• We are sorry, but NCBI web applications do not support your browser and may not function properly. More information
Logo of canvetjReference to the Publisher site.Journal Web siteJournal Web siteHow to Submit
Can Vet J. Dec 2003; 44(12): 984–986.
PMCID: PMC340367

Osteochondrosis of the occipital condyles and atlanto-occipital dysplasia in a Belgian horse


A lesion in the cervical region of a 14-month-old Belgian gelding with severe ataxia was suspected. Necropsy revealed symmetric focal cartilage defects compatible with osteochondrosis of the occipital condyles and atlanto-occipital dysplasia. To our knowledge this is the first equine report of symmetrical osteochondrosis of the occipital condyles causing neurologic signs.

Osteochondrosis refers to single or multifocal area of abnormal endochondral ossification affecting the nonarticular epiphysis, the articular cartilage of the epiphysis, and/or the growth plate or physis. It is the failure of endochondral ossification and the loss of normal differentiation into cartilage cells that results in the lack of transitional calcification of the matrix. Consequently, there is a lack of vascularization, which ultimately leads to necrosis in basal layers of the thickened cartilage and the development of osteolytic lesions, such as subchondral bone cysts or osteochondritis dessicans (1,2). These lesions are often diagnosed with the use of radiology. On gross examination, osteochondrosis is generally classified as either typical or atypical. Typical osteochondrosis refers to 1 or 2 lesions that are in a characteristic location. These lesions can be bilaterally symmetrical. Equine osteochondrosis is typically found in familiar regions of the appendicular skeleton. Atypical osteochondrosis is defined as multiple articular and sometimes physeal lesions in characteristic, other random locations, or both (1,2). The osteochondrosis observed in this case is atypical, due to the rare location on the occipital bone.

A 14-month-old, Belgian gelding weighing approximately 500 kg was presented to the Atlantic Veterinary College with a history of progressive ataxia. During the winter, he was placed outside in an area with deep snow, where, the owner noted, he experienced difficulty moving. Over a period of 6 mo, the abnormal gait progressed, at which time the gelding was referred to the Atlantic Veterinary College Large Animal Teaching Hospital. On presentation, his vital signs were within normal limits. Neurological evaluation showed the presence of grade III/IV ataxia with proprioceptive deficits in all 4 limbs. Proprioceptive deficits were enhanced when he moved in tight circles, walked with his head elevated, and was subjected to a tail pull. Cranial nerve examination was normal, as was assessment of mentation. No weakness was identified. The spinal reflexes were considered normal, based on a normal panniculus reflex response, and the horse was able to dorsoflex and ventroflex in a normal manner when stimulus was applied along the dorsum. These findings were consistent with a lesion localized to the cervical spinal cord. The chief differential diagnoses considered at this time included cervical vertebral malformation (“Wobblers”), equine degenerative myeloencephalopathy, and cervical trauma. Other less likely differential diagnoses were equine protozoal myelitis and equine herpes viral myelopathy. Other potential differentials, such as rabies, eastern equine encephalitis, western equine encephalitis, and West Nile virus disease were considered unlikely, based on the 6-month duration of the neurologic disease prior to presentation, the onset of the neurologic disease occurring in the winter, and the fact these etiologies are rare in our geographic location. Cervical radiographs of the entire cervical vertebral column revealed no significant abnormalities. A cervical myelogram and analysis of cerebrospinal fluid were not pursued, due to financial constraints. The severity and chronicity of the neurologic deficits indicated a poor prognosis. The horse was euthanized and a postmortem was performed.

