Anterior Interosseous Nerve Syndrome

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 flexor pollicis longus, the flexor digitorum profundus of the index finger, 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 distin- guished clinically from pseudo–anterior 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 perma- nent muscular atrophy, functional tendon transfers of the flexor digitorum superficialis of the ring or middle finger or of the brachioradialis may be helpful. Copyright © 2001 by the American Society for Surgery of the Hand

inel1 probably offered the original description peculiar triad of ﬁndings, identifying an isolated neu- of a characteristic pattern of weakness of me- ritis of the anterior interosseous nerve (AIN) as one Tdian innervated muscles, referring to it as a potential cause. Their anatomic correlation thus “dissociated paralysis of the median nerve.” Kiloh and named the syndrome, which now bears their eponym. Nevin2 offered a clear anatomic explanation for the Several other reports commonly are cited as early descriptions of AIN syndrome, such as the classic description of an acute brachial neuritis by Parsonage From the Division of Hand and Upper Exptremity Surgery, Depart- and Turner3 in 1948. Their description included a ment of Orthopedic Surgery, UCLA Center for Health Sciences, Los weakness of the shoulder girdle, making it impossible Angeles, CA. for this to have represented a neuropathy of the AIN. Address reprint requests to Roy A. Meals, MD, 100 UCLA Medical Plaza, Suite 305, Los Angeles, CA 90024. E-mail: [email protected] Others have reported observing the same constellation of ﬁndings associated with supracondylar humeral Copyright © 2001 by the American Society for Surgery of the Hand 4,5 6-8 1531-0914/01/0104-0004$35.00/0 fractures, forearm fractures, an anomalous median doi:10.1053/jssh.2001.28806 artery,9 the use of a lateral epicondylitis forearm

JOURNAL OF THE AMERICAN SOCIETY FOR SURGERY OF THE HAND ⅐ VOL. 1, NO. 4, NOVEMBER 2001 249 250 ANTERIOR INTEROSSEOUS NERVE SYNDROME ⅐ CHIN & MEALS

