The cauda equina is less frequently the site of neurologic dysfunction than the cervical or
thoracolumbar spine in small animals; however, it is not uncommon to see the condition in large breeds of dogs. Disease of the low lumbar spine has a pronounced effect in that several nerves
controlling locomotion, fecal and urinary continence, and sensation to the hind quarters can be
involved simultaneously or individually. Therefore, the syndrome of cauda equina compression can
result in diverse symptoms and is often difficult to diagnose. In order to understand diagnosis and
treatment of the problem better, this discussion reviews the anatomic features, pathomechanics,
diagnostic aids, and treatment of this syndrome.
Anatomic Features:
The cauda equina is a leash of nerve roots of the low lumbar spine. These nerve roots
descend from their spinal cord segment origins to their site of emergence from the spinal canal.
Early in the development of the embryo, the spinal nerves leave the spinal cord at right angles to exit
at the respective foramina. As the embryo continues to develop, the spinal cord ceases to grow
before the vertebral column. It is because of this differential growth of the two structures that the
spinal cord of the dog extends only to the level of the fifth or sixth lumbar vertebra. Thus, the spinal
nerves of the mature dog have to course obliquely and caudally to exit at the respective foramina.
Nerves included in the cauda equina are L7, S1 to 3, and coccygeal nerves 1 to 5. The L6,
L7, and S1 nerve roots contribute fibers to the sciatic nerve. The pudendal nerve, which innervates
the perineum, is composed of the S1 and S2 nerve roots. The pelvic nerve, which carries
parasympathetic fibers to the bowel and bladder, is composed of fibers from S2 and S3. The tail is
innervated by the nerve roots originating from the coccygeal segments. The cauda equina is enclosed
within the spinal canal whose boundaries are (1) dorsally, the lamina of the vertebrae, ligamentum
flavum, and articular facets; (2) laterally, the pedicles of the vertebrae and ligamentum flavum; and
(3) ventrally, the body of the vertebrae, dorsal longitudinal ligament, and the annulus fibrosus. The
cross section of the spinal canal is triangular in shape, and the facets form lateral recesses in which
nerves lie just prior to their exit through the foramina.
The intervertebral foramina form short restricting canals for exit of spinal nerves and blood
vessels to and from the spinal canal. Articular facets, ligamentum flavum, pedicles, vertebral bodies,
and intervertebral disks make up the boundaries of the foramina. In the
sacrum, the nerves exit through the foramina in the bone. Deformities and injuries, whether
congenital or acquired, of any of these structures comprising the canal or foramina may result in
attenuation of the cauda equina and structures in the intervertebral foramina.
Causes of Compression:
Attenuation of the cauda equina may have several causes. Neoplasia, infection
(discospondylitis), acute disk extrusion, spondylosis, trauma, or congenital spinal stenosis are among
the lesions that may attenuate the cauda equina and may cause neurologic dysfunction. Infectious
processes such as discospondylitis may be of bacterial or, less frequently, of fungal origin. The
source of these infections may be systemic or may be spread from local wounds in the area, such as
from tail docking and bite wounds over and around the dorsum of the pelvis. The subsequent
inflammatory, destructive, and proliferative processes may cause instability as well as nerve root
compression.
Although neoplasia os not commonly the cause of cauda equina compression,
chondrosarcomas, osteosarcomas, and metastatic choroid plexus carcinoma of the lumbosacral spine
have been reported. Trauma from various causes can result in fracture dislocations of the
lumbosacral spine.
Other than the aforementioned etiologic factors, spinal stenosis can be either acquired or
congenital. Acquired forms of lumbar spinal stenosis can be caused by primary degenerative
spondylosis (multifocal), focal spondylosis secondary to or associated with degenerative disk
disease, spondylolytic spondylolisthesis, or pseudospondylolisthesis. These changes basically result
from instability of one or more segments of the lumbar spine. In an effort to afford stability, the
body responds to the proliferative changes in several structures (that is, thickened lamina, pedicles,
facets, and ligaments). In veterinary medicine, some of the causes of acquired stenosis have been documented.
