Paralysis of one limb is referred to as monoplegia and is most often associated with diseases of the peripheral spinal nerves. Paralysis of the thoracic limb is usually associated with a lesion of the C6 to T2 nerve roots, the brachial plexus, or musculocutaneous, radial, median, or ulnar nerves. Paralysis of the pelvic limb is usually associated with a lesion of the L4 to S2 nerve roots, the lumbosacral plexus, or femoral, sciatic, peroneal (fibular), or tibial nerves.
Evaluation of the posture and gait, spinal reflexes, superficial and deep nociception, and muscle mass of the affected limb can localize the lesion to the nerve roots or plexus or to a specific nerve branch. Determining the exact location of the lesion is important for an accurate prognosis because the closer a nerve injury is to the muscle to be reinnervated, the better the prognosis for recovery. In general, nerve root or plexus lesions have a poorer prognosis than do peripheral nerve lesions.
Muscle atrophy from denervation develops within a few days and is faster to develop and more severe than disuse atrophy. With disease of the suprascapular nerve, the supraspinatus and infraspinatus muscles are atrophied; generally, little gait deficit is noted in small animals. However, in horses, the shoulder drops ventrally and rotates laterally, and the hoof may scuff or drag the ground slightly. If the musculocutaneous nerve is affected, the animal is unable to flex the elbow, and the biceps muscle is atrophied. With radial nerve disease, the elbow is dropped, the digits are knuckled onto their dorsal surface, and the limb is unable to bear weight. The thoracic limb flexor reflex (withdrawal reflex) is depressed or absent with lesions of the radial nerve (sensory portion), axillary nerve (shoulder flexion), musculocutaneous nerve (elbow flexion), or median and ulnar (carpal and digit flexion) nerves. The triceps and extensor carpi muscles may also atrophy in radial nerve disease. Superficial and deep digital flexor muscles atrophy with lesions of the median and ulnar nerves. There is little gait abnormality with ulnar nerve injury.
Superficial sensation is tested by observing a behavioral response (such as looking, wincing, crying, or biting) when the skin is pinched with hemostatic forceps or pricked with a needle. Regions of skin sensation associated with specific nerves are less distinct in equine and food animal species than in small animals. A loss of sensation on the rostral skin surface of the thoracic limb from the elbows to the paws indicates radial nerve disease. The skin of the caudal aspect of the limb, from the elbow to the pads, is desensitized in median and ulnar nerve disease, and the skin of the lateral aspect of the antebrachium and paw is desensitized with damage to the ulnar nerve.
Deep pain is tested by applying hemostatic forceps to the bones of the digits or hoof testers to the hoof and observing a behavioral response. The presence of deep pain from the fifth digit in small animals indicates integrity of the ulnar nerve. The presence of deep pain from the other digits of the thoracic limb indicates integrity of the radial and median nerves.
The eye on the side of the thoracic limb paralysis will show Horner syndrome (ptosis, miosis, and enophthalmos) when the lesion involves the T1 to T2 nerve roots as they exit the spinal cord. Horner syndrome is manifest in horses by ocular changes and ipsilateral sweating of the face and neck and in cattle by ocular changes and a unilateral loss of moisture on the muzzle.
Inability to extend the stifle to support weight in the pelvic limb is seen with L4 to L5 nerve root or femoral nerve disease; the patellar reflex is reduced or absent, the quadriceps muscle is atrophied, and sensation of the skin is reduced or absent on the medial surface of the limb. Inability to actively flex the stifle, hock, and digits or to extend the hock and digits is seen with lesions of the sciatic nerve, L6 to S2 nerve roots. The animal will support some weight if the femoral nerve is spared but will stand knuckled on the dorsum of the paw or hoof with the hock excessively flexed. If only the peroneal branch of the sciatic nerve is affected, the hock will be overextended and the digits knuckled. If only the tibial branch of the sciatic nerve is affected, the hock will be overflexed and the digits overextended. The prognosis for tibial or peroneal nerve lesions may be better than that for sciatic lesions, so differentiation is important.
The pelvic limb flexor reflex is diminished or absent with sciatic nerve lesions. The gastrocnemius reflex is diminished or absent with lesions of the sciatic or tibial nerve. The cranial tibial muscle reflex is diminished or absent with lesions of the sciatic or peroneal nerve. The distribution of denervation muscle atrophy can indicate whether the sciatic or only one of its branches is involved. Atrophy of gluteal, semimembranosus, semitendinosus, and all muscles below the stifle indicates a lesion of the L6 to S2 nerve roots as they exit the spinal cord. If the gluteal muscles are normal but the others are atrophied, then a lesion of the sciatic nerve is located at the sciatic notch or the proximal two-thirds of the femur. Atrophy of the cranial tibial or gastrocnemius muscles alone indicates a lesion of the peroneal or tibial nerve, respectively. If superficial sensation is reduced or absent on the cranial and caudal aspects of the limb and in the perineal region on the same side, then a lesion of the L6 to S2 nerve roots is likely. With peroneal nerve lesions, superficial sensation on the cranial surface of the hock and tibia and on the dorsal aspect of the foot is reduced or absent. With tibial nerve lesions, superficial sensation of the caudal surface of the hock and tibia and plantar surface of the paw is reduced or absent. Sciatic nerve lesions cause a loss of superficial sensation in the cranial, caudal, dorsal, and plantar regions. A loss of deep pain may be associated with sciatic nerve lesions. Preservation of sensation on the medial aspect of the pelvic limb is attributable to preservation of the saphenous nerve.
