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 login to view 2 more bullets pathoanatomy potential sites of entrapment of AIN login to view 7 more bullets patient with complete AIN palsy should have no motor function to all muscles innervated by AIN login to view 2 more bullets 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 login to view 1 more bullet 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 login to view 1 more bullet 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 login to view 1 more bullet Studies EMG/NCS indications helpful to make diagnosis login to view 1 more bullet assess severity of neuropathy assess for nerve recovery findings EMG may reveal abnormalities in the FPL and FDP index and middle finger login to view 1 more bullet 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 login to view 1 more bullet prognosis login to view 3 more bullets Operative surgical decompression of AIN indications login to view 3 more bullets prognosis login to view 1 more bullet 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 login to view 5 more bullets 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 login to view 1 more bullet 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