Lumbosacral Stenosis and Injury of the Cauda Equina

Common Neurologic Problems

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Lumbosacral Stenosis and Injury of the Cauda Equina

Richard J. Indrieri, DVM*

"Cauda equina" is the term applied to the collection of dorsal and ventral spinal roots of the more caudal spinal nerves that lie within the spinal canal caudal to and beyond the tapered terminal end of the spinal cord (conus medullaris).12. 14 It includes the roots of spinal nerves lumbar (L) 7, sacral (S) 1-3, and coccygeal (Cy) 1-5, but does not include the spinal nerves themselves . The cauda equina is vulnerable to compression, entrapment, displacement, and traumatic injury within the spinal canal at vertebral level L6 and caudally. Spinal nerves L7, SI-3, and Cyl-5 are vulnerable to injury from similar causes as they emerge from the spinal canal through their respective vertebral or intervertebral foramina . In order to understand how lesions of the cauda equina can produce the clinical signs often observed, it is important to consider the anatomy of the area.

ANATOMIC CONSiDERATIONS

The tapered terminal end of the spinal cord is called the "conus medullaris." It consists of sacral and coccygeal spinal cord segments (SI-3 and Cyl-5).17 The conus medullaris continues caudally as a non-neural band of pia mater (filum terminale), which unites with the arachnoid and dura mater to form the coccygeal ligament at vertebral level S1. The coccygeal ligament passes through the caudal spinal canal and fuses with the periosteum and dorsal longitudinal ligament at vertebral level C71 CyS.14. 17 It serves to anchor the spinal cord and conus medullaris caudally. During early embryonic development, the spinal cord and the vertebral column are of equal length. As the fetus grows, nonuniform differential growth of certain areas of the spinal cord results in the spinal cord being shorter in length than the vertebral column at birth. ll For this reason, in *Diplomate, American College of Veterinary Internal Medicine (Neurology); Staff Neurologist, Neurology and Neurosurgical Referral Service of Long Island, J\mityville, New York Veterinary Clinics of North America: Small Animal Practice-Vol. 18, No.3, May 1988

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dogs the conus medullaris ends between the mid to caudal half of the sixth lumbar vertebra and the cranial half of L7 (Fig. 1) . 8,17 In small breeds of dogs, it may end one half a vertebral body length more caudal. 8 In cats, the conus medullaris ends at the level of the middle of the seventh lumbar vertebra, 15 As a result of the "ascensus" of the spinal cord during fetal development, spinal roots of more caudal spinal cord segments traverse the spinal canal in increasingly greater distances before leaving the canal as spinal nerves, These roots form the cauda equina.

FUNCTIONAL CONSIDERATIONS The sciatic nerve of the pelvic limb is formed primarily by lumbar spinal roots L6 and L7. A smaller contribution is made by SI and occasionally S2 spinal roots. 17 The sciatic nerve is a mixed nerve containing motor (efferent) and sensory (afferent) nerve fibers, The nerve mediates extensor movements of the hip, hock, and digits and flexion of the stifle, It also provides cutaneous sensation to all of the pelvic limb (except medially), and it carries sensory impulses from muscles, joints, and tendons to the spinal cord. Lesions involving L7 and SI spinal roots will produce motor and sensory disturbances in the limb. Signs of root dysfunction include decreased position sense (conscious proprioception), flexor hyporeflexia, paresis, ataxia, hypotonia, atrophy in muscles innervated by the sciatic nerve (gluteal, biceps femoris, semitendinosus, semimembranosus, cranial tibial, and gastrocnemius muscles), and areas of paresthesia or anesthesia, 8, 13, 14, 17