band,10 thrombophlebitis,11 and antecubital vein example of the pseudo–anterior interosseous neurop- catheterization or phlebotomy.12 athies.3 From the numerous reports supposing a broad range of causes—inflammatory, compressive, post- ANATOMY traumatic—it becomes clear that AIN syndrome refers not to a single pathologic entity, but to a ust after coursing between the two heads of the common clinical manifestation of several different Jpronator teres muscle, the median nerve gives rise pathologies. These may or may not affect the AIN to the AIN from its radial aspect. This take-off of the itself. AIN from the median nerve occurs 5 to 8 cm distal to Much of the controversy surrounding the manage- the lateral epicondyle14 and 22.4 to 23.4 cm proximal ment of anterior interosseous nerve syndrome arises to the radial styloid.15,16 Coursing beneath the fibrous from subtle but important semantic differences be- arch of the flexor digitorum superficialis muscle, the tween the terms anterior interosseous nerve syndrome and AIN then enters the flexor digitorum profundus mus- anterior interosseous neuropathy, which, unfortunately, cle belly an average of 30% the forearm length distal 17 have tended even among experienced hand surgeons to to the medial epicondyle. The nerve then courses be used rather interchangeably. Many types of pathol- distally on the volar surface of the interosseous mem- ogies may result in the signature triad of palsies brane. Approximately 4 cm distal to its takeoff from representing the syndrome. the median nerve, the AIN gives rise to motor Strictly speaking, anterior interosseous syndrome branches to the flexor pollicis longus, the flexor digitorum profundus to the index finger, and, variably, refers to that constellation of signs and symptoms the flexor digitorum profundus to the middle finger.14 referable to weakness of the pronator quadratus, the It then supplies a motor branch to the pronator quad- flexor pollicis longus, and the flexor digitorum pro- ratus before terminating as sensory branches to the fundus to the index finger. Although the AIN sup- radiocarpal, midcarpal, and carpometacarpal joints. plies sensory fibers to the radiocarpal, midcarpal, and At the level of the elbow, motor fibers of the carpometacarpal joints, AIN syndrome by definition median nerve that are destined to become the constit- refers to a purely motor constellation of signs and uents of the AIN distally lie posteriorly relative to the symptoms. main nerve trunk.18 Sunderland reported that fibers Although AIN syndrome is strictly motor, it may ultimately becoming the AIN form a distinct bundle be associated with additional extrasyndromic signs within the median nerve 2.5 cm proximal to its and symptoms. Additional findings may suggest ei- take-off as the AIN.19 Spinner20 has shown that this ther that the underlying pathology resides outside of anatomic feature makes it possible for this fascicular the AIN itself (median nerve or brachial plexus) or component of the median nerve to sustain an isolated that aberrant anatomic features exist distal to the injury, giving rise to a clinical pattern mimicking an pathologic lesion in the AIN. anterior interosseous neuropathy. Wertsch and col- Among the many potential underlying pathologies leagues13 reported cases of AIN syndrome associated manifesting as AIN syndrome are abnormalities either with sensibility deficits in a median nerve distribu- within or proximal to the AIN. Thus, causes of AIN tion. On exploration, the median nerve, including syndrome are appropriately divided into 2 broad cat- fascicles comprising the AIN distally, were com- egories. Anterior interosseous neuropathies include pressed at the antecubital fossa, proximal to the take- those compression neuropathies, neuritides, congeni- off of the AIN. tal anomalies, and anatomic lesions and discontinui- Spinner and Schrieber 4,20 have identified at least 8 ties of the AIN itself. Pseudo–anterior interosseous anatomic features that seem to predispose an individ- neuropathies,13 on the other hand, represent patholo- ual toward an anterior interosseous palsy (Table 1). gies affecting more proximal anatomic sites, but in- Among a series of patients with AIN syndrome, Hill volve nerve fascicles contributing to the anterior in- and associates21 reported fibrous bands spanning from terosseous nerve more distally. Parsonage-Turner the deep head of the pronator teres to the brachialis syndrome, in which AIN syndrome is associated with fascia to be the most common source of anatomic weakness of the parascapular muscles, is a classic compression. Less common causes of compression were ANTERIOR INTEROSSEOUS NERVE SYNDROME ⅐ CHIN & MEALS 251

With anterior interosseous or pseudo–anterior in- TABLE 1 terosseous neuritides, onset of neurologic symptoms is Anatomic Features Predisponsing Toward Anterior Interosseous Compression Neuropathy typically sudden and rapidly progressive. Patients often relate an antecedent prodrome of proximal volar Tendinous origin of the deep head of the pronator forearm or shoulder pain, and these patients are gen- teres Tendinous origin of the flexor superficialis to the long erally suspected of exhibiting an inflammatory neu- finger ropathy. Pain will often be of sudden onset and may Tendinous origin of variant muscles (palmaris pro- be related to minor trauma. The prodrome may con- fundus, flexor carpi radialis brevis) Thrombosis of crossing ulnar collateral vessels sist of systemic complaints, including generalized fa- Accessory muscle and tendon from the flexor digitorum tigue and fever. Hepatitis has been reported to be superficialis to the flexor pollicis longus associated with acute brachial neuritis.23 Gantzer’s muscle (accessory head of the flexor pollicis longus) Aberrant radial artery EXAMINATION Enlarged bicipital bursa near the origin of the AIN

