Loss of voluntary motor control (weakness or paralysis) of a single limb is called monoplegia (when complete) or monoparesis (when partial). Trauma and neoplasia are the most common causes of monoplegia. Diagnosis is based on medical history and careful neurological examination. The nature and severity of monoplegia depends on which nerves are affected. Management of the underlying problem and physical rehabilitation are potentially useful for treatment.
Loss of voluntary motor control in a single limb is termed monoparesis when motor function is partially impaired (weakness) and monoplegia when motor function is completely absent (paralysis).
Bilateral motor dysfunction of the pelvic limbs is referred to as paraparesis when motor function is partially preserved and paraplegia when motor function is completely lost. Similarly, "tetraparesis" (or quadriparesis) and "tetraplegia" (or quadriplegia) denote partial and complete loss of voluntary motor function, respectively, affecting all four limbs.
Hemiparesis and hemiplegia describe partial and complete loss of voluntary motor function, respectively, affecting the thoracic and pelvic limbs on the same side of the body.
Monoplegia and monoparesis result from a neurological lesion and should be distinguished from lameness or other forms of impaired limb function caused by musculoskeletal disease or injury.
Mononeuropathy is a neurological disorder characterized by disease, dysfunction, or injury affecting a single peripheral nerve or its corresponding nerve root.
Etiology and Pathophysiology of Monoplegia
Monoparesis or monoplegia is most often associated with diseases of the peripheral nerves, commonly trauma and neoplasia.
Monoparesis or monoplegia of a thoracic limb is usually associated with a lesion of the C6-T2 nerve roots or spinal nerves; the brachial plexus; or musculocutaneous, radial, median, or ulnar nerves. Injury to the brachial plexus or to the C6-T2 nerve roots is common in most species because of direct shoulder trauma or abnormal shoulder abduction (eg, in small animals hit by cars).
Horses and cattle positioned in recumbency on hard surfaces for foot or other surgeries can develop iatrogenic brachial plexus injuries. Usually the lesion is not actually in the brachial plexus, but rather some or all of the C6-T2 nerve roots are avulsed from the spinal cord.
Monoparesis or monoplegia of a pelvic limb is usually associated with a lesion of the L4-S2 nerve roots or spinal nerves; the lumbosacral plexus; or femoral, sciatic, peroneal (fibular), or tibial nerves.
Lumbosacral plexus injuries are less common than brachial plexus injuries but can be associated with vehicular accidents or extreme limb abduction. Pelvic fractures and sacroiliac luxations can damage the sciatic nerve.
Intramedullary pinning to repair a femoral fracture can be associated with nerve injury if the proximal portion of the pin is not flush with the bone. As the patient flexes the hip, the tip of the pin can snag the sciatic nerve, causing severe pain and nerve dysfunction.
Intramuscular injections in the caudal thigh can also damage the sciatic nerve. Such damage can happen even if the needle does not contact the nerve, because the injected substance can flow along fascial planes to pool around the sciatic nerve, causing an inflammatory response that can directly damage the nerve or induce progressive scarring that entraps the nerve.
Trauma is the most common cause of acute monoparesis or monoplegia in animals. Traumatic loss of nerve function can be due, in order of severity, to neuropraxia, axonotmesis, or neurotmesis.
Neuropraxia is a focal block of nerve conduction with no loss of axons. Transient neuropraxia is usually caused by a brief period of ischemia, such as ischemia resulting from compression, or by traction of the nerve that compromises microcirculation to the nerve. With prolonged neuropraxia, there is focal demyelination of axons; in these cases, recovery requires remyelination, which can take several weeks to several months.
Axonotmesis is a disruption of axons while continuity of the nerve connective tissue is maintained. With axonotmesis, the portion of the axon distal to the site of injury degenerates in a process called Wallerian degeneration.
Recovery from axonotmesis occurs by two mechanisms:
When 20–30% of the axons are damaged, the primary mechanism of recovery is collateral branching from intact axons. Collateral branching begins within 4 days after injury, and recovery can take 3–6 months.
When more axons are disrupted, recovery involves axon regeneration, which occurs at a rate of 1–4 mm per day. Therefore, the amount of recovery time depends on the location of the injury.
Relatively more proximal injuries, a longer duration of injury, and disruption of endoneural tubes all decrease the chance of recovery from axonotmesis.
Neurotmesis is full transection of the nerve and connective tissue resulting in complete discontinuity of the nerve. Most cases of neurotmesis require surgical repair to reconnect the severed nerve, followed by regeneration of the distal portion of the axons; even then, the prognosis for full recovery is usually poor.
