Median nerve mononeuropathies

Author(s): Nassim Rad, MD

Originally published:09/20/2014

Last updated:11/05/2019

1. DISEASE/DISORDER:

Definition

The most common median nerve mononeuropathy results from chronic compression at the level of the wrist1 and is referred to as carpal tunnel syndrome. More proximal lesions of the median nerve can occur above the elbow (from compression by a dense band of connective tissue called the ligament of Struthers), immediately below the elbow (from compression between the two heads of the pronator teres muscle) and distal to the elbow (an isolated injury to the anterior interosseous nerve (AIN)). High median nerve lesions in the region of the shoulder and proximal humerus are uncommon and usually secondary to trauma.

Etiology

Pronator syndrome

Proximal lesions of the median nerve may result from:

  1. Compression at the following sites:
    • Under the ligament of Struthers
    • Under the lacertus fibrosus (biceps aponeurosis) in the antebrachial fossa*
    • Between the two heads of the pronator teres muscle*
    • Under the proximal arch of the flexor digitorum superficialis (FDS) (sublimis arch) *
  2. Trauma
  3. Inflammatory conditions
  4. Anterior interosseus neuropathy is most commonly seen as a result of idiopathic brachial neuritis

*Collectively these areas of entrapment are known as pronator syndrome

Epidemiology including risk factors and primary prevention

Pronator syndrome

  1. Less than 1% of all median nerve entrapments2
  2. Second most common entrapment site of the median nerve after the carpal tunnel3
  3. Most common in ages 40 to 50 years3
  4. Risk factors include the following:
    • Female sex
    • Repetitive use of elbow, wrist, and hand
    • Volar forearm muscle hypertrophy, specifically the pronator teres

Anterior interosseous syndrome

  1. Incidence is rare
  2. Risk factors include the following:
    • Anomalous fibrous bands arising from the pronator teres or FDS muscles
    • Compression at Gantzer muscles (variant muscles located in anterior forearm inserting into the flexor pollicis longus)
    • Post infectious (CMV, Zoster, Hepatitis E infections)
    • Trauma (e.g., supracondylar fractures4)
    • Inflammatory process (e.g., idiopathic brachial neuritis)
    • Multifocal motor neuropathy

Patho-anatomy/physiology

  1. As the median nerve descends through the medial arm it runs beneath the *ligament of Struthers, an aberrant ligament present in 1 to 13% of individuals5 which attaches from a supracondylar bony spur to the medial epicondyle.Branches to the pronator teres and flexor carpi radialis (FCR) may arise slightly above the elbow.
  2. The median nerve continues beneath the *lacertus fibrosus or biceps aponeurosis and then runs *between the two head of the pronator teres.
  3. 4 to 6 cm distal to the medial epicondyle, the AIN divides from the main trunk of the median nerve. The anterior interosseous branch contains no superficial sensory branches. It dives posteriorly to provide innervation to the flexor pollicis longus (FPL), flexor digitorum profundus (FDP) (index/middle), and pronator quadratus muscles.
  4. The median nerve passes deep to the FDS muscle and its aponeurotic tendinous edge, known as the *sublimus bridge6
  5. It innervates the FCR and FDS and continues through the forearm to the hand to innervate the abductor pollicis brevis (APB), opponens pollicis (OP), flexor pollicis brevis superficial head and first and second lumbricals.
  6. Proximal to the wrist, the palmar cutaneous branch divides and provides sensation to the thenar eminence. Terminal fibers of the median nerve provide sensation to the palmar surface of the thumb and second, third, and radial half of the fourth digit.

*Areas of possible compression.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Disease progression depends on etiology.

  1. Compressive
    • Insidious onset
    • Pain is less severe and worsened by repetitive activity
    • Slowly progressive weakness, loss of dexterity, clumsiness, and fatigue
    • Surgical decompression may provide relief7,8
  1. Inflammatory
    • Acute onset
    • Pain can be severe but short lasting
    • Muscle weakness may be quite severe in the acute phase

Some advocate that conservative treatment be considered for a year or more because late spontaneous recovery can occur.9,10

2. ESSENTIALS OF ASSESSMENT

History

Pronator syndrome

  1. Insidious onset
  2. Symptoms are not typically worse at night and paresthesias not as well localized as in carpal tunnel syndrome6
  3. Aching discomfort in the forearm, can be described as tiredness or heaviness
  4. Mild weakness
  5. Exacerbation by repeated or resisted forearm pronation and/or resisted or repeated proximal interphalangeal flexion of digits 2 and 37

Anterior interosseous syndrome

  1. Compressive1
    • Slow onset of symptoms
    • Pain is often not severe and localized to the forearm
    • Deficits are strictly confined to the AIN: no sensory changes
  2. Inflammatory: focal neuritis or part of acute brachial plexus neuropathy1
    • Acute onset of severe pain in the forearm (if part of brachial plexopathy, pain can involve the shoulder and/or elbow)
    • Pain typically precedes weakness
    • May have sensory symptoms if more than the AIN is involved

