Pronator syndrome is a compressive neuropathy of the median nerve at the elbow and refers to a constellation of signs and symptoms. This syndrome was initially attributed to entrapment of the nerve by the pronator teres muscle. However, there are several potential sites of compression [4–9]. These include the ligament of Struthers (a fibrous band from an anomalous supracondylar process of the distal humerus to the medial epicondyle), the proximal fibrous arch of the pronator teres, intramuscular aponeurotic bands of the pronator teres, the proximal arch of the FDS (which may be an indistinct fibrous arch), and the leading edge of the bicipital aponeurosis (lacertus fibrosus ). Additionally, a mass effect, caused by an accessory head of the flexor pollicis longus (Gantzer’s muscle ), or vascular structures such as a persistent median artery are other potential causes of compression [10–12].

Patients with pronator syndrome typically complain of vague aching pain of the proximal forearm and the antecubital fossa, as well as numbness and paresthesias that emanate to the radial 3½ digits. Frequently, these complaints may be mistaken for carpal tunnel syndrome. However, these symptoms are exacerbated by use and rarely occur at night. Additionally, there is decreased sensation over the palm and thenar eminence due to disruption of the innervation of the palmar cutaneous branch of the median nerve over this area, differentiating it from more distal compression (carpal tunnel syndrome).

This syndrome generally occurs in physically active patients such as professional bicyclists. Additionally, motor weakness is generally absent in pronator syndrome. Tenderness in the antecubital fossa and a positive Tinel sign over the course of the nerve in this area may further differentiate pronator syndrome from carpal tunnel syndrome.

There are several clinical maneuvers described in the literature to determine if a patient has suspected pronator syndrome. However, there is no evidence regarding the diagnostic performance characteristics of these tests. The pronator compression test is performed by manually compressing the median nerve at the proximal aspect of the pronator muscle for 30 s and is positive if paresthesias result [13]. There are several other provocative tests that can be performed including resisted forearm pronation with the elbow extended, resisted forearm supination, and resisted middle finger proximal interphalangeal flexion, which are positive if they result in paresthesias in the median nerve distribution. Electrodiagnostic studies may be obtained to rule out more proximal compression or carpal tunnel syndrome at the level of the wrist. Notably, only 30–65% of abnormalities are seen in electrodiagnostic studies for patients with suspected pronator syndrome including slowed conduction velocity in the forearm [14]. In one particular study, there was no significant difference in the success of median nerve decompression when comparing patients who had abnormal nerve conduction studies with patients who had normal studies [15].

In general, given the lack of objective evidence for pronator syndrome, the diagnosis and treatment are controversial, especially since operative findings are subjective (pathology seen at the described sites of nerve compression) [16]. The initial treatment for pronator syndrome is typically nonsurgical (with a period of at least 3 months). This includes a combination of rest, activity modification, splinting, and anti-inflammatory medications, which may result in symptom relief in approximately 50% of cases. Injection into the tender site of the pronator teres muscle with a corticosteroid and local anesthetic (0.7 ml of betamethasone 6 mg/ml and 0.7 ml of 1% lidocaine hydrochloride ) may be useful both diagnostically and therapeutically if the pain continues.

In refractory cases, surgical management is performed through a curvilinear incision across the antecubital fossa, starting 5 cm proximal to the elbow and extending distally to the mid-forearm. All potential sites of compression are then released from the ligament of Struthers, through the heads of the pronator teres and through the FDS arcades. The AIN is also identified and decompressed through its path deep to the head of the pronator and the FDS arch. After surgery, active range of motion as early as day 2 and full return to activity by 6–8 weeks has been advocated [17]. Overall, several case series have demonstrated that 70% of patients that had undergone nerve decompression had either complete resolution or reduced symptoms [5, 6, 15]. Several groups have also demonstrated endoscopically assisted decompression (with a 4.0 mm endoscope), with a 3 cm longitudinal incision, may be adequate and safe [18, 19].

AIN syndrome is a compressive neuropathy of the AIN (as it branches off the median nerve 4 cm distal to the medial epicondyle) that results in the loss of motor function of the FPL, FDP to the index finger and the middle finger, and the pronator quadratus. The most noticeable sign is FPL weakness manifesting as difficulty with pinch. Although some pain in the antecubital fossa may be present, given that the AIN is a motor nerve, the paresthesias or sensory loss that is typically seen in carpal tunnel and pronator syndrome are absent in AIN syndrome.

AIN syndrome results in patients having difficulty flexing the thumb interphalangeal (IP) joint and index finger distal interphalangeal joint (DIP) joint, which results in difficulty when asked to create an “OK” sign (Fig. 28.2). Long finger DIP joint flexion weakness is typically less severe when compared to the index finger. Testing the pronator quadratus is performed by resisting forearm pronation with the elbow in full flexion (which relaxes the pronator teres).

Given that AIN syndrome may result as a compressive neuropathy, other etiologies such as compression of the median nerve more proximally, or a peripheral neuritis (that may mimic the clinical manifestations of AIN neuropathy), have been reported in the literature as causes of AIN dysfunction resulting in an unclear natural history [20, 21]. Parsonage-Turner syndrome (neuralgic amyotrophy) is an autoimmune inflammation of the brachial plexus (with varying degrees of weakness of the scapular muscles) of unknown etiology. This may be considered if the patient has sudden symptom onset accompanied by severe pain and often following a viral illness [22, 23]. Trauma is another cause of AIN dysfunction [24, 25] due to a penetrating laceration of the nerve or an iatrogenic injury during elbow arthroscopy [26, 27]. Additionally, attritional ruptures of the FPL and FDP may be seen in settings of rheumatoid arthritis and may mimic the motor deficits seen in AIN syndrome. When diagnosing AIN syndrome, tendon integrity should be confirmed with an intact thumb and index finger tenodesis effect with wrist extension.

Electrodiagnostic studies may confirm the diagnosis and objectively assess the severity of neuropathy. The affected muscles will exhibit fibrillations, abnormal latency, and abnormal compound motor action potentials on electrodiagnostic testing [28].

Given the natural history of AIN syndrome has not been fully elucidated and often due to a neuritic etiology, the treatment of AIN syndrome is typically nonsurgical given the high probability of resolution after one year of onset of symptoms. Most patients will improve without surgical intervention [29–31]. Periods of at least 3 months and even up to 12 months of nonsurgical management have been recommended given the favorable natural history. However, if there is a compressive lesion or no signs of motor improvement after 6–12 months, then surgical management should be undertaken.