Volume 44 | Issue 2 Article 1

1982 Differential Diagnosis of Conditions Mimicking Intervertebral Disc Disease in the Canine Phil Olson Iowa State University

Robert W. Carithers Iowa State University

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Recommended Citation Olson, Phil and Carithers, Robert W. (1982) "Differential Diagnosis of Conditions Mimicking Intervertebral Disc Disease in the Canine," Iowa State University Veterinarian: Vol. 44 : Iss. 2 , Article 1. Available at: https://lib.dr.iastate.edu/iowastate_veterinarian/vol44/iss2/1

This Article is brought to you for free and open access by the Journals at Iowa State University Digital Repository. It has been accepted for inclusion in Iowa State University Veterinarian by an authorized editor of Iowa State University Digital Repository. For more information, please contact [email protected]. Differential Diagnosis of Conditions Mimicking Intervertebral Disc Disease In the Canine

by Phil Olson, DVM* Robert W. Carithers, DVM, MS, PhD**

Many abnormal conditions ofthe canine can Ataxia and paresis along with forced exercise produce clinical signs that in some way mimic is likely to cause falling and greater subluxa­ those associated with intervertebral disc tion. Anesthesia eliminates support of muscle disease. This oftentimes leads to unnecessary tone, increasing the danger further. 5.7 confusion and frustration in the diagnosis and "Wobbler Syndrome" is another common subsequent treatment of these cases by prac­ cervical problem. The condition most common­ ticing veterinarians. The purpose of this paper ly occurs in Great Danes and Doberman is to summarize the signs associated with those Pinschers, and clinical signs are due to com­ seen most commonly and thereby to clarify the pression of the cervical spinal cord caused by

manner in which these can be most readily vertebral malformation-malarticulation of C 5 , 2 5 6 differentiated in a clinical situation. This paper C 6 , and C 7 • • • is not intended to be an in-depth analysis ofall Clinical signs are usually seen at less than canine spinal cord problems, but only to pro­ one year of age, often by two, and occasional­ vide a review of clinical signs, pathogenesis, ly later. Owners generally recognize ataxia of and diagnosis of certain conditions which pre­ the pelvic limbs. The onset is usually insidious sent in a similar manner. but sometimes acute, with signs normally pro­ gressive. The pelvic limbs are seen to cross each CERVICAL VERTEBRAL other, abduct or collapse on walking and INSTABILITY especially on turning. The hind quarters sway Atlanto-axial subluxation occurs in awkwardly. The dog may knuckle over. The miniature and toy breeds, resulting from frac­ impression given is that the animal doesn't ture, degeneration, or malformation of the know where the limbs are because of a pro­ dens. The pathogenesis of absence of the dens prioceptive deficit. Thoracic limb signs, if pre­ is unknown, although some speculation exists sent, are similar but less marked. Occasional­ 2 5 6 that the mechanism is similar to femoral head ly, limb cro~sing and knuckling over occur. • • 5 6 necrosis of Legg-Perthes Disease. • Neurological exam reveals abnormal Luxation most commonly occurs at six to postural reactions present, especially hopping eight months of age. Absence of the dens or and proprioceptive positioning. Manipulation fracture allows the cranial aspect of the body of the neck usually does not elicit pain. Blood, of the axis to rotate dorsally into the vertebral urine and CSF parameters are normal (possibly canal, with subluxation sometimes a result. slightly elevated protein in the CSF). There is Clinical signs include severe neck pain, spastic involvement of ascending proprioceptive and tetraparesis, and recumbency. Thoracic limb descending motor tracts.2,5.6 paresis often is the most profound sign. The Intervertebral disc protrusion may be animal walks with a short stiff stride.5,6,7 associated with the condition. Unrelated cer­ Handling should be done with extreme care, vical disc extrusion occurs in older dogs and with no manipulation ofthe atlantoaxial region. may be readily identified on plain radiographs. Cervical pain in this case is prominent. The *Dr. Olson is a 1982 graduate of the College of primary neurological disease to differentiate Veterinary Medicine at Iowa State University. **Dr. Carithers is a Professor in Veterinary Clinical from in young dogs is canine distemper Sciences at Iowa State University. myelitis .. Neurological exam reveals other ab-