Necropsy revealed 2 bilaterally symmetrical, 2 cm in diameter, ovoid, well-demarcated, and slightly raised cartilaginous lesions involving the occipital condyles (Figure 1). Both defects were adherent to the underlying bone but moved slightly when pressure was applied. The opposing cranial articular surfaces of the atlas were moderately flattened; thus resulting in abnormal articulation with the atlanto-occipital joint. The remaining cervical vertebrae were inspected for gross lesions, instability, and stenosis; no abnormalities were noted. The gross pathologic diagnosis was bilaterally symmetrical osteochondrosis of the occipital condyles and atlanto-occipital dysplasia. Joints of the extremities were examined on necropsy and demonstrated no gross pathology.

figure 24FF1
Figure 1. Photograph showing occipital condyles. Arrows indicate bilaterally symmetrical ovoid cartilaginous defects measuring ~2 cm in diameter. Note thickening and fibrosis of the joint capsule.

Histologic lesions were confined to the caudal brain stem and cervical spinal cord to the level of cervical vertebra II. There was locally extensive vacuolation of the white matter involving mainly the ventral and lateral funniculi. Irregularly swollen myelin sheaths that sometimes contained scattered, moderately to markedly enlarged axons were often present. A loss of axons was evident in many areas, and vacuolated myelin sheaths often contained large, foamy macrophages, small amounts of karyorrhectic debris, or both. There were occasional, shrunken eosinophilic neurons in the adjacent grey matter. The histologic diagnosis was focal degenerative leukomyelopathy. Histologic examination of the gross lesions of the occipital bone and atlas was not performed, due to loss of the tissue samples.

Osteochondrosis and its manifestations as osteochondritis dessicans (OCD) and subchrondral bone cysts are frequently diagnosed in the horse. Common joints affected include the femoropatellar, tarsocrural, shoulder, fetlock, carpus, elbow, and coxofemoral joints. Lesions in the lateral trochlear ridge of the femur, lateral trochlea of the talus, and the distal intermediate ridge of the tibia account for a high percentage of the clinical cases (1). Most cases have been documented in the standard bred, Thoroughbred, and warm-blooded breeds, with few reports in draft breeds. One retrospective study on 51 draft horses reviewing the prevalence of osteochondrosis stated that the tibiotarsal joints were the most commonly affected. There was no mention of cervical vertebral osteochondrosis in this particular report (3). Several reports have documented osteochondritic lesions of the cervical vertebrae, but these lesions were confined mainly to cervical vertebrae III to VII in ataxic horses (1,4,5). A recent article documented osteochondrosis in the cranial articular surface of cervical vertebra II of a 2-year-old Thoroughbred that manifested severe neck pain without any neurologic abnormalities (6).

The osteochondritic lesions of the occipital condyles identified in this case were unique. The horse had no evidence of osteochondrosis in any other joint; the atlanto-occipital joint was the only joint affected. The other joints in the cervical spine were all investigated and found to be normal. To our knowledge, there is only 1 report of osteochondrosis of the atlanto-occipital joint (7). This involved a 24-month-old standard bred gelding, which also had lesions in the femoropatellar joint, the distal tibia, and the ribs. The abnormality in the atlanto-occipital joint was an incidental finding and not associated with clinical nervous deficits (7). In another paper, atlanto-occipital OCD in feedlot cattle was reported and its frequency over different seasons was compared (8). Of the cattle observed, 3.8% of the population was found to have occipital osteochondrosis lesions, with fewer lesions being seen in the cattle fattened during the summer. The decreased frequency during the summer was postulated to be due to slower growth rates at that time. The author concluded that varying concentrations of dietary protein did not influence the prevalence of the lesions, but that a high caloric diet and rapid growth rate were contributing factors in the development of osteochondritic lesions (8). The diet of the horse in this case was not known; however, the size of this horse for his age was above average, signifying a rapid growth rate.

The underlying etiology for the abnormal endochondral ossification leading to the development of equine osteochondrosis has not been established. Multiple factors, however, have been implicated repeatedly: genetics, nutrition, growth rates, endocrinology, biomechanics, and toxicosis (1,2,3).