The pudendal nerve is formed by contributions from all three sacral roots , 17 The ventral roots contain voluntary motor axons that innervate the external anal sphincter (caudal rectal nerve, branch of pudendal) and skeletal muscles of the penis, vulva, and urethra. Ventral sacral root lesions cause loss of voluntary control of anal and urethral sphincters and weakness of penile and vulvar musculature, 8, 13, 14, 17 The ventral roots also contain autonomic preganglionic parasympathetic fibers, These fibers combine to form the pelvic nerve located on the distal wall of the rectum , 17 Autonomic fibers of the pelvic nerve innervate involuntary smooth muscle of the rectum , bladder, descending colon, and accessory reproductive organs, They are important in reflex control of urination, defecation, erection, and ejaculation. 2, 17, 22 Dorsal sacral roots contain sensory nerve fibers from the pudendal nerve and visceral (parasympathetic) affer~nt fibers from the pelvic nerve, The sensory distribution of the pudendal nerve includes the perineum (perineal nerve), the scrotum, the vulva, and the inguinal area, 17 Sensory disturbances in these areas, as well as loss of the sensory arm of the anal reflex, result from lesions involving the dorsal sacral roots, Visceral afferent fibers ascend from pelvic organs by way of the pelvic nerve and dorsal roots to the conus medullaris, They playa major role in reflex control of bladder, colorectal and genital functions, and are involved in conscious sensation of distention and fullness of the bladder and colon. 17, 22 To recapitulate, lesions involving the sacral roots may produce volun-

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Ventral root 3L-

L3

L4

Lumbosacralenlargement

L5

Segment

L6

Dorsal root ICoFilum terminale-

L7

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Figure 1. Dorsal aspect of distal end of spinal cord. The dura mater has been cut middorsally and reflected. The dorsal roots have been cut on the left side to expose the ventral roots. The conus medullaris (L7, 51-3, Cy1-5 spinal cord segments), filum terminale, and cauda equina are shown in relationship to the vertebral column . (From Fletcher TF: The spinal cord and meninges. In Miller's Anatomy of the Dog. Edition 2. Philadelphia, WB • Saunders Co., 1979; with permission.)

tary and reflex abnormalities of the bladder, the urethra, and the anus, resulting in urinary and fecal incontinence, as well as failure to obtain erection or to ejaculate. Sensory disturbances in the perineal, vulvar, scrotal, preputial, and inguinal areas are observed. The dorsal and ventral coccygeal roots (Cyl-5) form the dorsal and ventral coccygeal nerve trunks. They provide motor and sensory innervation to the tail. Lesions of Cy 1-5 spinal roots cause partial or complete paralysis localized exclusively to the tail. 2. 13

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It is important to emphasize that peripheral nerve lesions involving the sciatic, pudendal, caudal rectal , perineal, or pelvic nerves, and lesions that involve spinal cord segments L7, SI-3, and Cyl-5 can produce abnormal function and clinical signs identical to those produced by lesions of spinal roots of the cauda equina. Therefore, distinguishing cauda equina lesions from those of the spinal cord or the peripheral nerves may offer the clinician considerable diagnostic challenge.