Data from Spinner.24 IN syndrome is suggested by the resting repose Aof the hand, which will exhibit an unnatural extension of the distal interphalangeal (DIP) joint of the index finger and interphalangeal (IP) joint of the fibrous bands arising from the superficial head of the thumb, compared with the gentle flexion arcade of the pronator teres, a nerve running deep to both heads of remaining fingers. The metacarpophalangeal joint of the pronator teres, and a double lacertus fibrosus. the thumb may compensate by assuming hyperflexion. The signature finding on physical examination is weakness of the flexor pollicis longus, flexor digitorum CLINICAL PRESENTATION profundus indicis, and pronator quadratus. Weakness of the flexor pollicis longus and flexor digitorum he only consistent finding in true AIN syndrome profundus to the index finger is indicated by an by definition is paresis or paralysis of the prona- T inability to make the “OK” sign. Rather, the DIP tor quadratus, the flexor pollicis longus, and the flexor joint of the index finger and the IP joint of the thumb digitorum of the index finger. In addition, Hill et al21 are hyperextended during attempted tip-to-tip pinch. have reported a series of 33 patients with incomplete The area of contact between the thumb and index AIN syndromes who presented with weakness of ei- finger is a flatter, broader area found more proximally. ther the flexor pollicis longus or flexor digitorum The “OK” sign on the affected hand has more the profundus indicis only. Weakness may initially be appearance of a Playboy bunny (Fig 1). In addition, noted as difficulty, fatigue, or clumsiness with writing Spinner24 has described a sign that, for all his contri- or with fine pinch activities, such as sewing. Deteri- butions to our understanding of anterior interosseous oration of handwriting has been described as a classic syndrome, should rightly bear his name: upon making presentation in a series of patients with AIN syn- a fist, the tips of the index finger and thumb remain drome.22 conspicuously excluded (Fig 2). Although there is no consistent history of onset of Examination of the pronator quadratus is difficult neuropathy, there are several different patterns of on- and unreliable. Theoretically, contributions to resisted set that provide important clues for determining eti- forearm pronation from the pronator quadratus and ology. A history of trauma obviously suggests either from the pronator teres are distinguishable. With the mechanical disruption of the nerve, injury to the elbow bent at 90°, the patient is asked to forcibly nerve, or compression neuropathy. Injuries associated pronate the forearm, against the resistance of the with anterior interosseous neuropathy include pene- examiner. Flexion of the elbow at 90° delivers the trating trauma, blunt injury, and traction injury. The pronator teres, which originates from the medial hu- association between fractures of the supracondylar humerus, out of its optimal sarcomere length on the merus4,5 and proximal forearm6-8 have classic associa- Starling length:tension curve, thus isolating contributions with anterior interosseous syndrome. tions from the pronator quadratus distally. However, 252 ANTERIOR INTEROSSEOUS NERVE SYNDROME ⅐ CHIN & MEALS

dent in any patient with anterior interosseous syndrome.

VARIANTS

n the presence of anterior interosseous syndrome, Iadditional findings 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 nerve—for example, acute brachial neuropathy—tend to be self-limited. On the other hand, because of FIGURE 1. Playboy bunny sign. Classic repose of a left hand certain well-described variations in forearm innerva- affected by AIN syndrome. Note the extension of the index tion, specific clinical findings in addition to anterior finger DIP joint and thumb IP joint. The contact point between interosseous syndrome itself are completely consistent the thumb and index finger has migrated more proximally and has become a broad surface. Instead of the “OK” sign formed with a true anterior interosseous neuropathy and do by the unaffected right side, the thumb and index finger of the not imply pathology more proximally. left hand form the elongated nose of a Playboy bunny, and A meticulous physical examination and a knowl- the gently flexed middle and ring fingers form floppy bunny ears. edge of important anatomic variants can allow the clinician to distinguish a pseudo–anterior interosseous neuropathy from a true anterior interosseous neurop- Stewart25 finds this maneuver to be unreliable and athy. Some additional features known to be associated 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 fibers to the skin. Therefore, an abnormal sensibility testing result de- finitively 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 flexor digitorum superficialis 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 flexor digitorum superficialis. Careful objective testing of the parascapular muscles can reveal subtle weakness of the shoulder girdle, FIGURE 2. Spinner’s sign. The patient is asked to make a fist. Typically the tips of the small, ring, and middle fingers are a finding that also would argue strongly against a able to achieve flexion to the distal palmar crease. However, diagnosis of anterior interosseous neuropathy. Addi- the tips of the index finger is conspicuously excluded. The tional testing to exclude Parsonage-Turner syndrome, thumb remains straight. This patient has a partial AIN syndrome, because he has sufficient strength of the flexor digi- acute brachial neuritides, or other proximal pseudo– torum profundus of the index finger to cause some active anterior interosseous neuropathies is clinically pru- flexion of its DIP joint. ANTERIOR INTEROSSEOUS NERVE SYNDROME ⅐ CHIN & MEALS 253