60 Iowa State Veterinarian normalities not explained by a localized lesion, CANINE DISTEMPER as distemper lesions are usually disseminated. Signs of this disease may present due to pre­ For example, the examiner may see paraplegia dominant action ofthe virus on the spinal cord, with mild thoracic limb deficit, suggesting \vith no history of systemic illness. Dogs less separate lesions, one thoraco-Iumbar, and one than one year old are especially suspect ofhav­ cervical. Head tilt, tremor, and abnormal ing the disease. The history should be of signs nystagmus may be present, suggesting a of segmental myelopathy, with progressive 5 6 16 cerebello-vestibular lesion. Also, with worsening. • • distemper, the CSF is often abnormal. 5.6 Information helping to differentiate this etiology from a focal thoraco-Iumbar spinal cord lesion, such as intervertebral disc disease, often is neurological deficits at multifocal areas. NEOPLASIA An example is mild thoracic limb deficit in a Neoplasia may occur as extramedullary ex­ paraplegic dog. This suggests a mild cervical pansive masses, compressing the spinal cord to spinal cord lesion and a severe thoraco-Iumbar 5 6 produce an ischemic myelopathy. lesion. • Classification is either of vertebral or spinal Most often additional signs are present which cord neoplasia. Vertebral neoplasia character­ make diagnosis much easier. Head tilt, abnor­ istically shows compression myelitis of the mal nystagmus and head tremor suggest cere­ spinal cord due to invasive bony growth. It may bellovestibular dysfunction. Nasal or ocular be primary or metastic. Osteosarcoma, chon­ discharge, harsh lung sounds, hyperkeratosis drosarcoma, and fibrosarcoma are most com­ ofthe nose and foot pads and chorioretinopathy mon. Spinal cord or meningeal neoplasms are may be seen. Myoclonus is a nearly pathog­ seen in the dog, most often in the thoracic cord. nomonic sign. Diffuse lesion distribution and Meningiomas are most common. Medullary progressive nature suggest inflammatory neoplasms are rare and when present, are disease. The CSF is many times normal, but usually neurofibromas or neurofibro­ may show a mild increase in mononuclear cells, 6 7 5 6 16 sarcomas. • protein or both. • • Typical signs of neoplastic spinal cord com­ pression are slow in onset and progression. TOXOPLASMOSIS However, they often show acute signs and can Toxoplasmosis can produce unlimited progress rapidly. Necropsies have shown a neurological clinical signs. It is much less com­ mass may grow slowly a considerable time, mon than canine distemper. As with distemper, with the spinal cord adapting. Suddenly a signs may manifest as segmental myelopathy. 5 critical point is reached, where spinal cord cir­ Possible clinical signs include seizures, blind­ culation is compromised, resulting in lesions ness, tremor, hemi- or paraparesis and hind­ and clinical signs. Adaptation can be phe­ quarter paralysis. Spinal reflexes may be ab­ nomenal, showing an amazing decrease in cord sent and extensor rigidity present in one or both diameter on necropsy. Often the neoplasm is hindlimbs. The history is usually of a dog less lateral, therefore initial signs are likely to be than one year of age, showing gradual pro­ asymmetrical, with paresis and ataxia more gressive paralysis. Some common signs that pronounced ipsilaterally. Signs later progress when present with CNS signs are suggestive of to bilateral.2.5.6 toxoplasmosis include abortions, stunted Plain radiographs are normal unless young, iritis, retinitis, recurrent fever, lym­ vertebral invasion or origination has occurred. phadenopathy, diarrhea, pneumonia, myocar­ 5 6 A myelogram usually demonstrates the lesion. ditis, and icterus. • A thorough physical exam and thoracic radio­ Positive diagnosis is difficult. Serum titers graphs are important to diagnose metastasis.2.5 can be taken but interpretation is uncertain, Neoplasia may be confused with vertebral in­ although rising titers are suggestive. Systemic fection as a slowly progressive lesion. If signs mycoses may also produce CNS signs and appear acutely, then an intervertebral disc retinitis. 6 problem, vascular accident and others must be included in the initial ruleouts. The fact that POLYRADICULONEUROPATHY­ neoplasia generally occurs in older animals filay COONHOUND PARALYSIS also aid in the initial analysis of the case. The etiology of Coonhound Paralysis IS