Neoplasia of the nervous system (nerve roots and peripheral nerves) can cause chronic, progressive, often painful paresis of a thoracic or pelvic limb. Nerve sheath tumors are common in dogs. Lymphosarcoma of the brachial or lumbosacral plexus occurs in dogs, cattle, and cats.
Horses with equine protozoal myeloencephalitis (EPM) can develop monoparesis or monoplegia and focal muscle atrophy.
Clinical Findings and Lesions of Monoplegia
Clinical signs of monoparesis or monoplegia in animals include ataxia, abnormal gait, or dragging a limb, which arise because of weakness or paralysis of the involved limb. Other neurological signs might occur concurrently. The nature and severity depend on the specific nerves involved.
Muscle atrophy from denervation develops within a few days and is faster to develop and more severe than disuse atrophy.
The first sign of nerve sheath tumors of the cervicothoracic or lumbosacral nerves is lameness, often with no neurological deficits. Orthopedic disease can be mistaken as the cause. Eventually, animals with nerve sheath tumors develop neurological deficits.
A nerve sheath tumor should always be considered in older dogs with obscure, persistent lameness. Patients with brachial plexus tumors often have pain when the limb is extended or abducted—maneuvers that stretch the brachial plexus. Deep palpation of the axilla might reveal pain or even a palpable mass.
Clinical Findings of Thoracic Limb Monoplegia
Thoracic limb monoparesis or monoplegia can involve the suprascapular, musculocutaneous, radial, or median and ulnar nerves, or the T1-T2 nerve roots.
In cases of brachial plexus injury, the specific deficits depend on how severe the injury is and which nerve roots are affected. With a complete lesion, there is monoplegia, loss of sensation distal to the elbow, ipsilateral Horner syndrome, and loss of the ipsilateral cutaneous trunci reflex.
With disease of the suprascapular nerve, the supraspinatus and infraspinatus muscles are atrophied. In small animals, the gait is relatively normal. In horses, the shoulder drops ventrally and rotates laterally, and the hoof might scuff or drag along the ground slightly.
If the musculocutaneous nerve is affected, the animal is unable to flex the elbow, and the biceps muscle is atrophied.
With a radial nerve lesion, the elbow is dropped, the digits are knuckled onto their dorsal surface, and the limb is unable to bear weight. The triceps and extensor carpi muscles atrophy. There is loss of sensation on the cranial surface of the limb from the elbow to the foot.
A lesion of the median and ulnar nerves causes loss of flexion of the carpus and digits and atrophy of the flexor muscles. There is loss of sensation on the caudal aspect of the limb, from the elbow to the pads
A lesion of the T1-T2 nerve roots can cause Horner syndrome and ipsilateral loss of the cutaneous trunci reflex. Horner syndrome is characterized as ptosis, miosis, enophthalmos, and elevation of the third eyelid. Horses also show ipsilateral sweating on the face and neck. In cattle, Horner syndrome also causes loss of sweating on the ipsilateral side of the muzzle.
Clinical Findings of Pelvic Limb Monoplegia
Pelvic limb monoparesis or monoplegia can involve the femoral, sciatic, peroneal, or tibial nerve.
A lesion of the femoral nerve (L4-L5 nerve roots) causes an inability to extend the stifle and a weak to absent patellar reflex. The quadriceps muscle atrophies, and sensation is absent on the very medial surface of the foot.
A lesion of the sciatic nerve (L6-S2 nerve roots) causes an inability to flex the stifle and an inability to flex or extend the hock and digits. Affected animals can 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. The withdrawal reflex is weak to absent.
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 distribution of denervation muscle atrophy can indicate whether the sciatic nerve or only one of its branches is involved:
Atrophy of the gluteal, semimembranosus, and semitendinosus muscles, as well as all muscles below the stifle joint, indicates alesion of the L6-S2 nerve roots as they exit the spinal cord.
Atrophy of the semimembranosus and semitendinosus muscles but normal gluteal musclesindicates a lesion of the sciatic nerve at the sciatic notch or the proximal two-thirds of the femur.
Atrophy of either the cranial tibial or the gastrocnemius muscle alone indicates a lesion of the peroneal or tibial nerve, respectively.
If superficial sensation is decreased or absent on the cranial and caudal aspects of the limb and in the perineal region on the same side, a lesion of the L6-S2 nerve roots is likely.
If superficial sensation is lost, the location of the loss can indicate which nerve has a lesion:
Peroneal nerve lesions cause a decrease or loss of superficial sensation on the cranial surface of the hock and tibia and on the dorsal aspect of the foot.
Tibial nerve lesions cause a decrease or loss of superficial sensation on the caudal surface of the hock and tibia and on the plantar surface of the paw.
Sciatic nerve lesions cause a loss of sensation in the cranial, caudal, dorsal, and plantar regions.