LUMBOSACRAL STENOSIS A common cause of compression of the cauda equina is dorsoventral narrowing of the lumbosacral (LIS) spinal canal. Narrowing is referred to as spinal stenosis. In general, stenosis is defined as inadequate space to accommodate neural structures. 6 Stenosis has also been used to describe narrowing of intervertebral foramina. 25 Within the past decade, a number of reports have appeared in veterinary journals describing a syndrome of nerve root (cauda equina) compression in small- and large-breed dogs. 2.9.21. 25 In all cases, compression of the cauda equina has been attributed to stenosis of the LIS spinal canal or intervertebral foramina, or both. Although the exact pathogenesis of stenosis in these cases is unknown, two explanations are currently accepted. In small and medium-sized dogs, stenosis is considered similar to congenital LIS stenosis in man. 6 • 25 In congenital stenosis, narrowing results from failure in development of a neural arch of adequate dimension. In these dogs, stenosis is observed at the LIS junction and at L6-7 and L7/S1 intervertebral foramina. It is characterized by short, thick pedicles; thickened, sclerotic laminae and articular processes; hypertrophy and infolding of the ligamentum flavum; and sclerotic, bulbous articular facets that bulge into the dorsal half of the spinal canal. The condition has been called idiopathic LIS stenosis .25 The problem in large-breed dogs is similar to acquired LIS stenosis in man. In man, acquired LIS stenosis results from bony or soft tissue changes associated with chronic, degenerative processes that gradually reduce the size of the spinal canal or intervertebral foramina. 6 In dogs, stenosis is attributed to chronic, degenerative changes associated with type II disc protrusion, hypertrophy and ventral displacement of the ligamentum flavum, connective tissue proliferation around roots of the cauda equina, spondylosis of intervertebral foramina, and ventral sacral displacement or subluxation (Fig. 2).2, 9, 21 This condition in dogs is referred to as LIS malarticulation and malformation, LIS instability, and LIS spondylolisthesis,9, 21, 28 Lumbosacral spondylolisthesis is technically incorrect and should not be used in referring to acquired LIS stenosis, 21, 28 Idiopathic LIS stenosis has been observed in small dogs, such as the Poodle, Beagle, and Lhasa Apso, and in mixed-breed dogs , In these animals, signs have appeared between 3 and 8 years of age. An approximately equal number of male and female dogs have been affected , In the only report of idiopathic LIS stenosis in dogs, 15 cases were grouped according to presenting clinical signs . These groups included dogs with lameness, dogs

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Figure 2. Midline saggital cut through the US vertebral column of necropsy specimen from a dog with signs of cauda equina dysfunction. Stenosis at L7-S1 is the result of chronic degenerative changes. A, Type II disc degeneration and protrusion (arrow) into the spinal canal. B, Hypertrophy and ventral displacement of the ligamentum flavum. C, Spondylosis deformans and connective tissue proliferation ventral to L7-Sl. Note the end of the conus medullaris (D , arrow), at the level of the L6 vertebral body.

with paresthesia, dogs with lameness and paresthesia, and dogs with sphincter dysfunction. 25 Acquired US stenosis occurs in large-breed dogs between 2 and 13 years of age. The average age of onset is 6 to 7 years, and more male than female dogs are affected. 21 The most commonly affected breed is the German Shepherd dog. However, the problem has also been seen in the Great Dane, Airedale Terrier, Irish Setter, English Springer Spaniel, Labrador and Golden Retrievers, the Boxer, and others. 2. 9. 21 Paresthesia and self-mutilation observed in some dogs with idiopathic US stenosis are not observed and have not been reported as a finding in dogs with acquired US stenosis. Regardless of the cause of stenosis, clinical signs are usually insidious in onset and gradually progressive. They may be unilateral or bilateral in manifestation. Before overt signs of neurologic dysfunction occur, nonspecific pelvic limb abnormalities are often observed. Difficulty in rising from sitting or recumbent positions, exercise intolerance, lameness during or follOWing exercise, stilted pelvic limb gait, reluctance to go up or down stairs, difficulty climbing or jumping into vehicles, and soreness on manipulation (especially extension) of the hips are often observed. These signs frequently lead to a presumptive preliminary diagnosis of arthritis or hip dysplasia. 2. 21 These nonspecific pelvic limb signs can be attributed to several factors that compromise the L7 and SI spinal roots or spinal nerves. Pain and

