An abnormal gait is a common reason for owners to seek veterinary attention. The challenge is in localizing the cause of the altered gait such that effective therapy can be applied. The musculoskeletal and nervous systems contribute the most to gait, and there is obviously a great deal of overlap between the two, but the role of organ systems such as cardiopulmonary and endocrine, should not be ignored.
As much historical information as possible should be gleaned from questioning the owner such that one can get an idea of what signs were first apparent, the time-line, and details of progression. Response, or lack thereof, to previously prescribed anti-inflammatory or analgesic therapies can provide clues. Differences in climbing versus descending stairs, reluctance to jumping onto furniture, and postural changes during defecation can alert one to lumbosacral issues but hip dysplasia could also result in similar signs. An inability to move versus reluctance to move is often not appreciated and differentiating between the two will often provide clues as to whether a neurological condition or an orthopaedic condition exists. Both neurological and orthopaedic conditions can be associated with variable degrees of pain, or not be painful at all. Generally, orthopaedic conditions resulting in lameness will improve with exercise but the signs will remain or even be exacerbated by activity in the neurological patient.
Observation of the patient is often the key - evaluate the mental status and responsiveness, and most important, evaluate the gait.
Have the owner or a technician/nurse walk the patient - away from you, towards you, and also observe the patient from the side. A level surface should be selected first and should abnormalities of gait not be appreciated, walk the patient on an incline, if possible. Only use stairs if it is unlikely to result in patient/client distress. With orthopaedic conditions, a faster pace of walking or even jogging will often reveal the lameness, whereas a slower pace may be required for neurological assessment since the patient may not show subtle deficits at a fast pace. Observe the patient rising from a laying position since an orthopaedic lameness may only be noticeable when initiating movement and as exercise continues the lameness is less evident or disappears. Orthopaedic and neuromuscular diseases tend to result in a shorter stride than spinal disease.
Common Orthopaedic Conditions that Mimic Neurological Disease
Bilateral Cranial Cruciate Rupture
Acute onset of difficulty rising and walking will mimic a paraparetic patient. A short pelvic limb stride is noted and these patients tend to pull themselves up from a recumbent position, primarily using their thoracic limbs. When sitting, they do so with great deliberation, slowly allowing the pelvis to lower to the floor as though sitting down on a hot surface. Postural deficits or ataxia are not noted on examination, and the gait is abnormal on initiation of walking, to distinguish it from myasthenia gravis, where the gait may be normal on initiation and then becomes short and choppy and the patient sits/collapses in the rear. Complete cranial cruciate ruptures will show an anterior drawer sign or positive tibial thrust sign - partial tears are sometimes more difficult to confirm, but stifle pain in the acutely presented patient in addition to radiographic evidence of joint effusion or osteoarthritic changes; medial buttress and joint cytology in the chronic cases can provide clues. On rare occasions MRI may be required for confirmation.
Bilateral Elbow/Hip Disease
Elbow dysplasia is a leading cause of thoracic limb lameness and includes the following conditions: fragmented coronoid process, radial-ulnar incongruence, medial compartment syndrome, osteochondrosis dissecans, ununited anconeal process. If bilaterally affected (as many are), signs comparable to a caudal cervical myelopathy could be evidenced since both thoracic limbs take on a shorter stride and stiffness becomes evident.
Hip dysplasia can not only mimic the exercise intolerance of neuromuscular disease but is often erroneously thought to be the cause in many patients with paraparesis secondary to either spinal or lumbosacral disease. In young dogs the pain results from articular cartilage wear exposing the subchondral bone pain fibres, and the stretching of the soft tissues due to laxity of the joint. Degenerative joint disease and osteoarthritic changes are responsible for the pain of hip dysplasia in the older dog.
Carpal Subluxation/Tarsal Subluxation
Loss of palmer ligamentous and muscle support and variable palmigrade (carpus) or plantigrade (tarsus) stance may be noted in older dogs secondary to severe end-stage polyarthritis. Bilateral involvement could mimic neuromuscular disease, but could also be associated with chronic displacement of weight to the thoracic limbs in overweight patients with either chronic thoracolumbar disease or painful orthopaedic disease. In young growing dogs, carpal laxity syndrome will present with similar bilateral signs and is thought to be a combination of poor nutrition and inadequate exercise. Traumatic hyperextension (carpus) or hyperflexion (tarsus) injuries are differentials.
Infraspinatus Muscle Contracture
Fibrosis of the infraspinatus muscle with contracture may occur as an acute onset of thoracic limb lameness after strenuous activity, most commonly in hunting dogs. Invariably, a weight-bearing lameness is initially noted which will resolve only to return as an abnormal gait develops about 3–4 weeks later. As the muscle contracts, the shoulder rotates outwards and the elbow becomes abducted, resulting in outward rotation of the paw. The gait/posture and palpation of an atrophied infraspinatus with no other neurological deficits usually allows for differentiation of a brachial plexus neuropathy. Characteristic changes are noted to the muscle on MRI, should it be required for confirmation.
Gracilis or semitendinosus myopathy occurs in German Shepherd and Belgian Shepherd dogs, usually as an athletic injury, and appears to be more common in young adult males. An immune-mediated or neurological mechanism has been postulated but not confirmed. Since the signs are slow in onset, the owners often don't recall a traumatic event. An abnormal pelvic limb gait occurs where the stride is shortened and in the mid to late stage of advancing the limb, the limb snaps down to the floor with medial rotation of the paw, the hock rotates outwards, and the stifle inwards. A tight, fibrous band of tissue is palpated at the caudal border of the gracilis or in place of the semitendinosus muscle.
Non-erosive polyarthritis, (including tick-borne, immune-mediated, idiopathic immune-mediated, plasmatic-lymphocytic synovitis), and the erosive (rheumatoid, feline progressive) polyarthritidies result in a painful gait and reluctance to walk. Many patients walk gingerly, or as though walking on eggshells/hot surface, with a shortened stride, often in all limbs. Spinal pain may be elicited if the disease process affects the vertebral synovia but importantly, proprioceptive and spinal reflex deficits are not appreciated. Joint pain and/or palpable joint effusion may not necessary be present, requiring joint aspiration and cytology/joint fluid analysis a requirement for confirmation/exclusion. The presence or absence of pyrexia is also not a reliable indicator.
Differentiation between a neurological versus an orthopaedic condition is not always easy. One should not underestimate the importance of obtaining a good history, which may require more pointed questioning of the owner. Observation of the patient's gait is paramount, and just as important as the hands-on neurological and orthopaedic examination. Generally, orthopaedic conditions improve with exercise, and do not have proprioceptive or reflex deficits - the difficulty is in patients with both orthopaedic and neurological disease, and if nothing fits, remember to exclude neuromuscular disease.
1. Fossum TW. ed. In: Small Animal Surgery. 4th ed. St. Louis, MO: Elsevier; 2013.