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 Martin-Gruber Communications contradistinction to specific findings that exclude its Martin-Gruber communications between the ulnar diagnosis (Fig 3). and median nerves in the proximal forearm are present in approximately 15% of upper limbs.26 Motor fibers Weakness of the Deep Flexor of the Middle Finger targeted for typically ulnarly innervated muscles of the hand (most notably the adductor pollicis, abductor According to Sunderland’s classic studies on up- digiti quinti, and first dorsal interosseous,27 as well as per extremity innervation, “the portion of the flexor the second and third dorsal interossei24) may be car- digitorum profundus serving the index finger is the ried temporarily in the median nerve. Therefore, when only part of this muscle that is exclusively and afflicted with either a neuritis or compression neurop- constantly supplied by the median nerve.”15,16 The athy of the AIN, patients with a Martin-Gruber com- deep flexors to the small and ring fingers are con- municating branch may exhibit weakness or paralysis sistently innervated by the ulnar nerve. Deep flexors of these intrinsic muscles in addition to signature to the ring and middle fingers receive variable weakness of the flexor pollicis longus, pronator quad- contributions from the AIN and ulnar nerve. Re- ratus, and flexor digitorum profundus of the index cently, Bhadra and coworkers17 performed cadaver finger. Conversely, in the rare patient with ulnar dissections confirming this: in only 5% of forearms innervation of the flexor digitorum profundus of the did the AIN supply the deep flexor to the index index finger, an anterior interosseous neuropathy may finger alone. In 75% of forearms, the AIN supplied manifest as isolated weakness of thumb IP flexion and the index and middle fingers, and the ulnar nerve forearm pronation.19 supplied the deep flexors to the small, ring, and middle fingers. In 20% of forearms, the AIN ex- Involvement of the Flexor Digitorum Superficialis clusively innervated the deep flexors to the index In approximately 30% of forearms, the flexor digi- and middle fingers. Consequently, with a lesion of torum superficialis is supplied by a separate branch the anterior interosseous nerve, there may be some deriving from the AIN.19 Therefore, weakness of flex- weakness of the flexor digitorum profundus to the ion of all of the proximal IP joints (with blockade of middle finger, as well as to the deep flexors to the profundus contributions) is possible with an anterior thumb and index finger. interosseous neuropathy. Even with anterior interosse- 254 ANTERIOR INTEROSSEOUS NERVE SYNDROME ⅐ CHIN & MEALS

ous innervation of the superficial flexors, however, thumb and index finger after penetrating wounds of functionally significant weakness of all fingers is ex- the upper forearm. Kiloh and Nevin2 reported 2 cases tremely rare because of the continued activity of deep of acute interstitial neuritis of the AIN, manifesting flexors to the small, ring, and—generally—middle with a similar pattern of thumb/index long flexor fingers. weakness, identifying an inflammatory etiology of anterior interosseous syndrome. Parsonage and Turn- Shoulder Girdle Weakness er3 described an acute brachial plexus neuritis mani- 3 Parsonage and Turner were the first to describe festing as AIN syndrome in association with weakness anterior interosseous syndrome arising from a diffuse of the shoulder girdle. neuritis, presumably of anterior horn cells. In such Gunther and colleagues18 have aptly shown that, cases, weakness of the deep flexors to the thumb and at the level of the elbow, motor fibers of the median index finger is associated with varying degrees of nerve destined to become the AIN lie posteriorly weakness of the scapular muscles (Parsonage-Turner with respect to the main nerve trunk. Hence, post- syndrome) and usually is preceded or accompanied by traumatic median neuropathy after supracondylar pain.23 humerus fractures or proximal radius fractures may ETIOLOGIES result in a pattern of clinical weakness representa- tive of a pseudo–anterior interosseous neuropathy. he key to treatment of anterior interosseous syn- In one series of supracondylar humerus fractures Tdrome is the recognition of a variety of potential associated with anterior interosseous syndrome, 24 anatomic, inflammatory, infectious, posttraumatic, Spinner reviewed patterns of fracture displace- and compressive causes (Table 2). These may affect ment. He concluded that prerequisites for nerve either the AIN itself (anterior interosseous neuropa- injury were a distal point of fixation of the anterior thy) or the median nerve or brachial plexus more interosseous nerve and posterior displacement of the proximally (pseudo–anterior interosseous neuropa- distal fragment. In such cases, the median nerve thy).13,25,28 Borchardt and Wjasmenski28 described a slipped between the fracture fragments; isolated similar clinical weakness of the deep flexors of the injury to the AIN itself was not noted.

