Common Causes of Neurogenic Lameness
World Small Animal Veterinary Association Congress Proceedings, 2016
Steven De Decker
Royal Veterinary College, Hatfield, UK

Although most dogs with lameness have orthopaedic disease, certain neurological disorders can also cause lameness. It is not always straightforward to differentiate orthopaedic from neurogenic lameness and many patients with neurogenic lameness will not demonstrate clear neurological deficits.

Thoracic Neurogenic Lameness

Malignant Peripheral Nerve Sheath Tumour (MPNST)

The vast majority of MPNSTs occur in the thoracic limbs. They commonly affect the brachial plexus and associated nerve roots. Large-breed dogs are overrepresented and most are >7 years old. The most common clinical sign is chronic progressive lameness. Muscle atrophy is often more severe than observed with orthopaedic disorders, while decreased muscle tone and decreased spinal reflexes may also be observed. Painful axillary palpation and pain on extension of the shoulder are occasionally seen. Horner's syndrome may be seen if the tumour involves the T1-T3 nerve roots. As the tumour grows it can invade the vertebral canal. When spinal cord compression occurs, neurological deficits may develop in the ipsilateral pelvic limb. The cutaneous trunci reflex may be interrupted ipsilaterally.

Survey radiographs can occasionally demonstrate an enlarged intervertebral foramen. Ultrasonography can be useful for more peripherally located MPNSTs and typically demonstrates a hypoechogenic tubular mass that displaces vessels and destroys normal architecture. The contralateral area can be examined for comparison. Ultrasound-guided fine needle aspiration biopsy has been reported to aid in reaching a final diagnosis.1 One limitation of ultrasound is that it only identifies MPNSTs at the level of the brachial plexus or distal to it; therefore a normal ultrasound will not rule out a more proximal MPNST. Imaging techniques that can be used to diagnose a more proximally located MPNST are myelography (occasionally), CT and MRI.

Although prognosis is guarded, the treatment of choice is surgical resection. Amputation is usually required. Nerve sheath tumours are locally invasive and rarely metastasize. Incomplete resection and postoperative local recurrence are unfortunately very common. Dogs with more proximally located tumours respond less favourably to surgery and will relapse earlier than dogs with peripherally located tumours.2

A metronomic chemotherapy protocol with cyclophosphamide and piroxicam has shown to delay tumour recurrence. Corticosteroids in combination with analgesia can be used as a palliative measure in nonsurgical cases.

Cervical Intervertebral Disk Disease and Cervical Spondylomyelopathy

Lateralised cervical intervertebral disk herniation or articular process hypertrophy resulting in intervertebral foraminal stenosis with compression of the nerve roots, can be a cause of neurogenic lameness in dogs. Usually, the lameness in these cases is associated with spinal pain and is called "nerve root signature." Clinical signs can be intermittent in nature. In an attempt to enlarge the intervertebral foramen, dogs often hold the affected limb in a characteristic "in-toe-posture." Myelography is often unrewarding in these cases. Diagnosis is best confirmed by CT or MRI. Medical treatment is usually preferred initially.3

Peripheral Nerve Trauma

1. Pathophysiology and Treatment

Peripheral nerve injuries can be classified based on the degree of physical and functional integrity of the nerve.

 Neuropraxia: interruption of nerve conduction without physical disruption of the axon. Recovery is usually spontaneous and complete, within 1–5 weeks.

 Axonotmesis: physical interruption of the axon, but surrounding supportive tissues remain intact. Recovery will be slow and occurs at a rate of 1–4 mm/day.

 Neuronotmesis: complete transection of the nerve and supporting structures. Recovery is unlikely.

It is clinically or electrophysiologically impossible to differentiate between these 3 gradations of peripheral nerve injury. The preservation of nociception makes axonotmesis and neuronotmesis unlikely. Loss of nociception does, however, not rule out neuropraxia and these dogs should be given the opportunity to improve.

Treatment involves (1) intense physical therapy and (2) supportive measures to protect the foot from injury. If no improvement is seen within 2–4 months, recovery becomes unlikely.

2. Brachial Plexus Avulsion

This is seen after road traffic accidents, which cause abduction and simultaneous caudal movement of the thoracic limb. The majority of dogs have avulsion of all roots of the brachial plexus (C6-T2). Thoracic limb monoparesis or monoplegia will be seen, instead of lameness. Cranial avulsions are rare and result in few clinical signs (C6-C8). These animals will be able to support weight and demonstrate abnormalities similar to lameness. Other signs can include decreased muscle tone, analgesia of the limb, absence of the withdrawal reflex, Horner's syndrome, and absence of the ipsilateral cutaneus trunci reflex.

Every animal unable to use a thoracic limb following trauma should be examined to detect orthopaedic as well as neurologic abnormalities. It is not uncommon for dogs with a brachial plexus avulsion to also have orthopaedic injuries. The most reliable prognostic indicator is analgesia distal to the elbow.4 Amputation of the limb should be considered if no improvement has occurred after 2 to 3 months or when the dog starts to self-mutilate the limb.

