ANTERIOR INTEROSSEOUS NERVE SYNDROME

BY DOUGLAS H.C.L. CHIN, MD, AND ROY A. MEALS, MD

Anterior interosseous nerve syndrome (Kiloh-Nevin Syndrome) is the triad of weakness of the exor pollicis longus, the exor digitorum profundus of the index nger, and the pronator quadratus. It is a manifestation of neuropathy affecting either the anterior interosseous nerve itself (anterior interosseous neuropathy) or its fascicles more proximally within the median nerve or brachial plexus (pseudo anterior interosseous neuropathy). Anterior interosseous neuropathy in the presence of normal anatomic variation of the anterior interosseous nerve must be distinguished clinically from pseudoanterior interosseous neuropathy, which can present with telltale signs in addition to the signature weaknesses of anterior interosseous nerve syndrome. A history of penetrating injury mitigates toward early exploration and nerve repair. A history of sudden onset and rapid progression, particularly when accompanied by a prodrome of pain and fatigue, suggests the presence of a focal neuritis, which typically resolves completely within 6 to 12 months without surgical intervention. If no improvement is noted within 6 to 12 months or if the neurologic condition worsens, surgical exploration may be warranted. In the presence of untreatable injury to the anterior interosseous nerve, with permanent muscular atrophy, functional tendon transfers of the exor digitorum supercialis of the ring or middle nger or of the brachioradialis may be helpful. Copyright 2001 by the American Society for Surgery of the Hand
inel1 probably offered the original description of a characteristic pattern of weakness of median innervated muscles, referring to it as a dissociated paralysis of the median nerve. Kiloh and Nevin2 offered a clear anatomic explanation for the

From the Division of Hand and Upper Exptremity Surgery, Department of Orthopedic Surgery, UCLA Center for Health Sciences, Los Angeles, CA. Address reprint requests to Roy A. Meals, MD, 100 UCLA Medical Plaza, Suite 305, Los Angeles, CA 90024. E-mail: rmeals@ucla.edu Copyright 2001 by the American Society for Surgery of the Hand 1531-0914/01/0104-0004$35.00/0 doi:10.1053/jssh.2001.28806

peculiar triad of ndings, identifying an isolated neuritis of the anterior interosseous nerve (AIN) as one potential cause. Their anatomic correlation thus named the syndrome, which now bears their eponym. Several other reports commonly are cited as early descriptions of AIN syndrome, such as the classic description of an acute brachial neuritis by Parsonage and Turner3 in 1948. Their description included a weakness of the shoulder girdle, making it impossible for this to have represented a neuropathy of the AIN. Others have reported observing the same constellation of ndings associated with supracondylar humeral fractures,4,5 forearm fractures,6-8 an anomalous median artery,9 the use of a lateral epicondylitis forearm
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band,10 thrombophlebitis,11 and antecubital vein catheterization or phlebotomy.12 From the numerous reports supposing a broad range of causesinammatory, compressive, posttraumaticit becomes clear that AIN syndrome refers not to a single pathologic entity, but to a common clinical manifestation of several different pathologies. These may or may not affect the AIN itself. Much of the controversy surrounding the management of anterior interosseous nerve syndrome arises from subtle but important semantic differences between the terms anterior interosseous nerve syndrome and anterior interosseous neuropathy, which, unfortunately, have tended even among experienced hand surgeons to be used rather interchangeably. Many types of pathologies may result in the signature triad of palsies representing the syndrome. Strictly speaking, anterior interosseous syndrome refers to that constellation of signs and symptoms referable to weakness of the pronator quadratus, the exor pollicis longus, and the exor digitorum profundus to the index nger. Although the AIN supplies sensory bers to the radiocarpal, midcarpal, and carpometacarpal joints, AIN syndrome by denition refers to a purely motor constellation of signs and symptoms. Although AIN syndrome is strictly motor, it may be associated with additional extrasyndromic signs and symptoms. Additional ndings may suggest either that the underlying pathology resides outside of the AIN itself (median nerve or brachial plexus) or that aberrant anatomic features exist distal to the pathologic lesion in the AIN. Among the many potential underlying pathologies manifesting as AIN syndrome are abnormalities either within or proximal to the AIN. Thus, causes of AIN syndrome are appropriately divided into 2 broad categories. Anterior interosseous neuropathies include those compression neuropathies, neuritides, congenital anomalies, and anatomic lesions and discontinuities of the AIN itself. Pseudoanterior interosseous neuropathies,13 on the other hand, represent pathologies affecting more proximal anatomic sites, but involve nerve fascicles contributing to the anterior interosseous nerve more distally. Parsonage-Turner syndrome, in which AIN syndrome is associated with weakness of the parascapular muscles, is a classic