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discomfort originating in the spinal roots can be caused by mechanical pressure at points of stenosis. Nerve roots and spinal nerves become inflamed and swollen due to reduced mobility and failure to yield to tension exerted at points of compression during exercise. 21 • 25 Finally, swelling of spinal roots and spinal nerves at points of compression reduces blood flow along radicular arteries at a time when there is increased demand (during exercise), resulting in ischemia. This phenomenon is referred to as neurogenic intermittent claudication. 6. 25. 27 As stenosis increases, clinical signs of neurologic dysfunction occur. Signs commonly seen include scuffing the toes of the pelvic limbs, ataxia, paresis, atrophy in muscles innervated by the sciatic nerve, weakness or paralysis of the tail, urinary incontinence, and fecal incontinence. These signs may occur individually or in any combination. Neurologic examination at this time may elicit a variety of responses . No two patients are exactly the same. The patellar reflex is usually normal because the L4 and L5 nerve roots and the femoral nerve are not involved. Occasionally, the patellar reflex is exaggerated. This can happen as a result of paresis and loss of reciprocal antagonism from muscles innervated by the sciatic nerve (that is, quadriceps override). The flexor reflex may be normal, slow, or absent. The quality of the reflex depends upon the degree of L7 and Sl root involvement. Flexor areflexia indicates that the L6 spinal roots, or spinal nerves, or both are also involved. If ataxia is present, there is usually a reduction in conscious proprioception on examination. The anal reflex may be present or absent. Anal tone may be decreased even though the anal reflex is present. Therefore, it is important to do a rectal examination, as well as test the anal reflex, in suspected cases. The tail may be weak or paralyzed. Soiling of the perineum with urine and/or feces may indicate the presence of weakness when the tail is not flaccid . The most consistent finding in dogs with US stenosis is the presence of a painful response when pressure is applied over the US junction. It is observed in dogs with idiopathic and acquired forms of stenosis. When pressure is applied in these animals, they often wheel around in pain and may even attempt to bite (Fig. 3). Diagnosis A tentative diagnosis of US stenosis and cauda equina compression is based upon the history, clinical signs, and examination findings. Radiographs of the US spine are needed to further assess the animal with suspected stenosis. Radiographs are obtained with dogs under general anesthesia. Lateral views with the hips extended and fle~ed and ventrodorsal views are obtained. Flexed hip lateral views are most apt to demonstrate the presence of ventral sacral displacement or subluxation. In small dogs with idiopathic US stenosis, radiographs show no evidence of degenerative disc disease, spondylosis, instability, tumor, or infection. An area of stenosis of the canal is usually seen at L6, L7, or Sl in every case. 25 In large dogs with acquired US stenosis,_ radiographs may also be normal. More often, however, chronic, degenerative changes are seen. These changes include spondylosis, which frequently extends from the

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Figure 3. In dogs with idiopathic or acquired US stenosis, a painful response is the most consistent finding when pressure is exerted over the US junction.

ventral to the lateral aspects of L7 and S1, narrowing of the L7-S1 disc space, sclerosis of the end plates at L7-S1, a change in the shape of L7, and ventral sacral displacement (Fig. 4). Spondylosis at L7-S1, sclerotic end plates, and ventral sacral displacement are often incidental radiographic findings in normal dogs. 18. 28 Therefore, these radiographic changes must be interpreted cautiously in dogs without clinical signs of stenosis. If the diagnosis is still in doubt after radiographs are obtained, contrast radiographic procedures such as epidurography23 and intraosseous venographyl6, 23 (Fig, 5) can be helpful in demonstrating the presence of US stenosis, These procedures are not particularly difficult; however, incom-

Figure 4. Lateral radiograph of a 6-year-old male German Shepherd with signs of cauda equina dysfunction. Collapse of the disc space at L7-S1, sclerotic end plates, change in the shape of L7, spondylosis deformans, and ventral sacral displacement (arrow) are seen. Radiographic changes like these may also be incidental findings in normal dogs.

