Animals with neurological disease often present for problems walking, moving, and standing. This discussion will focus upon the clinical diagnosis of these abnormalities in dogs and cats.

Neuroanatomy of Gait

Gait is commonly defined as a regularly repeating series of leg movements during walking or running. The nervous system controls the actions of the muscles, bones, joints and associated connective tissue important for walking. Normal walking is produced by the recruitment of stepping reflexes which alternate between the extensor and flexor muscles. The vestibulospinal and reticulospinal tracts are facilitatory to the extensor muscles, important for maintenance of the body tone against gravity (the stance or propulsive phase). The corticospinal and the rubrospinal tracts are facilitatory to the flexor muscles, important for the protraction (flight) phase of limb movement.

Locomotion is thought to be controlled at the level of the brain stem; however, a discrete anatomic gait center (nucleus) has not been identified. Supratentorial (forebrain) structures are important for voluntary initiation of movement. The cerebellum, while not necessary for the initiation of movement, is important for coordination of movement. Cerebellar influences coordinate and smooth body movements by controlling rate, range, and force of limb motion. The cerebellum helps to "smooth" movements.

Clinical Evaluation of Abnormalities of Gait

Clinical evaluation of gait usually involves observation of the animal's movements during walking, and, when indicated, running. This is best accomplished by having a handler walk the animal over a flat, non-slippery area (such as concrete or carpet). An overall assessment is made of how the animal moves and clues are obtained to abnormalities present.

General Abnormalities of Gait

Ataxia literally means lack of an axis, and is sometime described as incoordination. Ataxia can result from a variety of anatomic lesions within the nervous system, most commonly of the cerebellum, vestibular system and spinal cord sensory pathways. Ataxia, without motor involvement (paresis), usually implies cerebellar or cerebellar pathway disease. Sensory ataxia due to loss of joint position sense is often made worse by blindfolding the animal, effectively preventing visual compensatory mechanisms.

Dysmetria is improper estimation of distance during muscular activity. Dysmetria includes both hypo- and hypermetria. With hypermetria, voluntary muscular movement overreaches the intended goal; with hypometria, voluntary movement falls short of the intended goal. Hypermetria is more commonly recognized than hypometria. Both of these abnormalities are most often associated with lesions of the cerebellum or cerebellar pathways. In the instance of hypermetria, for example, the loss of cerebellar input, which normally stops the flexion phase of gait, results in the exaggerated movement.

Spasticity is a state of increased muscle tone and commonly results from upper motor neuron (UMN) lesions. Spasticity is observed in the gait as a lack of normal flexion or floating (failure to adequately flex the limbs during gait).

Stiffness associated with decreased step length is commonly seen with diseases of the peripheral neuromuscular apparatus (LMN cell body, nerve roots, peripheral nerve, neuromuscular junction and muscle). Dogs with neuromuscular disease may also have a stiff, stilted, choppy gait due primarily to muscle weakness. These abnormalities may be episodic and occur, as in the case of myasthenia gravis, as the level of exercise increases. A similar appearance may occur in dogs with pain, primarily from musculoskeletal disease.

Paresis is derived from the Greek word for relaxation and suggests neurological weakness without complete paralysis (implies that some voluntary motion remains). Varying degrees of paresis can occur with some animals retaining the ability to walk while others are unable to support their own weight and stand. Paresis may be observed at gait as dragging of the toes or feet. Abnormal toenail wear may suggest underlying paresis.

Paresis at gait first occurs with lesions in the midbrain caudal to the level of the red nucleus. The severity of the gait impairment increases as the lesion occurs progressively more caudally in the central nervous system. For example, supratentorial lesions may result in significant hemiparesis when postural reactions are tested, however, gait remains relatively normal. With brain stem or spinal cord lesions, the associated paresis usually results in obvious gait impairment.

Lameness (decreased or non-weight bearing on a limb(s)) is usually associated with pain of the limb from musculoskeletal disease. A similar clinical abnormality can also occur with nervous system dysfunction (and presumably pain), referred to as nerve root signature. This abnormality often occurs in a single thoracic limb due to cervical spinal compressive disorders (intervertebral disk extrusion). The same phenomenon may affect a pelvic limb. Often, the affected limb may appear painful upon manipulation, mimicking an orthopedic problem.

