Spinal Nerves & Plexuses

The spinal nerves are the bridges between the central nervous system and the body. Thirty-one pairs of them emerge from the cord, each carrying motor fibers from the ventral horn, sensory fibers to the dorsal horn (with cell bodies in the dorsal root ganglia), and autonomic fibers at the appropriate levels. In most regions, the nerves run directly to their targets. At the limbs, they reorganize themselves through complex plexuses — the brachial plexus for the upper extremity and the lumbosacral plexus for the lower — that mix fibers from multiple roots before sending them out as the named peripheral nerves. Understanding these plexuses is essential for recognizing the clinical pattern when something goes wrong with them.

This page covers the segmental anatomy of spinal nerves, the dermatome and myotome maps, and the architecture of the brachial and lumbosacral plexuses.

Segmental Spinal Nerves

Each spinal nerve is formed by the union of a dorsal root (sensory) and a ventral root (motor) just outside the spinal cord. The combined nerve passes through the intervertebral foramen and then divides into:

• Dorsal ramus: innervates the deep muscles of the back and the overlying skin in a strip along the back.
• Ventral ramus: innervates everything else — the limbs, the body wall, and the anterior trunk. In the thoracic region, the ventral rami remain as discrete intercostal nerves. In cervical and lumbosacral regions, they reorganize into the plexuses.
• Meningeal branch (recurrent meningeal nerve, sinuvertebral nerve): small, supplying the dura and the local intervertebral structures.
• Rami communicantes: at T1-L2, connecting to the sympathetic chain. White rami communicantes carry preganglionic sympathetic fibers from the cord to the chain; gray rami communicantes carry postganglionic sympathetic fibers back to the spinal nerve for distribution to skin and blood vessels.

Dermatomes and Myotomes

Each spinal nerve supplies a defined region of skin (its dermatome) and contributes to a defined set of muscles (its myotome).

Key Dermatome Landmarks

Key Myotomes

The Brachial Plexus

The brachial plexus is formed by the ventral rami of C5-T1, with contributions from C4 and T2 in some individuals. It is the source of all motor and sensory innervation to the upper limb (with the exception of skin innervation to the upper shoulder, which comes from the cervical plexus). The plexus has a layered architecture:

Roots → Trunks → Divisions → Cords → Branches

(Memorized as “Real Texans Drink Cold Beer” — Roots, Trunks, Divisions, Cords, Branches.)

• Roots (C5, C6, C7, C8, T1): the ventral rami of these segments.
• Trunks (three):
  • Upper trunk: from C5 + C6.
  • Middle trunk: from C7.
  • Lower trunk: from C8 + T1.
• Divisions (six): each trunk divides into an anterior and a posterior division. Anterior divisions tend to supply flexors; posterior divisions supply extensors.
• Cords (three):
  • Lateral cord: from anterior divisions of upper and middle trunks (C5-C7).
  • Medial cord: from anterior division of lower trunk (C8-T1).
  • Posterior cord: from posterior divisions of all three trunks (C5-T1).
• Branches (the named peripheral nerves): emerge from the cords.

Major Branches

Brachial Plexopathy Patterns

• Upper trunk (C5-C6, Erb palsy): from obstetric injury or motorcycle accident with shoulder depression. Weakness of shoulder abduction, elbow flexion, supination, and external rotation. Arm hangs in the “waiter’s tip” position. Sensory loss in lateral arm.
• Lower trunk (C8-T1, Klumpke palsy): from traction on an abducted arm. Weakness of intrinsic hand muscles. Sensory loss in medial arm. T1 involvement may produce Horner syndrome.
• Pancoast tumor: superior sulcus lung cancer invading the lower brachial plexus plus the sympathetic chain. Lower trunk plexopathy with Horner syndrome.
• Neuralgic amyotrophy (Parsonage-Turner syndrome): idiopathic, often after immunization or surgery. Sudden shoulder pain followed by patchy weakness in brachial plexus distribution, often involving long thoracic nerve (winged scapula) or suprascapular nerve. Recovery usually substantial but slow.
• Thoracic outlet syndrome: compression of the lower trunk by a cervical rib, fibrous band, or other anomaly. Vascular compression may coexist.

