Brachial Plexus Injury — Klumpke's Paralysis

Populations and Risk Factors

• Neonates during breech deliveries with arm trapped overhead (hyperabduction mechanism) — rarer than Erb's palsy in obstetric injuries; incidence approximately 0.5 per 1,000 live births for all lower trunk palsies
• Adults after falls with the arm outstretched and forcefully abducted overhead — grabbing a fixed object during a fall (e.g., a tree branch, railing) applies upward traction on the lower trunk
• Motorcycle and high-speed vehicle accidents — the arm is hyperabducted and forced upward on impact
• Individuals with cervical ribs or anomalous fibrous bands — the C8–T1 roots and lower trunk are compressed against the rib or band, producing a chronic compressive lower trunk plexopathy (overlaps with neurogenic thoracic outlet syndrome)
• Pancoast tumor (superior sulcus lung tumor) — the tumor invades the lower trunk from below, producing progressive C8–T1 deficit with Horner's syndrome; this is a critical differential because it mimics traumatic Klumpke's but requires oncological, not rehabilitative, management
• Median sternotomy and cardiac surgery — retraction of the sternal halves can stretch the lower trunk, producing postoperative hand weakness

Causes and Pathophysiology

Lower Trunk Anatomy and Vulnerability

The inferior trunk of the brachial plexus forms from the union of C8 and T1 ventral rami. It descends over the first rib behind the subclavian artery, where it is anatomically constrained:

• Inferior position: The lower trunk crosses the first rib at the lowest point of the plexus, making it the most vulnerable to upward traction forces — when the arm is hyperabducted, the lower trunk is stretched over the first rib like a rope over a pulley
• Proximity to the sympathetic chain: The T1 root passes close to the stellate ganglion (inferior cervical/first thoracic sympathetic ganglion) as it exits the T1 foramen; severe traction that avulses the T1 root frequently disrupts the sympathetic fibers, producing Horner's syndrome
• Derivation pathway: The lower trunk continues as the medial cord, giving rise to the medial pectoral nerve, the medial cutaneous nerves of the arm and forearm, the ulnar nerve (C8–T1), and the medial contribution to the median nerve (C8–T1 fibers that form the medial head of the median nerve). The lower trunk also contributes C8 fibers to the posterior cord (radial nerve)

This means a complete lower trunk injury affects all ulnar nerve-innervated muscles, the C8–T1 median nerve-innervated muscles (thenar group, lateral two lumbricals via the anterior interosseous nerve), and potentially the C8 contribution to the radial nerve (finger extensors, thumb extensors).

Traction Injury Mechanism

The classic mechanism is forceful hyperabduction of the arm — the arm is pulled upward and away from the trunk, stretching the lower trunk over the first rib. The sequence of injury severity follows the same neurapraxia → axonotmesis → neurotmesis/avulsion progression as Erb's palsy, but the lower trunk position makes avulsion more likely because:

• The C8 and T1 roots have shorter intradural segments than the upper roots, providing less slack before the tethering point at the spinal cord is reached
• The T1 root exits the spinal cord at the cervicothoracic junction where the cord is relatively fixed, further reducing the available stretch tolerance
• Avulsion of C8–T1 roots disconnects the motor neurons from the spinal cord — the denervated hand muscles undergo irreversible atrophy without surgical nerve transfer

Claw Hand Deformity Mechanism

The claw hand in Klumpke's paralysis follows the same mechanism as the ulnar claw but is more severe because both the ulnar and median nerve C8–T1 contributions are lost:

• MCP hyperextension: The interossei and lumbricals (which flex the MCP joints) are paralyzed; the extrinsic extensors (extensor digitorum, innervated by the radial nerve via C7, typically intact) are unopposed and hyperextend the MCP joints
• IP flexion: In a pure lower trunk lesion, the long flexors (FDP, FDS) may be partially affected (C8 contribution lost), which paradoxically reduces the severity of the claw compared to a distal ulnar nerve lesion (the "ulnar paradox" in reverse — a proximal lesion produces less severe clawing than a distal lesion because the FDP is also weakened)
• Digits 4–5 most affected: The ulnar nerve innervates the interossei and medial two lumbricals; digits 4–5 show the most pronounced clawing because both the lumbrical and interosseous function is lost
• Digits 2–3 variably affected: If the C8–T1 median nerve fibers are also disrupted, the lateral two lumbricals (median nerve) are lost, and all four digits develop clawing — this distinguishes Klumpke's from an isolated ulnar nerve lesion where digits 2–3 are spared