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Figure 5. Intraosseous venogram showing elevation of the venous sinus and stenosis of the US spinal canal due to type II intervertebral disc protrusion (arrow).

plete filling of the epidural space or vertebral sinuses can make radiographic interpretation difficult. Myelography is usually of little benefit because the conus medullaris ends cranial to the LIS junction. Ancillary diagnostic tests such as electromyography (EMG),3. 17. 19 evoked potentials,' cystometry (CMG),19. 20 and electromyelography (EMyG)4 may also be of some diagnostic help. These electrophysiologic tests can assist in localizing the abnormalities to specific spinal roots, and can be especially helpful when radiographs are normaL When the diagnosis is reasonably certain based upon the history, clinical signs, examination findings , radiographs, and ancillary tests, the therapy recommended is dependent upon the severity of clinical signs . Dogs without neurologic disturbance or self-multilating paresthesia and whose signs are limited to soreness, lameness, or stiffness that is intermittent frequently respond favorably to rest or restriction of exercise. Shortterm treatment with aspirin or corticosteroids can be used to completely arrest clinical signs when rest is insufficient. Conservative management does not eliminate the underlying cause of clinical signs but is often a very satisfactory alternative to more aggressive surgical intervention. In dogs with persistent pain, self-mutilation, or more significant neurologic dysfunction, decompressive dorsal laminectomy is recommended. These dogs rarely respond satisfactorily to conservative treatment. 9. 21. 25 The objective of surgery is to reduce compression on the cauda equina and free roots that may be entrapped by connective tissue. Foraminotomy is indicated to release spinal nerves compressed at stenotic intervertebral foramina or entrapped by connective tissue. The prognosis with surgical intervention is usually good to excellent. Postoperative complications include wound infection, seroma formation, and recurrence of clinical signs. Infection is rarely a problem. Seroma formation is best handled by open surgical drainage, debridement of granulation tissue, and closure of dead space. Recurrence of signs is infrequent. Recurrence is usually the result of fibrosis and adhesions, which form a laminectomy membrane over and around the cauda equina. Metic-

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ulous attention to hemostasis during surgery and the use of a fat graft 25 reduce the likelihood of this problem. INJURY OF THE CAUDA EQUINA Injury of the cauda equina occurs with displaced or nondisplaced fractures of L7 and the sacrum, with LIS and sacrococcygeal luxations, and with coccygeal fracture/luxation (Fig. 6A, B, and C). 1, 2.9,13 In dogs, vertebral injuries in this area occur most commonly as a result of motor vehicle accidents. !O In cats, falls from extreme heights (for example, from buildings) are also responsible. 1 Extreme caudal lumbar or LIS flexion, forced axial rotation, and severe coccygeal traction exert forces on the vertebral column that combine to cause these fractures andluxations. 7 , 26 Evidence of vertebral displacement may. be obvious at the time of presentation (Fig. 7). Signs of neurologic dysfunction vary and depend upon the location of vertebral injury and the type of damage sustained by spinal roots or nerves. Traction and shearing forces exerted on the cauda equina can cause partial or complete avulsion of roots and spinal nerves (Fig. 8). Avulsion produces irreversible injury and causes permanent neurologic dysfunction. Spinal roots and spinal nerves that are stretched mayor may not be irreversibly damaged. Occasionally, the filum terminale is avulsed from the conus medullaris and the caudal aspect of the spinal cord becomes swollen and hemorrhagic (Figs. 8 and 9). Other factors that contribute to neural injury and neurologic dysfunction include contusion, hemorrhage, and swelling along spinal roots; traumatic disc rupture with compression from ruptured nucleus pulposus and vertebral sinus hemorrhage; mechanical compression on spinal roots or nerves due to vertebral displacement, soft tissue bruising, hemorrhage, . and swelling around spinal nerves at vertebral and intervertebral foramina; and spinal cord contusion and hemorrhage. Differentiation of the type and severity of root and spinal nerve injury is difficult or impossible to achieve on routine neurologic examination immediately after the trauma. Neuropraxia resulting from neural or extraneural swelling can produce clinical signs indistinguishable from nerve root avulsion. Functional recovery over several days with conservative treatment indicates that injury to the cauda equina may be reversible. As a practical matter, however, owners are usually anxious to have some indication about prognosis before signs of recovery are observed. Exploratory laminectomy with visualization and examination of the cauda equina may be the only way of resolving this dilemma. When signs of cauda equina dysfunction are present follo~ing trauma, lateral radiographs of the LIS area are obtained with the animal under general anesthesia. A ventrodorsal or dorsoventral view is also obtained. Care must be exercised in moving and positioning the animal for radiographs. This prevents aggravation of injury to the cauda equina as a result of abrupt displacement of fractured and unstable segments of the vertebral column. . No matter how severe fractures and luxations appear radiographically, they must always be viewed with due regard for neurologic signs and

