arm over a chair back), producing wrist drop with sparing of the triceps. Its deep motor branch, the posterior interosseous nerve, can be trapped under the arcade of the supinator muscle, producing weak finger extension with no sensory loss.

Thoracic outlet syndrome describes compression of the brachial plexus, subclavian artery or subclavian vein as they pass through the interscalene triangle, the costoclavicular space or the space under pectoralis minor. Most cases are neurogenic, with symptoms often in the lower trunk (C8 and T1) distribution: medial arm and hand tingling, worse with overhead activity or carrying. Vascular forms are rarer but more serious. The classic provocative tests have high false positive rates in healthy people, so diagnosis requires a consistent overall picture.

Lower limb entrapments

Meralgia paresthetica is compression of the lateral femoral cutaneous nerve (L2 to L3) where it passes under or through the inguinal ligament near the anterior superior iliac spine. It is purely sensory: burning, tingling or numbness of the anterolateral thigh, with normal strength and reflexes. Tight belts, obesity, pregnancy and diabetes are typical contributors. Its sharply bordered patch of altered sensation and its normal motor exam separate it from an L2 or L3 radiculopathy.

The common fibular (peroneal) nerve winds around the neck of the fibula just under the skin, where it can be compressed by habitual leg crossing, a tight cast or brace, prolonged squatting or kneeling, or rapid weight loss that removes its fat padding. The result is foot drop (weak dorsiflexion and eversion) with numbness of the lateral leg and dorsum of the foot, which mimics L5 radiculopathy. In a fibular nerve palsy, foot inversion (tibialis posterior, tibial nerve) and hip abduction (gluteus medius, superior gluteal nerve) are normal, because those muscles are not supplied by the fibular nerve. In an L5 radiculopathy they are often weak, because they share the L5 root. Back pain and a positive straight leg raise also favor the root.

Other entrapments include tarsal tunnel syndrome (the tibial nerve beneath the flexor retinaculum behind the medial malleolus, causing burning in the sole), Morton neuroma (thickening of an interdigital nerve, most often between the third and fourth metatarsal heads, causing burning forefoot pain with tight shoes), and deep gluteal syndrome, a broader and more accurate term for sciatic nerve irritation in the buttock that includes the older idea of piriformis syndrome. It causes buttock pain that is worse with sitting; no single test is accurate.

Double crush and systemic risk

The debated double crush hypothesis proposes that compression at one point, such as the root, makes the distal nerve more vulnerable to a second compression, so examine the whole nerve when one lesion does not fit. Diabetes, hypothyroidism, kidney disease and vitamin B12 deficiency also make nerves more susceptible, so multiple entrapments should prompt a search for a cause.

Words worth knowing