Vol. 44, No. 2 61 unknown. The functional lesion is apparently this condition is not completely understood. on the ventral nerve roots and peripheral Clinical signs depend on the location of the le­ nerves. The disease is initiated by coon bites sion, with trauma more easily causing injury one to two weeks before signs appear. Hall­ to the spinal cord becasue of lack of bony pro­ marks are pain without motor function. Nine­ tection. Diagnosis is by radiography of the ty percent show paresis and hyporeflexia in the spine, myelography, and breed. The condition posterior limbs first and dysphonia. Progres­ is most common in the "screw-tailed" breeds sion is to tetraplegia with areflexia, normal (Boston Terrier, Pug, French and English mental altertness, and normal temperature. 'Bulldog).2,4,6 Most commonly affected are adult hunting dogs.4,6 SPINAL DYSRAPHISM Spinal dysraphism is an inherited incomplete TOXIC POLYNEUROPATHY­ closure of the neural tube in Weimaraners. It may be associated with syringomyelia, which TICK PARALYSIS 4 The exact mode ofpathogenesis is unknown, is seen as tube-like cavities in the spinal cord. however, the initiating agent is a neurotoxin Clinical signs include a hopping gait on the hind legs, crouching wide stance, and scratch­ from a female tick (usually Dermacentor ander­ ing reflex in both hind legs at once with paresis. soni). Only one tick is needed to show signs.4,6 Clinical presentation is ofan ascending flac­ The signs do not improve or worsen. Diagnosis cid paralysis, with little or no sensory impair­ is subjective and ascertained by breed, clinical ment. Progression is from hyporeflexia and signs and history. Radiographs and CSF tap ataxia to paresis to paralysis and areflexia. help determine that no treatable disease is present.4,6 Signs are seen five to seven days after attach­ ment of the ticks. Differential diagnosis must include coonhound paralysis. Finding ticks on HEMIVERTEBRAE the dog is suggestive.4,6 Hemivertebrae is a condition of uncertain pathogenesis, consisting of failure of fusion of right and left halves of vertebrae. The "screw­ INFECTIOUS VERTEBRAL tailed" breeds, Boston Terriers, Pugs, French OSTEOMYELITIS­ and English Bulldogs, are most often afRicted.4 DISKOSPONDYLITIS Clinical signs are rare. They are caused by Diskospondylitis is an inflammation of the intermittent trauma to the spinal cord due to vertebral bodies and associated intervertebral instability of the vertebral column. Clinical discs. Typically the source is hematogenous, signs are usually progressive and include although contiguous tissue infection may be posterior paresis, urinary and fecal incon­ associated. A variety of organisms have been tinence, muscle atrophy, abnormal conforma­ cultured, including Staph. aureus) Strep. canis) tion and pain. Paresis may be acute. Diagnosis Brucella canis) Corynebacterium spp.) Pseudomonas is by myelography.2,4 and others. Cultures are negative twenty-five percent ofthe time and sepsis may not be dem­ CAUDA EQUINA SYNDROME onstrated by biopsy.2,5,6 Cauda equina syndrome is a nerological con­ Diagnostically, the most important sign is dition that results from the compression, severe vertebral column pain associated with destruction, or displacement ofthe nerve roots a progressive paraparesis and ataxia. Neuro­ forming the cauda equina. The condition logic deficits result from compression due to usually occurs in older dogs, presenting as bone proliferation associated with the lesion. spinal nerve root signs resulting in disorders of Fever and blood chemistry abnormalities may the pelvic limbs, sphincters, and tail/perineal be absent. Radiographs may reveal bony pro­ areas.2,6 liferation of vertebral bodies with lysis The most common sign i~ pain in the lum­ present.2,5,6 bosacral area and tail. Other signs include pelvic limb lameness, difficulty rising, paresis SPINAL BIFIDA of the tail, urinary and/or fecal incontinence, Spinal bifida is a congenital defect in the dor­ perineal hyperalgesia, self-mutilation oftail and sal laminae ofthe vertebrae, often resulting in perineal area and decreased lumbosacral spinal herniation of meninges. The pathogenesis of reflexes. The clinical signs vary greatly due to

