Abnormalities of Voluntary Movement--Part II
World Small Animal Veterinary Association World Congress Proceedings, 2007
Rodney S. Bagley, DVM, DACVIM (Neurology and Internal Medicine)
Professor, Washington State University, College of Veterinary Medicine
Pullman, WA, USA

Functional Areas and Associated Clinical Signs of the Spinal Cord

 C1-C5--UMN tetraparesis/plegia, neck pain

 C6-T2--UMN signs to pelvic limbs; LMN signs to thoracic limbs

 T3-L3--UMN signs to pelvic limbs; thoracic limbs normal

 L4-S3--LMN signs to pelvic limbs and/or bladder

 Caudal--Tail abnormalities

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

An UMN is a neuron or group of neurons which does not exit the central nervous system, and influences, either positively or negatively, the LMN. Clinical signs of UMN include proprioceptive abnormalities, hyper- or normoreflexia, hyper- or normotonia, and disuse atrophy (slow and minimal). Hyperreflexia is due to loss of descending UMN inhibitory influence over the gamma neurons to the intrafusal muscle spindles.

The LMN is analogous to the peripheral nervous system and the effector organs (primarily muscles) however, also includes the cell bodies of the peripheral nervous system in the gray matter of either the spinal cord or brain stem. The LMN is similar to factory workers, which are under the direction of their bosses (i.e., the UMN), but without which the factory could not function. Clinical signs of LMN disease include proprioceptive abnormalities, hypo- to areflexia, hypo- to atonia, and neurogenic atrophy (quick and severe atrophy).

Both UMN and LMN abnormalities can result in proprioceptive deficits. Therefore, evaluation of spinal reflexes becomes important in separating the two lesions.

Lesions of Selected Spinal Areas

Lesions of the C1-C5 segments result in tetraparesis. Tetraplegia is uncommon as respiratory function is severely compromised and death may occur prior to presentation. If the lesion occurs unilaterally within the spinal cord, a hemiparesis is found ipsilateral to the lesion. Cervical hyperesthesia is common with extradural compressive lesions and inflammatory diseases (meningitis). Horner's syndrome may be present due to involvement of the descending sympathetic fibers in the lateral tectotegmental spinal tract. Reflexes in the affected limbs, being normal to exaggerated, will reflect UMN disease.

Lesions of the C6-T2 segments (cervical intumescence) may also result in tetraparesis; however, reflexes in the pelvic limb will be UMN while those in the thoracic limbs will be LMN. If the lesion is unilateral, a hemiparesis is seen with similar reflex changes. Horner's syndrome may be present as the caudal cervical intumescence is where the preganglionic cell bodies lie and these nerves exit the spinal cord. If the lesion involves the C8-T1 segments or nerves, the cutaneous trunci reflex may be abnormal. If the lesion is unilateral, the ipsilateral cutaneous trunci muscle will not contract with stimulation on either side of the body. The non-affected side, however, should still contract with stimulation on either side of the dorsum confirming the integrity of the T3-L3 spinal segments.

Lesions of the T3-L3 spinal segments will result in paraparesis/plegia. Reflexes in the pelvic limbs will be UMN in character. The cutaneous trunci reflex may be absent caudal to the lesion, especially with more severe lesions. Also, with severe lesions, Schiff-Sherrington posture may be seen. Focal hyperesthesia in the area of the lesion is often seen with extradural compressive and inflammatory diseases. With unilateral lesions, an UMN monoparesis of the pelvic limb may be found.

Lesions of the L4-S3 spinal segments (lumbar intumescence) will result in paraparesis/plegia. Pelvic limb reflexes, however, will be LMN in character. Depending upon which area of the intumescence is involved, specific reflexes may be abnormal. With a lesion of the L4-L6 segments (femoral nerve), the patella reflex is reduced or absent. Quadriceps muscle atrophy may be present. Sensation on the medial toe of the pelvic limb may be reduced or absent due to involvement of the saphenous nerve (sensory) which is a branch of the femoral.

With lesions of the L6-S1-2 segments (sciatic nerve), the withdrawal reflex is reduced or absent. The patellar reflex may appear exaggerated due to the loss of antagonist muscles to this reflex as a result of the sciatic involvement (pseudo-hyperreflexia). Atrophy of the muscles innervated by the sciatic nerve may be present. Atrophy is often most obvious in the cranial tibial muscle.

