Spinal and Peripheral Nerves

Part 5 · Head, neck and the nervous system

The plexuses, dermatomes and myotomes, and nerve injury and repair

The last chapter, and the one that ties the book together

Everything in this book converges here. The bone chapters told you where nerves are tethered and compressed. The muscle chapters told you what each nerve does. The regional chapters gave you the courses. This chapter gives you the system: how the 31 pairs of spinal nerves are organised into plexuses, how to map a lesion from the pattern of loss, and what happens to a nerve when it is injured.

The clinical question this chapter answers is the one you will ask most often in practice:

Is this a nerve root, a plexus, or a peripheral nerve — and how do I tell?

Learning outcomes

• Describe the structure of a peripheral nerve and its connective tissue sheaths.
• Describe the formation of a spinal nerve and the destinations of its rami.
• Describe the cervical, brachial, lumbar and sacral plexuses and their major branches.
• Map the dermatomes and myotomes and use them to localise a lesion.
• Distinguish radiculopathy from plexopathy from peripheral neuropathy.
• Classify nerve injury by the Seddon and Sunderland systems and predict recovery.
• Describe the mechanisms of nerve regeneration and the timeline of reinnervation.
• Describe the autonomic nervous system and its clinical manifestations.
• Explain entrapment neuropathies, the double crush hypothesis and neurodynamic testing.
• Describe the common polyneuropathies and their rehabilitation implications.

Structure of a peripheral nerve

The connective tissue architecture mirrors that of muscle (Chapter 5), and it determines everything about injury and repair.

Nerves are designed to move. A peripheral nerve must accommodate up to 10–20% strain and several millimetres to centimetres of excursion during limb movement (the median nerve moves ~7 mm at the elbow, the sciatic nerve ~10 mm at the hip). It does this by unfolding its undulating course, then unfolding the fascicles’ own undulation, and finally by gliding. Only after all three are exhausted does the nerve stretch.

Nerves are also metabolically demanding and vulnerable to ischaemia. Intraneural blood flow is impaired at as little as 20–30 mmHg of external pressure, and at 50 mmHg conduction begins to fail. This — not “pinching” — is the mechanism of most entrapment neuropathies, and it explains why symptoms are often worse at night (when limb positions are sustained and blood pressure falls) and why they resolve so quickly on position change.

The spinal nerve

Figure 1 · A typical spinal nerve

31 pairs: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal.

Formed in the intervertebral foramen by the union of:

• Dorsal (posterior) root — sensory, bearing the dorsal root ganglion (the cell bodies of primary afferents, which lie outside the cord — which is why root lesions proximal to the DRG spare the sensory nerve action potential on nerve conduction studies, a key electrodiagnostic discriminator)
• Ventral (anterior) root — motor, from the anterior horn

It divides almost immediately into:

Exit rule (Chapter 17, repeated because it is examined every year): C1–C7 exit ABOVE their corresponding vertebra; C8 exits between C7 and T1; from T1 down, nerves exit BELOW their corresponding vertebra.

The plexuses

Figure 2 · Dermatomes, and the brachial plexus

Cervical plexus (C1–C4)

Lies deep to sternocleidomastoid, on scalenus medius and levator scapulae.

The supraclavicular nerves (C3–C4) supply skin down to the second rib — which is why shoulder-tip pain refers from the diaphragm (Chapters 8 and 18), and why a patient may point to the clavicle when the problem is subphrenic.

Brachial plexus (C5–T1)

Roots → Trunks → Divisions → Cords → Branches (Really Tired? Drink Coffee Before).

Branches worth knowing by level, because the level of a branch localises the lesion:

Mnemonic for posterior cord branches: ULTRA — Upper subscapular, Lower subscapular, Thoracodorsal, Radial, Axillary.

Plexus injury patterns:

Lumbar plexus (L1–L4)

Within psoas major (Chapter 20).