example of the pseudoanterior interosseous neuropathies.3

ANATOMY
ust after coursing between the two heads of the pronator teres muscle, the median nerve gives rise to the AIN from its radial aspect. This take-off of the AIN from the median nerve occurs 5 to 8 cm distal to the lateral epicondyle14 and 22.4 to 23.4 cm proximal to the radial styloid.15,16 Coursing beneath the brous arch of the exor digitorum supercialis muscle, the AIN then enters the exor digitorum profundus muscle belly an average of 30% the forearm length distal to the medial epicondyle.17 The nerve then courses distally on the volar surface of the interosseous membrane. Approximately 4 cm distal to its takeoff from the median nerve, the AIN gives rise to motor branches to the exor pollicis longus, the exor digitorum profundus to the index nger, and, variably, the exor digitorum profundus to the middle nger.14 It then supplies a motor branch to the pronator quadratus before terminating as sensory branches to the radiocarpal, midcarpal, and carpometacarpal joints. At the level of the elbow, motor bers of the median nerve that are destined to become the constituents of the AIN distally lie posteriorly relative to the main nerve trunk.18 Sunderland reported that bers ultimately becoming the AIN form a distinct bundle within the median nerve 2.5 cm proximal to its take-off as the AIN.19 Spinner20 has shown that this anatomic feature makes it possible for this fascicular component of the median nerve to sustain an isolated injury, giving rise to a clinical pattern mimicking an anterior interosseous neuropathy. Wertsch and colleagues13 reported cases of AIN syndrome associated with sensibility decits in a median nerve distribution. On exploration, the median nerve, including fascicles comprising the AIN distally, were compressed at the antecubital fossa, proximal to the takeoff of the AIN. Spinner and Schrieber 4,20 have identied at least 8 anatomic features that seem to predispose an individual toward an anterior interosseous palsy (Table 1). Among a series of patients with AIN syndrome, Hill and associates21 reported brous bands spanning from the deep head of the pronator teres to the brachialis fascia to be the most common source of anatomic compression. Less common causes of compression were

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TABLE 1
Anatomic Features Predisponsing Toward Anterior Interosseous Compression Neuropathy Tendinous origin of the deep head of the pronator teres Tendinous origin of the exor supercialis to the long nger Tendinous origin of variant muscles (palmaris profundus, exor carpi radialis brevis) Thrombosis of crossing ulnar collateral vessels Accessory muscle and tendon from the exor digitorum supercialis to the exor pollicis longus Gantzers muscle (accessory head of the exor pollicis longus) Aberrant radial artery Enlarged bicipital bursa near the origin of the AIN Data from Spinner.24

With anterior interosseous or pseudoanterior interosseous neuritides, onset of neurologic symptoms is typically sudden and rapidly progressive. Patients often relate an antecedent prodrome of proximal volar forearm or shoulder pain, and these patients are generally suspected of exhibiting an inammatory neuropathy. Pain will often be of sudden onset and may be related to minor trauma. The prodrome may consist of systemic complaints, including generalized fatigue and fever. Hepatitis has been reported to be associated with acute brachial neuritis.23

EXAMINATION
IN syndrome is suggested by the resting repose of the hand, which will exhibit an unnatural extension of the distal interphalangeal (DIP) joint of the index nger and interphalangeal (IP) joint of the thumb, compared with the gentle exion arcade of the remaining ngers. The metacarpophalangeal joint of the thumb may compensate by assuming hyperexion. The signature nding on physical examination is weakness of the exor pollicis longus, exor digitorum profundus indicis, and pronator quadratus. Weakness of the exor pollicis longus and exor digitorum profundus to the index nger is indicated by an inability to make the OK sign. Rather, the DIP joint of the index nger and the IP joint of the thumb are hyperextended during attempted tip-to-tip pinch. The area of contact between the thumb and index nger is a atter, broader area found more proximally. The OK sign on the affected hand has more the appearance of a Playboy bunny (Fig 1). In addition, Spinner24 has described a sign that, for all his contributions to our understanding of anterior interosseous syndrome, should rightly bear his name: upon making a st, the tips of the index nger and thumb remain conspicuously excluded (Fig 2). Examination of the pronator quadratus is difcult and unreliable. Theoretically, contributions to resisted forearm pronation from the pronator quadratus and from the pronator teres are distinguishable. With the elbow bent at 90, the patient is asked to forcibly pronate the forearm, against the resistance of the examiner. Flexion of the elbow at 90 delivers the pronator teres, which originates from the medial humerus, out of its optimal sarcomere length on the Starling length:tension curve, thus isolating contributions from the pronator quadratus distally. However,

