Clinical signs such as abnormal gait and discomfort are often neurologic in origin but are not exclusive to disorders of the nervous system. It is important to establish whether or not the signs are neurologic in origin to determine the appropriate diagnostic approach. An abnormal gait is a relatively common and often challenging presenting problem in veterinarymedicine.

A complicated combination of body systems including musculoskeletal, neurologic, cardiovascular and metabolic/endocrine contribute to the development of gait. Of these body systems, the musculoskeletal and nervous systems are the most significant contributors to gait and are therefore the most common systems involved in an abnormal gait. These two systems are also the most likely to overlap and be present in the same case resulting in a combination of both orthopedic and neurologic factors such as the German shepherd with both hip dysplasia and degenerative radiculomyelopathy. In these cases the history will often help to establish the relative significance of these two systems to the presenting problem.

When evaluating gait, neurologic disorders are best observed at a slow walk so that forward limb momentum does not obscure the neurologic deficit. Evaluation should start on a level surface then progress to an uneven surface and/or slope such as a ramp or gentle hill, if appropriate for the patient. Stairs are also helpful in the evaluation of gait as long as it is safe for the patient to perform this task. Orthopedic disease is usually best observed at a faster walk or trot on a level surface and then gentle slope.

Evaluation of step or stride length can be especially useful since upper motor neuron diseases (i.e., descending spinal cord motor tract disorders) tend to have a normal to increased stride length while neuromuscular and orthopedic disorders tend to have a decreased stride length. Videotape of the patient in the clinic and/or at home can be an invaluable tool for evaluating gait, especially when assessing stride length.

Remember that not all "down" or recumbent patients have neurologic disease. It is important to distinguish the patient that is unwilling or reluctant to get up and walk from the patient that is unable to get up and walk.

Abnormal Gait: Neurologic

Since the majority of patients with neurologic disease as the cause of their abnormal gait have a neurologic deficit, the neurologic examinationplays a crucial role in their evaluation.

Ataxia: The presence of ataxia (i.e., incoordination, loss of the orientation of the body/axis) establishes the presence of a neurologic deficit. The sources of ataxia within the nervous system include spinal cord sensory pathways, vestibular system and the cerebellum.

Spinal cord sensory ataxia involves the ascending spinal cord pathways causing ataxia and usually postural reaction deficits. Since disorders affecting these ascending pathways often involve the descending motor tracts or the upper motor neuron (UMN), the spinal cord sensory ataxia is often associated with UMN signs including paresis, normal to increased spinal reflexes, normal to increased tone and disuse atrophy.

Vestibular ataxia is characterized by a dysequilibrium; imbalance or "drunk" gait. Additional signs of vestibular disease such as a head tilt and abnormal nystagmus are often present.

Cerebellar ataxia is typified by a spastic incoordination usually with hypermetria (exaggerated range of flexion) without paresis.Additional cerebellar signs that may be present includeintention tremor, truncal ataxia, ipsilateral menace deficit, and abnormal nystagmus.

Lower motor neuron: Lower motor neuron (LMN) disorders may present with a lameness and/or weakness so these signs can potentially overlap with an orthopedic disorder. The LMN disorder can usually be distinguished from an orthopedic disorder by identifying a LMN deficit. These LMN deficits include decreased to absent spinal reflexes, decreased tone, paresis to paralysis of affected limb(s) and possible neurogenic atrophy.

In the thoracic limb, a LMN musculocutaneous nerve deficit involves decreased to absent flexion of the elbow. Radial nerve LMN deficits include abnormal extensor function of the limb causing a dropped elbow posture if the lesion is proximal to the elbow, inability to extend the carpus and to flex and extend the digits. Deficits from LMN disorders affecting the median and ulnar nerves are minimal such as mild hyperextension of the carpus. In the pelvic limb, a LMN femoral nerve deficit causes inability to maintain the stifle in extension during weight bearing. A LMN deficit of the sciatic nerve can allow for over flexion of the hip joint and cause underflexion of the tarsus, plantigrade posture and inability to adequately flex and extend the digits.

Abnormal Gait: Orthopedic

Stiffness as demonstrated by decreased stride length is usually, but not exclusively, an indicator of non-neurologic disease.

Muscle weakness is a complex clinical sign that can have considerable overlap between non-neurologic and neurologic disorders. Primary disorders of muscle such as myositis can cause weakness and are sometimes associated with discomfort. Endocrine myopathies that can potentially cause weakness include hypothyroidism, hyperadrenocorticism and hypoadrenocorticism. Metabolic causes of weakness include hypoglycemia, hyperkalemia and hypokalemia.

Lameness is usually, but not exclusively,orthopedic in origin. Nonweight bearing lameness usually reflects musculoskeletal disease such as osteosarcoma, fracture, degenerative joint disease and cruciate ligament disease. In addition, decreased range of motion is usually a sign of musculoskeletal disease.

The examiner should be particularly careful when evaluating a thoracic limb lameness that involves knuckling onto the dorsum of the paw. This posture is usually a LMN deficit of the radial nerve, in which case the digits cannot be adequately extended. The limb may, however, be postured this way with painful orthopedic disorders of the shoulder and humerus such as osteosarcoma of the humerus or scapula, in which case the digits can be extended when the patient is forced to bear weight on the limb.