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Figure 6. A, Lateral radiograph showing ·fracture of L7 with cranioventral displacement of the caudal fracture segments. (From Walker TL, Tomlinson J Jr, Sorjonen DC, et al: Diseases of the spinal column. In Slatter DH (ed): Textbook of Small Animal Surgery. Volume 1. Philadelphia, WB Saunders Co, 1985; with permission.) B, Lateral radiograph of a dog with lumbosacral fracture-dislocation . (From Simpson SE, Kornegay JN, Rafl'e MR: Surgical diseases of peripheral nerves. In Slatter DH (ed): Textbook of Small Animal Surgery. Volume 1. Philadelphia, WB Saunders Co, 1985; with permission.) C, Lateral radiograph showing sacral fracture in a dog with paraparesis, urinary incontinence, fecal incontinence, and coccygeal paralysis.

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Figure 7. Vertebral displacement in a 3-year-old dog that was struck by an automobile,. Pelvic limb ataxia and paresis were present. The dog was able to walk with assistance. Urinary incontinence, fecal incontinence, and coccygeal paralysis were present. Sacrococcygeal fracture-dislocation was observed on radiographs.

examination findings . Radiographic assessment must not be used as the sole criterion for offering a prognosis. Despite complete luxation and malalignment of the vertebral column, as shown in Figure 6A and B, animals with these injuries often retain the ability to stand. Some need assistance and support to do so, while others may stand and walk with little assistance or support. Occasionally, bladder and anal control is maintained. 9. 24 The prognosis in these cases is not as grave as the radiographs may initially indicate. Surgical intervention to decompress the cauda equina and stabilize the vertebral column can lead to excellent functional recovery. 24 In select cases, functional recovery is also possible without surgery. 1.9. 24 Vertebral injuries of the US, sacral, and sacrococcygeal areas are

Figure 8. Surgical exploration of the dog seen in Figure 7. The dorsal laminae of L6, L7, and the sacrum have been removed. The filum terminale and caudal aspect of the conus medullaris have been avulsed (arrows), and only a few roots of the cauda equina remain intact.

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Figure 9. Postmortem specimen of conus medullaris and cauda equina from the dog shown in Figures 7 and 8. Extensive subarachnoid hemorrhage and cord contusion are eVident where nerve roots and the filum terminale have been avulsed (arrow A). Evidence of contusion and parenchymal hemorrhage are present on cut section of the spinal cord several segments cranial to the injury site (arrow B).

usually associated with neurologic abnormalities in one or both pelvic limbs. Abnormalities are generally localized to areas of sciatic nerve distribution and result from damage to L 7 and S1 spinal roots or nerves. The L6 spinal roots and nerves are often involved. The L4 and L5 spinal roots and nerves are usually spared. Thus, quadriceps function is not impaired. As long as avulsion has not occurred, the long-term prognosis for partial or complete functional recovery, although not absolute, is optimistic. Hemorrhage and bone fragments in the spinal canal can be removed at the time of surgery. Swelling, inflammation, and bruising of the cauda equina will gradually resolve with pharmacologic treatment and time. Owners will be concerned about recovery of motor function. If the animals are functionally ambulatory, most owners are willing to accept some degree of ataxia and paresis in their pets. A matter of greater concern to the owner and to the veterinarian is the extent of damage to the sacral roots and the functional status of the bladder, the urethra, and the anal sphincter. Urinary or fecal incontinence is an unacceptable problem to most owners, even in the ambulatory or ataxic animal. Unfortunately, fractures and luxations of the caudal vertebral column almost invariably produce sacral root injury, which causes incontinence of urine, feces, or both. Furthermore, incontinence is often permanent. 1. 2, 7, 9, 23. 24 Spontaneous recovery following conservative treatmentl. 9. 24 and following surgery9. 24 has been seen however. As with all other traumatic injuries to the cauda equina, there is no easy way to determine the reversibility of clinical signs. Electrophysiologic tests such as EMG, CMG, and EMyG may be helpful, but are not readily available to most practitioners. The immediate benefit of EMG is doubtful, because spontaneous electrical activity and de nervation potentials in denervated muscle do not appear for 1 to 3 weeks follOwing denervation. 3 , 5 Examination of the sacral roots during surgery provides the best way of assessing potential for