brous bands arising from the supercial head of the pronator teres, a nerve running deep to both heads of the pronator teres, and a double lacertus brosus.

CLINICAL PRESENTATION
he only consistent nding in true AIN syndrome by denition is paresis or paralysis of the pronator quadratus, the exor pollicis longus, and the exor digitorum of the index nger. In addition, Hill et al21 have reported a series of 33 patients with incomplete AIN syndromes who presented with weakness of either the exor pollicis longus or exor digitorum profundus indicis only. Weakness may initially be noted as difculty, fatigue, or clumsiness with writing or with ne pinch activities, such as sewing. Deterioration of handwriting has been described as a classic presentation in a series of patients with AIN syndrome.22 Although there is no consistent history of onset of neuropathy, there are several different patterns of onset that provide important clues for determining etiology. A history of trauma obviously suggests either mechanical disruption of the nerve, injury to the nerve, or compression neuropathy. Injuries associated with anterior interosseous neuropathy include penetrating trauma, blunt injury, and traction injury. The association between fractures of the supracondylar humerus4,5 and proximal forearm6-8 have classic associations with anterior interosseous syndrome.

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dent in any patient with anterior interosseous syndrome.

VARIANTS

FIGURE 1. Playboy bunny sign. Classic repose of a left hand affected by AIN syndrome. Note the extension of the index nger DIP joint and thumb IP joint. The contact point between the thumb and index nger has migrated more proximally and has become a broad surface. Instead of the OK sign formed by the unaffected right side, the thumb and index nger of the left hand form the elongated nose of a Playboy bunny, and the gently exed middle and ring ngers form oppy bunny ears.

Stewart25 nds this maneuver to be unreliable and states rather that if weakness of pronation is detected, the pronator teres is involved; this indicates a lesion of the main trunk of the median nerve or an anatomic anomaly with the pronator teres being innervated by the AIN. The AIN provides no sensory bers to the skin. Therefore, an abnormal sensibility testing result denitively rules out an anterior interosseous neuropathy. Abnormal sensibility in the median distribution in the presence of an anterior interosseous syndrome strongly suggests a proximal median compression neuropathy involving fascicles of the AIN. Abnormalities of other typically median nerve functions, such as exor digitorum supercialis activity, do not necessarily exclude a diagnosis of anterior interosseous neuropathy. As stated above, the pronator teres may be aberrantly innervated by the AIN, as may the exor digitorum supercialis. Careful objective testing of the parascapular muscles can reveal subtle weakness of the shoulder girdle, a nding that also would argue strongly against a diagnosis of anterior interosseous neuropathy. Additional testing to exclude Parsonage-Turner syndrome, acute brachial neuritides, or other proximal pseudo anterior interosseous neuropathies is clinically pru-

n the presence of anterior interosseous syndrome, additional ndings or symptoms can provide important clues to determining whether the pathology resides within or proximal to the AIN. This is an important distinction clinically, because certain neuropathies proximal to the anterior interosseous nervefor example, acute brachial neuropathytend to be self-limited. On the other hand, because of certain well-described variations in forearm innervation, specic clinical ndings in addition to anterior interosseous syndrome itself are completely consistent with a true anterior interosseous neuropathy and do not imply pathology more proximally. A meticulous physical examination and a knowledge of important anatomic variants can allow the clinician to distinguish a pseudoanterior interosseous neuropathy from a true anterior interosseous neuropathy. Some additional features known to be associated

FIGURE 2. Spinners sign. The patient is asked to make a st. Typically the tips of the small, ring, and middle ngers are able to achieve exion to the distal palmar crease. However, the tips of the index nger is conspicuously excluded. The thumb remains straight. This patient has a partial AIN syndrome, because he has sufcient strength of the exor digitorum profundus of the index nger to cause some active exion of its DIP joint.

