Cervical Intervertebral Disc Protrusion in Two Horses

CASE REPORT Cervical Intervertebral Disc Protrusion in Two Horses

R.R. FOSS, R.M. GENETZKY, E.A. RIEDESEL AND C. GRAHAM Department of Clinical Sciences (Foss, Genetzky and Riedesel) and Department of Pathology (Graham), Iowa State University, College of Veterinary Medicine, Ames, Iowa 50011

Summary epiniere, au niveau du deuxieme tion and cranial nerve function were Two horses with ataxia of all four espace intervertebral. Dans l'autre cas, within normal limits. Although the limbs were found to have cervical la necropsie revela une protrusion du horse was alert, he was reluctant to intervertebral disc protrusion. Severe disque intervertebral entre les sixieme move. There was a proprioceptive pelvic limb ataxia, proprioceptive et septieme vertebres cervicales. Les deficit in the rear limbs as evidenced by deficits and spasticity were present in lesions microscopiques de la moelle delayed foot replacement from the both horses with similar but less severe epiniere se caracterisaient par de la cross-legged stance and a positive signs in the thoracic limbs. Cerebros- degenerescence des fibres nerveuses et sway response. All hooves scuffed dur- pinal fluid analysis was within normal une mauvaise coloration de la myeline. ing limb protraction, and when circled limits. Metrizamide myelography the rearlimbs exhibited excessive cir- allowed definitive diagnosis in one Introduction cumduction. The horse resented hav- case when a compression of the spinal Intervertebral disc protrusion has ing the head turned to the left. A lesion cord was demonstrated at the level of been described in several species but is of the cranial portion of the cervical the second intervertebral space. In the apparently rare in the horse, as there is spinal cord was suspected. second case, an intervertebral disc pro- only one report (1). The following is a Creatine phosphokinase, serum trusion between cervical vertebrae 6 report of two horses with cervical glutamic-oxalocetic transaminase, and 7 was found at necropsy. Fiber intervertebral disc protrusion. blood ureau nitrogen and venous pH degeneration with poor myelin stain- values were slightly elevated, other- ing characterized the spinal cords Case I wise routine hematology and serum histologically. A six year old Paint stallion was chemistries were within normal limits. admitted to the Iowa State University Approximately three weeks after Resume College of Veterinary Medicine with onset of signs the horse was anesthet- Protrusion de disques intervertebraux the complaint of pelvic limb ataxia ized with glyceryl guaicolate and cervicaux, chez deux chevaux and spasticity. The horse had been maintained with halothane for cervical Les auteurs ont decele une protru- found down in his stall approximately radiography and myelography. Cere- sion de quelques disques interver- one week earlier. A tentative diagnosis brospinal fluid (CSF) was withdrawn tebraux cervicaux, chez deux chevaux of myositis had been made and treat- from the atlanto-occipital site for qui manifestaient une ataxie locomo- ment initiated with flunixin rneglum- analysis and cytology. All CSF trice des quatre membres. Les mem- ine,' B-vitamins, furosemide,2 pro- parameters were within normal limits bres pelviens de ces deux chevaux affi- caine penicillin G and sodium (2). chaient de l'ataxie locomotrice, des bicarbonate. The horse stood up Plain radiographs of the cervical deficits proprioceptifs et de la spas- within a day, but remained very stiff vertebrae showed an active collapse of ticite; leurs membres thoraciques and ataxic. Over the next several days the C-2/3 intervertebral disc space manifestaient des signes similaires, no improvement was noted and the with accompanying sclerosis of the mais moins prononces. U ne analyse du horse was referred for further opposing endplates. There were no liquide cephalo-rachidien ne revela diagnostics. obvious signs of cervical vertebral rien d'anormal. Une myelographie, At admission, a spastic, dysmetric, malformation. The appearance at C- avec de la metrizamide, permit de ataxic gait was noted in both the pelvic 2/3 was interpreted as a possible disc poser un diagnostic definitif, dans un and thoracic limbs, with the pelvic protrusion (Figure 1). cas, parce qu'elle demontra la presence limbs being more severely affected. No A myelogram using metrizamide3 d'une compression de la moelle paresis was evident. Cutaneous sensa- demonstrated a ventral extradural

Dr. Foss's current address is: Rolling Hills Veterinary Hospital, 210 Keene, Columbia Missouri 65201. Dr. Graham's current address is: 163 Oakwood Lane, Ithaca, New York 14850. 'Banamine@, Schering Corporation, Kenilworth, New Jersey. 2Lasix@, Taylor Pharmaceutical, Decatur, Illinois. 3Nyegaard & Co., Oslo, Norway.

