Anterior interosseous nerve syndrome: retrospective analysis of 14 patients

Duchenne de Boulogne [8] in 1872 reported an isolated palsy of the FPL in 1872. This was the first description of an AIN neuropathy. In 1952, Kiloh and Nevin [17] described the clinical manifestations of an isolated compression of the AIN in detail. A patient with a complete AIN palsy would present with no motor function to the FPL, FDP to the index and middle fingers, and pronator quadratus. Patients with incomplete palsies or with Martin–Gruber anastomoses may present differently [24]. In addition, the FDP to the middle finger may not be always exclusively innervated by the median nerve. Thus, intact middle finger distal interphalangeal joint flexion does not itself exclude AIN syndrome as a potential diagnosis [7].

As in our group, most patients with AIN syndrome present with weakness or absence of FPL function. Although no sensory loss occurs, pain may be present in the forearm along the course of the nerve. This was also true in eight of our patients. The characteristic physical examination finding is a patient’s inability to make an “OK” sign when asked to flex his thumb interphalangeal joint and index finger distal interphalangeal joint. Another clinical test is to ask the patient to pinch a sheet of paper between thumb and index finger using only the fingertips and then trying to pull the paper away. A patient with AIN may be unable to hold on to the sheet of paper with just his fingertips and may compensate by using a more adaptive grip in which the interphalangeal joint of the thumb and distal interphalangeal joint of the index finger remain extended [7].

Causes for AIN palsy can be divided in traumatic and non traumatic/spontaneous. Palsy of the AIN has been described in association with the neuralgic amyotrophy [10, 27], isolated neuritis [27], and entrapment neuropathy [18]. The nerve is susceptible to entrapment by soft tissue and by vascular and bony structures. According to Spinner [33], it is vulnerable to injury or compression by the following:

Collins and Weber [6] considered entrapment to be by far the most common cause of AIN palsy. In all of our patients explored operatively, compression structures could be found. Hill et al. [13] observed it in 24 of 28 cases of incomplete palsy. Schantz and Riegels-Nielson [29] found evidence of nerve compression in nine of 15 patients.

An incomplete syndrome in which only the FLP or the FDP of the index finger is paralysed must be distinguished from flexor tendon rupture, flexor tendon adherence or adhesion, and stenosing tenosynovitis. The nerve is usually compressed by fibrous bands that most commonly originate from the deep head of the pronator teres and the brachialis fascia [13, 33].

Differential diagnosis consists of a noncompressive neuropathy, such as brachial neuritis, which may mimic the clinical manifestations of an AIN neuropathy [27]. A rupture of the FPL tendon is also possible in patients with rheumatoid arthritis. To exclude this differential diagnosis, the wrist should be passively flexed and extended to confirm that the patient has an intact tenodesis effect. A sudden onset of AIN compression symptoms associated with a viral prodrome suggests the diagnosis of such a viral neuritis (Parsonage–Turner syndrome [27]).

Important elements in the diagnosis of AIN syndrome are electrodiagnostic studies. They confirm the diagnosis and objectively assess the severity of the neuropathy. More proximal lesions can be ruled out by EMG. Also, EMG is helpful for distinguishing AIN syndrome from a flexor tendon rupture in patients with severe rheumatoid disease who have such limited wrist motion that the determination of an intact tenodesis effect is impossible. MRI is not commonly used in the diagnosis of AIN syndrome, although there is literature describing the MRI findings associated with AIN syndrome in which increased signal intensity can be seen in the AIN-innervated muscles on T2-weighted, fat-saturated images or short inversion time inversion recovery sequences [9, 12].

The indications of operative treatment for spontaneous AIN palsy remain controversial. Once the diagnosis of AIN syndrome is made, observation with an avoidance of aggravating activities, rest, and anti-inflammatory medication for several months has been suggested before decompression [19]. Most of the patients with AIN syndrome have an improvement without any surgical intervention [21, 24]. This was also true for our patients. There is a role for physiotherapy and this should be directed specifically towards the pattern of pain and symptoms. Soft tissue massage, stretches and exercises in order to directly mobilise the nerve tissue may be used. Spinner et al. [34] recommended exploration if no signs of clinical and electromyographical improvement occur within 6–8 weeks. Nigst and Dick [25] recommended operative treatment in patients in whom there was no improvement after the conservative treatment for 8 weeks, since surgical decompression reduces the time needed for recovery. Hill et al. [13] recommended that exploration and external neurolysis be undertaken when there is no clinical and/or electromyographical improvement by 12 weeks after onset. However, spontaneous recovery in a later course has been described by several authors [21, 30, 32]. For patients who have a space-occupying mass in the area, or who fail a several month course of nonsurgical treatment, surgical decompression has been recommended [21]. Randomized, controlled trials concerning the ideal duration of nonsurgical management and the timing of surgical intervention are still missing. In the absence of evidence suggesting neuritis, most authors still recommend a trial of conservative management for at least 12 weeks [32]. We also performed operative exploration in our patients after 12 weeks if no clinical and electromyographical signs of improvement were visible. During the operation, the AIN should be thoroughly decompressed from any overlying tissue and completely visualised as it travels into the distal forearm (Fig. 1). The surgical approach and extent of proximal exploration can be tailored to the surgeon’s specific areas of preoperative concern. Nearly all of the median nerve’s branches course off its ulnar side at this level, with the notable exception being the AIN, which branches off the radial side of the nerve. Meticulous haemostasis is essential during nerve decompression in the forearm to minimize a postoperative haematoma. Early active range of motion is allowed.

If motor function does not recover, tendon transfer will restore the function satisfactorily. The brachioradialis is a good substitute for restoring flexion of the interphalangeal joint of the thumb. The transfer of the tendon of FDP of the ring or middle finger to that of the index finger at the wrist can provide satisfactory flexion of the distal phalanx of the index finger [23]. Schantz and Riegels-Nielson [29] recommend delay in the use of tendon transfer until one year after the onset of palsy.