Mnemonic: I, I Get Laid On Fridays — Iliohypogastric, Ilioinguinal, Genitofemoral, Lateral femoral cutaneous, Obturator, Femoral.

Sacral plexus (L4–S4)

On the posterior pelvic wall, anterior to piriformis.

Dermatomes and myotomes

Figure 3 · Dermatome and myotome

Dermatomes — the reliable landmarks

Maps disagree because adjacent dermatomes overlap substantially (Chapter 8). Learn the reliable single points — the ASIA key sensory points — rather than trying to memorise boundaries.

Myotomes — the movements to test

Reflexes

Note that sclerotomes (Chapter 8) explain the deep, aching, poorly localised bone pain that follows neither a dermatome nor a peripheral nerve territory — a common source of confusion.

Localising the lesion: root, plexus or peripheral nerve

This table is the practical heart of the chapter.

The single most useful discriminator, worked through

A patient has weak wrist extension. Is it a C7 radiculopathy or a radial nerve palsy?

• Both weaken wrist and finger extension.
• But C7 also supplies triceps (radial nerve), flexor carpi radialis (median nerve) and latissimus dorsi (thoracodorsal nerve). In a C7 radiculopathy those are also weak, and the triceps reflex is reduced.
• In a radial nerve palsy at the spiral groove, flexor carpi radialis and latissimus dorsi are normal, and there is a sensory deficit confined to the dorsal first web space.

Test a muscle that shares the root but not the nerve. That one manoeuvre separates root from nerve more reliably than any special test.

Similarly, weak ankle dorsiflexion: L5 radiculopathy also weakens hip abduction (superior gluteal nerve) and inversion (tibialis posterior, tibial nerve); common fibular nerve palsy spares both (Chapter 15).

Nerve injury and repair

Classification

Wallerian degeneration begins within 24–48 hours distal to the lesion: axonal and myelin breakdown, macrophage clearance, and Schwann cell proliferation into bands of Büngner within the surviving endoneurial tubes. The cell body undergoes chromatolysis and shifts to a regenerative phenotype.

Regeneration and its timeline

Axonal sprouts advance at approximately 1 mm per day (~1 inch per month), after an initial delay of 2–4 weeks at the injury site.

Practical prediction: a radial nerve injury at the spiral groove is roughly 30 cm from the wrist extensors → around 10–12 months to reinnervation. This is not an academic calculation; it is what you tell the patient, what determines the splinting plan, and what tells you when to become concerned that recovery is not happening.

The advancing front is tracked by a progressing Tinel’s sign — the point of maximal paraesthesia on percussion moves distally as regeneration proceeds. A Tinel’s that fails to advance over successive months indicates that repair is not occurring and warrants surgical review.

The limiting factor is time, not distance. Denervated muscle loses its capacity to be reinnervated after roughly 12–18 months, as motor endplates degrade and the muscle is replaced by fibrofatty tissue. This is why proximal injuries have a worse prognosis than distal ones — the axons simply cannot arrive in time — and why nerve transfer surgery (bringing a donor nerve close to the target) has transformed the management of proximal brachial plexus injury.

Sensory recovery sequence: pain and temperature → vibration → moving touch → static touch → two-point discrimination. Sensory re-education is delivered along this sequence.

Physiotherapy management of peripheral nerve injury

A note on electrical stimulation of denervated muscle: the evidence is genuinely equivocal. It may retard atrophy, but there is also evidence it can impair reinnervation, and it is uncomfortable and time-consuming. It is not a substitute for range maintenance and splinting.

Entrapment neuropathies and neurodynamics

The common entrapments (collected from across the book)

The double crush hypothesis

Upton and McComas (1973) proposed that a proximal lesion of an axon makes it more vulnerable to a second, distal compression, because axonal transport is impaired along its whole length. Clinically it is invoked for the coexistence of cervical radiculopathy and carpal tunnel syndrome, which is more common than chance would predict.

