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Musculocutaneous nerve: paralysis

ISSN 2398-2977


Introduction

  • Cause: this is a rare condition as an isolated paralysis and is more commonly involved with other nerve dysfunction. Brachial plexus injuries and spinal cord lesions involving the brachial intumescence may affect this nerve. External trauma directly or indirectly (via upper forelimb fractures) to this nerve individually are very uncommon.
  • Signs: no gait deficits to very mild gait deficits, unilateral unusually, an overextension of the elbow, atrophy of the biceps and brachialis muscles, hypoalgesia of the craniomedial carpus and cannon.
  • Diagnosis: clinical signs, neurological examination and electrodiagnostics.
  • Treatment: DMSO, corticosteroids, physiotherapy, rest.
  • Prognosis: good.

Presenting signs

  • The clinical signs can include no to very mild gait deficits due to decreased elbow flexion.
  • Toe dragging is associated with decreased elbow flexion.
  • With more severe injury, overextension of the elbow may occur at rest and exercise.
  • Atrophy of the biceps and brachialis muscles may be found in severe and long-term cases.
  • Hypoalgesia of the craniomedial carpus and cannon.
  • Other abnormalities may be present if other peripheral nerves are involved   Brachial plexus: trauma      Median / ulnar nerve: paralysis  .

Acute presentation

  • Sudden onset unilateral gait deficits, inability to flex elbow and hypoalgesia.
  • Signs of trauma or injury in upper forelimb.

Geographic incidence

  • Worldwide.

Cost considerations

  • Costs of diagnosis and treatment.
  • Permanent loss of function and use.

Special risks

  • Upper forelimb fractures or severe trauma.

Pathogenesis

Etiology

  • This is a rare condition as an isolated paralysis and is more commonly involved with other nerve dysfunction.
  • Brachial plexus injuries and spinal cord lesions involving the gray matter of the brachial intumescence may affect this nerve.
  • External trauma directly or indirectly (via upper forelimb fractures) to this nerve individually are very uncommon.

Pathophysiology

  • Paralysis of any of this nerve rarely occurs as a single event.
  • Paralysis of this nerve can be associated with dynsfunction of other peripheral nerves such as the median ulnar nerves.
  • The musculocutaneous nerve supplies the muscles extending the shoulder and flexing the elbow. Section of the proximal part of the nerve experimentally results in decreased elbow flexion and subsequent toe dragging. Partial sensory loss occurred in the skin over the craniomedial carpus and cannon.

Timecourse

  • Experimental studies showed that the gait deficits may disappear within 2 or 3 months due to compensation and adaptation.

Diagnosis

Presenting problems

  • Gait deficits in the forelimb.
  • Chronic loss of muscle in the upper forearm.

Client history

  • Upper forelimb trauma.
  • Sudden onset forelimb gait change.

Clinical signs

  • The clinical and lameness examinations may detect characteristic gait abnormalities or sensory deficits as result of nerve injury.
  • No gait deficits to very mild gait deficits.
  • Usually unilateral.
  • Overextension or lack of flexion of the elbow. The horse lifts the limb at the level of the shoulder to allow the carpus and lower limb to be flipped forward during the walk/trot.
  • Toe dragging in the forelimb.
  • Backing the horse up emphasis the inability to flex the elbow and as the horse attempts to move caudally it drags the foot on the ground.
  • Atrophy of the biceps and brachialis muscles   Chest: pectoral muscle atrophy    Sweeney: shoulder muscle atrophy  .
  • Partial sensory loss is expected in the skin over the craniomedial aspect of the knee and metacarpal region, possibly distally to the fetlock.

A close inspection of cutaneous sensation is important.

Diagnostic investigation

  • Neurologic examination  Neurology: examination - adult  .
  • Electrodiagnostic aids  Electrodiagnostic testing  (EMG and nerve conduction velocity) may be helpful in diagnosing diseases of the nerves   →   because the muscle is the end organ of the peripheral nerve, damage to the nerve can lead to abnormal muscle electrical potentials such as positive sharp waves and fibrillation potentials.
  • Needle electromyographycan disclose denervation potentials in the biceps and brachialis muscles.
  • Muscle biopsy  Muscle: biopsy  may reveal muscle fiber atrophy, angular fibers, and fiber type grouping characteristics of denervation.