Physical examination

  1. Cervical spine, shoulder, elbow, and wrist evaluation
  2. Findings may be normal in mild cases
  3. Sensory findings
    • Pronator syndrome/entrapment at ligament of Struthers
      • Sensory deficits may be detected in the entire median territory including thenar eminence which is spared in carpal tunnel syndrome (palmar cutaneous branch leaves median nerve proximal to carpal tunnel)
    • Anterior interosseous syndrome
      • No sensory deficits
  4. Motor findings
    • Pronator syndrome/entrapment at ligament of Struthers
      • Weakness may be detected in entire median territory
      • Pronator teres muscle weakness is usually spared in pronator syndrome (There is variable innervation to the pronator teres with the main branch of the median nerve providing innervation either proximal to or within the muscle itself.1)
      • Significant weakness rare, mild weakness of FPL and APB most common6
      • Muscle bulk of pronator teres may be greater in symptomatic volar forearm
    • Anterior interosseous syndrome
      • Weakness may be detected in the FPL, pronator quadratus, and FDP (index and middle)
      • OK sign: inability to flex first and second distal interphalangeal joints

Functional assessment

  1. Review type of work performed, including tools used, forceful gripping, or twisting forearm movements
  2. Assess recreational activities that may involve repetitive use including, but not limited, to the following:
    • Racquet sports
    • Rowing
    • Weight lifting
    • Chopping wood
    • Throwing

Laboratory studies

Laboratory studies may be used to evaluate for conditions that may predispose to compressive/inflammatory neuropathies.

Imaging

Magnetic resonance imaging (MRI)

  1. MRI allows visualization of mass lesions and nerve enlargement or inflammation11
  2. Signal changes or atrophy of the muscle innervated by the nerve in question is also seen on MRI12

Ultrasound

  1. Less expensive than MRI
  2. Can be more easily accessed when done in the office
  3. Can detect mass lesions and nerve enlargement
  4. Can provide dynamic imaging

Supplemental assessment tools

Electrodiagnostic Testing

Nerve Conduction Studies/ Needle Electromyography (EMG)

  1. Include routine median sensory nerve conductions to the digits and at least one median vs ulnar comparison at the wrist to exclude carpal tunnel.
  2. Include routine median motor studies at wrist and antecubital fossa to the APB. May need to stimulate at the axilla if question of entrapment at ligament of Struthers.
  3. Consider medial antebrachial cutaneous nerve conduction studies to rule out lower trunk/median plexopathy.
  4. Perform needle EMG of the APB, pronator teres, and one of the following: FPL, FCR, or FDS.6
  5. If the APB is abnormal, rule out lower trunk brachial plexopathy, polyneuropathy, or C8-T1 radiculopathy by testing other nonmedian lower trunk/C8-T1 muscles.
  6. If the proximal median muscles are abnormal, rule out proximal brachial plexopathy or C6-C8 radiculopathy by testing nonmedian C6-C7 and C7-C8 muscles.

Pronator syndrome

  1. Reduced median compound muscle action potentials (CMAPs) and/or sensory nerve action potentials (SNAPs) amplitudes with relatively normal distal latencies.6
  2. Conduction block/temporal dispersion or marked conduction velocity slowing between the wrist and elbow or between the elbow and axilla, with relatively normal CMAP distal latency.
  3. Prolonged median F waves despite a relatively normal distal CMAP and distal latency.
  4. Muscles distal to the lesion should demonstrate abnormalities on needle EMG

Anterior interosseous syndrome

  1. Routine median SNAPs and CMAPs are normal.
  2. Median motor study to the pronator quadratus may demonstrate evidence of demyelination and/or axon loss.1
  3. Needle EMG abnormalities seen in the pronator quadratus, FPL, and FDP of digits 2 and 3.

The following limitations exist:

  1. If nerve conduction studies show a nonlocalized median neuropathy, needle EMG can only localize a lesion if motor axon damage is involved.
  2. Variability of pronator teres innervation complicates lesion localization.
  3. Axonal injury may result in distal conduction slowing via loss of fastest axons.
  4. Concomitant median neuropathy at the wrist challenges localization of proximal lesion.

Early predictions of outcomes

Not reported.

Environmental

  1. Controversy remains regarding the role of muscle hypertrophy and overuse in the development of pronator syndrome.
  2. Controversy remains regarding true entrapment of the AIN versus inflammatory etiology (focal neuritis, acute brachial plexus neuropathy) given the lack of abnormalities intraoperatively and variable response with surgery.1

3. REHABILITATION MANAGEMENT AND TREATMENTS

Available or current treatment guidelines

No official guidelines.