Congenital stenosis can be subdivided into those episodes that occur in dogs with
achrondroplasia and those considered to be idiopathic. Whatever the cause, congenital stenosis is
characterized by a shortening of the pedicles, thickened and sclerotic apposition of the lamina and
articular processes, infolding and hypertrophy of the ligamentum flavum adjoining the lamina, and
sclerotic and bulbous articular facets that bulge into the dorsal half of the canal. The most common
sites of involvement in dogs are the L6-L7 and L7-S1 spinal cord segments. Idiopathic lumbar
spinal stenosis does not usually manifest itself until middle or late age. In these patients, the bony
changes are present at birth with further attenuation, as evidenced by a thickened ligamentum
flavum, occurring later in life and resulting in clinical signs.
Spinal stenosis not only causes mechanical compression of the dural tube and nerve roots,
but also produces intermittent ischemia of the nerve roots. Dilation of the vessels of the nerve roots
and spinal cord occurs subsequent to the increased demand imposed on neural function during
exercise. The nerve roots and associated vessels, being abnormally confined by the stenosed canal
or intervertebral foramen, are further attenuated when exercise is induced. The subsequent overall
increased diameter of the nerve roots, confined by the stenotic canal, reduces the effective blood
flow to roots and causes an ischemic phenomenon.
Ischemia produces root pain and subsequent reflex pain (paresthesias, dysesthesias) to the
part innervated by that nerve(s). Various states of paresis may also be associated with the ischemic
and pressure phenomena. In each instance, early in the course of the disease, the referred pain or
paresis is intermittent and is associated with exercise. The severity of pain or paresis progresses
with increased stenosis, which is associated with degenerative disease of the ligamentous and bony
structure of the stenotic canal. In the latter instance, the pain or paresis may be persistent.
Therefore, adequate historical information is mandatory to establish the initial intermittency of the
deficits. Signs referable to the extremities, tail, bowel or bladder function, and genitals have been
reported.
Diagnosis of Compression:
Animals presented to the veterinarian with stenosis of the cauda equina usually exhibit
intermittent lameness, fecal or urinary incontinence, or paresthesias and dysesthesias, such as
evidenced by tail biting, leg biting, genital licking, conscious proprioception deficits, and motor
weakness. These animals all have lumbosacral pain. The lameness is usually related to dysfunction
of the nerve roots comprising the sciatic nerve, whereas fecal and urinary incontinence are the result
of attenuation of the S2 and S3 nerve roots.
Paresthesias are unpleasant sensory disturbances that often manifest as referred pain
(lameness) or in various forms of self-mutilation of the tail, leg, or extremity. More often than not,
dogs are treated for various obscure dermatologic problems. Dysesthesias are even less pleasant
sensory disturbances enhanced by manipulation of the affected part by the clinician. Each condition
has been demonstrated in previous literature.
The cauda equina is unique because a large number of nerve roots are contained in a small
area (L6 through S3). A single lesion can involve several nerves and may result in one or all of the
aforementioned signs. Thus, the presenting symptoms are often bizarre and mimic other problems,
such as orthopedic disorders, anal sacculitis, and tail-head dermatitis.
In order to arrive at a correct diagnosis, a general examination of the entire animal and an orthopedic examination of the hind
limbs should be performed first.
Once the more common causes are ruled out, a critical neurologic examination is indicated,
including an evaluation of conscious proprioception, motor function, reflexes, sensory status, anal
tone, and state of continence (from the patient's medical history). Most important, the clinician must
manipulate the lumbosacral spine to establish the presence or absence of pain. This finding was the
most consistent on all reported cases.
Electromyographic studies have also been used to localize the lesions to specific nerves and
segments in animals with this syndrome. Whenever facilities are available, this tool can provide
useful information to support a diagnosis. In our experience, however, confirmation with such
studies is not the rule.