Honest appraisal: the epidemiological association is real; the causal mechanism remains contested and the concept has been over-applied. Use it as a prompt to examine the whole neural pathway rather than as a diagnosis in itself — the practical value is that it stops you treating a wrist while ignoring a neck.

Neurodynamics

Peripheral nerves must glide, elongate and tolerate compression during movement. When that mechanical or physiological capacity is impaired — by adhesion, oedema, inflammation or ischaemia — movements that load the nerve reproduce symptoms.

Interpretation requires care. A test is positive only if it reproduces the patient’s symptoms, and if those symptoms change with a structurally differentiating movement at a distant joint (adding cervical lateral flexion changes arm symptoms; adding ankle dorsiflexion changes posterior thigh symptoms). Discomfort at end range is normal — most asymptomatic people feel a stretch on ULNT 1 and slump.

Treatment uses sliders (tensioning at one end while releasing at the other, producing excursion with minimal strain — the gentler option for irritable presentations) and tensioners (loading both ends, increasing strain — used later for capacity). The evidence supports them as an adjunct within a broader programme, particularly in carpal tunnel syndrome and in nerve-related leg pain, not as a stand-alone treatment.

The autonomic nervous system

Figure 4 · The autonomic outflow

Referred visceral pain travels with the sympathetics, which is the anatomical basis of the referral patterns in Chapters 8, 19 and 20.

Clinical syndromes:

Polyneuropathies worth recognising

A shared principle: in most polyneuropathies and in post-polio syndrome, overwork weakness is a real phenomenon — excessive eccentric or maximal loading of a partially denervated muscle can produce lasting loss. Prescribe moderate-intensity, submaximal, well-spaced work with careful monitoring, not maximal strengthening.

Afterword — how to use this book

Twenty-four chapters, five parts. If you take four things from all of it:

• Structure explains function, and function explains pathology. A tuberosity means something pulls there. A watershed zone means something ruptures there. A retrograde blood supply means something dies there. Learn the reason and the fact comes free.
• The clinically decisive facts are usually the ones about position, level and exception. Which nerve at which level of the humerus. Which root a posterolateral disc herniation actually compresses. Which lung is dependent. Which side the walking stick goes in. Which position the hand is splinted in. These are what separate a safe clinician from a well-read one.
• Anatomy tells you when NOT to treat. Cauda equina, septic arthritis, compartment syndrome, cervical arterial dissection, autonomic dysreflexia, abdominal aortic aneurysm, Charcot neuroarthropathy, cardiac referred pain. Recognising these is the most valuable use to which this entire book can be put.
• Where the evidence has moved, the teaching should move with it. Impingement, tendinitis, core stability, degenerative meniscal surgery, ITB stretching, sternal precautions, imaging in low back pain — the anatomy did not change, but what we do with it did. Hold both: the structure firmly, and the practice provisionally.

Chapter 24 of 24 · Human Anatomy · Physiotherapist India End of Part 5 — and of the series.

Where students consistently go wrong

• Forgetting the dorsal root ganglion lies outside the cord — the basis of the SNAP discriminator.
• Getting the exit rule wrong. C1–C7 above, C8 between C7 and T1, T1 downwards below.
• Not testing a muscle that shares the root but not the nerve. This is the discriminator.
• Treating dermatome maps as exact boundaries. Use the reliable key points.
• Missing Horner’s syndrome in a brachial plexus injury — it signals root avulsion.
• Forgetting the 1 mm/day rule and therefore giving patients no realistic timeline.
• Forgetting the 12–18-month endplate window. Proximal injuries are a race against it.
• Calling a neurodynamic test positive on stretch alone. It must reproduce the symptoms and change with structural differentiation.
• Over-applying the double crush concept as a diagnosis rather than a prompt to examine the whole pathway.
• Maximally strengthening a partially denervated muscle. Overwork weakness is real.

Check yourself

15 questions on this chapter. Tap one to see the answer and the reasoning.

Quick review

Further reading

Reviewed by the Physiotherapist India Team. · Human Anatomy contents