Diseases of the Peripheral Nerves, Neuromuscular Junction, or Uncertain Sites: Relevant Examination Techniques and Illustrative Video Segments

1. Introduction

Mechanical injuries to peripheral nerves occur because of compression, entrapment, transection, laceration, ischemia, crushing, stretching, or chemical or burn damage.^1,2  Neurapractic lesions are characterized by a failure of conduction of the action potential across the injured axonal segment.³  Axonotmesis is axonal interruption caused by axon and myelin sheath injury, whereas neurotmesis reflects complete disruption of endoneurium, perineurium, and/or epineurium. Recovery by axonal regrowth is unlikely after neurotmesis.⁴  After axonotmesis of motor nerves, muscle reinnervation is to be expected and occurs by 2 separate mechanisms: collateral sprouting and axonal regrowth.¹  If there is incomplete loss of axons, reinnervation of muscle units by sprouting occurs in days to weeks. Reinnervation by axonal regrowth occurs at a rate of 1 millimeter per day (approximately 1 inch per month). Skeletal muscle cells deprived of nerve supply ultimately undergo fibroblastic transformation; thus, reinnervation may not be possible after more than 12 months, although this remains a controversial issue. Peripheral nerve injuries are characterized by weakness of the innervated muscle accompanied within 2 to 4 weeks by appreciable atrophy. When the injured nerve supplies important extensor muscles of the limbs (e.g., as is the case for radial, femoral, sciatic, and peroneal nerves), there is obvious alteration of gait. Areas of cutaneous anesthesia occasionally accompany peripheral nerve injuries. Over the neck and trunk, cutaneous sensory innervation occurs in defined bands associated with segmental dermatomes. Damage to a peripheral spinal nerve or dorsal nerve root results in cutaneous anesthesia/hypalgesia over the supplied dermatome. With damage to the pudendal nerve or its sacral nerve roots, there is anesthesia/hypalgesia of the perineal area. In contrast, relatively small autonomous zones have been defined for sensory components of the ulnar, musculocutaneous, median, femoral, tibial, and peroneal nerves.^5,6 Sympathetic fibers are distributed with peripheral nerves, so denervated skin also may be evident as circumscribed spontaneous sweating. The most common and important syndromes of mechanical injury to peripheral nerves of the limbs are described below.^6-8 

2. Suprascapular Nerve

The suprascapular nerve arises from C6 and C7 spinal cord segments. Injury occurs most commonly when a horse’s shoulder is impacted at speed such that the nerve is injured as it curls around the front of the neck of the scapula. There immediately is laxity and lateral instability of the shoulder joint, which bows out or “pops” as the affected limb bears weight. Within 2 to 4 weeks of injury, there is obvious atrophy of the supraspinatus and infraspinatus muscles (Sweeney). At least 50% of such injuries are predominantly neurapractic, and recovery of function (and muscle mass as there is atrophy) is evident within 30 days of injury and is complete within 60 days. In more severe injuries with morbid axonal injury, successful reinnervation is evident as recovery of muscle bulk in the ventral part of the supraspinatus muscle beginning within 3 months of injury. Maximal recovery takes an additional 3 to 12 months. Regrowth of the suprascapular nerve can be facilitated by surgery to resect scar tissue and a constricting band (external neurolysis) and reduce tension on the nerve as it crosses the front of the scapula (often performed 3 to 6 months after injury). Removal of a piece of bone from the neck of the scapula may further relax the injured nerve, but the scapular notch created by this procedure creates a potential nidus for scapular fractures during recovery from anesthesia.

3. Radial Nerve

The radial nerve innervates a flexor of the shoulder and the extensors of the elbow, carpal, and digital joints. It arises from T1. The nerve root may be lacerated by fractures of the C7 or T1 vertebrae or first rib. The nerve is commonly damaged as a result of humeral fracture⁹ and can be injured within the brachial plexus by trauma to the shoulder region. Ischemic damage may occur in horses anesthetized in lateral recumbency.¹⁰ The lower part of the nerve may be injured by dislocation or fractures that involve the elbow.

Horses with complete radial paralysis stand with the shoulder extended, the elbow “dropped,” and the dorsum of the hoof resting on the ground. When forced to walk, the horse may partially protract the limb by exaggerated extension of the shoulder; however, the toe drags and the horse collapses on the limb during the weight-bearing phase of the stride. If the site of damage is distal, the shoulder and elbow are normal. Although the radial nerve has numerous cutaneous sensory branches, injury to this nerve does not result in any consistent area of cutaneous anesthesia.

4. Musculocutaneous Nerve

The musculocutaneous nerve arises from C7 and C8 and supplies flexors of the elbow. Injury is uncommon and causes only transient toe-dragging. The shoulder may be held in a flexed position and the elbow in an extended position. There is hypalgesia/ anesthesia over the dorsomedial aspect of the knee and proximal metacarpus and atrophy of the biceps and brachialis muscles.

5. Median and Ulnar Nerves

The median nerve arises from C8 and T1 and the ulnar nerve from T1 and T2. Injury to either can be caused by injury to the brachial plexus or along the medial aspect of the upper limb. Clinical findings include a “tin soldier” gait, with decreased flexion and dragging of the toe during protraction of the limb and hypalgesia/analgesia of the skin of the caudal forearm, lateral metacarpus, and medial pastern areas and atrophy of the carpal and digital flexors.

6. Femoral Nerve

The femoral nerve arises from L3 to L5 and innervates muscles that flex the hip and extend the stifle. The nerve can be damaged by ilial, femoral, or vertebral fractures. Ischemic injury is caused by prolonged stretch or increased tissue pressure during anesthesia in dorsal recumbency or after severe prolonged dystocia.¹¹ With unilateral paralysis, the pelvic limb is abnormally flexed, usually with the foot flat on the ground, and buckles when the limb bears weight. In the case of bilateral involvement, the horse is either unable to rise or stands uncomfortably in a crouched position. If the nerve injury occurs proximal to the saphenous branch, there is anesthesia/hypalgesia of the skin over the medial surface of the thigh and atrophy of the quadriceps muscle.

7. Sciatic Nerve

The sciatic nerve arises from L5-S1 and supplies important extensors of the hip and flexors of the stifle. Damage usually is a result of deep injections into the caudal thigh.¹ The nerve also may be injured by fractures of the ilium or ischium or sacroiliac or coxofemoral dislocations. The limb is held slightly caudal with the dorsum of the hoof resting on the ground. The stifle and hock are extended, whereas the distal joints are flexed. The leg is dragged forward by the actions of the quadriceps and biceps femoris muscles. These muscles, in concert with the reciprocal apparatus, allow the horse to bear some weight on the limb if the foot is first placed in normal position. There is cutaneous hypalgesia/anesthesia over most of the limb except for the medial thigh.

8. Peroneal Nerve

The peroneal nerve arises from the sciatic trunk deep to the biceps femoris and is motor to the flexors of the tarsus and the extensors of the digit. Paralysis results in extension of the tarsus and flexion of the distal joints of the pelvic limb. [...]