Anterior Interosseous #Nerve OK Signs

Courtesy:Prof Nabile Ebraheim, University of Toledo, Ohio, USA

Anterior Interosseous Nerve (AIN) Syndrome

(Kiloh–Nevin Syndrome)

Introduction

Kiloh–Nevin syndrome was first described in 1948 by Parsonage and Turner and later defined in 1952 by Kiloh and Nevin.
It represents a compressive forearm neuropathy affecting the anterior interosseous nerve (AIN).
Characterized by pure motor deficits without sensory involvement.
Also known as Anterior Interosseous Nerve Syndrome.

Origin & Course

Motor branch of the median nerve.
Arises approximately 4–6 cm distal to the elbow (about one-third down the forearm).
Exits from the anterolateral aspect of the median nerve.
Travels along the interosseous membrane between the radius and ulna.
Lies deep between flexor digitorum profundus (FDP) and flexor pollicis longus (FPL).
Accompanies the anterior interosseous artery.

Innervation

Purely motor nerve (no cutaneous sensory supply).
Supplies three muscles:
- Flexor Digitorum Profundus (index & middle fingers)
- Flexor Pollicis Longus
- Pronator Quadratus
Terminal branches also supply:
- Volar wrist capsule
- Carpal joint capsule

Epidemiology

Rare condition
Accounts for <1% of all median nerve neuropathies

Etiology

Common Sites of AIN Entrapment

Tendinous edge of the deep head of pronator teres (most common)
Fibrous arch of the flexor digitorum superficialis (FDS)
Thrombosed radial, ulnar, or anterior interosseous artery
Accessory head of FPL (Gantzer’s muscle)
Accessory muscle slips from FDS to FDP
Aberrant muscles (e.g., FCR brevis, palmaris profundus)

Causes

Idiopathic or spontaneous compression
Anatomical variations
Trauma (especially supracondylar fractures, usually traction injury)
Infections (e.g., CMV)
Iatrogenic causes (venipuncture or catheterization in cubital fossa)
Compartment syndrome and Volkmann ischemic contracture

Associated Conditions

Parsonage–Turner Syndrome

Viral brachial neuritis
May cause bilateral AIN palsy
Suspected when:
- Motor weakness follows severe shoulder pain
- Viral prodrome present

Martin–Gruber Anastomosis

Communicating branch between median/AIN and ulnar nerve
Fibers travel from median nerve across forearm to ulnar nerve
Primarily motor fibers
Can:
- Confuse clinical diagnosis
- Alter EMG interpretation
- Cause AIN palsy to mimic ulnar nerve dysfunction

Clinical Presentation

Motor weakness without sensory loss
Vague deep forearm pain may be present
Pain often absent or short-lived (typically 2–3 weeks)
Unlike:
- Carpal tunnel syndrome
- Pronator syndrome

Physical Examination

Inspection

Severe cases may show forearm muscle atrophy

Motor Findings

Weak grip and pinch strength
Weak flexion of:
- Thumb
- Index finger
- Middle finger

Characteristic Signs

Inability to form a proper “OK sign”
Also called:
- Kiloh–Nevin sign
- Peacock’s eye sign
Median nerve sensory examination is normal

Provocative & Differentiating Tests

Weak resisted pronation with elbow maximally flexed (tests pronator quadratus)
Differentiate from FPL tendon rupture:
- Passive wrist extension should flex thumb IP and index DIP joints (tenodesis effect)

Imaging

MRI

Indications

Suspected space-occupying lesion

Findings

Increased T2/STIR signal in:
- FPL
- FDP
- Pronator quadratus
Most reliable sign: edema in pronator quadratus

Electrodiagnostic Studies (EMG/NCS)

Role

Confirms diagnosis
Rules out proximal lesions
Assesses severity and recovery

Findings

Median nerve conduction: normal
Needle EMG:
- Abnormalities in FPL and FDP (index & middle finger)
- Fibrillations and sharp waves
- Prolonged latency

Differential Diagnosis

Flexor tendon rupture
Cervical spine or brachial plexus pathology
Pronator syndrome
Carpal tunnel syndrome

Key Clinical Distinctions

AIN Syndrome vs Pronator Syndrome

AIN: pure motor palsy
Pronator syndrome: motor + sensory involvement

AIN Injury vs High Median Nerve Injury

AIN Injury
- Pure motor deficit
- No sensory loss
- Cannot form OK sign
High Median Nerve Injury
- Motor + sensory loss
- OK sign deficit with sensory symptoms

Important Clinical Signs

OK Sign vs Froment’s Sign

OK Sign
- Tests AIN (FPL + FDP)
- Flattened pinch instead of circle
Froment’s Sign
- Indicates ulnar nerve injury
- Thumb IP flexes due to FPL compensation

Benediction Sign vs Ulnar Claw Hand

Benediction Sign
- Seen in AIN/high median nerve injury
- Index and middle fingers fail to flex when making a fist
Ulnar Claw Hand
- Seen in ulnar nerve injury
- Ring and little fingers remain flexed on attempted extension

Management

Non-Operative (First Line)

Observation, rest, and physiotherapy
Indicated in absence of space-occupying lesion
Most patients improve with conservative care
Recovery timeline:
- Improvement begins: 3–12 months
- Full recovery: up to 18 months
- Mean recovery: ~9 months
Pyridoxine (Vitamin B6) 100 mg for 6–8 weeks may be added

Operative Management

Indications

Space-occupying lesion
Failure of conservative treatment after 12 months
Surgery controversial in patients <40 years, as many recover non-operatively

Outcomes

Approximately 75% success rate

Surgical Technique (AIN Decompression)

Lazy-S incision over proximal volar forearm
Structures released:
- Lacertus fibrosus
- Superficial head of pronator teres
- FDS fibrous arch
- Gantzer’s muscle (if present)
- Crossing vessels
- Any compressive mass
AIN visualized from proximal to distal
Early active motion encouraged post-operatively

Complications

Persistent AIN palsy (very rare; 5–10 cases reported)
Managed with tendon transfer:
- Brachioradialis to FPL

Prognosis

Recovery typically begins 3–12 months after onset
Full recovery may take up to 18 months
Better prognosis in patients <40 years

Examples of Compression Neuropathies

Carpal tunnel syndrome
Cubital tunnel syndrome
Pronator syndrome
Radial tunnel syndrome
Posterior interosseous nerve syndrome
Tarsal tunnel syndrome
Meralgia paresthetica
Thoracic outlet syndrome

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