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FIGURE 3. AIN neuropathy versus pseudoneuropathy. Findings in addition to the classic triad may indicate that the lesion resides proximal to the AIN. However, certain anatomic variants allow for additional features in the presence of a true anterior interosseous neuropathy.

with anterior interosseous neuropathy stand in notable contradistinction to specic ndings that exclude its diagnosis (Fig 3). Weakness of the Deep Flexor of the Middle Finger According to Sunderlands classic studies on upper extremity innervation, the portion of the exor digitorum profundus serving the index nger is the only part of this muscle that is exclusively and constantly supplied by the median nerve.15,16 The deep exors to the small and ring ngers are consistently innervated by the ulnar nerve. Deep exors to the ring and middle ngers receive variable contributions from the AIN and ulnar nerve. Recently, Bhadra and coworkers17 performed cadaver dissections conrming this: in only 5% of forearms did the AIN supply the deep exor to the index nger alone. In 75% of forearms, the AIN supplied the index and middle ngers, and the ulnar nerve supplied the deep exors to the small, ring, and middle ngers. In 20% of forearms, the AIN exclusively innervated the deep exors to the index and middle ngers. Consequently, with a lesion of the anterior interosseous nerve, there may be some weakness of the exor digitorum profundus to the middle nger, as well as to the deep exors to the thumb and index nger.

Martin-Gruber Communications Martin-Gruber communications between the ulnar and median nerves in the proximal forearm are present in approximately 15% of upper limbs.26 Motor bers targeted for typically ulnarly innervated muscles of the hand (most notably the adductor pollicis, abductor digiti quinti, and rst dorsal interosseous,27 as well as the second and third dorsal interossei24) may be carried temporarily in the median nerve. Therefore, when aficted with either a neuritis or compression neuropathy of the AIN, patients with a Martin-Gruber communicating branch may exhibit weakness or paralysis of these intrinsic muscles in addition to signature weakness of the exor pollicis longus, pronator quadratus, and exor digitorum profundus of the index nger. Conversely, in the rare patient with ulnar innervation of the exor digitorum profundus of the index nger, an anterior interosseous neuropathy may manifest as isolated weakness of thumb IP exion and forearm pronation.19 Involvement of the Flexor Digitorum Supercialis In approximately 30% of forearms, the exor digitorum supercialis is supplied by a separate branch deriving from the AIN.19 Therefore, weakness of exion of all of the proximal IP joints (with blockade of profundus contributions) is possible with an anterior interosseous neuropathy. Even with anterior interosse-

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ous innervation of the supercial exors, however, functionally signicant weakness of all ngers is extremely rare because of the continued activity of deep exors to the small, ring, and generallymiddle ngers. Shoulder Girdle Weakness Parsonage and Turner3 were the rst to describe anterior interosseous syndrome arising from a diffuse neuritis, presumably of anterior horn cells. In such cases, weakness of the deep exors to the thumb and index nger is associated with varying degrees of weakness of the scapular muscles (Parsonage-Turner syndrome) and usually is preceded or accompanied by pain.23

ETIOLOGIES
he key to treatment of anterior interosseous syndrome is the recognition of a variety of potential anatomic, inammatory, infectious, posttraumatic, and compressive causes (Table 2). These may affect either the AIN itself (anterior interosseous neuropathy) or the median nerve or brachial plexus more proximally (pseudoanterior interosseous neuropathy).13,25,28 Borchardt and Wjasmenski28 described a similar clinical weakness of the deep exors of the

thumb and index nger after penetrating wounds of the upper forearm. Kiloh and Nevin2 reported 2 cases of acute interstitial neuritis of the AIN, manifesting with a similar pattern of thumb/index long exor weakness, identifying an inammatory etiology of anterior interosseous syndrome. Parsonage and Turner3 described an acute brachial plexus neuritis manifesting as AIN syndrome in association with weakness of the shoulder girdle. Gunther and colleagues18 have aptly shown that, at the level of the elbow, motor bers of the median nerve destined to become the AIN lie posteriorly with respect to the main nerve trunk. Hence, posttraumatic median neuropathy after supracondylar humerus fractures or proximal radius fractures may result in a pattern of clinical weakness representative of a pseudoanterior interosseous neuropathy. In one series of supracondylar humerus fractures associated with anterior interosseous syndrome, Spinner24 reviewed patterns of fracture displacement. He concluded that prerequisites for nerve injury were a distal point of xation of the anterior interosseous nerve and posterior displacement of the distal fragment. In such cases, the median nerve slipped between the fracture fragments; isolated injury to the AIN itself was not noted.