Having established historical and clinical neurologic signs referable to the cauda equina,
plain radiographs, taken when the patient is under general anesthesia, are indicated to evaluate
potential existing disease of the lumbosacral spine. Neoplasia, fractures, congenital lesions,
herniated disks, spondylosis, discospondylitis, and lumbosacral stenosis can often be confirmed by
radiographic means alone. In numerous cases of congenital stenosis, however, little if any bony
pathologic tissue may be demonstrated.
Myelographic studies in this area are of little value because
it is often difficult to obtain an adequate dye column this far caudally.
Intraosseous venography may
be of value in some patients; however, it does not permit adequate study of the dorsal aspect of the
canal. Consideration should be given to epidural dye studies.
CT scans and MRI scans offer the best
method to accurately examine the cauda equina and to determine the extend of involvement of the
various anatomic structures in the disease process. They do not allow dynamic studies which can
be done with other radiographic techniques, but dynamic studies are not often needed.
Surgical Treatment of Compression:
In patients demonstrating neurologic dysfunction of the cauda equina, several factors should
be considered in deciding the optimal mode of therapy:
1. Duration and severity of the dysfunction. An animal with mild proprioceptive deficits
of short duration (1 to 2 days) has a better prognosis than an animal with no sensation to the hind
quarters.
2. Etiologic factors. Neoplastic processes, such as osteogenic sarcoma, may offer a poor
prognosis. Congenital stenosis and some other disorders offer a good prognosis if a surgical
procedure is performed early in the course of the disease. Discospondylitis responds, in our
experience, most favorably to analgesics, muscle relaxants, and antibiotics. Patients that respond
poorly are candidates for surgical treatment, culture, and biopsy.
3. Economics and aftercare. Especially in the case of traumatic luxations or fractures of
the area, surgical decompression, stabilization, and aftercare are costly and time-consuming. If the
patient's owners are unwilling or unable to make financial commitments or fail to understand their
role in postoperative care, surgical treatment is not warranted.
It should be remembered that each case is to be evaluated on an individual basis; not all are
clear cut with regard to prognosis, and individual decisions must be made.
Surgical exposure of the cauda equina is best accomplished by laminectomy, facetectomy and foraminotomy.
The epiaxial musculature is subperiosteally elevated and is retracted laterally.
The dorsal spinous processes are removed with a ronguer.
The dorsal lamina is removed with a
ronguer or a high-speed bur. In cases of congenital stenosis, a thickened ligamentum flavurn may
be encountered.
The ligament can be resected using a No. 11 Bard-Parker scalpel blade. The extent
of the laminectomy should continue cranially and caudally until the dural contents are free of
compression. Laterally, the facets must be removed, effecting a foraminotomy and subsequently
decompressing the nerve roots. Biopsy specimens can be taken in cases of suspected neoplasia or
infection.
Curettage and culture of the interspace in cases of discospondylitis can be accomplished
by working lateral to the sheath of nerves.
Prior to closure, the spine is evaluated for stability.
Rarely is instability a feature in patients with stenosis of the spinal canal. If the spine is unstable,
the technique used in the repair of spinal fractures can be employed. The wound is copiously lavaged
with normothermic saline solution. A free graft of fat is taken from the subcutaneous tissue near the
incision and is placed over the laminectomy site to effectively decrease scar formation.
The
lumbosacral fascia is closed on the midline with 2-0 or 3-0 monofilarnent nylon suture material. The
remainder of the closure is routine.
Postoperative Care:
As with all surgical cases, proper postoperative care is essential to obtain satisfactory results.
Strict rest and confinement should be enforced especially in active dogs for 4 to 8 weeks. In dogs
that are unable to ambulate, straw bedding helps to prevent decubitus ulcers and urine burns, and
bladder expressions or intermittent catheterization and assisted fecal evacuation may be indicated
to prevent adverse sequella. |
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