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recovery of neurologic function . Surgery only permits an assessment of the structural integrity, not the functional integrity of the sacral roots, however. Coccygeal fractures and luxations beyond the sacrococcygeal junction usually cause damage to the coccygeal nerve trunks only. The result is loss of sensory and motor function from the site of injury caudally. Efforts can be made to salvage and preserve the tail for cosmetic reasons. However, it is wise to consider amputation because paresthesia may cause self-multilation of the denervated tail. 23 Amputation is also indicated for fractures causing paralysis from the base of the tail caudally. In this case, amputation is performed to prevent soiling of the perineum and tail during defecation and urination. Treatment After thorough neurologic examination is performed and radiographs are obtained, treatment with corticosteroids is indicated. Treatment may be helpful in reducing swelling of injured spinal roots and nerves. Corticosteroids will also reduce the inflammatory reaction and swelling in soft tissues adjacent to the fracture site. Conservative treatment consisting of cage rest, antibiotics, corticosteroids" urinary catheterization, evacuation of urine, prevention of decubital ulcers, and general hygiene may give excellent results in selected cases. 1. 9. 24 Paresis and incontinence have resolved within 1 to 4 weeks in some animals. 1.9 Conservative treatment is most rewarding in animals with minimal neurologic deficits localized to the pelvic limbs and without urinary or fecal incontinence. 24 When neurologic deficits are more severe, surgery is indicated to visualize the cauda equina. Hemorrhage, disc material, and bone fragments are removed from the spinal canal. If spinal roots are intact, stabilization of the vertebral column can be achieved using techniques described elsewhere. 24, 26 Despite aggressive surgical intervention, decompression of the cauda equina, and stabilization, many animals fail to recover sufficiently and are euthanatized. Even though injury of the cauda equina often produces permanent neurologic deficits, each case must be evaluated and treated individually. The impressions and biases one has developed as a result of previous experience with similar cases must not cloud one's assessment of the case nor preclude thorough examination, Every case is new, and every case is unique. SUMMARY ,

Idiopathic (congenital) US stenosis, acquired (degenerative) US stenosis, and traumatic injury to the vertebral column caudal to L6 often produce signs of neurologic dysfunction attributed to compression, displacement, entrapment, or trauma of the cauda equina. Clinical signs vary from animal to animal and depend upon which roots of the cauda equina are involved and the nature of the compromise. An understanding of the anatomy of the area and an appreciation for the fUllctional relationship between the cauda equina and structures innervated are essential for accurate evaluation, workup, diagnosis, treatment, and outcome.