Diagnosis of Monoplegia
Neurological examination and neurolocalization
Electrodiagnostic testing (eg, electromyography)
Other diagnostic testing, depending on the underlying cause
In cases of monoparesis or monoplegia, evaluation of the posture and gait, spinal reflexes, superficial and deep pain perception, and muscle mass of the affected limb can localize the lesion to the nerve roots or plexus or to a specific nerve branch. Superficial sensation is tested by observing a behavioral response (such as looking, wincing, crying, or biting) when the skin is pinched with hemostats. Deep pain is tested by applying hemostats to the bones of the digits or hoof testers to the hoof and observing a behavioral response.
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 chances are for recovery. In general, animals with nerve root or plexus lesions have a poorer prognosis than do animals with peripheral nerve lesions.
Pearls & Pitfalls
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If no nerve function is found on the initial neurological examination, neuropraxia, axonotmesis, and neurotmesis can be difficult to differentiate. Electromyography and motor nerve conduction of a nerve with neuropraxia is usually normal, and the prognosis is good. Finding denervation on electromyography 7–10 days after injury indicates a disruption of axons (axonotmesis or neurotmesis) and therefore prolonged recovery time and a more guarded prognosis.
Serial neurological examinations after the injury can help to determine the prognosis if electrodiagnostic testing is not pursued. Axonal regeneration is evident by return of motor function and pain sensation starting near the site of the injury and progressing distally at approximately 30 mm per month (1).Lack of improvement within 6 months after injury suggests a poor prognosis (1).
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.
Electric stimulation of the nerve can be used to determine nerve integrity. If there is some nerve integrity, the prognosis for patients with monoparesis or monoplegia is better if the motor nerve conduction velocity is normal than if it is slowed.
Tumors of the nerve roots within the vertebral canal can be visualized with myelography, CT, or MRI in dogs and cats. MRI is the best way to identify tumors of the brachial or lumbosacral plexus. Surgical removal or biopsy can help confirm a diagnosis of nerve sheath tumor.
Pearls & Pitfalls
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For horses with EPM, CSF analysis and CSF and serum EPM titers should be evaluated to determine the appropriate treatment.
Treatment of Monoplegia
Physical rehabilitation
Medical management of clinical signs
Treatment of the underlying cause
In most cases of peripheral nerve injury, treatment is time and physical rehabilitation. Prompt surgery to decompress the nerve is indicated when the nerve is entrapped by a fracture or orthopedic implant. Daily passive range-of-motion exercises help decrease muscle and joint contractures. Bandages or braces can help prevent damage to the foot from dragging.
Animals with nerve damage should be monitored closely for self-mutilation of the affected limb, which can occur as a result of paresthesia and loss of pain perception. Gabapentin, anti-inflammatory medications, and analgesics can help with paresthesia.
Pearls & Pitfalls
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If voluntary movement, pain perception, and spinal reflexes improve within 1–2 months, the prognosis is good. If nerve injury is suspected to be permanent and the patient is mutilating the limb, amputation is recommended in small animals (2).
When a brachial plexus injury lesion is complete, the prognosis for neurological recovery is very poor. In small animals, amputation is often required eventually. When lesions are incomplete and pain perception is preserved, some patients recover with supportive care and physical rehabilitation.
The long-term prognosis for animals with nerve sheath tumors that extend to the spinal cord is poor, even after attempted surgical removal and limb amputation, because the tumors eventually recur. The prognosis is better with surgical excision of more distal nerve sheath tumors, especially those affecting only one nerve.
Nerve sheath tumors often affect multiple nerve roots, making the tumors difficult to remove completely. Chemotherapy is not very helpful to treat these tumors; however, radiation therapy can have some benefit.
If appropriate chemotherapy is instituted in cases of lymphosarcoma, the patient's length and quality of life can be improved.
Key Points
Treatment of peripheral nerve trauma is usually time and physical rehabilitation.
Medication—including gabapentin, anti-inflammatory agents, and analgesics—can be helpful to manage pain and paresthesia.
Nerve sheath tumors often initially present as chronic lameness that can be mistaken for orthopedic disease.
For More Information
Also see pet owner content regarding leg paralysis in dogs.
References
Gordon T. Peripheral nerve regeneration and muscle reinnervation. Int J Mol Sci. 2020;21(22):8652. doi:10.3390/ijms21228652
Troupel T, Van Caenegem N, Jeandel A, Thibaud JL, Nicolle A, Blot S. Epidemiological, clinical, and electrophysiological findings in dogs and cats with traumatic brachial plexus injury: a retrospective study of 226 cases. J Vet Intern Med. 2021;35(6):2837-2845. doi:10.1111/jvim.16254
