Brachial Plexus Injuries: Clinical Anatomy of Upper vs. Lower Trunk Lesions

Most students approach the brachial plexus as a brute-force memorization challenge: five roots, three trunks, six divisions, three cords, five terminal branches, and dozens of smaller branches along the way. This produces fragile knowledge that breaks under exam pressure. A better approach treats the plexus as a logical wiring diagram where nerve fibers from specific spinal levels are progressively reorganized as they travel from the neck to the arm. The fundamental principle is that each spinal nerve root (C5, C6, C7, C8, T1) contributes motor fibers to specific muscles and sensory fibers to specific skin areas. When those roots combine into trunks, the fibers are sorted — lateral cord fibers generally come from C5-C7 and supply anterior arm and forearm muscles, while medial cord fibers generally come from C8-T1 and supply hand muscles. The posterior cord receives contributions from all levels and supplies the extensors. If you understand this sorting logic, you can predict what will be lost with any plexus injury without having memorized every branch.

C5 is the 'shoulder root.' Its fibers contribute to the suprascapular nerve (supraspinatus and infraspinatus for shoulder abduction and external rotation), the axillary nerve (deltoid for shoulder abduction above 15 degrees), and the musculocutaneous nerve (biceps for elbow flexion and supination). Sensory territory includes the lateral arm via the superior lateral cutaneous nerve of arm (from axillary) and the lateral forearm via the lateral cutaneous nerve of forearm (from musculocutaneous). C6 is the 'elbow flexion root' that works closely with C5. It adds power to the biceps and brachioradialis for elbow flexion, and provides the wrist extensors (extensor carpi radialis longus and brevis). The brachioradialis reflex and biceps reflex primarily test C6 (with C5 contribution). C6 also supplies sensation to the thumb and index finger via the median nerve's digital branches. C7 is the 'extension root.' It is the primary supply to the triceps (elbow extension), the wrist flexors (flexor carpi radialis), and contributes to the finger extensors. The triceps reflex primarily tests C7. Loss of C7 alone causes a noticeable but not devastating weakness because C6 and C8 provide backup to many C7-supplied muscles. Sensory territory is the middle finger. C8 is the 'finger flexion root.' It supplies the flexor digitorum superficialis and profundus for grip strength, and contributes to the intrinsic hand muscles. Loss of C8 significantly weakens grip and fine finger movements. Sensory territory includes the ring and little finger via the ulnar nerve. T1 is the 'hand intrinsic root.' It is the primary supply to the small muscles of the hand — the interossei, lumbricals (via ulnar nerve), thenar muscles (via median nerve), and hypothenar muscles (via ulnar nerve). Loss of T1 causes devastating loss of fine motor control even though the long flexors (powered by C8) may still work. The finger adduction and abduction that allows you to spread your fingers apart and squeeze them together is primarily T1.

Erb-Duchenne palsy results from traction injury to the upper trunk, damaging the C5 and C6 fibers. In adults, this typically occurs from motorcycle accidents, falls onto the shoulder, or any mechanism that forcefully widens the angle between the neck and shoulder (depressing the shoulder while the head is pushed to the opposite side). In neonates, it occurs during difficult deliveries when lateral traction on the head during shoulder dystocia stretches the upper trunk. The clinical presentation is the 'waiter's tip' position, which is not arbitrary — it is the logical result of losing specific muscles while their antagonists remain intact. The arm hangs at the side (loss of deltoid and supraspinatus for abduction), is medially rotated (loss of infraspinatus and teres minor for lateral rotation, while subscapularis and pectoralis major are intact), the elbow is extended (loss of biceps and brachialis for flexion, while triceps from C7 is intact), and the forearm is pronated (loss of biceps supination, while pronators from C7-C8 are intact). The wrist may be flexed because the wrist extensors (C6) are weakened. Sensory loss in Erb-Duchenne palsy follows the C5-C6 dermatomes: the lateral arm, lateral forearm, and often the thumb and index finger. The biceps reflex (C5-C6) and brachioradialis reflex (C5-C6) are absent, while the triceps reflex (C7) is preserved. This reflex pattern is a classic exam question and the fastest way to localize the lesion level. Recovery depends on the severity of the stretch. Neurapraxia (bruising without structural damage) can recover completely within weeks to months. Axonotmesis (axon disruption with intact nerve sheaths) recovers more slowly as axons regenerate at approximately 1 mm per day. Neurotmesis (complete disruption) requires surgical repair and has a more guarded prognosis.

