Anterior interosseous nerve syndrome (Kiloh-Nevin Syndrome)
Dr. KS Dhillon
The anterior interosseous nerve syndrome is a constellation of signs and symptoms that refers to weakness of the flexor pollicis longus, pronator quadratus, and the flexor digitorum profundus to the index finger. The anterior interosseous nerve does supply sensory fibers to the radiocarpal, midcarpal, and carpometacarpal joints, though the syndrome by definition refers to a purely motor constellation of signs and symptoms.
The strictly motor anterior interosseous syndrome can be associated with additional extrasyndromic signs and symptoms. The additional findings suggest that the underlying pathology resides outside of the anterior interosseous nerve (median nerve or brachial plexus) or that the aberrant anatomic features exist distal to the pathologic lesion in the anterior interosseous nerve.
The causes of anterior interosseous nerve syndrome can be divided into 2 broad categories. The anterior interosseous neuropathies include those compression neuropathies, neuritides, congenital anomalies, and anatomic lesions, and discontinuities of the anterior interosseous nerve itself. The pseudo–anterior interosseous neuropathies [1] represent pathologies affecting more proximal anatomic sites, but involve nerve fascicles contributing to the anterior interosseous nerve more distally. The Parsonage-Turner syndrome, in which anterior interosseous nerve syndrome is associated with weakness of the parascapular muscles, is a classic example of the pseudo–anterior interosseous neuropathies [2].
Anatomy
The median nerve gives rise to the anterior interosseous nerve from its radial aspect just after coursing between the two heads of the pronator teres muscle. This take-off of the anterior interosseous nerve from the median nerve occurs 5 to 8 cm distal to the lateral epicondyle [3] and 22.4 to 23.4 cm proximal to the radial styloid [4,5]. It passes beneath the fibrous arch of the flexor digitorum superficialis muscle and then enters the flexor digitorum profundus muscle belly at about 30% of the forearm length distal to the medial epicondyle [6]. The nerve then passes distally on the volar surface of the interosseous membrane. About 4 cm distal to its takeoff from the median nerve, the anterior interosseous nerve gives rise to motor branches to the flexor pollicis longus, the flexor digitorum profundus to the index finger, and, the flexor digitorum profundus to the middle finger [3].
The nerve then supplies a motor branch to the pronator quadratus before terminating as sensory branches to the radiocarpal, midcarpal, and carpometacarpal joints.
Clinical presentation
The only consistent finding in the anterior interosseous syndrome is
paresis or paralysis of the flexor pollicis longus, pronator quadratus, and the flexor digitorum of the index finger. In patients with incomplete anterior interosseous syndrome, there may be weakness of either the flexor pollicis longus or the flexor digitorum profundus indicis [7]. Weakness initially manifests as difficulty or clumsiness with writing or with fine pinch activities such as sewing. A history of trauma suggests either mechanical disruption of the nerve, injury to the nerve, or compression neuropathy. Injuries causing anterior interosseous neuropathy include penetrating trauma, blunt injury, and traction injury. The association between supracondylar fractures of the humerus [8,9] and fractures of the proximal forearm [10-12] have classic associations with the anterior interosseous syndrome. With anterior interosseous or pseudo–anterior interosseous neuritides, the onset of neurologic symptoms is typically sudden and rapidly progressive. Patients usually complain of proximal volar forearm or shoulder pain. Pain is often of sudden onset and may be related to minor trauma.
Examination
In patients with anterior interosseous syndrome, the resting repose of the hand will exhibit an unnatural extension of the distal interphalangeal joint (DIP) of the index finger and interphalangeal joint (IP) of the thumb, as compared with the gentle flexion arcade of the remaining fingers.
The main finding on physical examination is weakness of the flexor pollicis longus, flexor digitorum profundus indicis, and pronator quadratus. Weakness of the flexor pollicis longus and flexor digitorum profundus to the index finger is indicated by an inability to make the “OK” sign. The DIP joint of the index finger and the IP joint of the thumb are hyperextended during attempted tip-to-tip pinch. The area of contact between the index finger and thumb is a flatter, broader area found more proximally.
Spinner [13] has described a sign where the patient is asked to make a fist. When making a fist the tips of the small, ring, and middle fingers are able to achieve flexion to the distal palmar crease. However, the tips of the index finger is conspicuously excluded. The thumb remains straight. It is usually difficult to examine the pronator quadratus.
Etiology
For the treatment of anterior interosseous nerve syndrome, the cause has to be identified.
The causes of anterior interosseous syndrome include:
Direct injury to the nerve
Midshaft radius fracture
Compression due to fibrous bands (pronator, FDS), enlarged median artery, hematoma (trauma, coagulopathy), and tumors
Idiopathic inflammatory anterior interosseous neuropathy
The causes of pseudo–anterior interosseous neuropathies include:
Supracondylar humerus fracture
Proximal radius fracture
Antebrachial venipuncture or catheterization
Inflammatory- Acute brachial neuropathy and Parsonage-Turner syndrome
Differential diagnosis
Anterior interosseous neuropathy must be distinguished from a tendon rupture. A tendon rupture can easily be excluded by careful examination for tenodesis. When the flexor tendon is intact, passive wrist extension should produce passive thumb and finger IP joint flexion. Tendon rupture should be suspected in patients with rheumatoid arthritis and Kienbo¨ck disease [3]. In patients with rheumatoid disease, attritional rupture can occur as a result of volar carpal subluxation. In patients with Kienbo¨ck disease, proximal carpal pathology may lead to attritional tendon rupture. Tendon rupture due to scaphoid nonunion also has been reported [14,15].