188 Can Vet J 1983; 24: 188-191. vical segment and at the point of dis.c protrusion. Necrosis of individual neurons within the gray matter was noted at the level of the second and third cervical vertebrae. Case 2 A three year old Arabian-saddle- bred cross gelding was presented with a history of pelvic limb ataxia of sud- den onset and two weeks duration. Treatment had consisted of furosemide, phenylbutazone, and dexametha- sone with no response. At admission physical examination revealed severe ataxia and proprioceptive deficits in the pelvic limbs with similar but slightly less severe signs in the thoracic limbs. Movement of all limbs was spastic and dysmetric. No paresis was evident. A positive sway FIGURE 1. Survey cervical radiograph of horse 1, showing collapse of the intervertebral disc space response and delayed foot replace- between C-2/3. The opposing endplates are markedly sclerotic when compared to C-3/4. ment from the cross-legged stance was exhibited most notably in the pelvic lesion at the level of C-2/3. With the Due to an unfavorable prognosis limbs. Pain was not apparent during neck in a neutral lateral position the the owners elected euthanasia one cervical palpation and manipulation. degree of compression on the spinal month after the initial episode. At Anesthesia was induced with gly- cord was minimal. With the head and necropsy the intervertebral disc mate- ceryl guaicolate and thiamylal and neck in ventral flexion the degree of rial and cartilage was absent on the maintained with halothane for cervical spinal cord compression was slightly opposing surfaces of cervical vertebral radiography and collection of CSF increased (Figures 2a and 2b). No bodies 2 and 3, protruding dorsally from the atlanto-occipital space. The other lesions were identified on the about 5 mm into the vertebral canal. CSF was within normal limits (2). No myelogram. Measurement of the min- Approximately 2 mm of underlying abnormalities were noted on plain imum flexion diameter (MFD), min- bone was eburnated on both sides of radiographs, with or without cervical imum sagittal diameter (MSD) were the joint space (Figure 3). flexion, although insufficient expo- within the normal ranges reported in Histologically the white matter of sure of the caudal cervical vertebrae the literature for a horse of greater the cervical cord was characterized by hampered evaluation. The owner than 320 kg body weight (3,4). These fiber degeneration with poor myelin elected not to have myelography myelographic findings supported the staining and scattered throughout all performed. suspicion of an intervertebral disc funiculi, but concentrated in the ven- Routine hematology and serum protrusion. tral and lateral funiculi in the first cer- enzyme levels were within normal lim-

U.?l.

FIGURE 2a. Myelographic study of horse 1, demonstrating some narrow- FIGURE 2b. With ventral flexion of the head the narrowing of the ventral ing of the ventral subarachnoid contrast column at the C-2/ 3 disc space. subarachnoid space is accentuated.

189 The histological spinal cord lesions exhibited were similar to those noted in cervical disc protrusions in the canine. In the dog, the clinical signs o:~~~M seen are dependent on the location, force, extent, speed, and duration of the protrusion (29). After the initial edema subsides, the spinal cord lesion can be produced in several ways. An

