Summary Compression of the AIN nerve (also known as Kiloh-Nevin's syndrome) is a forearm compressive neuropathy that results in motor deficits of the AIN nerve. Diagnosis can be made with a careful neurological exam (weakness of thumb, index and middle finger flexion) with inability to make OK sign and normal median nerve sensory exam. Treatment involves a prolonged nonoperative course, and rarely, surgical decompression. Epideomology Incidence rare (<1% of median nerve neuropathies) Etiology Pathophysiology pathophysiology common causes transient neuritis (Parsonage-Turner syndrome) various anatomical cites of compression (see below) pathoanatomy potential sites of entrapment of AIN tendinous edge of deep head of pronator teres most common cause fibrous arch of the FDS thrombosed radial, ulnar or anterior interosseous artery accessory head of FPL (Gantzer's muscle) accessory muscle from FDS to FDP abberant muscles (FCRB, palmaris profundus) patient with complete AIN palsy should have no motor function to all muscles innervated by AIN patients with Martin-Gruber anastomoses may also present with intrinsic weakness this is an anomalous anatomy in 15% of population where axons of AIN may cross over and connect to ulnar nerve and innervate other muscle groups (mainly adductor pollicis and dorsal interossei) Associated conditions Parsonage-Turner Syndrome bilateral AIN signs caused by viral brachial neuritis be suspicious if motor loss is preceded by intense shoulder pain and viral prodrome Anatomy Median nerve originates from the lateral and medial cords of the brachial plexus and travels between the biceps and brachialis as it heads towards the antecubital fossa The nerve travels deep to the lacertus fibrosis and gives a branch to the pronator teres AIN is terminal motor branch of median nerve AIN arises from the median nerve approximately 4 cm distal to the medial epicondyle (and 5-8 cm distal to lateral epicondyle) Travels between FDS and FDP initially, then between FPL and FDP, then it lies on the anterior surface of the interosseous membrane traveling with the anterior interoseous artery to pronator quadratus Terminal branches innervate the joint capsule and the intercarpal, radiocarpal and distal radioulnar joints. AIN has principally motor innervation (no cutaneous sensory) and innervates 3 muscles FDP (index and middle finger) FPL pronator quadratus Presentation Symptoms common symptoms motor deficits without sensory loss may have vague complaints of deep forearm pain, but unlike other median compression neuropathies (carpal tunnel syndrome and pronator syndrome) pain can be absent if pain present, typically last only 2-3 weeks Physical exam inspection severe disease may show forearm atrophy neurovascular weakness of grip and pinch, specifically thumb, index and middle finger flexion patient unable to make OK sign (test FDP and FPL) normal median nerve sensory exam provocative tests pronator quadratus weakness shown with weak resisted pronation with elbow maximally flexed distinguish from FPL attritional rupture (seen in rheumatoids) by passively flexing and extending wrist to confirm tenodesis effect in intact tendon if tendons intact, passive wrist extension brings thumb IP joint and index finger DIP joint into relatively flexed position MRI indications when concerned for a compressive mass lesion findings T2 or STIR images may show increased signal intensity in the FPL, FDP and PQ most reliable finding is edema in the PQ Studies EMG/NCS indications helpful to make diagnosis may rule out more proximal lesions assess severity of neuropathy assess for nerve recovery findings EMG may reveal abnormalities in the FPL and FDP index and middle finger fibrillations, sharp waves, abnormal latency in the FPL and FDP Differential Flexor tendon rupture Proximal sites of nerve compression (i.e cervical spine, brachial plexus) Pronator syndrome AIN syndrome differs from pronator syndrome in that it is a pure motor palsy pronator syndrome also involves sensory changes Carpal tunnel syndrome Diagnosis Clinical and EMG/NCS diagnosis can be made based on history, physical examination and EMG/NCS. Treatment Nonoperative observation, rest and physical therapy indications first line treatment in all patients who do not have a space occupying lesion prognosis majority will improve with nonoperative management symptom resolution begins 3 to 12 months from onset of symptoms with full recovery taking up to 18 months mean full recovery is ~9 months Operative surgical decompression of AIN indications clear space occupying mass if nonoperative treatment fails after 12 months controversial in patients < 40 years old since some studies show patients in this age group uniformly respond to non-operative management. prognosis approximately 75% success rate of surgical decompression Techniques Observation, rest and physical therapy technique given symptoms may take up to a year to improve, a prolonged course of observation is generally recommended in most patients massage and forearm stretches recommended during observation period Surgical decompression of AIN approach lazy-S incision over the proximal volar forearm centered over the anatomical area of most concern technique the AIN needs to be visualized proximal to distal with the following structures released detachment of superficial head of pronator teres lacertus fibrosus superficial arch of FDS Gantzer's muscle (if present) ligation of any crossing vessels removal of any space occupying lesion post-operative rehab early motion encouraged with elbow ROM beginning post-op day 2 Complications Persistent AIN motor deficit incidence only ~5-10 cases reported in literature treatment tendon transfer brachioradialis to FPL transfer Prognosis Recovery generally begins 3 to 12 months after onset of symptoms with full resolution taking up to 18 months. Positive prognostic variables patients < 40 years old noted to have faster recovery