DIFFERENTIAL DIAGNOSIS TABLE 2 Causes of Anterior Interosseous Syndrome nterior interosseous neuropathy must also be dis- Atinguished from tendon rupture. The latter is Anterior interosseous neuropathies Direct injury to nerve easily excluded from the diagnosis by careful exam- Midshaft radius fracture ination for tenodesis: with intact flexor tendons, Compression passive wrist extension should effect passive thumb Fibrous bands (pronator, FDS) Enlarged median artery and finger IP joint flexion. In addition, tendon Hematoma rupture should be suspected in patients with rheu- Trauma 14 Coagulopathy matoid arthritis and Kienbo¨ck disease. In the Tumor former instance, attritional rupture may occur as a Idiopathic inflammatory anterior interosseous result of volar carpal subluxation. In the latter case, neuropathy PseudoÐanterior interosseous neuropathies proximal carpal pathology may lead similarly to Supracondylar humerus fracture attritional tendon rupture. Tendon rupture second- Proximal radius fracture Antebrachial venipuncture or catheterization ary to scaphoid nonunion also has been de- Inflammatory scribed.29,30 In the above instances of secondary Acute brachial neuropathy tendon rupture, limitation of passive extension of Parsonage-Turner syndrome the wrist due to underlying wrist pathology may Abbreviation: FDS, flexor digitorum superficialis. make it difficult to exclude tendon rupture on the Data from Spinner.24 basis of an observed tenodesis effect. ANTERIOR INTEROSSEOUS NERVE SYNDROME ⅐ CHIN & MEALS 255

ELECTRODIAGNOSTIC STUDIES neurolysis resulted in motor recovery in every case.19 Stern discussed 3 cases of AIN syndrome due to ill et al21 have described 33 cases of incomplete proximal median compression neuropathy. These HAIN syndrome in which either the flexor pollicis proved to be uniformly unresponsive to conservative longus or the flexor digitorum profundus to the index management, but rapid and long-term recovery oc- finger was paretic or paralyzed. Because of the above curred in all cases managed surgically.22 On the other types of variations in forearm muscle innervation and hand, Miller-Breslow et al32 reported their results of because it is possible to exhibit an incomplete anterior nonoperative management in 10 patients with spon- interosseous neuropathy, it is prudent to sample elec- taneous AIN paralysis. Eight patients recovered fully tromyographically all muscles typically innervated by within 1 year. However, all of their patients reported the AIN. Electrodiagnostic studies at a minimum a prodrome of forearm pain and probably suffered should include electromyography of the flexor pollicis from anterior interosseous neuritis rather than com- longus, pronator quadratus, and flexor digitorum pro- pression neuropathy. Hence, controversy relating the fundus indicis. Because the pronator teres is typically surgical versus nonoperative treatment of AIN syn- innervated by the median nerve, electromyographic drome may in large part be due to the broad range of testing of the pronator teres should logically distin- pathologies resulting in a common triad of findings. guish anterior interosseous neuropathy from proximal Therefore, the probability and extent of motor re- compression of the median nerve affecting fascicles of covery from AIN syndrome is predicated on the es- the AIN. However, Ashworth et al31 have described a tablishment of a correct and precise diagnosis. One case in which compression of the AIN by a fibrous must recognize that AIN syndrome represents a con- band arising from the deep head of the pronator teres stellation of findings and does not refer to a single resulted in weakness and denervation of the pronator distinct pathology. A thorough and directed neuro- teres. On exploration, the AIN was found to innervate logic examination in combination with a thorough the pronator teres. history and well-considered electrodiagnostic study Electromyographic studies may be most helpful will distinguish pseudo–anterior interosseous neurop- after a history of trauma, particularly blunt injury. athies from focal lesions of the AIN itself. Complete lesions are probably most amenable to im- Once an accurate diagnosis is established, etiologic mediate exploration, whereas surgical exploration of factors must guide therapy. A history of penetrating incomplete lesions may be deferred for several months. trauma suggests mechanical disruption or compres- As with most other neuropathies, the presence of sion of the nerve and mitigates strongly toward sur- positive sharp waves or fibrillation potentials indicate gical exploration and nerve decompression or repair. nerve degeneration and may provide an indication for In the presence of blunt trauma, management of an- surgical exploration. terior interosseous palsy is less straightforward. Elec- North and Kaul14 suggest that any patient sus- tromyography suggestive of a complete lesion may pected of having AIN syndrome should receive elec- mandate early surgical exploration. Partial injuries tromyographic studies of the shoulder girdle to rule may be given an opportunity to recover spontane- out neuralgic amyotrophy. Among patients manifest- ously. If no improvement is noted either clinically or ing signs and symptoms suggestive of anterior in- electromyographically after 6 to 12 weeks, surgical terosseous–like neuropathy, Parsonage-Turner syn- exploration may be warranted. If positive sharp waves drome is found with relatively high frequency. or fibrillation potentials are present on electromyography, surgical exploration and neurolysis may be indi- TREATMENT cated. Spontaneous or rapid onset of weakness is sugges- eview of the literature shows considerable con- tive of an anterior interosseous neuritis or pseudo– Rtroversy surrounding the treatment of AIN syn- anterior interosseous neuritis. In such cases, neuro- drome. Sunderland reported that when fibrous bands logic symptoms are typically preceded by proximal constricting the AIN were found at operation, resec- anterior forearm or shoulder pain and tenderness. Pain tion of these bands followed by anterior interosseous generally has subsided by the time weakness of pinch 256 ANTERIOR INTEROSSEOUS NERVE SYNDROME ⅐ CHIN & MEALS