DIFFERENTIAL DIAGNOSIS
TABLE 2
Causes of Anterior Interosseous Syndrome Anterior interosseous neuropathies Direct injury to nerve Midshaft radius fracture Compression Fibrous bands (pronator, FDS) Enlarged median artery Hematoma Trauma Coagulopathy Tumor Idiopathic inammatory anterior interosseous neuropathy Pseudoanterior interosseous neuropathies Supracondylar humerus fracture Proximal radius fracture Antebrachial venipuncture or catheterization Inammatory Acute brachial neuropathy Parsonage-Turner syndrome Abbreviation: FDS, exor digitorum supercialis. Data from Spinner.24

nterior interosseous neuropathy must also be distinguished from tendon rupture. The latter is easily excluded from the diagnosis by careful examination for tenodesis: with intact exor tendons, passive wrist extension should effect passive thumb and nger IP joint exion. In addition, tendon rupture should be suspected in patients with rheumatoid arthritis and Kienbock disease.14 In the former instance, attritional rupture may occur as a result of volar carpal subluxation. In the latter case, proximal carpal pathology may lead similarly to attritional tendon rupture. Tendon rupture secondary to scaphoid nonunion also has been described.29,30 In the above instances of secondary tendon rupture, limitation of passive extension of the wrist due to underlying wrist pathology may make it difcult to exclude tendon rupture on the basis of an observed tenodesis effect.

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ELECTRODIAGNOSTIC STUDIES
ill et al21 have described 33 cases of incomplete AIN syndrome in which either the exor pollicis longus or the exor digitorum profundus to the index nger was paretic or paralyzed. Because of the above types of variations in forearm muscle innervation and because it is possible to exhibit an incomplete anterior interosseous neuropathy, it is prudent to sample electromyographically all muscles typically innervated by the AIN. Electrodiagnostic studies at a minimum should include electromyography of the exor pollicis longus, pronator quadratus, and exor digitorum profundus indicis. Because the pronator teres is typically innervated by the median nerve, electromyographic testing of the pronator teres should logically distinguish anterior interosseous neuropathy from proximal compression of the median nerve affecting fascicles of the AIN. However, Ashworth et al31 have described a case in which compression of the AIN by a brous band arising from the deep head of the pronator teres resulted in weakness and denervation of the pronator teres. On exploration, the AIN was found to innervate the pronator teres. Electromyographic studies may be most helpful after a history of trauma, particularly blunt injury. Complete lesions are probably most amenable to immediate exploration, whereas surgical exploration of incomplete lesions may be deferred for several months. As with most other neuropathies, the presence of positive sharp waves or brillation potentials indicate nerve degeneration and may provide an indication for surgical exploration. North and Kaul14 suggest that any patient suspected of having AIN syndrome should receive electromyographic studies of the shoulder girdle to rule out neuralgic amyotrophy. Among patients manifesting signs and symptoms suggestive of anterior interosseouslike neuropathy, Parsonage-Turner syndrome is found with relatively high frequency.

TREATMENT
eview of the literature shows considerable controversy surrounding the treatment of AIN syndrome. Sunderland reported that when brous bands constricting the AIN were found at operation, resection of these bands followed by anterior interosseous