.:. .4 ~~~~~~~~~~~~~~~A extruded nucleus causes an epidural inflammatory reaction. The physical presence of the disc with resulting compression of the cord is important. Vascular derangements such as reduced blood flow in the ventral spinal artery and intramedullary branches with resultant ischemia, as well as venous obstruction causing edema, have also been incriminated (30-33). Although cervical intervertebral disc protrusion is apparently a rare FIGURE 3. Sagittal section through the spinal column of horse 1. C-3/4 (left) and C-2/3 (right) occurrence, it warrants addition to the showing collapse of the C-2/3 intervertebral disc space with subchondral eburnation as well as list of causes of ataxia in the horse. protrusion of the disc. References its. Clinical improvement myelitis was not (3,19), parasitic myelitis 1. McKELVEY WAC, OWEN RapR. Acquired torti- noted over the next two weeks and the (3,19,24,25), equine infectious anemia collis in eleven horses. J Am Vet Med Assoc owner requested that the horse be (26) congenital abnormalities of 1979; 175: 295-297. euthanized. venous drainage (27) and degenerative 2. MAYHEW IG, WHITLOCK RH, TASKER JB. Intervertebral disc protrusion myeloencephalopathy (3,28) should Equine cerebrospinal fluid: reference values between cervical vertebrae 6 and 7 also be considered in the differential of normal horses. Am J Vet Res 1977; 38: compressed the spinal cord in that diagnosis. 1271-1274. area. Histologically, there was fiber Diagnosis in these cases, after the 3. MAYHEW IG, DELAHUNTA A, WHITLOCK RH, degeneration ofthe dorsal, lateral, and lesion was localized to the cervical spi- KROOKER L, TASKER JB. Spinal cord disease ventral columns of the spinal cord in nal cord, was based on history, cere- in the horse. Cornell Vet 1978; 68 suppl. 6. the 4. NYLAND TG, BLYTHE LL, POOL RR, HELPHREY area ofprotrusion. Microglial cells brospinal fluid analysis and cytology, MG, OBRIEN TR. Metrizamide myelography were scattered, sometimes occurring in apparent neck pain, radiography, and in the horse: Clinical radiographic and clumps of three to five. Myelin balls, postmortem evaluation. History of a pathologic changes. Am J Vet Res 1977; 41: swollen axons and empty spaces were relatively rapid onset when combined 204-211. numerous. with equine herpesvirus 1 serology and 5. WAGNER PC, GRANT BD, BAGBY GW, GALLINA CSF analysis helped rule out infec- AM. SANDE RD. Evaluation of cervical spinal Discussion tious, inflammatory and neoplastic fusion as a treatment in the equine With the advent of surgical treat- spinal cord disease. The apparent neck "wobbler" syndrome. Vet Surg 1979; 8: ment of selected spinal cord disease in pain in horse 1 could be attributed to a 84-88. the horse (5,6), accurate diagnosis is fracture, vertebral 6. WAGNER PC, BAGBY GW, GRANT BD, GALLINA osteoarthritis, or a A. Surgical stabilization of the equine cervi- becoming increasingly more impor- compressive lesion causing meningeal cal spine. Vet Surg 1979; 8: 7-12. tant to provide appropriate therapy or nerve root pain (29). The definitive 7. BEECH J. Cervical cord compression and and prognosis. The clinical signs diagnosis was reached with myelo- wobbles in horses. Proc Am Assoc Eq Pract shown by these horses with cervical graphy in the first horse and necropsy 1976; 22: 78-79. intervertebral disc protrusion mim- in the second. 8. FRASER J, PALMER AC. Equine incoordina- icked those of cervical spinal cord Although intervertebral disc degen- tion and wobbler disease in young horses. compression from other causes, eration in the horse has been reported Vet Rec 1967; 80: 338-355. including cervical stenotic myelopathy in association with thromboembolism 9. YAMIGIWA J, YOSHIKAWA R. OYAMADA T. (3,7-1 1), vertebral fractures (12-14), (18) and in asymptomatic older horses Pathological studies on equine ataxia in vertebral luxations (15), occipitoatlan- (30) no evidence was found in these Japan. Jpn J Vet Sci 1980; 42: 681-694. toaxial malformation 10. SAKURA Y. Histopathological changes in the (16) and neopla- animals that the protrusions were nervous system in "equine incoordination" sia (17). Noncompressive entities such secondary to degeneration, as is often - observations on eight affected foals as thromboembolic ischemic myelo- the case in the chondrodystrophoid including cases of the earliest neonatal pathy (18), rhinopneumonitis mye- dog (29). Instead, these protrusions onset. Jpn J Vet Res 1967; 25: 30-35. loencephalopathy (19-23), protozoal may be of traumatic origin. 11. MORDRAKOWOKI A, KSZUBIEWICZ C. Correla-

