Gross Anatomy · Applied Anatomy
The brachial plexus is a complex network of nerves formed by the anterior rami of the C5 to T1 spinal nerves, with variable contributions from C4 and T2. It provides motor and sensory innervation to the entire upper limb. Injuries to the brachial plexus, whether traumatic (birth injuries, road traffic accidents, penetrating wounds) or atraumatic (inflammation, tumors, radiation), result in characteristic patterns of paralysis, sensory loss, and deformity. Understanding the anatomical organisation of the plexus—roots, trunks, divisions, cords, and terminal branches—is fundamental to localising lesions, predicting deficits, and planning management.
This module covers the applied anatomy of brachial plexus injuries, including classification, mechanisms, specific syndromes (Erb‑Duchenne palsy, Klumpke’s palsy, total plexus lesions), clinical evaluation, and the anatomical basis of surgical reconstruction.
The brachial plexus is formed by the union of the anterior primary rami of C5, C6, C7, C8, and T1. These roots combine to form three trunks: upper (C5, C6), middle (C7), and lower (C8, T1). Each trunk divides into anterior and posterior divisions. The divisions then regroup into three cords: lateral cord (anterior divisions of upper and middle trunks), medial cord (anterior division of lower trunk), and posterior cord (posterior divisions of all three trunks). The terminal branches arise from these cords and supply the muscles and skin of the upper limb.
Key branches from the roots and trunks include the dorsal scapular nerve (C5), long thoracic nerve (C5, C6, C7), nerve to subclavius (C5, C6), and suprascapular nerve (C5, C6). The lateral cord gives off the lateral pectoral nerve and then divides into the musculocutaneous nerve and the lateral root of the median nerve. The medial cord gives off the medial pectoral nerve, medial cutaneous nerve of arm and forearm, and then divides into the ulnar nerve and medial root of the median nerve. The posterior cord gives off the upper subscapular, thoracodorsal (middle subscapular), and lower subscapular nerves, and then divides into the axillary nerve and the radial nerve.
Brachial plexus injuries can be classified by mechanism: (1) Traction injuries, where the head is forcibly separated from the shoulder, stretching or avulsing the roots; (2) Compression injuries, such as from a Pancoast tumour or a cervical rib; (3) Penetrating injuries from stab or gunshot wounds; (4) Birth injuries (obstetric brachial plexus palsy), usually from shoulder dystocia; (5) Iatrogenic injuries, including during surgical positioning or radiation therapy; and (6) Inflammatory or neoplastic plexopathies (e.g., Parsonage‑Turner syndrome).
The level of injury—preganglionic (root avulsion) or postganglionic (rupture or neuroma distal to the dorsal root ganglion)—determines the potential for spontaneous recovery and surgical options. Preganglionic avulsions have a poor prognosis and may require nerve transfers, whereas postganglionic injuries may recover or benefit from nerve grafting.
Injury to the upper trunk (C5, C6) is the most common pattern. It results in paralysis of the shoulder abductors and external rotators (deltoid, supraspinatus, infraspinatus, teres minor), the elbow flexors (biceps, brachialis), and the supinator. The arm hangs adducted and internally rotated, with the forearm pronated and the wrist and fingers flexed—the classic ‘waiter’s tip’ or ‘policeman’s tip’ posture. Sensory loss occurs over the lateral aspect of the shoulder and the lateral forearm.
This lesion is commonly caused by excessive lateral flexion of the neck to the opposite side with shoulder depression (e.g., in motorcycle accidents or difficult childbirth). The shoulder dystocia during delivery can produce an obstetric Erb’s palsy. Associated Horner’s syndrome suggests a preganglionic injury at T1.
Injury to the lower trunk (C8, T1) is less common. It results in paralysis of the intrinsic hand muscles (thenar, hypothenar, interossei, lumbricals) and the long flexors of the fingers (flexor digitorum profundus to the ulnar side, flexor pollicis longus). The result is a claw hand deformity with hyperextension at the MCP joints and flexion at the IP joints. Sensory loss occurs over the medial forearm and the medial one and a half digits. Horner’s syndrome (ptosis, miosis, anhidrosis) is often present due to involvement of the sympathetic fibres to the head that run with the T1 root.
Common causes include hyperabduction of the arm (e.g., grabbing a tree branch during a fall) or a Pancoast tumour compressing the lower trunk. In birth injuries, it may result from traction on the abducted arm.
Complete involvement of C5–T1 leads to a flail, anaesthetic limb. All motor function from the shoulder to the hand is lost. Sensory loss covers the entire arm except for the axillary border of the upper arm (supplied by the intercostobrachial nerve from T2). This devastating injury is most commonly caused by high‑velocity trauma, such as motorcycle accidents. Surgical reconstruction aims to restore some elbow flexion and shoulder stability, often using nerve transfers (e.g., spinal accessory nerve to suprascapular nerve, intercostal nerves to musculocutaneous nerve).
A thorough neurological examination is critical to localise the level and extent of injury. Motor testing should systematically assess myotomes and peripheral nerves. Sensory examination maps dermatomes and the autonomous zones of the major nerves. The presence of Horner’s syndrome indicates proximal injury (T1 root avulsion). Winged scapula suggests damage to the long thoracic nerve (C5, C6, C7). A positive Tinel’s sign over the supraclavicular fossa may indicate a postganglionic lesion. Electromyography and nerve conduction studies, along with MRI and CT myelography, confirm the diagnosis and help differentiate preganglionic from postganglionic lesions.
Prognosis depends on the severity (neuropraxia, axonotmesis, neurotmesis, avulsion), level (preganglionic vs postganglionic), and time to intervention. Neuropraxia often recovers spontaneously within weeks to months. Axonotmesis may regenerate over months if the endoneurial tubes remain intact. Neurotmesis and avulsions require surgical intervention. Options include primary nerve repair, nerve grafting (e.g., sural nerve grafts), nerve transfers (neurotisation), and tendon transfers for late presentations. Physiotherapy and splinting prevent contractures and maintain joint mobility.
Brachial plexus injuries vary from mild traction neuropraxia to complete avulsion of nerve roots. The pattern of deficit depends on the level: upper trunk (C5, C6) leads to Erb‑Duchenne palsy with waiter’s tip deformity; lower trunk (C8, T1) produces Klumpke’s palsy with claw hand; total plexus injury results in a flail limb. Horner’s syndrome signifies preganglionic T1 avulsion. Management ranges from conservative monitoring to complex nerve reconstruction. Applied anatomical knowledge is essential for accurate diagnosis, prediction of recovery, and surgical planning.