Paralysis is the loss of voluntary motor function due to dysfunction of neural or muscular systems. The term “paralysis” does not include sensory dysfunction or response to a noxious stimulus. Paresis results from the same mechanisms as paralysis but the lesion(s) are less severe. It is commonly referred to as weakness and may be severe enough to result in nonambulation (animal cannot support weight and walk) or the patient may still be able to walk but with varying degrees of loss of strength. Terms used to define the location/degree of paresis or paralysis are monoparesis/plegia (one limb that is weak or paralyzed), para-paresis/plegia (both pelvic limbs are weak or paralyzed), tetraparesis/plegia (all four limbs are weak or paralyzed), hemiparesis/plegia (the two limbs of the same side are weak or paralyzed), and paresis/paralysis of specific cranial nerves (e.g., facial paresis/plegia and mandibular paralysis).

The final common pathway for all motor function is the lower motor neuron (LMN), which ultimately consists of an efferent nerve and the neuromuscular junction that connect the central nervous system to a muscle. All voluntary motor activity is expressed through LMNs, which begin in the ventral and intermediate columns of the gray matter of the spinal cord and/or in the cranial nerve nuclei located in the brain stem. Axons of the LMN neurons in the ventral horns or cranial nerve nuclei then form a peripheral nerve or cranial nerve, respectively. The LMN unit therefore includes (1) the nerve cell body in the ventral gray column/horn or cranial nerve nuclei, (2) the ventral root or cranial nerve axon, (3) the peripheral nerve or cranial nerve, (4) muscle fibers, and finally (5) the neuromuscular junction/motor endplate. If damage occurs to any of these five regions, then LMN signs may manifest (see below).

Dysfunction of the LMN prevents activation of the muscle (paresis/plegia), abolishes or diminishes reflexes (areflexia/hyporeflexia), decreases or eliminates the normal tone in the muscle (hypotonia/flaccidity), and within a short time frame (7–10 days), results in severe muscle atrophy.

The nervous system is arranged in a segmented fashion. Each spinal cord segment is demarcated by a pair of spinal nerves; one for the left and one for the right side. The brain is less orderly in its segmentation, but anatomic and functional regions can be identified. Paresis of a muscle or group of muscles, if due to LMN damage (UMN damage can result in weakness too, see below), can usually be traced to a specific peripheral nerve, spinal nerve, spinal cord segment(s), or a cranial nerve nuclei or nerve. Lesions of peripheral nerves cause severe LMN signs in the muscles which they innervate. Peripheral nerves most commonly originate from several spinal cord segments; therefore, spinal nerve or cord lesions may affect portions of a muscle or an entire muscle group. Brain stem lesions are more likely to affect an entire nucleus and therefore the signs seen are usually that of a complete lesion.

Voluntary movement of muscles also requires control from the brain. The LMN is under the control of motor pathways originating from the cerebral cortex and brain stem. Nuclei in the brain stem form tracts referred to as long tracts or upper motor neuron (UMN) tracts. The more important UMN tracts in the dog and cat, which serve to initiate voluntary motor function, include the vestibulospinal, rubrospinal, and reticulospinal tracts (de Lahunta and Glass, 2009). The UMN system therefore serves to initiate voluntary movement, maintain muscle tone to support the body against gravity, maintain proper body and trunk posture, and lastly, to control muscular activity associated with the visceral functions, such as respiratory, cardiovascular, and excretory (de Lahunta and Glass, 2009). The locomotor systems important for initiation and maintenance of gait are located in the brain stem. This is why dogs and cats are referred to as “brain stem walkers.” The cortical influence (e.g., the corticospinal tract) is much less important in the dog and cat than it is in primates for initiation of voluntary muscle activity and movement. The brain stem locomotor centers are in the midbrain and pons. The pathways, which extend through the brain stem and spinal cord, are responsible for the initiation and maintenance of normal movements. Pathways from the vestibular nuclei maintain tone in the extensor muscles to support the body against gravity. The UMN system thus includes the nuclei in the brain stem and the long axons that travel down the spinal cord, influencing the LMN along the way; hence, the name long tracts.

The diagnostic plan for paresis or paralysis requires localization of the lesion, the anatomic diagnosis, and then the cause (etiology) of the lesion.

Anatomic Diagnosis

The first step is to determine that the problem is truly neurologic in origin. Lameness (which may first appear as weakness) and weakness may be caused by a variety of musculoskeletal and/or systemic problems. The neurologic examination, especially postural reactions and spinal and cranial nerve reflexes, provides the necessary information. Abnormal postural test reactions or depressed reflexes are virtually always the result of neuromuscular disease.