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Limb Paralysis in Animals


William B. Thomas

, DVM, DACVIM-Neurology, Small Animal Neurology, College of Veterinary Medicine, University of Tennessee

Reviewed/Revised Apr 2021 | Modified Nov 2022

Monoplegia is paralysis of one limb. Trauma and neoplasia are the most common causes of monoplegia. Diagnosis is based on medical history and careful neurologic examination.

Monoplegia is most often associated with diseases of the peripheral nerves. Paralysis of the 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. Paralysis of the 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.

Clinical Findings and Lesions in Animals with Limb Paralysis

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. 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.

Superficial sensation is tested by observing a behavioral response (such as looking, wincing, crying, or biting) when the skin is pinched with hemostatic forceps.

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.

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.

Thoracic Limb

With disease of the suprascapular nerve, the supraspinatus and infraspinatus muscles are atrophied. In small animals, the gait is relatively normal. 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 a radial nerve lesion, the elbow is dropped, the digits are knuckled onto their dorsal surface, and the limb is unable to bear weight. There is atrophy of the triceps and extensor carpi muscles. There is loss of sensation on the rostral 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. In horses, there is also ipsilateral sweating of the face and neck. In cattle, Horner syndrome also causes loss of sweating on the ipsilateral side of the muzzle.

Pelvic Limb

A lesion of the femoral nerve (L4–L5 nerve roots) causes inability to extend the stifle and a weak to absent patellar reflex. The quadriceps muscle will atrophy, and sensation is absent on the very medial surface of the foot.

A lesion of the sciatic nerve (L6–S2 nerve roots) causes inability to flex the stifle and inability to flex or extend the hock and digits. 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. 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 gluteal, semimembranosus, semitendinosus, and all muscles below the stifle indicates a lesion of the L6–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–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 sensation in the cranial, caudal, dorsal, and plantar regions.

Diagnosis and Treatment of Limb Paralysis in Animals

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 dysfunction of nerve conduction dysfunction that can last several weeks. 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 recovery depends on the integrity and diameter of the nerve sheath and on the distance between the 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-month period are necessary if electromyographic evaluation is not performed.

Injury to the brachial plexus or 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 may develop an iatrogenic brachial plexus injury. In most cases, 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. The specific deficits depend on which particular nerve roots are affected. With complete lesion, there is monoplegia, loss of sensation distal to the elbow, ipsilateral Horner syndrome, and loss of the ipsilateral cutaneous trunci reflex. In these cases, prognosis for neurologic recovery is very poor. Amputation is often required eventually in small animals. With incomplete lesions where pain perception is preserved, some patients will recover with nursing care and physical rehabilitation.

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. This 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. This causes an inflammatory response that can directly damage the nerve or induce progressive scarring that entraps the nerve.

In most cases of peripheral nerve injury, treatment is passage of 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 reduce muscle and joint contractures. Bandages or braces can help prevent damage to the foot from dragging. Self-mutilation of the affected limb may occur as a result of paresthesia and loss of pain perception, and should be monitored for closely. Gabapentin, anti-inflammatory medication, and analgesics can help with paresthesia. 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 animal is mutilating the limb, amputation is recommended in small animals.

Neoplasia of the nervous system Neoplasia of the Nervous System in Animals Primary neoplasia of the nervous system includes tumors originating from the brain, spinal cord, and peripheral nerves. Clinical signs are related to location: causing seizures, affecting mentation... read more (nerve roots and peripheral nerves) can cause a chronic, progressive, often painful paresis of a thoracic or pelvic limb. Nerve sheath tumors are common in dogs. Affected patients initially develop lameness, often with no neurologic deficits, which can be mistaken for orthopedic disease. Eventually, the patient develops neurologic deficits. A nerve sheath tumor should always be considered in older dogs with obscure, persistent lameness. Patients with brachial plexus tumors will often be in pain when the limb is extended or abducted, a maneuver that stretches the brachial plexus. There may be pain or even a palpable mass on deep palpation of the axilla.

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. MRI is the best way to identify tumors of the brachial or lumbosacral plexus. Surgical exploration and removal or biopsy can help with diagnosis and 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 Equine Protozoal Myeloencephalitis (EPM) may develop monoparesis and focal muscle atrophy. CSF analysis and CSF and serum EPM titers should be evaluated so appropriate therapy can be administered.

Key Points

  • Treatment of peripheral nerve trauma is usually time and physical rehabilitation.

  • Medication can be helpful to manage pain and paresthesia, and includes gabapentin, anti-inflammatory agents, and analgesics.

  • Nerve sheath tumors often initially present as chronic lameness that can be mistaken for orthopedic disease.

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