Peripheral nerves of animals can be injured as a result of external trauma. Surgery and intramuscular injections can also cause nerve injury.
Peripheral nerve injuries are some of the most common neuropathies in animals.
The immediate effect of injury to a peripheral nerve is a variable degree of nerve dysfunction, depending on the severity of the injury. The mildest form of injury is neuropraxia, which temporarily disrupts function but causes minimal morphological alterations in the nerve. Axonotmesis is disruption of axons without disruption of the surrounding connective tissue of the nerve. The most severe form of peripheral nerve injury is neurotmesis, which is complete severance of the nerve. With both axonotmesis and neurotmesis, there is subsequent degeneration of the axons distal to the injury site and in a portion of the nerve proximal to the injury site.
Diagnosis of peripheral nerve trauma is based on the history and clinical assessment of the motor and sensory function of the affected nerves. Electromyographic evaluation often helps identify denervated muscles 5–10 days after nerve injury. Nerve conduction studies can also be useful in diagnosis.
The prognosis for patients with peripheral nerve trauma is guarded. Patients with neuropraxia usually recover completely within 3 weeks. For function to return after axons are disrupted (axonotmesis, neurotmesis), the nerve must regenerate from the point of injury all the way to the innervated muscle. The growth rate of regenerating axons in the distal stump is 1–3 mm every 24 hours. Recovery is unlikely if the severed axons are substantially separated or if scar tissue interferes with axonal growth.
Although various anti-inflammatory drugs have been recommended for treatment of traumatic nerve injuries, there is little evidence that they provide any benefit.
Surgery to appose the nerve stumps should be performed promptly in patients with sharply transected nerves. In instances of blunt trauma, surgical exploration and excision of scar tissue might help. Surgery is often successful in horses with fibrous compression of the suprascapular nerve.
Long-term management of peripheral nerve injury consists of physical rehabilitation to minimize both muscle atrophy and decreased mobility of joints. Bandages, splints, or various other methods of external coaptation might be necessary to help protect the affected limb.
Brachial Plexus Injury
Brachial plexus injury occurs when the C6-T2 nerve roots that innervate the thoracic limb are traumatically injured. With severe extension or abduction of the limb, the nerve roots stretch or tear from their attachment to the spinal cord. Brachial plexus injuries include stretching, compression, contusion, laceration, or in the most severe case, avulsion (detachment) of the nerve roots.
Brachial plexus injuries have been reported in a number of species, including dogs, cats, birds, horses, and cattle (see Brachial Plexus Injury in Cattle).
Clinical signs of brachial plexus injury vary with the extent of root involvement. Complete avulsion results in flaccid paralysis of the limb, anesthesia distal to the elbow, ipsilateral Horner syndrome, and ipsilateral loss of the cutaneous trunci (panniculus) reflex. The injured animal bears little or no weight on the limb and drags the dorsal surface of the paw on the ground. Sensation to the ventral surface of the paw is spared if only the cranial nerve roots are affected. Avulsion of the caudal nerve roots causes loss of sensation on the caudal surface of the limb and variable loss on the cranial surface.
There is no treatment for brachial plexus injury, and for patients with complete avulsion, the prognosis is poor. Amputation of the limb might be necessary because of damage from dragging or self-mutilating the limb. Recovery is possible in mild cases in which the roots are contused rather than avulsed.
Calving Paralysis in Cattle
Calving paralysis occurs in heifers with oversize fetuses. It has previously been attributed to bilateral compression of the obturator nerve; however, damage to the L6 nerve root, which contributes to the obturator and sciatic nerves, likely accounts for most of the paralysis (1).
Ischemic necrosis of muscles secondary to compression and rupture of muscles during attempts to rise also contribute to the paraparesis. In addition, metabolic derangements, such as hypocalcemia, can complicate the clinical picture. (Also see Bovine Secondary Recumbency.)
Facial Nerve Trauma
Facial nerve trauma is most common in large animals that become recumbent, which leads to subsequent compression of the side of the face. Sustained pressure can additionally compromise the nerve's blood supply and produce ischemic injury. Although it is often known as recumbency-associated facial nerve paralysis, facial nerve trauma can also be caused by pressure from a halter that is left on a horse during general anesthesia.
Clinical signs of facial nerve trauma include ipsilateral lip paralysis, deviation of the muzzle to the contralateral side (see ), and weak to absent palpebral reflex. A drooping ear can result from injuries to the proximal aspect of the nerve.
Horse with right facial nerve paralysis due to facial nerve trauma secondary to recumbency. Note deviation of the upper lip to the left and drooping of the right ear.
Courtesy of Dr. Carla Sommardahl (University of Tennessee).
Other Peripheral Nerve Injuries
The sciatic nerve or its branches can be injured by pelvic fractures or during or after retrograde placement of intramedullary pins in the femur. Intramuscular injections in the caudal aspect of the thigh also risk injury to the sciatic nerve. The sciatic nerve lies in a fascial plane between the biceps femoris and adductor muscles. Any material injected into the caudal thigh tends to accumulate in this fascial plane surrounding the nerve, causing immediate nerve damage or delayed injury as a result of local inflammation and fibrosis.
Pearls & Pitfalls
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Damage to the proximal aspect of the sciatic nerve causes monoparesis with an inability to flex the stifle joint. The tarsus (hock) and digits cannot be flexed or extended, and weight is supported on the dorsal surface of the foot with the hock excessively flexed. There might be loss of sensation below the stifle joint, except for the medial aspect, which is innervated by a branch of the femoral nerve.
Injury to the tibial nerve results in an inability to extend the hock or flex the digits, as well as decreased sensation over the plantar surface of the foot.
Injury to the peroneal nerve results in an inability to flex the hock or extend the digits, as well as decreased sensation over the craniodorsal surface of the foot, hock, and stifle joint.
The femoral nerve can be injured in calves and foals during dystocia if excessive traction stretches or otherwise damages it. This results in an inability to bear weight on the limb because of an inability to extend the stifle joint. The patellar reflex is weak or absent. Sensation is lost along the medial surface of the limb (saphenous nerve).
The suprascapular nerve is most commonly injured in large animals secondary to trauma of the shoulder region. This results in atrophy of the supraspinatus and infraspinatus muscles and instability of the shoulder joint (a condition also called "sweeney"; see Suprascapular Neuropathy in Horses). In horses, the nerve can be entrapped by connective tissue that develops in the region of the supraspinous fossa.
Key Points
Caudal thigh injections can damage the sciatic nerve.
The facial nerve in large animals can be damaged by compression during recumbency.
Damage to the brachial plexus nerve roots is a common cause of monoplegia in dogs and cats.
For More Information
References
Cox VS, Breazile JE, Hoover TR. Surgical and anatomic study of calving paralysis. Am J Vet Res. 1975;36(4 Pt.1):427-430.