At different disease stages

Pronator syndrome

  1. New onset/acute
    • Avoidance of provocative activity
    • Splinting to neutralize forearm pronation/supination and elbow flexion
    • Physical therapy: modalities for inflammation and swelling, soft tissue mobilization, gentle range of motion, and graduated strengthening
    • Patient education
  2. Subacute
    • Corticosteroid injections have been reported to give relief13
  3. No clinical improvement after conservative treatment with median nerve dysfunction
    • Extensive surgical exploration and decompression1

Anterior interosseous neuropathy

  1. New onset/acute
    • Same as above
  2. No clinical improvement after conservative treatment
    • Surgical exploration and decompression
      • Timing for surgical intervention varies from after 8 weeks to up to 12 months8-10

Patient & family education

  1. Ergonomics education
  2. Modification of recreational and work-related activities

Emerging/unique Interventions

  1. Impairment-based measurement
    • American Medical Association’s Guides to the Evaluation of Permanent Impairment
  2. Measurement of patient outcomes
    • Disabilities of the Arm, Shoulder, and Hand score14

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

  1. Thenar eminence sensory changes should warrant proximal investigation.
  2. Check the “OK” sign.
  3. In anterior interosseous syndrome, when a Martin-Gruber anastomosis is present, there may be associated weakness of the second and fifth digit abduction and adduction of the first digit because of the ulnar fiber cross-over.
  4. A normal physical exam does not rule out proximal median mononeuropathies.

4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE

Cutting edge concepts and practice

  1. High-frequency ultrasound is becoming the imaging modality of choice for peripheral nerves and may be an additional tool to aid in diagnosis.15
  2. Ultrasound has been able to identify stenotic lesions of the AIN.16 Nagano20reported good recovery in patients who underwent surgical neurolysis of these lesions. Closer attention to identifying these lesions may lead to better patient outcomes.

5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE

Gaps in the evidence-based knowledge

More outcome studies are needed to guide management.

REFERENCES

  1. Stewart JD. Focal Peripheral Neuropathies. Philadelphia, PA: JBJ Publishing; 2010.
  2. Mercier LR. Practical Orthopedics. St Louis, MO: Mosby; 2005.
  3. Lee, MJ, LaStayo, PC. Compressions that mimic carpal tunnel syndrome. J Orthop Sports Phys Ther. 2004; 34:601-609.
  4. Lipscomb PR, Burleson RJ. Vascular and neural complications in supracondylar fractures in children. J Bone Joint Surg Am. 1955; 37:487-492.
  5. Dang AC, Rodner CM. Unusual compression neuropathies of the forearm, part II: median nerve. J Hang Surg Am. 2009; 34(10):1915-1920.
  6. Preston DC, Shapiro BE. Electromyography and Neuromuscular Disorders. Philadelphia, PA: Elsevier; 2005.
  7. Hartz CR, Linscheid RL, Gramse RR, Daube JR. The pronator teres syndrome: compressive neuropathy of the median nerve. J Bone Joint Surg Am. 1981; 63:885-890.
  8. Nigst H, Dick W. Syndromes of compression of the median nerve in the proximal forearm (pronator teres syndrome; anterior interosseous nerve syndrome). Arch Orthop Trauma Surg.1979; 93:307-312.
  9. Seror P. Anterior interosseous nerve lesion: clinical and electrophysiological features. J Bone Joint Surg Br. 1996; 78:238-241.
  10. Futami T, Kobayashi A, Itoman M, Shimajiri I, Fujita T. Clinical investigation on the anterior interosseous nerve syndrome. J Jpn Soc Surg Hand. 1993;10:338-341.
  11. Spratt JD, Stanley AJ, Grainger AJ, Hide IG, Campbell RS. The role of diagnostic radiology in compressive and entrapment neuropathies. Eur Radiol. 2002;12:2352-2364.
  12. Sallomi D, Janzen DL, Munk PL, Connell DG, Tirman PF. Muscle denervation patterns in upper limb nerve injuries: MR imaging findings and anatomic basis. AJR Am J Roentgenol. 1998;171:779-784.
  13. Morris HH, Peters BH. Pronator syndrome; clinical and electrophysiological features in seven cases. J Neurol Neurosurg Psychiatry. 1976;39:461-464
  14. Svernlov B, Nylander G, Adolfsson L. Patient-reported outcome of surgical treatment of nerve entrapments in the proximal forearm. Adv Orthop. 2011;2011:727689.
  15. Strakowski JA. Ultrasound Evaluation of Focal Neuropathies: Correlation with Electrodiagnosis. New York, NY: Demos Medical Publishing; 2014.
  16. Kodama A, Sunagawa T, Ochi M. Early treatment of anterior interosseous nerve palsy with hourglass-like fascicular constrictions by interfascicular neurolysis due to early diagnosis using ultrasonography: a case report. J Hand Surg Eur Vol. In press.
  17. Nagano A. Spontaneous anterior interosseous nerve palsy.Br J Bone Joint Surg.2003;85:313-318.

Original Version of the Topic

Christie M. Lehman, MD. Median nerve mononeuropathies. POriginal Publication Date 09/20/2014

Author Disclosure

Nassim Rad, MD
Nothing to Disclose

Related Articles