is noted. A history of fatigue, fever, myalgia, or other digitorum superficialis tendon from the ring or long prodromic systemic symptoms also strongly suggests finger to the tendon of either the flexor pollicis longus an inflammatory process, which may resolve sponta- or the flexor digitorum profundus indicis distally. neously or with systemic steroids. However, to date Obviously, this is possible only if the median nerve there have been no persuasive studies showing that the itself, with its innervation of the flexor digitorum use of systemic steroids has any effect on the rate, superficialis, is unaffected. Transfers of the brachiora- extent, or probability of motor recovery from AIN dialis to the flexor pollicis longus or the extensor carpi syndrome. As a general rule, Spinner24 treats sponta- radialis longus to the flexor digitorum profundus of neous paralysis of the AIN nonsurgically initially but the index finger are also acceptable alternatives for recommends surgical exploration within 12 weeks if functional restoration.24 no clinical or electromyographic improvement is evi- dent. However, spontaneous recovery after 12 months is well-documented,32,33 and some have considered SUMMARY waiting at least this long for spontaneous recovery before proceeding with surgical exploration. Miller- IN syndrome consists of a triad of clinical find- Breslow et al32 followed up 10 patients with sponta- Aings: weakness of the pronator quadratus, flexor neous anterior interosseous nerve paralysis, all of pollicis longus, and flexor digitorum profundus of the whom related an initial history of pain. Eight patients index finger. It is important to recognize that this recovered fully within 1 year. On the basis of their clinical constellation of findings does not refer to a experience, Miller-Breslow et al advocated nonsurgi- single distinct pathology. An understanding of com- cal management extending beyond 1 year. mon variants of forearm innervation combined with a Should the AIN fail to recover, should it be unre- thorough physical examination for accompanying fea- constructible, or should there be irreversible muscular tures can provide important clues as to whether pa- atrophy after a prolonged period of denervation, ten- thology resides within (anterior interosseous neurop- don transfers offer an acceptable means of functional athy) or proximal to (pseudo–anterior interosseous reconstruction of the thumb and index finger. In such neuropathy) the AIN. Proper treatment is predicated cases, Spinner24 advocates transfer of a slip of flexor on a precise and accurate diagnosis.

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