neurolysis resulted in motor recovery in every case.19 Stern discussed 3 cases of AIN syndrome due to proximal median compression neuropathy. These proved to be uniformly unresponsive to conservative management, but rapid and long-term recovery occurred in all cases managed surgically.22 On the other hand, Miller-Breslow et al32 reported their results of nonoperative management in 10 patients with spontaneous AIN paralysis. Eight patients recovered fully within 1 year. However, all of their patients reported a prodrome of forearm pain and probably suffered from anterior interosseous neuritis rather than compression neuropathy. Hence, controversy relating the surgical versus nonoperative treatment of AIN syndrome may in large part be due to the broad range of pathologies resulting in a common triad of ndings. Therefore, the probability and extent of motor recovery from AIN syndrome is predicated on the establishment of a correct and precise diagnosis. One must recognize that AIN syndrome represents a constellation of ndings and does not refer to a single distinct pathology. A thorough and directed neurologic examination in combination with a thorough history and well-considered electrodiagnostic study will distinguish pseudoanterior interosseous neuropathies from focal lesions of the AIN itself. Once an accurate diagnosis is established, etiologic factors must guide therapy. A history of penetrating trauma suggests mechanical disruption or compression of the nerve and mitigates strongly toward surgical exploration and nerve decompression or repair. In the presence of blunt trauma, management of anterior interosseous palsy is less straightforward. Electromyography suggestive of a complete lesion may mandate early surgical exploration. Partial injuries may be given an opportunity to recover spontaneously. If no improvement is noted either clinically or electromyographically after 6 to 12 weeks, surgical exploration may be warranted. If positive sharp waves or brillation potentials are present on electromyography, surgical exploration and neurolysis may be indicated. Spontaneous or rapid onset of weakness is suggestive of an anterior interosseous neuritis or pseudo anterior interosseous neuritis. In such cases, neurologic symptoms are typically preceded by proximal anterior forearm or shoulder pain and tenderness. Pain generally has subsided by the time weakness of pinch

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is noted. A history of fatigue, fever, myalgia, or other prodromic systemic symptoms also strongly suggests an inammatory process, which may resolve spontaneously or with systemic steroids. However, to date there have been no persuasive studies showing that the use of systemic steroids has any effect on the rate, extent, or probability of motor recovery from AIN syndrome. As a general rule, Spinner24 treats spontaneous paralysis of the AIN nonsurgically initially but recommends surgical exploration within 12 weeks if no clinical or electromyographic improvement is evident. However, spontaneous recovery after 12 months is well-documented,32,33 and some have considered waiting at least this long for spontaneous recovery before proceeding with surgical exploration. MillerBreslow et al32 followed up 10 patients with spontaneous anterior interosseous nerve paralysis, all of whom related an initial history of pain. Eight patients recovered fully within 1 year. On the basis of their experience, Miller-Breslow et al advocated nonsurgical management extending beyond 1 year. Should the AIN fail to recover, should it be unreconstructible, or should there be irreversible muscular atrophy after a prolonged period of denervation, tendon transfers offer an acceptable means of functional reconstruction of the thumb and index nger. In such cases, Spinner24 advocates transfer of a slip of exor

digitorum supercialis tendon from the ring or long nger to the tendon of either the exor pollicis longus or the exor digitorum profundus indicis distally. Obviously, this is possible only if the median nerve itself, with its innervation of the exor digitorum supercialis, is unaffected. Transfers of the brachioradialis to the exor pollicis longus or the extensor carpi radialis longus to the exor digitorum profundus of the index nger are also acceptable alternatives for functional restoration.24

SUMMARY
IN syndrome consists of a triad of clinical ndings: weakness of the pronator quadratus, exor pollicis longus, and exor digitorum profundus of the index nger. It is important to recognize that this clinical constellation of ndings does not refer to a single distinct pathology. An understanding of common variants of forearm innervation combined with a thorough physical examination for accompanying features can provide important clues as to whether pathology resides within (anterior interosseous neuropathy) or proximal to (pseudoanterior interosseous neuropathy) the AIN. Proper treatment is predicated on a precise and accurate diagnosis.

