A condition has been recognised in five young dogs in which the proximal tibia exhibited cranial bowing. This altered conformation, sometimes accompanied by bow legs (genu varum), occurs bilaterally, but to differing degrees. The deformity apparently altered the biomechanics of the stifle joint so that degenerative joint disease and rupture of the cranial cruciate ligament followed in four of the five dogs. The aetiology is unknown, but the most likely cause appears to be retardation of growth in the caudal aspect of the proximal tibial physis. Treatment involving surgical techniques to correct the joint instability was only moderately successful.

The clinical and radiographic findings associated with the presence of hemivertebra ("wedge-shaped"vertebra) in small and brachycephalic breeds of dogs are reported together with the results of post mortem examination in the availabel cases. The condition is characterised clinically by progressive hind-leg weakness, spinal pain, abnormalities of the nervous system and evidence of muscle atrophy or other abnormalities of conformation. Confirmation of the clinical diagnosis is by radiography. It is suggested that the condition is congenital in origin. Breed incidences are reported. The occurrence of the disorder in certain families of dogs suggests also that it may be hereditary. Other congenital abnormalities are seen in some dogs affected by hemivertebrae.

The clinical findings in 18 dogs with gracilis (n = 17) or semitendinosus (n = 1) myopathy are described. Each dog had a similar hind-limb gait abnormality characterized by a shortened stride with a rapid, elastic medial rotation of the paw, internal rotation of the hock and external rotation of the calcaneus [corrected] and internal rotation of the stifle during the mid-to-late swing phase of the stride. Medical management prior to or in lieu of surgery was attempted (n = 8) with no apparent response. Fifteen dogs had one or multiple surgical procedures. Although transection, partial excision, or complete resection of the affected muscle resulted in resolution of lameness following surgery, lameness recurred six weeks to five months (mean, 2.5 months; median, two months) following surgery. Adjunctive medical treatment did not prevent recurrence. Variable replacement of the affected muscle with fibrous connective tissue (predominantly along the caudolateral border of the muscle) was evident grossly, and replacement of myofibers with fibrous connective tissue was confirmed histologically. A definitive etiology could not be established.

To test the hypothesis that joint incongruity contributes to the pathogenesis of elbow osteochondrosis, the left and right radius and ulna of 20 young large breed dogs were measured to determine any variation in length and to observe any incongruity of the elbow joint. Both lame and normal dogs were included in the study. Nine of the 20 dogs had marked disparity in radial and ulnar lengths yet only one had obvious elbow joint incongruity. The use of a sliding osteotomy for the treatment of fragmented coronoid process and a lengthening osteotomy for the treatment of an ununited anconeal process is also discussed. All four dogs treated with a sliding osteotomy showed a marked clinical improvement, and two of the three dogs treated with a lengthening osteotomy showed radiographic fusion of the anconeal process.

Caudal cervical spondylo‐myelopathy was diagnosed in 30 cases admitted to the University of Queensland Veterinary Clinic (UQVC) over a four‐year period. The clinical signs at presentation and the radiographic changes detected varied considerably. A number of different surgical treatments were used and a small number of animals were treated conservatively. The results are presented, followed by some discussion concerning the aetiology and pathogenesis of this condition.