Electromyography can be used 7–10 days after a nerve insult to detect denervation in muscles and to outline the distribution of the nerve lesion. Denervation of limb and paravertebral muscles indicates nerve root lesions. Denervation of a specific muscle group indicates a lesion in its respective nerve. Electrical stimulation of the nerve can be used to determine nerve integrity. If some nerve integrity is present, the prognosis is better if motor nerve conduction velocity is normal than if it is slowed.
Trauma is the most common cause of acute monoplegia. Traumatic loss of nerve function may be due to neurapraxia, axonotmesis, axonostenosis, or neurotmesis. Neurapraxia is a temporary nerve conduction dysfunction that can last several weeks, but recovery is complete. Axonotmesis is rupture of some axons within the nerve but with an intact nerve sheath. Most closed nerve injuries from stretch or compression are a combination of neurapraxia and axonotmesis. Ruptured axons regenerate 1–4 mm/day, but functional recovery depends on the integrity and diameter of the nerve sheath and on the distance between injury and reinnervation sites. Nerves injured >180 mm from their respective muscles may be unable to make anatomic contact. If anatomic contact is made, the nerve sheath contracture, which develops over time, may not leave enough room to develop sufficient myelin to conduct an effective electrical impulse. Axonostenosis, or narrowed nerve sheaths with reduced nerve function, may be a sequela of nerve injuries. Neurotmesis is total nerve rupture, and surgical reattachment is required for regeneration. If no nerve function is found on the initial neurologic examination, neurapraxia, axonotmesis, and neurotmesis can be difficult to differentiate. Electrical stimulation of a nerve with neurapraxia is usually normal, and the prognosis is good, regardless of the findings of the initial neurologic examination. If the affected nerve does not respond to electrical stimulation distal to the site of the lesion ≥3 days after injury, the prognosis for recovery is guarded. Serial neurologic examinations throughout a 6-mo period are necessary if electromyographic evaluation is not performed.
Injury to the brachial plexus or the C6 to T2 nerve roots is common in most species due to direct shoulder trauma or abnormal shoulder abduction (eg, in small animals hit by automobiles). Horses and cattle cast on hard surfaces for foot or other surgeries may develop a brachial plexus injury. If Horner syndrome is present on the same side as a thoracic limb that has lost sensation and is areflexic and paralyzed, a brachial plexus avulsion is likely, and the prognosis for recovery grave. With brachial plexus avulsion, the nerve roots are torn from the spinal cord and cannot be repaired. If there is also no response to radial nerve stimulation, recovery is hopeless. If the limb drags on the ground, it can be held up with a neck sling or amputated in small animals to avoid laceration of the dorsal surface of the paw. Three-legged dogs and cats generally have a good quality of life. If no Horner syndrome is present with thoracic limb paralysis, the prognosis for recovery may be better.
Lumbosacral plexus injuries are less common than brachial plexus injuries but can be associated with automobile accidents or extreme limb abduction. Fractures of long bones can injure peripheral nerves locally. Surgical intervention for pelvic and hip disease and injection injuries are common causes of sciatic nerve injuries. Sustained pressure on the lateral aspect of the stifle can cause peroneal nerve injury. Heat application, massage, and stretching of tendons should be performed for 15 min 2–3 times/day to keep muscles, tendons, and joints healthy while the nerve is regenerating. A light bandage may prevent damage to the foot from dragging, but reduction of circulation should be avoided. No specific therapy is currently available to assist nerve regeneration, but recent studies with laser therapy, also known as cold laser, low level light therapy, or photobiomodulation, has shown some promise in assisting nerve regrowth. In traumatic injuries with accompanying swelling, small animals may be given NSAIDs or a short course of anti-inflammatory oral prednisone at 0.5 mg/kg/day for 5–7 days. This will help reduce edema, which can compromise circulation to the nerve. NSAIDs and corticosteroids should not be used concurrently. NSAIDs can be given to horses to reduce edema. If voluntary movement, nociception, and spinal reflexes improve within 1–2 mo, the prognosis is good. Limb mutilation can be transient in recovering nerve injuries and may be prevented by temporary use of an elizabethan collar. If nerve injury is suspected to be permanent and the animal is mutilating the limb, amputation is recommended in small animals. Enough time should be allowed to pass for possible regeneration of the nerve, typically 3–6 mo, before amputation.
Neoplasia of nerve roots and peripheral nerves can cause a chronic, progressive, often painful paresis of a thoracic or pelvic limb (See also Neoplasia of the Peripheral Nerve and Neuromuscular Junction and Neoplasia of the Nervous System.). Nerve sheath tumors are common in dogs. Lymphosarcoma of the brachial or lumbosacral plexus is seen in dogs, cattle, and cats. If the nerve roots within the spinal canal are affected, an extramedullary mass may be visualized with a myelogram, CT, or MRI in dogs and cats. Surgical exploration and removal or biopsy are essential to determine diagnosis or prognosis. The longterm prognosis for nerve sheath tumors is poor, even after attempted surgical removal and limb amputation. Nerve sheath tumors often affect multiple nerve roots, and the tumor is difficult to completely remove. If appropriate chemotherapy is instituted for lymphosarcoma, the length and quality of life may be improved. Chemotherapy is not very helpful to treat nerve sheath tumors, but radiation therapy may have some benefit.
Horses with equine protozoal myeloencephalitis (EPM, see Equine Protozoal Myeloencephalitis) may develop monoparesis and focal muscle atrophy. CSF analysis and CSF and serum EPM titers should be evaluated so appropriate therapy can be administered.