Klumpke's Palsy

Introduction

Introduction to Klumpke’s Palsy

Klumpke’s palsy, also known as Klumpke’s paralysis or Dejerine‑Klumpke palsy, is a lower trunk brachial plexus injury affecting the C8 and T1 nerve roots. It results in paralysis of the intrinsic hand muscles and the long flexors of the fingers, producing a characteristic claw hand deformity. Sensory loss involves the medial forearm and the medial one and a half digits. When the T1 root is injured close to the spinal cord, the associated sympathetic fibres are disrupted, leading to Horner’s syndrome (ipsilateral ptosis, miosis, and anhidrosis).

Although less common than Erb‑Duchenne palsy, Klumpke’s palsy is clinically significant because it produces profound hand dysfunction. This module covers the anatomical basis, aetiology, clinical features, diagnostic evaluation, and management of this lower trunk plexopathy.

Study

1. Anatomical Basis

The lower trunk of the brachial plexus is formed by the union of the C8 and T1 anterior rami. Its anterior division forms the medial cord, while its posterior division joins the posterior cord. The medial cord gives rise to the ulnar nerve (C8, T1), the medial root of the median nerve (C8, T1), the medial pectoral nerve, and the medial cutaneous nerves of the arm and forearm. The posterior cord contributes fibres to the radial nerve (C5–T1) and axillary nerve (C5, C6), but the lower trunk contribution to the radial nerve is primarily to the long extensors of the forearm and hand, while the intrinsic muscles of the hand are supplied by the ulnar nerve and the thenar muscles (via the median nerve) from C8, T1.

Therefore, a lower trunk injury paralyzes all intrinsic hand muscles (interossei, lumbricals, hypothenar muscles, adductor pollicis, deep head of flexor pollicis brevis, and the thenar muscles to a variable degree), the long flexors of the fingers (flexor digitorum profundus to the ring and little fingers, flexor pollicis longus), and the wrist and finger extensors (extensor digitorum, extensor pollicis longus, etc. to a variable extent). The sympathetic fibres destined for the head and neck travel via the T1 root, so a proximal avulsion causes Horner’s syndrome.

2. Mechanisms of Injury

Klumpke’s palsy occurs when the arm is forcibly hyperabducted, stretching the lower trunk. Common scenarios include: (1) traction on an abducted arm during a fall, as when grasping a tree branch to break a fall; (2) obstetric traction on the extended arm during a breech delivery; (3) compression by a Pancoast tumour at the lung apex; (4) cervical rib or fibrous band compressing the lower trunk (thoracic outlet syndrome); and (5) direct trauma or iatrogenic injury during surgery. The lesion can be a neuropraxia, axonotmesis, neurotmesis, or root avulsion.

3. Clinical Features

The classic deformity is a claw hand (main en griffe), characterised by hyperextension at the metacarpophalangeal (MCP) joints and flexion at the interphalangeal (IP) joints of the fingers. This results from paralysis of the intrinsic muscles (lumbricals and interossei) that normally flex the MCP joints and extend the IP joints, leaving the long extensors and flexors unopposed. Wasting of the thenar and hypothenar eminences is present. The patient is unable to abduct or adduct the fingers (loss of interossei), has a positive Froment’s sign (thumb IP flexion when pinching due to adductor pollicis paralysis), and cannot perform fine manipulative tasks.

Sensory loss follows the C8, T1 dermatomes: the medial aspect of the forearm and the medial one and a half digits. Horner’s syndrome is present if the T1 root is avulsed preganglionically; it consists of ptosis (drooping eyelid), miosis (constricted pupil), anhidrosis (lack of sweating) on the ipsilateral face, and sometimes enophthalmos. In obstetrical cases, the Moro reflex may be asymmetric, and the grasp reflex is absent on the affected side.

4. Differential Diagnosis

Klumpke’s palsy must be distinguished from an isolated ulnar nerve palsy or a median nerve lesion. In an ulnar nerve lesion, clawing is more pronounced in the ring and little fingers (because the median‑innervated lumbricals to the index and middle are intact), while in Klumpke’s palsy all fingers are affected. Sensory loss in ulnar neuropathy is limited to the palmar and dorsal aspects of the hand (sparing the forearm), while C8/T1 root involvement extends more proximally. Horner’s syndrome indicates a preganglionic T1 lesion and is not seen in peripheral nerve palsies. A Pancoast tumour should be excluded in adults.

5. Prognosis and Management

The prognosis depends on the nature and severity of the injury. Neuropraxia may recover spontaneously over weeks to months. Axonotmesis has a slower recovery over months; neurotmesis and root avulsions require surgical repair. Horner’s syndrome is a poor prognostic indicator as it signifies preganglionic avulsion.

Initial management includes physiotherapy to maintain passive range of motion, splinting to prevent contractures (e.g., MCP flexion splint to counteract clawing), and occupational therapy. Surgical options include nerve grafting for postganglionic ruptures and nerve transfers for root avulsions. Tendon transfers (e.g., using the extensor carpi radialis longus to restore thumb opposition) are considered in late presentations. For Pancoast tumours, treatment is directed at the underlying malignancy.

Summary

Summary of Klumpke’s Palsy

Klumpke’s palsy is a lower brachial plexus (C8, T1) injury producing claw hand deformity, intrinsic muscle wasting, sensory loss on the medial forearm and hand, and Horner’s syndrome in preganglionic T1 avulsions. It is caused by hyperabduction trauma, obstetric brachial plexus injuries, or Pancoast tumours. Management ranges from conservative physiotherapy to nerve surgery and tendon transfers. Differentiating it from isolated ulnar or median nerve lesions is crucial for appropriate treatment.