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Posterior interosseous nerve (PIN) palsy has been recognised at least since 1905 when Guillain and Courtellemont described a case in an orchestral conductor. In 1899 Gowers described involvement of the muscles of the forearm in radial nerve palsy but did not specifically note damage to its important branch, the PIN. During the first world war Tinel described the anatomy without mentioning the nerve by name and without discussion of causation. By the end of the second world war the PIN had been so named.1
The PIN consists of one bundle of motor nerve fibres at the arcade of Fröhse (the supinator arch ) but divides into two bundles near its point of exit from the supinator muscle. The recurrent superficial motor branch innervates the extensor digitorum, extensor digiti minimi, and extensor carpi ulnaris; the descending or deep motor branch innervates the abductor pollicis longus, extensor pollicis brevis, extensor pollicis longus, and extensor indicis.2
The syndrome is also known as the supinator syndrome. It is distinguished from a seventh cervical root syndrome in which the triceps is involved but the wrist extensors usually are spared.
Palsy of the PIN produces the characteristic syndrome of weakness of extension of the digits and thumb with preservation of extension of the wrist which, nevertheless, may deviate radially. Sensory function, supination, and brachioradialis are not affected. Pain is often felt lateral to the elbow.
Palsy of the PIN may be caused by acute trauma in gunshot wound or pressure from a space occupying lesion. Repetitive use of the forearm has caused PIN palsy in a bartender, violinist, swimmer, conductor, waiter, factory worker, and an embroiderer. It has also been reported with strenuous arm exercises, snow shovelling, in frisbee games and tennis playing, and after the prolonged carrying of an M60 machine gun. It has also been reported after cannulation of a forearm vein.3
We report a case of PIN palsy after repetitive movements of the forearm and we have named this variant “upholsterer's PIN”.
A 47 year old right handed woman, an enthusiastic pianist, at an upholstery class one evening used both hands to compress springs and apply clips to the springs. During that evening she noted aching around the lower part of the right arm and on the next day found she could not extend the right thumb and fingers. She had not slept heavily on that side and had not noted trauma to the elbow. She did not have cervical pain or numbness.
The region of the lateral epicondyle of the elbow was tender. Finger flexion and volar flexion at the wrist were strong as were flexion and extension of the elbow, supination, and pronation. Examination failed to show movement in the extensor digitorum and extensor pollicis longus.
An EMG showed changes typical of a PIN lesion—namely, active denervation in the extensor carpi radialis brevis, extensor digitorum communis, and extensor carpi ulnaris. The brachioradialis, biceps, and triceps brachii were normal as was sensory conduction in the superficial branch of the radial nerve. The active denervation noted in the extensor carpi radialis longus is an anomaly and suggests aberrant innervation or anatomical anomaly.
At exploration the PIN was degenerate from the origin of the superficial radial nerve to the branch of the brachioradialis although it did not seem compressed. An 8 to 10 mm segment of obvious abnormality within the PIN itself was resected and the nerve ends sutured together. The patient continued to recover function and did not require tendon transfer as her functional deficit substantially improved.
The histology of the excised segment showed very severe demyelination, presumed to be the primary pathology. Demyelination secondary to underlying axonal disease could not be excluded (figure1).
The clinical features were typical of a PIN palsy. However, EMG studies showed active denervation in extensor carpi radialis longus and extensor carpi radialis brevis. As the extensor carpi radialis longus is innervated by the radial nerve before the origin of the PIN, it is possible to distinguish a PIN palsy from a more proximal radial nerve injury, which typically produces wrist drop and has also been reported after repetitive muscle contraction.4
We suggest that focal demyelination in the PIN and conduction block resulted from ischaemia due to direct pressure on the nerve at an area of anatomical constriction as a result of the repetitive action of the surrounding muscles.
Patients with PIN palsy sometimes report a history of forceful, repetitive rotation of the forearm preceding the onset of symptoms. Because we do not know of a report of PIN palsy in association with the compressing of springs, we have named this palsy “Upholsterer's PIN”.
We are extremely grateful to Dr Elias Ragi for the nerve conduction studies and to Dr R Simpson for supplying the photographs illustrating nerve demyelination.
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