Horner's Syndrome Mechanism

The preganglionic sympathetic fibers that supply the head and face originate from the intermediolateral cell column at T1 (and T2), exit with the T1 ventral root, and synapse at the stellate ganglion. If the T1 root avulsion extends to disrupt these sympathetic fibers, the result is ipsilateral Horner's syndrome:

• Ptosis: Partial drooping of the upper eyelid (loss of Muller's muscle, smooth muscle innervated by sympathetic fibers — not the levator palpebrae, which is CN III)
• Miosis: Pupillary constriction (loss of sympathetic pupillodilator fibers; parasympathetic constrictor is unopposed)
• Anhidrosis: Absent sweating on the ipsilateral face (loss of sympathetic sudomotor fibers)

The presence of Horner's syndrome in the context of lower trunk plexopathy indicates T1 root avulsion — this is a poor prognostic sign because avulsion injuries do not recover spontaneously.

Signs and Symptoms

Motor Deficits

• Claw hand deformity: MCP hyperextension with IP flexion, most pronounced in digits 4–5; may extend to digits 2–3 if the median nerve C8–T1 contribution is also affected; the hand appears non-functional for grip and fine manipulation
• Intrinsic muscle paralysis: Loss of all interossei (finger abduction/adduction), lumbricals 3–4 (or all four), hypothenar group (abductor digiti minimi, flexor digiti minimi, opponens digiti minimi), and adductor pollicis — producing positive Froment's sign and Wartenberg sign
• Grip weakness: Loss of intrinsic contribution to power grip (interossei stabilize the MCP joints during grip); FDP may be weakened (C8 contribution) further reducing grip force
• Wrist flexor weakness: FCU (ulnar nerve, C8–T1) is weak or absent; wrist flexion may deviate radially due to unopposed FCR (median nerve, C6–C7)
• Finger extension may be affected: If C8 fibers to the posterior cord are disrupted, finger extensors (extensor digitorum, extensor indicis, extensor digiti minimi) may be weakened

Sensory Deficits

• Medial arm and forearm numbness: Medial cutaneous nerve of the arm (T1) and medial cutaneous nerve of the forearm (C8–T1) — numbness or paresthesia along the medial arm from the axilla to the elbow and medial forearm to the wrist
• Ulnar 1.5 digit numbness: Sensory loss in the little finger and ulnar half of the ring finger (ulnar nerve distribution)
• Median nerve C8–T1 territory: If the medial head of the median nerve is involved, there may be additional sensory changes in the index and middle fingers — though this is often masked by intact C6–C7 lateral head contribution

Horner's Syndrome (One-Third of Severe Cases)

• Ipsilateral ptosis (partial upper lid droop), miosis (constricted pupil), and anhidrosis (dry facial skin on the affected side)
• Indicates T1 root avulsion — the injury has extended to the sympathetic chain
• A critical finding because it changes the prognosis: root avulsion does not recover spontaneously

Assessment Profile

Subjective Presentation

• Chief complaint: "I can't grip anything — my hand feels useless"; "My fingers curl up and I can't straighten them"; in neonatal cases (parent report): "The baby's hand is curled up and doesn't move"
• Pain quality: Burning or lancinating neuropathic pain along the medial arm and forearm; deep aching in the hand from attempted use of paralyzed muscles; medial elbow pain may be present if compensatory overuse of remaining forearm muscles develops
• Onset: Acute traumatic event (fall with outstretched arm overhead, motorcycle accident, breech delivery) with immediate hand weakness; or insidious progressive hand weakness and wasting (suggests Pancoast tumor, cervical rib compression, or radiation plexopathy — requires urgent investigation)
• Aggravating factors: Any activity requiring grip strength, fine manipulation (buttons, keys, writing, typing); sustained arm elevation overhead may reproduce traction symptoms; cold exposure often worsens neuropathic pain
• Easing factors: Supporting the hand and wrist with a splint reduces the claw posture and protects the intrinsic muscles from overstretching; rest reduces neuropathic pain; warmth may ease neuropathic symptoms
• Red flags: Progressive hand weakness without trauma → suspect Pancoast tumor (superior sulcus lung tumor) compressing the lower trunk; refer for chest imaging immediately, especially if Horner's syndrome is present; bilateral hand weakness → consider motor neuron disease, cervical myelopathy, or bilateral plexopathy; refer for neurological evaluation