The Lumbar Plexus

Formed by the ventral rami of L1-L4 within the psoas muscle. Major branches:

• Iliohypogastric (L1): sensation to lateral hip area.
• Ilioinguinal (L1): sensation to inguinal region.
• Genitofemoral (L1-L2): sensation to upper thigh and (in males) the cremaster reflex.
• Lateral femoral cutaneous (L2-L3): sensation to anterolateral thigh. Compression at the inguinal ligament produces meralgia paresthetica.
• Femoral nerve (L2-L4): motor to iliopsoas, sartorius, quadriceps. Sensation (via saphenous branch) to medial leg.
• Obturator nerve (L2-L4): motor to thigh adductors. Sensation to medial thigh.

Lumbar Plexus Injury

• Femoral neuropathy: from diabetic amyotrophy, retroperitoneal hematoma (anticoagulation), surgical injury, prolonged lithotomy position, hip surgery. Weakness of knee extension and hip flexion, with reduced or absent knee jerk and sensory loss in medial leg.
• Diabetic amyotrophy (Bruns-Garland syndrome): subacute severe pain followed by proximal lower extremity weakness, often unilateral initially. Affects the lumbosacral plexus and roots.
• Retroperitoneal hematoma: in an anticoagulated patient, can compress the femoral nerve in the psoas. Acute femoral neuropathy.

The Sacral Plexus

Formed by the ventral rami of L4-S4, lying on the posterior wall of the pelvis. The lumbar and sacral plexuses are sometimes considered together as the lumbosacral plexus. Major branches:

• Sciatic nerve (L4-S3): the largest nerve in the body. Composed of two parts that share a common sheath:
  • Tibial division: motor to hamstrings (except short head of biceps), gastrocnemius, soleus, tibialis posterior, flexor digitorum longus, flexor hallucis longus, intrinsic foot muscles. Sensation to sole of foot. Below the popliteal fossa, becomes the tibial nerve.
  • Common peroneal (fibular) division: motor to short head of biceps, tibialis anterior (via deep peroneal), peroneus longus and brevis (via superficial peroneal). Sensation to lateral leg and dorsum of foot.
• Superior gluteal nerve (L4-S1): motor to gluteus medius and minimus (hip abductors). Damage produces Trendelenburg gait (the patient cannot stabilize the pelvis during the stance phase on the affected side).
• Inferior gluteal nerve (L5-S2): motor to gluteus maximus (hip extensor).
• Pudendal nerve (S2-S4): motor to external anal and urethral sphincters and pelvic floor muscles. Sensation to perineum.
• Posterior femoral cutaneous nerve (S1-S3): sensation to posterior thigh.

Sacral Plexus Injury

• Sciatic neuropathy: hip surgery, hip fracture, intramuscular injections, piriformis syndrome, sciatic nerve tumor. Combined tibial and peroneal deficit with sparing of hip flexion and knee extension (femoral nerve territory).
• Common peroneal nerve at the fibular head: prolonged crossing of legs, prolonged squatting, casts, weight loss with reduced subcutaneous fat. Foot drop with sensory loss on lateral leg and dorsum of foot.
• Obstetric injury: lumbosacral plexus can be injured during difficult delivery.
• Pelvic malignancy: invasion of the lumbosacral plexus by cervical, prostate, rectal cancers. Painful progressive lower extremity weakness.

The Cervical Plexus

Formed by the ventral rami of C1-C4. Less prominent than the brachial and lumbosacral plexuses. Major branches:

• Phrenic nerve (C3-C5): motor to diaphragm. Unilateral paralysis produces elevated hemidiaphragm; bilateral paralysis produces severe respiratory failure.
• Lesser occipital, great auricular, transverse cervical, supraclavicular nerves: sensory to scalp behind ear, lateral neck, anterior neck, upper shoulder.
• Ansa cervicalis: motor to strap muscles of the neck.