Pelvic Neurogenic Lameness

Caudal Lumbar Intervertebral Disk Disease

Because of an embryological uneven growth between the vertebral column and neural tissues, the spinal cord will terminate cranially from the lumbosacral intervertebral disk space. The spinal cord will usually terminate at the L5-L6 or L6-L7 intervertebral disk space and continues caudally as the cauda equina. Dogs with caudal lumbar intervertebral disk disease will therefore not experience spinal cord, but cauda equina compression. These dogs do not always demonstrate neurological signs, but can present with unilateral pelvic limb lameness. They can demonstrate decreased movement of the tail and a variable degree of caudal lumbar or lumbosacral pain. A large proportion of affected dogs will demonstrate severe pain on extension of the hips and dorsal extension of the tail. Although all dog breeds can be affected, the Cocker Spaniel is overrepresented for this type of intervertebral disk disease.5 A myelogram can be unrewarding in these dogs, because the dural sac does not always reach until the caudal lumbar intervertebral disk spaces. Little information is available about the medical management of these dogs. Outcome is good after surgery.5

Degenerative Lumbosacral Stenosis

Degenerative lumbosacral stenosis (DLSS) is a disorder in which a combination of bony and soft tissue abnormalities causes progressive lumbosacral vertebral canal stenosis with subsequent cauda equina compression. It typically affects older large-breed dogs, in particular the German shepherd. Dogs with DLSS can present with chronic pelvic limb lameness.6 Affected dogs often respond painfully on extension of the hips, complicating differentiation from orthopaedic disease. Specific findings suggestive for an underlying neurological disease are lumbosacral pain on palpation, pain on dorsal extension of the tail, proprioceptive deficits, decreased muscle tone, decreased withdrawal reflexes, flaccid tail and a decreased perianal reflex. Although radiographs may reveal many abnormalities, these abnormalities do not necessarily correlate with clinical signs and can also be seen in clinically normal dogs. Medical treatment is successful in approximately 55% of dogs.6 Surgical treatment is generally associated with good outcomes.

Traumatic Sciatic and Femoral Nerve Injury

Possible causes of sciatic nerve injury include pelvic or femoral fractures, pelvic or femoral surgery, and intramuscular injections in the caudal thigh.7 Animals will be able to support weight, but will walk with the paw knuckled over, the stifle joint will not flex, and the tarsus and digits will not flex or extend. The hock will have a typical "dropped" appearance. Sensation can be affected in the entire limb except for the medial aspect, which is supplied by the femoral nerve.

Extreme extension of the hip can cause femoral nerve dysfunction and a severe non-weight bearing gait abnormality.8 Animals will carry the limb flexed at the stifle and will demonstrate little hip flexion. Selective neurogenic atrophy of the quadriceps muscle can occur. Analgesia of the medial aspect of the limb and digit can occur.

References

1.  Da Costa RC, Parent JM, Dobson H, et al. Ultrasound-guided fine needle aspiration in the diagnosis of peripheral nerve sheath tumors in 4 dogs. Can Vet J. 2008;49:77–81.

2.  Elmslie RE, Glawe P, Dow SW. Metronomic therapy with cyclophosphamide and piroxicam effectively delays tumor recurrence in dogs with incompletely resected soft tissue sarcomas. J Vet Intern Med. 2008;22:1373–1379.

3.  Bersan E, McConnell F, Trevail R, et al. Cervical intervertebral foraminal disc extrusion in dogs: clinical presentation, MRI characteristics and outcome after medical management. Vet Rec. 2015;176:597.

4.  Van Soens I, Struys MM, Polis IE, et al. Magnetic stimulation of the radial nerve in dogs and cats with brachial plexus trauma: a report of 53 cases. Vet J. 2009;182:108–113.

5.  Cardy TJ, Tzounos CE, Volk HA, De Decker S. Clinical characterization of thoracolumbar and lumbar intervertebral disk extrusions in English Cocker Spaniels. J Am Vet Med Assoc. 2016;248:405–412.

6.  De Decker S, Wawrzenski LA, Volk HA. Clinical signs and outcome of dogs treated medically for degenerative lumbosacral stenosis (2004–2012). J Am Vet Med Assoc. 2014;245:408–413.

7.  Forterre F, Tomek A, Rytz U, et al. Iatrogenic sciatic nerve injury in eighteen dogs and nine cats. Vet Surg. 2007;36:464–471.

8.  Stepnik MW, Olby N, Thompson RR, Marcellin-Little DJ. Femoral neuropathy in a dog with iliopsoas muscle injury. Vet Surg. 2006;35:186–190.

  

Speaker Information
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Steven De Decker
Royal Veterinary College
Hatfield, UK


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