Eletrodiagnostic studies
Electrodiagnostic studies should include electromyography of the flexor pollicis longus, pronator quadratus, and flexor digitorum profundus indicis. The pronator teres is typically innervated by the median nerve, hence electromyographic testing of the pronator teres should distinguish anterior interosseous neuropathy from proximal compression of the median nerve affecting fascicles of the anterior introsseous nerve.
Electromyographic studies are most helpful after a history of trauma, especially blunt injury. Complete lesions of the nerve are amenable to immediate exploration and repair. Surgical exploration of incomplete lesions can be deferred for several months.
The presence of positive sharp waves or fibrillation potentials indicates
nerve degeneration and that provides an indication for surgical exploration.
Treatment
In the literature, there is considerable controversy surrounding the treatment of anterior interosseous syndrome. Sunderland [16] reported motor recovery in all patients following resection of fibrous bands that were constricting the anterior interosseous nerve followed by anterior interosseous neurolysis.
Stern [17] reported complete recovery in 3 patients with compression neuropathy of the anterior interosseous nerve after surgical treatment following the failure of conservative treatment.
Miller-Breslow et al [18], on the other hand, reported their results of
nonoperative management in 10 patients with spontaneous anterior interosseous nerve paralysis. Eight of their patients recovered fully within 1 year. Their patients reported a prodrome of forearm pain and they probably suffered from anterior interosseous neuritis rather than compression neuropathy.
This controversy relating to surgical versus nonoperative treatment of anterior interosseous syndrome may in large part be due to the broad range of pathologies that produce similar clinical findings.
Therefore, the probability and extent of motor recovery from anterior interosseous syndrome will depend on a correct and precise diagnosis.
Anterior interosseous syndrome represents a similar group of findings and does not refer to a single distinct pathology. A good history, thorough neurologic examination, and an electrodiagnostic study will distinguish pseudo–anterior interosseous neuropathies from focal lesions of the AIN itself.
Once the diagnosis is established, etiologic factors must guide therapy. A history of penetrating injury suggests mechanical disruption or compression of the nerve. Surgical exploration and nerve decompression or repair would be required.
When there is blunt trauma, management of anterior interosseous palsy is less straightforward. If electromyography is suggestive of a complete lesion then early surgical exploration would be indicated. Partial injuries can be given an opportunity to recover spontaneously. If there is no improvement after 6 to 12 weeks, surgical exploration may be warranted. If there are positive sharp waves or fibrillation potentials on electromyography, surgical exploration and neurolysis may be indicated.
Spontaneous or rapid onset of weakness is suggestive of anterior interosseous neuritis or pseudo–anterior interosseous neuritis. In such cases, neurologic symptoms are usually preceded by proximal anterior forearm or shoulder pain and tenderness. Pain usually subsides by the time weakness of the pinch is noted. If there is a history of fatigue, fever, myalgia, or other prodromic systemic symptoms then an inflammatory process is likely, which may resolve spontaneously or with systemic steroids.
There are, however, no persuasive studies that show that the use of systemic steroids has any effect on the rate, extent, or probability of motor recovery from anterior interosseous nerve syndrome.
Spinner [13] initially treats spontaneous paralysis of the anterior interosseous nerve nonsurgically but recommends surgical exploration within 12 weeks if no clinical or electromyographic improvement is evident. Spontaneous recovery after 12 months has been well-documented [18,19], and some have recommended waiting at least this long for spontaneous recovery before proceeding with surgical exploration.
Miller-Breslow et al [18] followed up 10 patients with spontaneous anterior interosseous nerve paralysis, all of whom had an initial history of pain. Eight of the 10 patients recovered fully within 1 year. Miller-Breslow et al [18] advocated nonsurgical management extending beyond 1 year.
When the anterior interosseous nerve fails to recover and it cannot be reconstructed, or should there be irreversible muscular atrophy after a prolonged period of denervation, tendon transfers to the thumb and index finger are recommended.
Spinner [13] recommends the transfer of a slip of flexor digitorum superficialis tendon from the ring or middle finger to the tendon of either the flexor pollicis longus or the flexor digitorum profundus indicis.
This is possible only if the median nerve itself, with its innervation to the flexor digitorum superficialis, is unaffected. Brachioradialis transfer to the flexor pollicis longus or the extensor carpi radialis longus to the flexor digitorum profundus of the index finger are acceptable alternatives [13].
Conclusion
Anterior interosseous nerve syndrome is characterized by a triad of clinical findings that include weakness of the flexor pollicis longus, pronator quadratus, and flexor digitorum profundus of the index finger. The findings do not refer to a single distinct pathology. A physical examination for accompanying features can provide important clues as to whether pathology resides within the nerve (anterior interosseous neuropathy) or proximal to the nerve (pseudo–anterior interosseous neuropathy). Proper treatment depends on a precise and accurate diagnosis.
References
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