Neurologic Disorders Commonly Associated with Lameness

Nerve root (sheath) neoplasia can be a particularly difficult diagnostic dilemma when evaluating lameness. The thoracic limb is more commonly involved than the pelvic limb. Affected dogs usually present with a monolimb lameness. This can be the only presenting sign for several months. A LMN deficit may not be present initially since only a single nerve root may be affected. As the disease progresses, LMN deficits including abnormal spinal reflex(es) and muscle atrophy will usually develop. Additional features may include palpable mass in the axilla, ipsilateral Horner's syndrome and cutaneous trunci reflex deficit. As the neoplasia progresses, invasion into the vertebral canal may cause ipsilateral ascending/descending spinal cord deficits such as pelvic limb postural reaction deficits, ataxia and paresis. Diagnosis of a nerve sheath tumour is made by biopsy of an axillary mass if palpable, electromyography (EMG), myelogram, or preferably by MRI.

Nerve root signature usually involves a thoracic limb. The patient presents with discomfort and holding up of a thoracic limb and/or lameness. Root signature is usually caused by entrapment of the spinal nerve(s) near the intervertebral foramen often secondary to lateralized cervical intervertebral disc extrusion. Thoracic limb root signature associated with intervertebral disc extrusion is usually associated with cervical discomfort.

Lumbosacral disease can be a challenging diagnosis. These cases can present with pelvic limb lameness but will usually have associated discomfort on palpation of the lumbosacral junction that will help to rule out orthopedic disease. Other less consistent signs of lumbosacral disease include LMN pelvic limb deficit(s), paresis of the tail, and urinary and/or fecal incontinence. Although electromyography, myelography and CT scan can be used in the diagnosis of lumbosacral disease, MRI provides the most accurate information.

Neuromuscular junction: Disorders affecting the neuromuscular junction such as myasthenia gravis can cause muscle weakness resulting in a stiff, stilted stride that can overlap with the signs of orthopedic disease.

Non-Neurologic Disorders that Present to Neurologists

Bilateral cranial cruciate disease: The patient with an acute bilateral cranial cruciate rupture can present as a "down" dog. Typically, however, these patients have a short, stilted pelvic limb stride and sit down very carefully ("as if sitting on a hot surface"). They tend to stand up using their thoracic limbs more than their pelvic limbs. They do not have any neurologic deficits (i.e., noataxia or postural reaction deficits). If the cruciate rupture is complete, then a positive anterior drawer sign and/or positive tibial compression test will be present. The partial cruciate tear can be very difficult to diagnose because joint laxity is often not present so look for subtle radiographic changes of DJD and on joint fluid analysis, possible mild inflammation.

Polyarthritis: The patient with polyarthritis may be unwilling to get up but is able to do so if encouraged. They have a normal neurologic examination. These patients tend to walk with a short, stilted stride ("as if walking on eggshells or a hot surface"). Usually all limbs are affected but occasionally just one limb/one joint is abnormal. They may have an arched back and/or low head carriage suggestive of cervical intervertebral disc disease or meningitis but remember that there are joints along the vertebral column that may be affected. While patients with polyarthritis often have joint effusion, discomfort and warmth on palpation of limb joints, and/or pyrexia, these signs can be inconsistent, making the clinical suspicion of polyarthritis elusive. Diagnosis of polyarthritis is made by joint fluid analysis.

Fibrotic myopathy: This is an uncommon disorder that results from fibrosis of the semimembranosis and semitendinosis muscles, and occasionally gracilus muscle. Fibrotic myopathy usually affects primarily the german shepherd breed with male dogs more common than females. A fibrotic band on the medial aspect of the thigh produces the classic gait that includes abrupt inward jerk motion of the pelvic limb paw with outward rotation of the tarsus at the end of a suspended anterior phase of the step. Typically one pelvic limb is affected but occasionally it is a bilateral disorder. The etiology is unknown but trauma to the muscle(s) is suspected. Surgical removal of the band resolves the problem for several months but with the surgical options currently available the signs always return. Fortunately, the affected dogs do not experience discomfort and can usually continue a normal life although their athletic ability may be limited by the gait.

Ruptured gastrocnemius tendon or inflammation of the gastrocnemius tendon: These patients present for evaluation of a unilateral or bilateral, mild to marked plantigrade ("dropped") tarsal posture. They may have a palpable irregularity or "pea-like" thickening near or at the insertion of the gastrocnemius tendon. Complete rupture of the tendon appears to be more common in the cat and inflammation at the insertion of the tendon appears to be more common in the dog. It is important to differentiate a gastrocnemius tendon disorder from a tibial neuropathy such as diabetic neuropathy in cat. In cases of gastrocnemius tendon disease, the digits may be drawn backwards into partial flexion as the affected limb bears weight ("claw effect") due to the pulley-like effect of the intact superficial digital flexor. This posture of the digits can help to distinguish gastrocnemius tendon disease from a tibial neuropathy.

Pseudomyotonia: Pseudomyotonia is an uncommon disorder of muscle that is usually associated with hyperadrenocorticism (Cushing's disease). It can affect one or multiple limbs but usually involves the pelvic limb more than the thoracic. The patient exhibits increased extensor tone of a limb(s) that can be intermittent in nature. Myotonic dimpling may occur with stimulation of the affected muscle group. Myotonic discharges are evident on electromyography (EMG). On muscle biopsy there is myofiber atrophy especially of type 2 fibers. The etiology is unclear but is presumed to be secondary to prolonged steroid exposure. The pseudomyotonia may improve with treatment of hyperadrenocorticism.

In Summary

Remember to ask yourself the fundamental question: Is there a neurologicdeficit?If a neurologic deficit is present, then neurologic disease is the sole cause or is a component of the abnormal gait. If no neurologic deficit is present, then consider either a neurologic disorder that can have a normal neurologic examination or a non-neurologic disorder to explain the abnormal gait.

References

References are available upon request.