62 Iowa State Veterinarian multiple etiologies and varying degrees ofcom­ The syndrome should be differentiated from pression. The early signs can be confused with other spinal cord lesions demonstrating acute hip dysplasia. Differential diagnosis includes onset. Possibilities include acute disc hernia- degenerative myelopathy, type II disc protru­ tion and osteomyelitis, vvhile neoplasia and 2 sion and spinal neoplasia. ,6 spinal cord infection more commonly manifest as deterioration over several months' time. DEGENERATIVE MYELOPATHY OF Since there is a large area over which this can GERMAN SHEPHERDS occur and thus show signs, the differential must Degenerative myelopathy occurs in aging be made more on the basis of acute onset with German Shepherds and is characterized by a improvement following and on unilateral signs slowly progressive paraparesis and ataxia ofthe rather than location.2 pelvic limbs. The onset is insidious and may continue for five to six months. Proprioception PATHOLOGICAL VERTEBRAL is the first reflex to go, along with crossed limbs FRACTURE and hyperreflexia ofthe pelvic limbs. Signs can Chronic renal insufficiency in older dogs be asymmetrical. Often a disuse atrophy ofthe from interstitial nephritis, glomerulonephritis muscles in the caudal thoracic and lumbosacral or amyloidosis results in hypocalcemia. The region is evident.5,6 resultant increase in parathormone (PTH) in­ Geriatric intervertebral disc disease can be duces accelerated release of stored calcium from ruled out by plain radiography and myelogram. bone. Skeletal involvement is general, but cer­ The myelogram would demonstrate a normal tain lesions are more apparent in given areas. subarachnoid space not compressed by space­ Loss of alveolar socket bone and lamina dura occupying mass (neoplasia) or excessive dural dentes occurs early, loosening the teeth. The ossification, or encroachment of spondylosis maxilla and mandible are softened and readily deformans. CSF is normal. 5 pliable (rubberjaw syndrome). Lameness and The lesion is of multisystemic degeneration stiffness of gait occur. Vertebral fractures after consisting ofdiffuse white matter degeneration relatively minor trauma can cause spinal cord in both ascending and descending spinal cord damage. The fracture may occur anywhere tracts in all segments of the cord. Both myelin along the vertebral column, thus signs may be sheaths and axons degenerate. Peripheral referable to most any area. Other signs that nerves may be involved, resulting in lower may aid in diagnosis include jaw softening, a motor neuron signs. Diagnosis is usually based generalized decrease in bone density, and ab­ on breed, age, typical history, clinical signs, 5 normalities found in urine analysis and on and inability to find other lesions. ,6 general workup. 6.11 Neoplasia can also cause lysis of vertebrae VASCULAR ACCIDENT­ FIBROCARTILAGINOUS EMBOLI and resultant fracture (see section on neoplasia). A vascular accident involving the spinal cord Differential diagnosis should again include is caused by occlusion of vessels of leptomen­ other spinal cord lesions demonstrating acute inges and spinal cord parenchyma by fibrocar­ onset, such as vascular accident, acute disc her­ tilaginous emboli derived from herniated disc niation, and osteomyelitis. material. Presenting signs are an acute (devel­ oping in less than six hours), unilateral hemiparesis or hemiplegia. This may occur TRAUMA from the cervical region caudal to the caudal The most likely sources of external trauma vertebrae, showing signs referable to C 3 to L 7 , are auto collision, gunshot, and fight wounds, 2 5 varying with the area affected. • presenting with sudden onset relating to the Often recovery is spontaneous, especially if time of incident or within a few hours. Signs some voluntary motion is retained in the are generally nonprogressive, especially greater affected limbs. Improvement is usually noted than twenty-four hours post-trauma. If signs during the first week, possibly due to resolu­ continue to develop over the next twenty-four tion ofhemorrhage and edema and to collateral hours, they indicate continual bleeding or ex­ circulation reaching ischemic areas. Later im­ cessive movement at the site ofvertebral injury, provement may be due to compensation for thus allowing continued cord trauma. 5 5 6 permanent loss of spinal cord parenchyma. Thereafter signs are stable or improved. • ,13

