Spinal Cord Diseases of the Horse: Relevant Examination Techniques and Illustrative Video Segments

1. Introduction

The white matter of the spinal cord relays information in both directions between the body and the brain. Upper motor neurons influence posture and gait by modulating lower motor neuron activity. General proprioceptive (mostly cuneocerebellar and spinocerebellar) and pain (spinothalamic) pathways convey sensory information from the torso and limbs to the brain. Limb reflexes (flexor, patella) and long spinal reflexes (slap, cervicofacial, back, cutaneous trunci) are the final determinant of gait and posture. Careful evaluation of these reflexes along with assessments of gait and limb strength allow accurate localization of spinal cord lesions. Localization of spinal cord lesions is an important step in the processes of diagnosis and treatment.

2. Functions

Upper Motor Neuron–Muscle Tone and Voluntary Movement

Axons of the upper motor neuron (UMN) extrapyramidal and vestibular systems travel from cell bodies throughout the brain and pass predominantly in reticulospinal and vestibulospinal tracts to lower motor neurons (LMN) in the ventral and intermediate columns of the gray matter of the spinal cord. This system provides tonic support of the body against gravity and recruits spinal reflexes for the initiation of voluntary movement. UMN act by influencing α and γ motor neurons in the spinal cord. These LMN, in combination with afferent nerves and stretch receptors in the neuromuscular spindles and tendons, control muscle tone and movement by myotatic and anti-myotatic reflexes. Most descending UMN tracts are inhibitory to extensor motor neurons. Basic locomotor activity involves recruitment and control of these reflexes by distinct postural and voluntary UMN systems. Interruption of UMN tracts in the spinal cord causes signs of ipsilateral weakness of the trunk and limbs. Signs of paresis range in severity from slight toe-dragging and delayed protraction to recumbency and inability to rise. Because myotatic reflexes are released from inhibitory UMN influences, there may also be spasticity (stiffness) of limb movement. This is most obvious in the thoracic limbs, which may appear to “float” during walking. Interference with UMN also may manifest as delayed initiation of voluntary movement or alterations in gait cadence. For example, some horses with spinal cord disease may have a lateral “pacing” gait at walking speed. If LMN are not affected, spinal reflexes are either normal or exaggerated on the side of the spinal cord lesion, and crossed extensor reflexes may be seen. In keeping with the basic principles of neuro-anatomic localization, UMN lesions from C1-T2 (inclusive) may cause neurologic signs in all 4 limbs, lesions from T3-S2 can only affect the pelvic limbs, and lesions caudal to S2 do not directly affect gait. With external compression of the cervical spinal cord as in horses with cervical vertebral stenotic myelopathy (i.e., wobblers), signs typically are worse in the pelvic limbs than in the thoracic limbs.^1-3

LMN and Spinal Cord Reflexes

The effector function of the central nervous system (CNS) is exerted entirely through the actions of LMN on skeletal and smooth muscle. LMN to skeletal muscles are found in the ventral columns of the gray matter, whereas those of the autonomic nervous system are located in the intermediate columns. LMN form a ventral root, which then exits the vertebral canal through the intervertebral foramen, usually of the vertebra of the same name. The ventral root joins with the dorsal sensory root to form the segmental spinal nerve. In the cervical vertebrae, this foramen is at the cranial end of each vertebra. For the remaining roots, the foramina are at the caudal end. The more caudal spinal cord segments have long nerve roots because the spinal cord segments are shifted cranially with respect to the vertebrae. The neurons of the afferent (sensory) component of reflexes course from receptors in the skin, muscle, or tendon, through the spinal nerve and dorsal root, into the dorsal horn of the gray matter, where they terminate on interneurons. The interneurons then complete the pathway by passing to the LMN. An exception to this is the patella reflex, wherein the sensory neuron terminates directly on the LMN in the ventral horn. Long (i.e., multi-segment) spinal cord reflexes, including “slap” tests, cervicofacial and cutaneous trunci reflexes, and caudal reflexes, including anal and tail-clamp, are routinely evaluated during neurologic examination. Limb reflexes, including withdrawal, patella, and triceps, are always evaluated in neonatal foals and in older horses that are recumbent. Abnormalities of LMN (in gray matter, ventral root, plexus, peripheral nerve, or neuromuscular junction) manifest as flaccid muscle weakness (paresis, paralysis) with hypotonia and hyporeflexia. Within 2 to 4 weeks, muscle atrophy is noticeable, and this neurogenic muscle atrophy progresses rapidly. Ventral nerve roots contribute to multiple peripheral nerves and peripheral nerves are derived from multiple roots, so injury to gray matter of an individual segment or to a ventral nerve root produces less severe neurologic signs than does loss of function in a peripheral nerve.

Proprioception

Through a system of receptors in muscles, tendons, and joints, the general proprioceptive system is able to monitor the position of the body or limbs in space. Proprioceptive information is passed centrally in sensory nerves that terminate in the dorsal gray column on cell bodies of neurons in the spinocerebellar (pelvic limbs) or cuneocerebellar (thoracic limbs) tracts. These tracts pass cranially and provide information for the cerebellum to use in its role of regulating posture, muscle tone, locomotion, and equilibrium. Other proprioceptive pathways that serve in conscious proprioception pass from the spinal cord to the somesthetic sensory cortex via relay nuclei in the midbrain and thalamus. Interruption of spinal cord proprioceptive pathways interferes with recognition by the brain of the positions in space of the body and limbs. This is manifest as ataxia. Signs of proprioceptive deficit in the horse include base-wide or base-narrow limb placement, swaying of the trunk and torso during walking (but not usually at rest), and overstriding, especially in the pelvic limbs. During circling, limb ataxia is evident as circumduction in the pelvic limbs and interference in the thoracic limbs.

Urination

Parasympathetic LMN to the bladder’s smooth muscle (detrusor) originate in the intermediate column of the gray matter of S2–4. These neurons exit in ventral roots and contribute to the pelvic plexus, a network that supplies autonomic innervation to the smooth muscle of the bladder and rectum. Sympathetic LMN to the bladder begin in the gray matter of L1–4, exit the vertebral canal, and course caudally to the pelvic plexus. Post-ganglionic sympathetic neurons terminate on smooth muscle in the body and neck of the bladder and proximal urethra. These autonomic LMN function in local reflexes. Afferent neurons pass from stretch receptors in the bladder wall and enter the spinal cord in dorsal sacral nerve roots to exert inhibitory influences on parasympathetic and sympathetic LMN. Striated muscle of the urethra is innervated by somatic LMN in the pudendal nerve. Urination occurs when there is stimulation of parasympathetic nerves to the detrusor muscle, inhibition of sympathetic nerves to the detrusor muscle, and inhibition of sympathetic and somatic nerves to the urethra. The net effect of this activity is contraction of the smooth muscle of the body of the bladder and relaxation of the proximal urethra. Centers in the midbrain and hindbrain receive sensory information from the bladder and modulate reflex activity via UMN passing caudally in the spinal cord. Forebrain influence on these centers is responsible for initiation of voluntary voiding. In horses with severe spinal cord disease cranial to S2, there may be loss of voluntary control of urination. [...]