190 tion between clinical symptoms and locali- 479-481. 26. McCLURE J, LINDSAY W, TAYLOR W, OCHOA R, zation ofanatomical lesions in spinal ataxia 19. DELAHUNTA A. Neurological problems of ISSEL C, COULTER J. Ataxia in four horses (wobbler disease in horses). Med Weter the horse. Proc Am Assoc Eq Pract 1977; with equine infectious anemia. J Am Vet 1977; 33: 712-716. (Vet Bull 1978; 48: 601). 19: 25-32. Med Assoc 1982; 180: 279-283. 12. SCHEBITZ H, DAHME E. Spinal ataxia in the 20. BITSCH V, DAM A. Nervous disturbances in 27. GILMOUR JS, FRASER JA. Ataxia in a welsh horse. Proc Am Assoc Eq Pract 1967; 13: horses in relation to injection with equine cob filly due to a venous malformation in 133-148. rhinopneumonitis virus. Acta Vet Scand the thoracic spinal cord. Eq Vet J 1977: 9: 13. FRASER H, PALMER AC. Equine incoordina- 1971; 12: 134-138. 4042. tion and wobbler disease of young horses. 21. JACKSON T, KENDRICK JW. Paralysis of 28. MAYHEW IG, DELAHUNTA A, WHITLOCK RH, Vet Rec 1967; 80: 338-353. horses associated with equine herpes virus I GEARY ic. Equine degenerative myeloence- 14. DEBOWES RM, WAGNER PC, GAVIN PR, RODER infection. J Am Vet Med Assoc 1971; 158: phalopathy. J Am Vet Med Assoc 1977; PH. Vertebral compression fracture in a foal 1351. 170: 195-201. following electric shock. J Vet Orth 1981; 2: 22. JACKSON TA, OSBURN Bl, CORDY DR, KEN- 29. HOERLEIN BF. Canine neurology. Philadel- 14-19. DRICK Jw. Equine herpes virus I infection of phia: W.B. Saunders, 1978: 470-560. 15. GUFFY M, COFFMAN J, STRAFUSS, A. Atlan- horses: Studies on the experimentally 30. ROONEY JR. The horse's back: biomechanics toaxial luxation in a foal. J Am Vet Med induced neurologic disease. Am J Vet Res of lameness. Eq Pract 1982; 4: 10-12. Assoc 1969; 155: 754-757. 1977; 38: 709-719. 31. LINDBALD G, LJUNGGREN G, OLSSON SE. On 16. MAYHEW IG, WATSON AG, HEISSAN JA. Con- 23. PURSELL AR, SANGSTER LT, BYARS TD, DIVERS spinal cord compression in the dog: an genital occipito-atlantoaxial malforma- TJ, COLE JR. Neurologic disease induced by angiographic study. Adv Small Anim Pract tions in the horse. Eq Vet J 1978; 10: equine herpes virus I. J Am Vet Med Assoc 1962; 3: 121-124. 103-113. 1979; 175: 473-474. 32. TARLOV IM. Spinal cord compression mech- 17. TRAVER D. MOORE J,THORNBURG L,JOHNSON 24. FRAUNFELDER HC, KAZACOS DR, LICHTEN- anisms of paralysis and treatment. Spring- J, COFFMAN J. Epidural melanoma causing FELS JR. Cerebrospinal nematodiasis caused field, Illinois: Charles C. Thomas, 1957. posterior paresis in a horse. J Am Vet Med by a filariid in a horse. J Am Vet Med Assoc 33. TARLOV IM, KLINGER H, VITALE S. Spinal cord Assoc 1977; 170: 1400-1403. 1980; 177: 359-362. compression studies. I. Experimental tech- 18. TAYLOR H, VANDEVELDE M, FIRTH E. Ischemic 25. LITTLE PB. Cerebrospinal nematodiasis of niques to produce acute and gradual com- Myelopathy caused by fibrocartilaginous equidae. J Am Vet Med APssoc 1972; 160: pression. Arch Neurol Psych 1950; 70: emboli in a horse. Vet Path 1977; 74: 1407-1413. 813-818.

BOOK REVIEWS Problems in SmallAnimal Neurology. each individual problem. This is spe- articles are by world renowned nutri- C.L. Chrisman. Published by Lea& cially well demonstrated in the chapter tionists. Half of the book is concerned Febiger, Philadelphia. 1982. 461 on Behavior and Personality Dis- with protein utilization by the dairy pages. Price US$37.50 and C$45.00. orders. All relevant changes, signs or cow and the modifying effects of symptoms are well studied, and rumen fermentation on dietary pro- The author uses a rational stepwise analyzed. teins. Veterinarians may prefer to read approach in the diagnoses and treat- Relevant references follow at the these chapters last because of the ment of the neurological problems end ofeach chapter for those who wish uncertainties in applying this informa- found in veterinary practice. The first more intensive information. tion in the field. There are excellent part of the book introduces the reader Although large parts of the book are chapters on milk fever, processing of to the nervous system and to the many addressed to the animal neurologists, feeds, silage, complete diets, body ways and means which can be used to the book itself allows a better under- condition and production, and con- investigate the complaints. The chap- standing, and will often clarify some centrate: forage rations. These chapter dealing with the medical manage- cases which are puzzling to the practi- ters will offer many veterinarians new ment of the patient will certainly be tioner. C. Gardell. insights into feeding dairy cattle. most useful to many practitioners, as it There is helpful information on the deals with the practical steps to be causes and prevention of butter fat taken at the time of the neurological depression and on the benefits of com- emergency and thereafter. Recent Developments in Ruminant plete rations versus self-feed grain sys- Much of the second part of the book Nutrition. W. Haresign and D.J.A tems for high producing cows. The deals with specialized examination Cole. Published by Butterworths benefits of feeding sodium bicarbo- and investigation practices which Inc., Massachusetts. 1981. 367 nate to dairy cows are described. belong to the realm of the reference pages. Price $21.50. Although the book is not aimed at the neurological clinic. However, it gives beef producer the chapter on process- an intense understanding ofthe neuro- This excellent book consists of a ser- ing of grains contains data on how to logical problems which may be ies of review articles drawn from the minimize rumenal upsets on high grain encountered. Diagnosis, prognosis Proceedings of the University of Not- diets, there is also a chapter on growth and patient care and treatment are all tingham Nutrition Conferences for promotants in cattle. Buy the book but considered, thus giving an overview of Feed Manufacturers. Many of the read it selectively. J. M. Naylor.

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