Vol. 44, No. 2 63 The thoraco-Iumbar junction is the most Thoracolumbar disc protrusion is likely to common fracture site. It should be realized that show less pain. The dog may show radiographs show only the present degree of aggressiveness, refusal to move, and pain when luxation and do not show the extent at the time handled. The lumbar muscles are rigid and ofinjury. Presenting signs may include Schiff­ kyphosis of the spine may be evident. Local Sherrington syndrome, with normal postural hyperesthesia at the site of herniation may be reactions and efforts of voluntary movement. present. Motor signs include changes in gait Spinal reflexes caudal to the lesion are normal and progression from ataxia to knuckling over or exaggerated. Lesion level may be de­ to paresis and finally paralysis. 2 5 termined by panniculus response. ,13 Eight percent of disc protrusions are at

"Spinal shock" is a physiological phenomena, T ll-L3 • An intercapitalligament coursing dor­ commonly seen in primates, that causes com­ sally over the discs from T 2-T 10 is a major fac­ plete atonia and areflexia caudal,to the lesion tor in low incidence ofdisc protrusion here. 13,14 for two to three weeks. While a distinct entity Pressure from protrusions or extrusions pro­ in primates, in domestic animals it is not duces varying degrees of ischemic myelopathy outstanding and carries no clinical significance. in the spinal cord by interfering with blood cir­ By the time the veterinarian examines the pa­ culation in the parenchyma. A sudden large ex­ tient, spinal reflexes are always present caudal trusion may produce focal hemorrhage and to the lesion. 5,6, 13 myelomalacia of grey and white matter. 5 Location of injuries associated with trauma In all cases spinal reflexes are intact. Most should be done with minimal patient manipula­ often they are hyperreactive and manipulating tion, with the animal in lateral recumbency. To limbs reveals hypertonia, ie. classic signs ofup­ differentiate the Schiff-Sherrington phenome­ per motor neuron disease. Pain sensation is non from cervical injury in cases of thoracic almost always intact in paraparetic cases. limb hypertonia, check for pain and voluntary Paraplegic animals with pain sensation have a n10vement. In the Schiff-Sherrington syndrome better prognosis than those with no cerebral they are present in the forelegs and not in the response to deep pain, such as that elicited by rear. With cervical spinal cord injury, pain and forceps pressure at the base of the toenail. In voluntary movement deficit is more equal.5,6,13 these cases, the panniculus test is helpful. 5 The examiner must establish the degree of INTERVERTEBRAL DISC DISEASE paresis, spinal reflex function and cerebral Intervertebral disc disease occurs in all response to pain in order to establish prognosis breeds, being seen more commonly in chondro­ and treatment. Radiographs and a myelogram dystrophic breeds (Dachshund, Pekinese, are also very helpful in precise localization of French Bulldog) and can occur at a young age. the lesion. The condition is thought to be related to the early spontaneous degeneration of the in­ CONCLUSION tervertebral discs that takes place in these A good history and clinical neurological ex­ breeds. Occurence is considered unlikely at less am are very important in cases of spinal cord than one year ofage, occasionally at two years disease. A knowledge of spinal column an­ of age, and quite often at three or more years atomy and physiology is necessary for an of age. Miniature poodles, beagles, and cocker understanding of clinical signs and interpreta­ spaniels also undergo this type ofdegeneration. tion ofneurological tests. This knowlege, along In nonchondrodystrophic breeds it is also seen with an understanding of the pathology and and is associated with aging, occurring in dogs clinical signs associated with spinal cord five years of age and older.5,10 disease, will enable the clinician to give an ac­ Signs ofdisc protrusion in the cervical region curate estimate of functional cord damage, lo­ calize the lesion, and suggest optimal therapy. from C 2 to T 1 include a "stiff neck" appearance as a classical sign. Also seen are an arched back, Spinal cord problem diagnosis and treatment reluctance to move, and pain with vocal can then become a very rewarding experience manifestations, which may even be elicited by for the practicing veterinarian. touch. Tremors of muscle groups of the REFERENCES thoracic limb and neck, along with knuckling 1. Berzon JL, Dueland R: Cauda Equina Syndrome: over, are seen. The C 2 -C3 disc and C 5 -C6 disc Pathophysiology and Report of Seven Cases. J ofAm most commonly are involved.2 Anim Hosp Assoc 15:635-643, 1979.