Remember that in the lumbar area, the spinal cord segments are in front of the corresponding vertebral segments. In dogs, the sacral segments lie over L 5 vertebra (remember an S looks like a 5) (S2-3 lie over L6 in cats). L 1 and L 2 segments overlie L 1 and L 2 vertebrae, respectively. Segments L 3-7 lie between L 3 and L 5 vertebrae. The spinal cord ends usually in the cranial 1/2 of L7 in dogs. In larger breeds it may terminate more cranially and in smaller breeds more caudal. In cats the spinal cord ends at L7 or the sacrum.

With lesions of the S1-3 segments, bladder and colonic dysfunction is seen. The bladder will have characteristics reflecting the LMN lesion. With lesions of the caudal segments, tail dysfunction and reduced or absent tail sensation is seen.

Once the lesion has been localized to the spinal cord, an appropriate group of differential diagnoses can be generated. There are some diseases that can affect the entire length of the spinal cord, whereas others affect only specific areas.

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.

Clinical Signs

Lower motor neuron signs are seen in the affected limbs or head. In animals, LMN disease primarily results in weakness. The gait is usually short-stepped and "choppy" if a gait is able to be generated. The limbs may appear flaccid, may tremor and buckle with weight bearing. With some diseases, weakness is exacerbated with exercise (e.g., Myasthenia gravis). Muscle weakness may be seen in visceral structures such as the esophagus.

When evaluating conscious proprioception, it is important to evaluate the animal when fully weight-bearing and again when the animal's weight is supported by the examiner as some diseases affect only the motor portion of the nerve. Diseases of the NMJ are one such example. Animals with disease of the NMJ or muscle may have proprioceptive deficits during weight bearing, but not when their weight is supported. With many peripheral nerve and UMN lesion, both motor and sensory weakness occurs concurrently, and postural reaction deficits will be seen regardless of weight-bearing status.

Spinal reflexes will be reduced or absent. Tone in the limbs will be poor with very little resistance to passive movement of the limb by the examiner. In some instances of disease of the NMJ (e.g., Myasthenia gravis) spinal reflexes are normal.

Atrophy of muscles that occurs is neurogenic in origin. This atrophy occurs quickly after a LMN injury (within 7 to 10 days) and is severe (muscle waste away). Electromyographic (EMG) abnormalities can be detected in denervated muscle as soon as 5 days after injury (fibrillation and positive sharp waves).

Other signs of nervous system weakness such as megaesophagus, dysphagia, facial muscle weakness, dysphonia, and respiratory abnormalities may be seen. Remember that many of the cranial nerves are peripheral nerves and can be affected by polyneuropathies and NMJ disease.

Individual peripheral nerves may be selectively involved with various pathological processes. Lesions of the femoral nerve result in an inability to extend the stifle and support weight. The animal may have difficulty bringing the limbs forward and may "bunny-hop" or be short-stepped in the affected limb (s). "Bunny-hopping" is the simultaneous advance of the pelvic limbs, and has classically been associated with UMN spinal cord disease (spinal dysraphism/myelodysplasia). Occasionally, animals with orthopedic disease (bilateral hip dysplasia or coxofemoral pain) will have the same gait abnormality.

Lesions of the obturator nerve often do not affect gait in dogs and cats. If an animal is placed on a slippery surface, however, the affected pelvic limb(s) may slide laterally with weight bearing. Lesions of the sciatic nerve result in a characteristic gait wherein the distal foot is almost "thrown" forward by the movements of the more proximal muscles of the limb. When the animal is weight bearing, the hock joint may over flex resulting in the "dropped-hock" appearance. Atrophy of the muscles of the limb is common with LMN disease. Atrophy associated with sciatic disease is often obvious in the cranial tibial muscle group.

With lesions of the cranial gluteal nerve, the stifle may become abducted during the stance phase of gait. Lesions of the radial nerve affect the animal's ability to extend the carpus. If the lesion occurs proximally in the radial nerve, the elbow may be held more ventrally than normal. The limb may be carried off of the ground with the elbow flexed if the musculocutaneous nerve is intact.

With lesions of the medial, ulnar, musculocutaneous and suprascapular nerves, gait is usually unaffected. The carpal joint may be overextended with medial and ulnar lesions. With musculocutaneous nerve paralysis, elbow flexion is poor and this joint may be held overextended.

Tumor of the nerves of the brachial plexus may initially show signs of lameness in the affected limb. Suspicion should be heightened for these tumors in dogs with undiagnosed thoracic limb lameness.

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Rodney S. Bagley, DVM, DACVIM (Neurology and Internal Medicine)
Washington State University
Washington, USA


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