Klumpke palsy results from traction on the lower trunk, damaging C8 and T1 fibers. The classic mechanism is forced arm abduction — grabbing something overhead during a fall or, in neonates, traction on the arm during a breech delivery. In adults, axillary lymph node dissection and Pancoast tumors (lung apex tumors invading the lower plexus) can also cause lower trunk injury. The clinical presentation is dominated by loss of hand function. The intrinsic hand muscles (interossei, lumbricals, thenar, hypothenar) are paralyzed, causing a 'claw hand' deformity — the metacarpophalangeal joints hyperextend (because the extensors from C7 are intact but the interossei that flex the MCPs are lost) while the interphalangeal joints flex (because the long flexors from C8 have partial innervation disruption but the lumbricals that extend the IPs are lost). The claw is most prominent in the ring and little fingers because these are most dependent on ulnar-innervated intrinsics. Grip strength is significantly weakened because the finger flexors (flexor digitorum profundus and superficialis, partially C8) are affected and the interossei that contribute to grip force are paralyzed. Fine motor tasks — buttoning a shirt, writing, picking up small objects — become extremely difficult or impossible. Sensory loss follows the C8-T1 dermatomes: the medial forearm and the ring and little fingers. If the T1 root is damaged proximal to the white ramus communicans (the sympathetic fiber connection), the patient may also develop Horner syndrome: miosis (constricted pupil), ptosis (drooping eyelid), and anhidrosis (absent sweating) on the ipsilateral face. This occurs because sympathetic fibers destined for the head and face travel with T1 before ascending in the sympathetic chain. The combination of claw hand plus Horner syndrome is virtually pathognomonic for a proximal lower trunk lesion — and it is a board-favorite question. The AnatomyIQ app provides interactive lesion-based scenarios where you select which muscles and sensory areas are affected at each plexus level, building the pattern recognition needed to answer these questions quickly.

Isolated middle trunk (C7) injuries are uncommon but do occur, typically from direct trauma. The presentation includes weakness of elbow extension (triceps), wrist flexion and extension (affecting both flexor carpi radialis and extensor digitorum), and finger extension. The triceps reflex is lost. Sensory loss involves the middle finger and the posterior forearm. Because C7 innervation overlaps extensively with C6 and C8, isolated C7 lesions produce less functional impairment than upper or lower trunk lesions. In practice, many brachial plexus injuries are not cleanly limited to a single trunk. Motorcycle accidents and high-energy trauma often damage multiple levels simultaneously. The approach to these combined injuries is the same: systematically test each myotome (C5 shoulder abduction, C6 elbow flexion and wrist extension, C7 elbow extension, C8 finger flexion, T1 finger abduction), check each reflex (biceps C5-6, brachioradialis C5-6, triceps C7), and map the sensory loss to identify which root levels are involved. Total plexus avulsion (all five roots torn from the spinal cord) produces a completely flail, anesthetic arm. Root avulsions have a worse prognosis than trunk injuries because the nerve roots cannot regenerate once torn from the cord. MRI and CT myelography distinguish avulsion (preganglionic injury) from trunk rupture (postganglionic injury), which is critical for surgical planning.

Brachial plexus questions follow predictable patterns. The question stem describes a mechanism of injury and a set of findings (muscle weakness, sensory loss, reflex changes), and you need to identify the lesion level. The fastest approach is a three-step process. Step one: check the reflexes. If biceps and brachioradialis reflexes are absent but triceps is intact, the lesion is at C5-C6 (upper trunk). If the triceps reflex is absent but biceps is intact, the lesion involves C7. If all reflexes are intact but there is hand weakness, the lesion is at C8-T1 (lower trunk). Step two: confirm with motor findings. Upper trunk lesions lose shoulder abduction and elbow flexion. Lower trunk lesions lose hand intrinsics and grip. This should match the reflex pattern. Step three: check for bonus findings. Horner syndrome localizes to a proximal T1 lesion. Winging of the scapula (long thoracic nerve, C5-C7) suggests root-level damage rather than trunk damage, because the long thoracic nerve branches directly from the roots before they form trunks. The most commonly missed detail on exams is the difference between an upper trunk lesion (C5-C6 only) and an upper trunk plus middle trunk lesion (C5-C6-C7). The addition of C7 damage adds triceps weakness and triceps reflex loss. If the question includes both waiter's tip positioning AND elbow extension weakness, the lesion extends beyond the upper trunk alone.