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EQUINE VETERINARY EDUCATION / AE / MAY 2019
Discussion
This case report is the first description of OAAM in a Warmblood horse. Key findings were hypoplasia and dysplasia of C1 and C2, partial fusion of the atlanto-occipital joint, bilateral aplasia of the rectus capitis ventralis and rectus capitis lateralis muscles, presence of an abnormal muscle extending from C2 to the occiput, sclerosis of the cranial oblique muscle of the head, scoliosis of the cranial cervical spine and local dynamic ventral compressive damage to the spinal cord leading to the clinical sign of a grade 3/5 spinal ataxia. Furthermore, in a flexed position a dorsal subluxation of the dens of C2 was detected. Most horses affected by OAAM develop ataxia due to
compressive damage to the spinal cord secondary to the bony malformations early in life. In many cases, ataxia has been observed while they are foals (Mayhew et al. 1978a; Gonda et al. 2001). In some cases, ataxia develops progressively to the age of 2–3 years (Wilson et al. 1985) as in the horse described in this case report. A few horses described in the literature had only mild proprioceptive deficits or did not show signs of ataxia up to age 5 years (Watson and Mayhew 1986). Affected horses are usually subjected to euthanasia as they cannot be used for riding. The ataxia can be progressive and is a risk for the patient and rider and in Arabians, the heritable nature of the condition is to be considered. Furthermore, there is no promising therapeutic option (Green 1995; Hahn 2006). Surgical intervention has been suggested in breeds other than Arabians to correct the atlantoaxial subluxation and scoliosis associated with OAAM (Rush 2012) but there is neither a description of such a procedure nor a report of a case treated with such an approach. Apart from radiographic information, there are some descriptions of post- mortem examinations but little information using other diagnostic modalities (Mayhew et al. 1978a; Wilson et al. 1985; Watson and Mayhew 1986; Gonda et al. 2001). This present report characterises OAAM in a Warmblood horse using multiple diagnostic imaging modalities and post- mortem examination. This allowed for very accurate illustration of the anatomical abnormalities including malformation of the adjacent musculature that has hitherto not been described in a case of OAAM. Using information obtained by clinical, radiological and
morphological studies, classification of OAAM into four types was suggested. These were defined as type A; atlanto-occipital fusion with hypoplasia and malformation of C2 including the dens and a modification of the atlanto-axial joint: type B; asymmetrical atlanto-occipital fusion, cervical scoliosis and presence of a wedge-shaped bone caudally at C2: and type C; asymmetrical atlanto-occipital fusion with aplasia of the occipital condyles and cervical scoliosis (Mayhew et al. 1978a). An additional type D characterised by duplication of C1 was documented in a young Arabian horse (Watson et al. 1985). It is difficult to assign the patient described in this report to
one of the types A–D mentioned above. The lack of a duplication of C1 rules out a type D form of OAAM. Similar to a type C variation, the mare had partial atlanto-occipital fusion and vertebral scoliosis. Aplasia of the occipital condyles was however, not present. Similarly, the mare had many features assigned to type B, i.e. atlanto-occipital fusion and cervical scoliosis, but the bone fragment at C2 typical
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for a type B abnormality was not found. Most abnormalities described in our case fulfil the criteria of a type A abnormality which is the typical hereditary form observed in Arabian horses. Wilson et al. (1985) described two cases of OAAM in two
mature non-Arabian horses (one Appaloosa and one Quarter Horse) that showed significant similarities with the mare presented in this case report. In all these horses, the head was carried in an extended position. The neurological signs (ataxia and proprioceptive deficits) did not appear in either of these horses before the age of 2 or 3 years, respectively. All three horses suffered from severe anatomical variations of the occiput, C1 and C2, with the most significant finding being the mineralised fusion between C1 and occiput. Additionally, the Quarter Horse described by Wilson et al. (1985) showed a fissure like longitudinal defect along the entire dorsal arch of C1 as described in our case report. Gonda et al. (2001) described another case of OAAM in
a 7-day-old Quarter Horse colt. Radiographic examination of this colt revealed deformation and shortening of the transverse processes and the dens of C2, thus inducing a subluxation of the dens ventral to C1. Post euthanasia, a severe compression of the spinal cord at the level of C1-C2 was detected, which explained the pronounced clinical signs. Similar to this colt, the Swiss Warmblood mare of this case report showed pathological variation in the dens of C2 with a subsequent subluxation of C2 toward dorsally. OAAM is most commonly diagnosed in Arabian foals, but
this and other case reports (Wilson et al. 1985; Gonda et al. 2001) show that it should be on the list of differential diagnoses for foals and young horses of other breeds showing signs of cervical spinal ataxia. Furthermore, this case report provides evidence that the malformations associated with OAAM are not restricted to the bones but can also involve the musculature.
Authors’ declaration of interests No conflicts of interest have been declared.
Ethical animal research
This is a case report where the horse was presented to the hospital for the condition described. The decision to submit the report was made after the horse was subjected to euthanasia.
Source of funding None.
Acknowledgements The skilful help of Urs M€
and the support of Elisabeth H€ procedures is highly acknowledged.
Authorship H.P. Br€
uller during the anatomical dissection ogger-Manser with histological
unisholz was the surgeon responsible for the case and
prepared the manuscript for submission together with N. Wildhaber, a student who presented this case for her Master’s thesis. S. Hoey was the radiologist involved in the case.
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