It can be a challenge for the clinician to unravel the various factors influencing a gait abnormality in a patient. Particular situations leading to difficulties are:
Where lameness is caused by an occult neurological problem, with or without concurrent orthopaedic disease. Case example--a seven-year-old Retriever with progressive forelimb lameness over several months, with mild osteoarthritis of the elbow. Eventual diagnosis is of brachial plexus tumour.
Where lameness is the presenting sign in a nervous system disease that usually manifests itself with clear neurological deficits. Case example--German shorthaired pointer with intermittent hindlimb lameness caused by a lumbosacral disc protrusion
Where neurological disease co-exists with orthopaedic disease and the significance of either is not clear. Case example--German shepherd dog with severe coxofemoral osteoarthritis being considered for total hip replacement, but also with degenerative myelopathy.
It can be very difficult to differentiate between orthopaedic and neurological causes of lameness, and in rare situations, vascular disease can underlie the problem. Of course, there is also the occasional case of a soft tissue lesion causing lameness. Some patients may have problems with several body systems. For this reason, it is vital that each patient be approached in a thorough and methodical manner. The clinician must complete a complete orthopaedic, neurological and soft tissue assessment on each case, which must start with a careful history.
Most nerve tumours in dogs and cats occur close to the spinal cord, although they may come to involve the brachial plexus. Any mature animal with a chronic forelimb lameness for which no orthopaedic cause can be found should be evaluated for the possible presence of a brachial plexus tumour. Pain in the axilla, muscle atrophy, loss of the panniculus reflex and Horner's syndrome all are indicative of a brachial plexus tumour. Clinical signs include lameness, paralysis distal to the lesion and pain or thickening on palpation. Surgical exploration, biopsy and resection are indicated in solitary tumours.
Working dogs seem prone to fibrotic myopathy of the infraspinatus muscle. This leads to forelimb lameness with a characteristic outward rotation of the distal limb.
The most common neurological causes of monoparesis and monoplegia lie in the nerves and spinal cord segments of the lumbosacral region. Deficits of the femoral innervation manifest as loss of the patellar reflex. There may also be sensory loss on the medial aspect of the limb. The animal is unable to extend the stifle, thus it cannot bear weight. Sciatic deficits lead to lack of the withdrawal reflex, often seen as an inability to flex the hock.
UMN vs. LMN
Upper motor neurone (UMN) lesions causing hindlimb neurological problems include:
Lower motor neuron (LMN) deficits can be caused by:
Ischaemic myelopathy and neoplasia as mentioned above.
This is a major cause of neurological damage to the hindlimbs. It can be very difficult to determine whether there are neurological complications of pelvic fractures because of the severe pain that many dogs suffer and the lack of mobility, which restricts neurological assessment. It is wise to attempt some sort of neurological examination in all patients with pelvic fractures, even if it is restricted to reflex evaluation and assessment of pain perception. Loss of sciatic reflexes and/or deep pain complicate the picture and may indicate a poor prognosis.
Intramuscular injections in the caudal thigh carry a significant risk of damaging the sciatic nerve. For this reason, other injection sites are preferable. Intrafascicular injection can result in severe nerve damage with permanent disability, particularly with certain preparations, for example, penicillin/streptomycin and anthelmintics. Other drugs, for example, soluble corticosteroids, seem to be less of an irritant. Treatment depends to a large degree on the progression of the patient. Any improvement, whether monitored clinically or electrophysiologically, is an indication not to interfere surgically. Remembering that nerve fibres regrow at approximately 1cm per week, adequate time must be given for recovery. If after such time significant improvement has not occurred, surgical exploration is indicated. Recovery after nerve injection, either spontaneous or following surgical intervention, is unlikely to be complete.
There are several situations where nerve injury is commonly seen following orthopaedic or other procedures.
Sciatic nerve injury may occur following retrograde intramedullary pin placement in the proximal fragment in femoral fracture repair. Similar lesions can occur if a femoral intramedullary pin migrates proximally. The initial clinical sign is severe pain on walking and on palpation over the greater trochanter. Apparently severely affected sciatic nerves can recover to a marked degree following this type of injury, and surgical intervention should be cautious, particularly when considering grafting. Other orthopaedic procedures likely to cause nerve injury are repair of distal humeral fractures via a medial approach (radial nerve); cranial cruciate repair by "over-the-top" techniques (peroneal nerve); and ileal shaft fractures (lumbosacral trunk).
Perineal hernia repair using sutures through the sacrotuberous ligament is particularly hazardous to the sciatic nerve. Sutures should be passed through this ligament, not around it. If following surgery the dog is lame, painful or has sciatic paralysis, the sutures on the affected site must be removed immediately and an alternative method used.