Confirmation of diagnosis

Discriminatory diagnostic features

  • History and clinical signs.

Definitive diagnostic features

Differential diagnosis

  • Brachial plexus injuries   Brachial plexus: trauma  and spinal cord lesions involving grey matter of the brachial intumescence may cause signs related to involvement of some or all of these nerves.

Treatment

Standard treatment

  • Therapy may not be indicated in mild or transient cases.

Medical management

Systemic anti-inflammatory treatment

  • Dimethyl sulfoxide (DMSO)  Dimethyl sulfoxide  :
    • Can be used in horses with acute injury to peripheral nerves.
    • Its principal action is to scavenge free oxygen radicals generated in damaged tissue.
    • Helps to maintain blood flow to hypoxic tissues by reducing generation of prostaglandins and thromboxane, thus preventing platelet aggregation.
    • Can be efficacious early in the onset of peripheral nerve trauma both intravenously (IV) (1 g/kg as a 10% solution) and topically over the affected area.
  • Corticosteroids:
    • Can be efficacious in acute peripheral nerve trauma.
    • Dexamethasone   Dexamethasone  (0.05-0.2 mg/kg IV) may be used initially.

Short-term administration of corticosteroids is best, but long-term administration may be necessary. When given at the recommended doses, corticosteroids can act synergistically with DMSO.

  • NSAIDs have been used in some acute cases.
  • Box rest with adequate bedding but not such that it will collect around the distal part of the affected leg.
  • Support other legs.
  • Physiotherapy of affected muscles to prevent atrophy and maintain function.
  • Specific treatment for any trauma of upper forelimb or other injuries/nerve dysfunction.

Surgical management

  • Although theoretically possible there are no published reports of this. Direct severance of the individual nerve is very rare and other causes are not applicable to surgical treatment.

Subsequent management

Treatment

Surgical management

  • Theoretically, surgical exploration of the area to free entrapped nerves or hematomas could be performed if the condition persists, but this has not been reported for this nerve. Removal of adhesions, neuromata, and possible re-anastomosis is potentially possible 2-8 weeks after injury.

Physical therapy

  • May be effective in developing compensatory mechanisms and strength in horses that have recovered from the initial nerve injury.
  • Horses may improve dramatically with regular and controlled exercise.
  • Exercise allows the unaffected parts of the nervous system to compensate for the affected muscles by increasing strength and conscious proprioception.
  • Electrical stimulation of the affected muscles of the upper forelimb may help to stop atrophy and maintain function.
  • Passive flexion and extension of the affected limb are also helpful in maintaining range of motion.

Prevention

Outcomes

Prognosis

  • Quite good as the gait alteration usually substantially decreases or disappears within 3 months of the injury. This seems at least partially to be due to crossing over of fibers between the musculocutaneous and median nerves with compensatory return of function to the affected muscles. Each individual case and the site of disruption will determine the likelihood and extent of this compensation.
  • If the brachial plexus or spinal cord are affected then the overall prognosis will be determined by the variety and extent of neurological dysfunction in addition to that of the musculocutaneous nerve damage.

Expected response to treatment

  • 2-3 months.

Reasons for treatment failure

  • Severe damage to nerve.
  • Damage to other nerves preventing compensation and increasing range of neurological deficits.

Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Hahn C (2008) Peripheral nerves in the horse. In Practice 30 (6), 322-329 BMJ Online.
  • Alexander K & Dobso N H (2003) Ultrasonography of peripheral nerves in the normal adult horse. Vet Radiol Ultrasound 44 (4), 456-464 PubMed.
  • Blythe L L & Kitchell R L (1982) Electrophysiologic studies of the thoracic limb of the horse. Am J Vet Res 43 (9), 1511-1524 PubMed.

Other sources of information

  • Mayhew I G (2009) Large Animal Neurology. 2nd edn. Wiley-Blackwell, UK. pp 309.
  • Blythe L L (1997) Peripheral Neuropathy. In: Current Therapy in Equine Medicine. 4th edn. Ed: Robinson N E. Saunders, USA. pp 314-318.