64 Iowa State Veterinarian 2. Bojrab MJ: Editor Pathophysiology in Small Animal Reproduction 2nd ed. Philadelphia: Lea and Febiger, Surgery. Philadelphia: Lea and Febiger, 1981, pp 1976 pp 90-100. 729-738, 747-759, 841-848. 12. Miller ME, Christensen GC, Evans HE: Anatomy of 3. Burt AD, Gammie JS, Ellis SE: A Case of Tick the Dog) 2nd ed. Philadelphia: WB Saunders Co., 1964 n C)~Q Paralysis in a Dog, Canadian Vet J 19:347, 1978. .t' -'-'...,. 4. Carithers RW: Lecture Notes, 1981. 13. Parker AJ: Diagnosis and Treatment ofCanine Spinal 5. De Lahunta A: Veterinary Neuroanatomy and Clinical Cord Disease. Scope 18:2-17, 1974. Neurology. Philadelphia: WB Saunders Co., 1977 pp 14. Parker AJ: Clinical Neurology in Small Animal Prac­ 169-205. tice, Part 7. Modern Veterinary Practice 61:826-829,1980. 6. Ettinger SJ: editor Textbook of Veterinary Internal Medicine 15. Parker AJ: Clinical Neurology in Small Animal Prac­ Volume 1, Philadelphia: WB Saunders Co., 1975 pp tice, Part 6. Modern Veterinary Practice 61 :738-743, 1980. 408,412-426,434-441,449,480. 16. Parker AJ: The Many Faces of Canine Distemper. 7. Gage ED: Paresis in the Older Dog. Proc Am Anim Canine Practice 5:25-28. 1978. Hospital Assoc. 1980 pp 287-290. 17. Patnaik AK, et al: Choroid Plexus Carcinoma with 8. Gotthelf LN: Diagnosis of Canine Wobbler Syndrome Meningeal Carcinomatosis in a Dog. Vet Path 17:381­ Using Myelography. Vet Med/Sm An Clin 385, 1980. 75: 1860-1861, 1980. 18. Van Bree H, et al: Successful Conservative Treatment 9. Hawe RS: Acute Idiopathic Polyradiculoneuritis in a of Cervical Discospondylitis in a Dog. J Small Animal Dog. Vet Med/Sm An Clin 74:675-680, 1979. Practice 22:59-65, 1981. 10. Hoerlein BF: editor Canine Neurology. Philadelphia: WB 19. Van Heerden J, Van Rensburg IB: Toxoplasmosis in Saunders Co., 1978 pp 470-560. a Dog. J ofSouth African Vet Assoc 50:211-214. 1979. 11. McDonald LE: editor Veterinary Endocrinology and

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