There is conflicting literature on what role specific nutrients play in the manifestation of osteochondrosis. One study illustrated a significantly greater occurrence of histologic osteochondrosis lesions in foals fed with high energy diets but not in those fed with high crude protein diets (9). Another study found that excessive dietary phosphorus significantly increased the prevalence of osteochondrosis in unexercised foals, while excessive levels of dietary calcium had no such effect (10). Copper deficiency has also been suggested to result in defective collagen cross-linking and altered matrix remodeling; however, conflicting reports on dietary copper and osteochondrosis development remain (11). In the eastern region of Canada, copper deficiency is not a common occurrence. In the present case, the diet offered to the horse was not known; therefore, it cannot be determined whether it played an intricate role in the development of osteochondrosis.

A genetic predisposition and growth rate have been associated with the occurrence of osteochondrosis. However, a specific gene defect affecting the orderly process of endochondral ossification has not yet been recognized (1) and recent investigations have shown that rapid growth and high body weight, or large size, are not implicated in the pathogenesis of this disease (1,3,10). The weight gain and growth rate for this horse were not recorded; however, for a 14-month-old draft horse, he was above average for both weight and size.

In summary, the clinical manifestation of ataxia in this case was consistent with cervical vertebral malformation, but the pathologic finding illustrated an atlanto-occipital instability associated with osteochondritic lesions on the occipital condyle and atlanto-occipital dysplasia. It is unknown as to which of these lesions was primary or secondary. There are numerous reports of equine atlanto-occipital dysplasia being the inciting cause of ataxia, primarily in Arabian foals. However, to the authors knowledge, there is only 1 published report of osteochondrosis of the occipital condyles in the horse. This case report suggests that occipital osteochondrosis should be considered as a differential diagnosis in horses that present with clinical signs consistent with cervical vertebral malformation. CVJ


Address all correspondence and reprint requests to Dr. Muirhead.


1. Stashak TS. Adams' Lameness in Horses. 5th edition. New York: Lippincott Williams and Wilkins, 2002:544–568.
2. McIlwraith CW, Trotter GW. Joint Disease in the Horse. Philadelphia: WB Saunders, 1996:335–358.
3. Riley CB, Scott WM, Caron JP, Fretz PB, Baily JV, Barber SM. Osteochondritis dessicans and subchondral cystic lesions in draft horses: a retrospective study. Can Vet J 1998;39:627–633. [PMC free article] [PubMed]
4. Girard C, Lepage OM, Rossier Y. Multiple vertebral osteochondrosis in a foal. J Vet Diag Invest 1997;9:436–438. [PubMed]
5. Tomizawa N, Nishimura R, Sasaki N, et al. Morphological analysis of cervical vertebrae in ataxic foals. J Vet Med Sci 1994;56:1081–1085. [PubMed]
6. Beck C, Middleton D, Maclean A, Lavelle R. Osteochondrosis of the second vertebra of a horse. Equine Vet J 2002;34:210–212. [PubMed]
7. Reiland S, Asheim A, Jeffcott LB, Ekman S. Spinal osteochondrosis in the horse. Svensk-Veterinartidning 1983;35:63–65.
8. Jensen R, Park RD, Lauerman LH, et al. Osteochondrosis in feedlot cattle. Vet Pathol 1981;18:529–535. [PubMed]
9. Savage CJ, McCarthy RN, Jeffcott LB. Effects of dietary energy and protein on induction of dyschondroplasia in foals. Equine Vet J 1993;16:74–79.
10. Savage CJ, McCarthy RN, Jeffcott LB. Effects of dietary phosphorus and calcium on induction of dyschondroplasia in foals. Equine Vet J 1993;16:80–83.
11. Jeffcott LB. Problems and pointers in equine osteochondrosis. Equine Vet J 1993;16:1–3.

Articles from The Canadian Veterinary Journal are provided here courtesy of Canadian Veterinary Medical Association
PubReader format: click here to try


Related citations in PubMed

See reviews...See all...


Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...