REFERENCES
1. Tinel J. Nerve wounds. New York: William Wood, 1918. 2. Kiloh L, Nevin S. Isolated neuritis of the anterior interosseous nerve. BMJ 1952;1:850-851. 3. Parsonage M, Turner JW. Neuralgic amyotrophy: the shoulder-girdle syndrome. Lancet 1948;1:973-978. 4. Spinner M, Schrieber SN. The anterior interosseous nerve paralysis as a complication of supracondylar fractures in children. J Bone Joint Surg Am 1969;51A:1584-1590. 5. Cramer K, Green N, Devito D. Incidence of anterior interosseous nerve palsy in supracondylar humerus fractures in children. J Ped Orthop 1993;13:502-505. 6. Geissler W, Fernandez DL, Graca R. Anterior interosseous nerve palsy complicating a forearm fracture in a child. J Hand Surg [Am] 1990;15A:44-47. 7. Gainor B, Olson S. Combined entrapment of the median and anterior interosseous nerves in a pediatric both-bone forearm fracture. J Orthop Trauma 1990;4:197-199. 8. Huang K, Pun WK, Coleman S. Entrapment and transection of the median nerve associated with greenstick fractures of the forearm: case report and review of the literature. J Trauma 1998;44:1101-1102. 9. Proudman T, Menz PJ. An anomaly of the median artery associated with the anterior interosseous nerve. J Hand Surg [Br] 1992;17:507-509. Enzenauer R, Nordstrom DM. Anterior interosseous nerve syndrome associated with forearm band treatment of lateral epicondylitis. Orthopedics 1991;14:788-790. Pavesi G, Medici D, Mancia D. Anterior interosseous nerve syndrome secondary to forearm thrombo-phlebitis. Ital J Neurol Sci 1989;10:221. Saeed M, Gatens PF. Anterior interosseous nerve syndrome: unusual etiologies. Arch Phys Med Rehabil 1983;64:182. Wertsch J, Sanger JR, Matloub HS. Pseudo-anterior interosseous nerve syndrome. Muscle Nerve 1985;8:68-70. North E, Kaul MP. Compression neuropathies: median. New York: McGraw-Hill, 1996. Sunderland S. The innervation of the exor digitorum profundus and lumbrical muscles. Anat Rec 1945;93:317-321. Sunderland S. The intraneural topography of the radial, median, and ulnar nerves. Brain 1945;68:243-299. Bhadra N, Keith M, Peckham P. Variations in innervation of the exor digitorum profundus muscle. J Hand Surg [Am] 1999;24:700-703. Gunther S, Dipasquale D, Martin R. The internal anatomy of

10.

11.

12. 13. 14. 15. 16. 17.

18.

ANTERIOR INTEROSSEOUS NERVE SYNDROME

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19. 20.

21.

22.

23. 24. 25. 26.

the median nerve in the region of the elbow. J Hand Surg [Am] 1992;17:648-456. Sunderland S. Nerves and nerve injuries. Edinburgh: Churchill Livingstone, 1978;660:695-696. Spinner M. The anterior interosseous nerve syndrome. With special attention to its variations. J Bone Joint Surg Am 1970;52A:84-94. Hill N, Howard FM, Huffer BR. The incomplete anterior interosseous nerve syndrome. J Hand Surg [Am] 1985;10: 4-16. Stern M. The anterior interosseous nerve syndrome (the Kiloh-Nevin syndrome). Report and follow-up study of three cases. Clin Orthop Rel Res 1984;187:223-227. Dillin L, Hoaglund F, Scheck M. Brachial neuritis. J Bone Joint Surg Am 1985;67A:878-880. Spinner M. Injuries to the major branches of peripheral nerves of the forearm. Philadelphia: Saunders, 1978;160-227. Stewart J. Focal peripheral neuropathies. New York: Lippincott Williams and Wilkins, 2000;183-239. Thomason A. Third annual report on the Committee of Collective Investigation of the Anatomical Society of Great

27. 28. 29. 30.

31. 32. 33.

Britain and Ireland for the year 1891-1892. J Anat Physiol 1893;27:183-194. Mannerfelt L. Studies on the hand in ulnar nerve paralysis: a clinical-experimental investigation in normal and anomalous innervation. Acta Orthop Scand 1966;87(suppl):1-176. Borchardt M, Wjasmenski P. Der Nervus Medianus. Beitr Klin Chir 1917;107:553-582. McLain R, Steyers CM. Tendon ruptures with scaphoid nonunion. A case report. Clin Orthop Rel Res 1990;255:117120. Mahring M, Semple C, Gray IC. Attritional exor tendon rupture due to a scaphoid nonunion imitating an anterior interosseous nerve syndrome: a case report. J Hand Surg [Br] 1985;10:62-64. Ashworth N, Marshall SC, Classen DA. Anterior interosseous nerve syndrome presenting with pronator teres weakness: a case report. Muscle and Nerve 1997;20:1591-1594. Miller-Breslow A, Terrono A, Millender LH. Nonoperative treatment of anterior interosseous nerve paralysis. J Hand Surg [Am] 1990;15:493-496. Sood M, Burke FD. Anterior interosseous nerve palsy: a review of 16 cases. J Hand Surg 1997;22:64-68.