Investigation of Plexopathies

When plexopathy is suspected, the bedside exam is supplemented by:

• EMG and nerve conduction studies: localize the lesion to a specific plexus region and distinguish plexopathy from radiculopathy or peripheral nerve injury.
• MRI of the plexus: shows masses, inflammation, hematoma, or other structural causes.
• Laboratory studies: blood glucose for diabetic amyotrophy, coagulation studies for retroperitoneal hematoma, infectious and autoimmune workup as appropriate.

🔍 Did You Know?

Neuralgic amyotrophy (also called Parsonage-Turner syndrome or idiopathic brachial neuritis) is an underrecognized cause of acute upper extremity weakness. The classical presentation is sudden, severe shoulder or upper arm pain — often described as the worst pain the patient has ever felt — lasting days to weeks, followed by patchy weakness in the brachial plexus distribution. The long thoracic nerve (producing scapular winging) and suprascapular nerve (weakness of shoulder abduction and external rotation) are particularly often involved. Triggers include recent viral infection, immunization, surgery, or childbirth — supporting an autoimmune or inflammatory mechanism. Imaging is often normal; the diagnosis is clinical. Recovery is usually substantial but slow, often taking 18 months to several years. Recognition matters because patients are often initially diagnosed with rotator cuff injury and treated with prolonged immobilization, which can produce frozen shoulder and worsen the eventual functional outcome.

Pitfalls and Pearls

• Dermatomes overlap by 1-2 segments. Loss of a single root may produce minimal sensory deficit because adjacent roots cover the area.
• “C3, 4, 5 keeps the diaphragm alive”: a high cervical cord injury above C3 produces respiratory failure.
• The brachial plexus has 5 roots, 3 trunks, 6 divisions, 3 cords, and 5 main branches: “Real Texans Drink Cold Beer.”
• Erb palsy (upper trunk, C5-C6) produces the “waiter’s tip” arm posture.
• Klumpke palsy (lower trunk, C8-T1) produces intrinsic hand weakness, often with Horner syndrome from T1 sympathetic involvement.
• Pancoast tumor presents with lower trunk plexopathy plus Horner syndrome. Always image the lung apex.
• Neuralgic amyotrophy presents with severe shoulder pain followed by patchy weakness, often in long thoracic or suprascapular distributions. Recovery is slow but usually substantial.
• L5 radiculopathy vs peroneal palsy: L5 weakens gluteus medius (hip abduction) and tibialis posterior (inversion); peroneal palsy spares both. Test these specifically.
• S1 radiculopathy weakens plantar flexion and the ankle jerk; sensory loss in the lateral foot and sole.
• Trendelenburg gait suggests superior gluteal nerve or L5 root weakness with gluteus medius involvement.
• Diabetic amyotrophy presents with subacute severe lower extremity pain followed by weakness, often unilateral initially. Treatment is supportive; gradual recovery is common.

References

1. Stewart JD. Focal Peripheral Neuropathies. 4th ed. JBJ Publishing; 2010.
2. Wilbourn AJ. Brachial plexus disorders. In: Dyck PJ, Thomas PK, eds. Peripheral Neuropathy. 4th ed. Elsevier; 2005.
3. van Alfen N, van Engelen BG. The clinical spectrum of neuralgic amyotrophy in 246 cases. Brain. 2006;129(2):438-450.
4. Said G. Diabetic neuropathy — a review. Nat Clin Pract Neurol. 2007;3(6):331-340.
5. Brazis PW, Masdeu JC, Biller J. Localization in Clinical Neurology. 7th ed. Wolters Kluwer; 2017.
6. Standring S, ed. Gray’s Anatomy. 42nd ed. Elsevier; 2021.