Posted because some might find this informative.
Localization of Spinal Cord Lesions
Richard A. Lecouteur, BVSc, PhD, DACVIM (Neurology)
University of California, Davis
Davis, CA, USA
Motor, sensory, reflex, and sphincter abnormalities may be used to determine the location of a lesion within one of four major longitudinal divisions of the spinal cord: cervical (C1 to C5 spinal cord segments); cervical enlargement (C6 to T2); thoracolumbar (T3 to L3); and lumbar enlargement (L4 to Cd5).
A disorder of each of these four regions results in a combination of neurological signs that is specific for the region involved. Recognition of a characteristic group of clinical signs therefore allows accurate localization of a spinal cord lesion. The presence of neurological deficits indicative of involvement of more than one region of the spinal cord is highly suggestive of multifocal or disseminated spinal cord disease.
The functional differences between upper motor neurons (UMNs) and lower motor neurons (LMNs) may be used to localize lesions to regions of the spinal cord. Cell bodies of spinal cord LMNs are located in the spinal cord gray matter. Their axons leave the spinal cord via the ventral nerve roots to become part of a peripheral nerve, and to terminate on a muscle. The LMNs of the thoracic limb have cell bodies in C6 to T2 spinal cord segments that form the cervical enlargement, while LMNs of the pelvic limb arise from the L4 through S1 spinal cord segments of the lumbar enlargement. Anal and urethral sphincter LMNs originate from S1 through S3 spinal cord segments. Signs of LMN dysfunction, which in diseases affecting the spinal cord reflect damage to the spinal cord segment(s) from which LMNs originate, are depression or loss of voluntary motor activity (paresis or paralysis), depression or loss of muscle tone, and rapid, severe atrophy of an affected muscle due to denervation. Upper motor neurons arise from cell bodies located in the brain. Their axons form descending pathways of the spinal cord and termination interneurons that in turn synapse with LMNs. Lesions affecting UMNs result in UMN signs. These UMN signs result predominantly from an increase in the excitatory state of LMNs. Upper motor neuron signs include depression or loss of voluntary motor activity (paresis or paralysis), normal or exaggerated segmental spinal reflexes, appearance of abnormal spinal reflexes (e.g., crossed extensor reflex), increased muscle tone, and muscle atrophy due to disuse.
Unilateral signs resulting from spinal cord disease are unusual; however, signs frequently are asymmetric. In the majority of cases, a lesion resulting in asymmetric signs is located on the side of greater motor and sensory deficit.
Cervical (C1 to C5)
Fatal respiratory paralysis resulting from interruption of descending respiratory motor pathways or damage to motor neurons of the phrenic nerve (C5 to C7 spinal cord segments) occurs in a complete transverse myelopathy. Lesions that are less than complete may not affect respiration, and in such cases other signs may be detectable.
Ataxia and paresis of all four limbs usually are seen. Tetraplegia rarely is seen, as lesions of sufficient severity to cause tetraplegia also may produce respiratory paralysis. Hemiparesis occasionally may be present in association with a cervical lesion. Rarely, lesions of the cervical spinal cord may result in paraparesis with minimal neurological deficits in thoracic limbs. The reasons for this are poorly understood.
Spinal reflexes and muscle tone are intact in all limbs, and may be normal or exaggerated. Muscle atrophy generally is not present; however, disuse atrophy may develop in cases that have a chronic course. Anal reflexes are intact and anal tone usually is normal. Bladder dysfunction may occur due to detrusor muscle areflexia, with normal or increased urinary sphincter tone, and loss of voluntary control of micturition. Reflex dyssynergia also may be seen. Although voluntary control of defecation may be lost, reflex defecation occurs when feces are present in the rectum.
Horner's syndrome (ptosis, miosis, and enophthalmos) rarely may be present in an animal with a severe destructive cervical lesion. Conscious proprioception and other postural reactions usually are depressed or absent in all limbs. Complete loss of conscious proprioception may occur without detectable loss of pain perception.
Cervical hyperesthesia ("spasms," apparent pain on palpation, cervical rigidity, and abnormal neck posture) may be seen in some animals with cervical myelopathy. Occasionally an animal may hold a thoracic limb in a partially flexed position, a posture that may be consistent with C1 to C5 nerve root or spinal nerve entrapment ("root signature"), although this posture is seen more commonly with a disorder of the cervical enlargement.
Disorders that affect the cervical region of the spinal cord must be differentiated from brain lesions that result in tetraparesis. This may be accomplished by doing a complete neurological examination. However, occasionally this distinction may be difficult. In most circumstances a cervical lesion does not result in neurological deficits attributable to involvement of the medulla oblongata. However, there are several notable exceptions to this rule. Positional strabismus, resulting from loss of the vertebral joint proprioceptive input to the attitudinal reflexes, may be seen in association with a cranial cervical lesion (C1 to C3 spinal cord segments). A cranial cervical lesion also may cause facial hypesthesia as a result of involvement of the spinal nucleus and tract of the trigeminal nerve. Cranial cervical trauma often results in clinical signs referable to injury of the caudal brain stem (head tilt, pharyngeal paresis, facial paresis) or cerebellum.
The Schiff-Sherrington sign (syndrome or phenomenon) consists of hypertonicity of thoracic limb muscles and hyperextension of the neck, and is seen in association with spinal cord lesions caudal to the cervical enlargement. It is essential to differentiate this sign from thoracic limb hypertonicity caused by a cervical lesion.