Clinical Assessment

Important clues as to the cause of the gait abnormality can be obtained by assessing the step distance (i.e., the distance between where both thoracic or both pelvic limbs are placed in relation to each other). This determination is best made when viewing the animal from a lateral direction and when the animal is perpendicular to the examiner's line of sight.

Generally, animals with UMN neurological disease have normal or increased step lengths, where dogs with orthopedic or neuromuscular disease have shorten step lengths. Animals with UMN disease may appear irregular and uncoordinated, having a tendency to sway from side-to side; some may fall to the side. Their feet may contact the ground with increased force. Doberman pinchers with cervical vertebral malformation--malarticulation, for example, may over flex the hock joints during weight-bearing, presumably the result of motor or sensory weakness.

Dogs with LMN disease may hold the head low (possibly because of neck muscle weakness) and take short ("choppy") steps. Some have a kyphotic posture. They may tire easily and appear unwilling to perform. Animals with orthopedic disease may have a similar gait abnormality wherein the limb step length is short. Normal conscious proprioception in the presence of a shorten step distance should suggest underlying orthopedic disease or neuromuscular weakness. Poor limb perfusion, such as from a partial bilateral iliac arterial thrombus or from a right-to-left PDA may also result in a short, choppy pelvic limb gait. The clinical signs may worsen with exercise (similar to myasthenia gravis) and differential cyanosis may be seen with the latter disease. Dogs with vertebral pain may also be short-strided and reluctant to move.

Depending upon where within the nervous system the lesion occurs, gait may be altered differently. Supratentorial disease will often not affect gait. Wide circling toward the side of a unilateral forebrain lesion is common. Occasionally, spasticity may be noticed, with the limb (primarily a thoracic limb) appearing stiff, floating and over-reaching. Also, apparent hypermetria may be found, usually in the thoracic limb opposite a supratentorial lesion.

Lesions of the brain stem and cervical spinal cord will often have dramatic affects on gait, frequently impairing the ability to stand and generate a gait. If the lesion occurs unilaterally, ipsilateral hemiparesis is noted. If pathways are affected bilaterally, tetraparesis will be present. Spinal reflexes should reflect the UMN nature of the lesion.

Neurologic Abnormalities Resulting in Abnormal Gait

Intracranial Disease

Depending upon where within the nervous system the lesion occurs, gait may be altered differently. Supratentorial disease will often not affect gait. Wide circling toward the side of a unilateral forebrain lesion is common. Occasionally, spasticity may be noticed, with the limb (primarily a thoracic limb) appearing stiff, floating and over-reaching.

Lesions of the brain stem and cervical spinal cord will often have dramatic affects on gait, frequently impairing the ability to stand and generate a gait. If the lesion occurs unilaterally, ipsilateral hemiparesis is noted. If pathways are affected bilaterally, tetraparesis will be present. Spinal reflexes should reflect the UMN nature of the lesion.

Spinal Cord Abnormalities

Animals are commonly presented for problems involving the spine and spinal cord. Often, these clinical signs are reflected as problems with walking or moving (limb motion). If there is abnormal function of a limb, the first determination made is whether there is, in fact, a neurologic problem. If a neurologic problem is encountered, then a determination of the location of lesion or lesions is made. Once the location of the lesion is determined, an appropriate differential diagnosis and diagnostic plan can be formulated.

The spinal cord can be functionally divided based upon the spinal segments and associated clinical signs of disease affecting these segments. The following is a summary of the clinical signs associated with lesions of selected spinal segments.

The functional division of the spinal cord is primarily dependent on the presence of either upper motor neuron (UMN) or lower motor neuron (LMN) clinical signs to the limbs. The presence or absence of these characteristic signs is based upon the concept of local reflex (does not require conscious control) function and the normal control of these reflex functions from higher nervous system centers.

Lower Motor Neuron Disease

Technically, the lower motor neuron includes the motor neuron cell body, the motor (efferent) peripheral nerve, the neuromuscular junction, and the muscle. As LMN signs can also occur with sensory (afferent) lesions of the peripheral nervous system, disease of these nerves are sometimes categorized under LMN disease in Part II.