Observation

• Local inspection: Claw hand deformity (MCP hyperextension, IP flexion, most pronounced digits 4–5); interosseous wasting visible as guttering between metacarpals on the dorsal hand; hypothenar atrophy (flattening of the medial palm); thenar wasting if median C8–T1 fibers are involved; Wartenberg sign (little finger held in abduction); check the ipsilateral eye for ptosis and pupil asymmetry (Horner's syndrome)
• Posture: No consistent whole-body postural pattern specific to Klumpke's; however, the patient may guard the affected hand against the body; assess for forward head posture and protracted shoulders if concurrent TOS or cervical rib is suspected
• Gait: Not applicable

Palpation

• Tone: Interosseous muscles — atrophic, soft, reduced bulk palpable between metacarpals. Hypothenar eminence — flattened and soft. Thenar eminence — may be atrophic if median C8–T1 involvement exists. Forearm flexor group — FCU may be flaccid while FCR remains normal. Forearm extensors — may be weak if C8 radial contribution is affected. Scalenes and pectoralis minor — assess for hypertonicity contributing to concurrent lower trunk compression.
• Tenderness: Supraclavicular fossa — tenderness over the lower trunk as it crosses the first rib; scalene triangle — may be tender if concurrent compression exists; referred path tenderness: with neural irritation, tenderness may extend along the medial arm (medial cutaneous nerve of arm, T1) and medial forearm (medial cutaneous nerve of forearm, C8–T1) to the ulnar wrist and hand — this maps the C8–T1 distribution and should be correlated with sensory testing to distinguish from isolated ulnar nerve entrapment; palpate for cervical rib (bony prominence above the first rib in the supraclavicular fossa)
• Temperature: The affected hand may feel cool due to sympathetic involvement (T1 fibers); in Horner's syndrome, the ipsilateral face may feel warmer initially (loss of vasoconstrictor tone produces vasodilation) but eventually equalizes; the medial hand and forearm may feel cool from reduced sympathetic tone
• Tissue quality: Intrinsic hand muscles — soft, wasted, inelastic in chronic cases. Interosseous spaces on the dorsal hand feel hollow compared contralaterally. Forearm flexors (FCU region) — may feel soft and atrophic. Skin of the medial forearm and hand may show trophic changes (shiny, thin, hairless) from chronic denervation.

Motion Assessment

• AROM: Finger abduction and adduction absent or markedly weak (interossei); grip strength severely reduced (loss of intrinsic MCP stabilization and FDP weakness); wrist flexion may deviate radially (FCU loss with intact FCR); thumb opposition may be weak if thenar C8–T1 contribution is lost; shoulder and elbow function typically preserved (C5–C7 intact) — this preservation of proximal function with severe distal hand deficit is the hallmark of lower trunk palsy
• PROM / end-feel: MCP joints may be passively hyperextensible from unopposed extensor pull; IP joints may resist passive extension if chronic claw posture has produced adaptive shortening of the flexor tendons and volar plates; wrist PROM typically full; cervical PROM — assess for reproduction of symptoms with lateral flexion toward the affected side (compresses lower trunk against first rib/cervical rib)
• Resisted testing: Finger abduction — absent or trace (T1: dorsal interossei); finger adduction — absent or trace (T1: palmar interossei); thumb adduction — absent (T1: adductor pollicis, positive Froment's); wrist flexion with ulnar deviation — weak (C8–T1: FCU); grip — markedly reduced; shoulder abduction, elbow flexion, forearm supination — normal (C5–C6 intact); triceps — may be mildly weak if C8 contribution is disrupted

Special Test Cluster

Cluster interpretation: Froment's sign + Wartenberg sign + C8–T1 myotomal weakness with preserved C5–C6 function confirms a lower trunk lesion. If Horner's syndrome is also present, T1 root avulsion is likely and prognosis for spontaneous recovery is poor. If Roos test is positive, assess for concurrent thoracic outlet syndrome — lower trunk symptoms may be vascular or compressive rather than traction-based.

Differential Diagnoses