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REFERENCES 1. Bennett D: Orthopaedic diseases affecting the pelvic region of the cat. J Small Anim Pract 16:723, 1975 2. Berzon JL, Dueland R: Cauda equina syndrome: Pathophysiology and report of seven cases. J Am Anim Hosp Assoc 15:635, 1979 3. Bowen JM: Peripheral nerve electrodiagnostics, electromyography, nerve conjunction velocity. In Hoerlein BF (ed): Canine Neurology: Diagnosis and Treatment. Edition 3. Philadelphia, WB Saunders Co, 1978, p 266 4. Bradley WE, Timm GW, Rockswold GL, et aI: Detrussor and urethral electromyelography. J Urol114:891, 1975 5. Buchthal F: An Introduction to Electromyography. Copenhagen, Scandinavian University Press, 1957 6. Camins MB, O'Leary PF (eds): The Lumbar Spine. New York, Raven Press, 1987 7. Chrisman CL: Problems in Small Animal Neurology. Philadelphia, Lea & Febiger, 1982 8. de Lahunta A: Veterinary Neuroanatomy and Clinical Neurology. Edition 2. Philadelphia, WB Saunders Co, 1983 9. Denny HR, Gibbs C, Holt PE: The diagnosis and treatment of cauda equina lesions in the dog. J Small Anim Pract 23:425, 1982 10. Fenney DA, Oliver JE: Blunt spinal trauma in the dog and cat. J Am Anim Hosp Assoc 16:664, 1980 11. Fletcher TF, Kitchell RL: Anatomical studies on the spinal cord segments of the dog. Am J Vet Res 27:1759, 1966 12. Goss CM (ed): Gray's Anatomy of the Human Body. Philadelphia, Lea & Febiger, 1973 13. Hoerlein BF (ed): Canine Neurology: Diagnosis and Treatment. Edition 3. Philadelphia, WB Saunders Co, 1978 14. Jenkins TW: Functional Mammalian Neuroanatomy. Philadelphia, Lea & Febiger, 1972 15. McClure RC, Dellman MJ, Garrett PG: Cat Anatomy. Philadelphia, Lea & Febiger, 1973 16. McNeel SV, Morgan JP: Intraosseous vertebral venography: A technique for examination of the canine lumbosacral junction. J Am Radiol Soc 19:168, 1978 17. Miller ME, Christensen GC, Evans HE (eds): Anatomy of the Dog. Philadelphia, WB Saunders Co, 1969 18. Morgan JP, Ljunggren G, Read R: Spondylosis deformans (vertebral osteophytes) in the dog. A radiographic study from England, Sweden and USA. J Small Anim Pract 8:57, 1967 19. Oliver JE: Disorders of micturition. In Hoerlein BF (ed): Canine Neurology: Diagnosis and Treatment. Edition 3. Philadelphia, WB Saunders Co, 1978, p 461 20. Oliver JE, Selcer RR: Neurogenic causes of abnormal micturition in the dog and cat. Vet Clin North Am (Small Anim Pract) 4(3):517, 1974 21. Oliver JE, Selcer RR, Simpson S: Cauda equina compression from lumbosacral malarticulation and malformation in the dog. J Am Vet Med Assoc 173:207, 1978 22. Segedy AK, Yano B, Jeraj K: Sacral spinal cord agenesis in a kitten. J Am Vet Med Assoc 174:510, 1979 23. Simpson SE, Kornegay IN, Raffe MR: Surgical diseases of peripheral nerves. In Slatter DH (ed): Textbook of Small Animal Surgery. Volume I. Philadelphia, WB Saunders Co, 1985, p 1335 24. Slocum B, Rudy RL: Fractures of the seventh lumbar vertebra in the dog. J Am Anim Hosp Assoc 11:167, . 1975. 25. Tarvin G, Prata RG: Lumbosacral stenosis in dogs. J Am Vet Ml!d Assoc 177:154, 1980 26. Walker TL, Tomlinson J Jr, Sorjonen DC, et al: Diseases of the spinal column. In Slatter DH (ed): Textbook of Small Animal Surgery. Volume I. Philadelphia, WB Saunders Co, 1985, p 1367 27. Weinstein PR, Ehni G, Wilson CB: Lumbar Spondylosis: Diagnosis, Management, and Surgical Treatment. Chicago, Year Book Medical Publications, Inc, 1977 28. Wright JA: Spondylosis deformans of the lumbosacral joint in dogs. J Small Anim Pract 21:45, 1980 Neurology and Neurosurgical Referral Service of Long Island 191 Sunrise Highway Amityville, New York, 11701