The electroretinographic phenotype of dogs with Golden Retriever muscular dystrophy

Objective To characterize the flash electroretinogram (ERG) in the Golden Retriever muscular dystrophy (GRMD) dog and to compare the results with those from a control group of Golden Retrievers. To investigate whether similar abnormalities of the ERG as those found in a majority of human patients with Duchenne muscular dystrophy (DMD) are also observed in the GRMD dog, the canine model for DMD. Animals Five GRMD dogs and five age‐matched clinically normal Golden Retrievers. Procedure An ophthalmic examination was carried out prior to performing electroretinography under general anesthesia. Rod, combined rod–cone and oscillatory potentials responses were recorded after dark adaptation. Responses to 30‐Hz‐flicker were recorded after light adaptation. The ERG responses of the GRMD dogs were compared with those of the control dogs by use of a Wilcoxon signed rank test. Results GRMD dogs had significantly reduced a and b‐wave amplitudes after dim white flash stimuli (rod response) and reduced a‐wave amplitude after bright white flash stimuli (rod–cone response). Conclusion and clinical relevance The ERG abnormalities observed in the GRMD dog suggest a dysfunction in the rod signaling pathway. These ERG alterations are different from those observed in human patients with DMD.     

Tissue Doppler assessment of diastolic and systolic alterations of radial and longitudinal left ventricular motions in Golden Retrievers during the preclinical phase of cardiomyopathy associated with muscular dystrophy

OBJECTIVE: To quantify radial and longitudinal left ventricular free wall (LVFW) velocities in dogs during the preclinical phase of Golden Retriever muscular dystrophy (GRMD)-associated cardiomyopathy by use of tissue Doppler imaging (TDI). ANIMALS: 9 dogs with GRMD and 6 healthy control dogs. PROCEDURE: All dogs (< 3 years old) were examined via conventional echocardiography and 2-dimensional color TDI. Myocardial velocities in the LVFW were recorded from right parasternal ventricular short-axis (radial motion) and left apical 4-chamber (longitudinal motion) views. Cardiac assessments via TDI included maximal systolic and early and late diastolic LVFW velocities in the endocardial and epicardial layers (for radial motion) and in the basal and apical segments (for longitudinal motion) (for longitudinal motion), RESULTS:-No notable ventricular dilatation or alteration of inotropism was detected in dogs with GRMD via conventional echocardiography. Compared with healthy dogs, endocardial velocities were significantly decreased in dogs with GRMD, resulting in marked decreases in radial myocardial velocity gradients during systole and early and late diastole. Similarly, basal and apical velocities were significantly decreased in systole and the former also in early diastole, resulting in significant decreases in the 2 corresponding longitudinal myocardial velocity gradients. The radial epicardial and longitudinal late diastolic velocities were comparable in the 2 groups. CONCLUSION AND CLINICAL RELEVANCE: Results indicated that GRMD-associated cardiomyopathy in dogs is associated with early marked dysfunction of both radial and longitudinal LVFW motions. These combined regional myocardial abnormalities might be useful criteria for detection of dilated cardiomyopathy at the preclinical stage of the disease in dogs.     

Evaluation of a short interspersed nucleotide element in the 3' untranslated region of the defective dystrophin gene of dogs with muscular dystrophy.

OBJECTIVES: To determine the distribution of a 231-base pair (bp) element in the dystrophin gene 3' untranslated region (UTR) in a colony of Golden Retrievers with muscular dystrophy and other unrelated dogs and to estimate the frequency of recombination for the canine dystrophin gene. ANIMALS: 77 dogs from the Golden Retriever Muscular Dystrophy (GRMD) colony at the Murdoch Veterinary School and 30 unrelated dogs from the Murdoch University Veterinary Clinic. PROCEDURE: Samples of blood or hair from dogs were used for amplification of DNA, using primers to the canine dystrophin 3' UTR. RESULTS: The DNA from affected dogs generated a larger PCR product than that obtained from clinically normal dogs. Products were cloned and sequenced, and the difference in size was found to be attributable to a 231-bp short interspersed nucleotide element (SINE). The SINE was found in all affected dogs in the colony but not in most unaffected puppies in the colony. Eighteen of 19 dogs in the colony were heterozygous for the GRMD mutation, and 7 of 30 unrelated dogs also were heterozygous for the SINE. CONCLUSION AND CLINICAL RELEVANCE: Evidence of recombination between the GRMD mutation and the SINE was observed in only 4 dogs (2 sets of littermates) in the GRMD colony. Incidence of this SINE in a few unrelated dogs suggests that this particular insertion into the dystrophin gene may have been a recent event. The SINE in the dystrophin 3' UTR did not have an apparent influence on dystrophin mRNA concentrations.     

Diagnostic potential of natriuretic peptides in the occult phase of golden retriever muscular dystrophy cardiomyopathy

The objective of the study was to determine whether the plasma concentrations of atrial and brain natriuretic peptides (ANP and BNP, respectively) could be reliable markers of cardiac alterations during occult cardiomyopathy in Golden Retriever Muscular Dystrophy (GRMD). Fifty Golden Retrievers without any clinical or radiographic sign of heart disease were included in this study (21 GRMD dogs and 29 controls). Controls and GRMD dogs were divided into 2 subgroups according to age (< and > or =12 months old, respectively). All dogs underwent echocardiography and determination of BNP and ANP plasma concentrations by radioimmunoassay. No ventricular dilatation or dysfunction was observed in either control or GRMD dogs. ANP plasma concentration did not differ significantly between controls and GRMD dogs (mean +/- SD = 72 +/- 49 versus 58 +/- 23 pg/mL, respectively, P = .21). This finding was confirmed in both subgroups of dogs (ie, those < and > or =12 months old). In contrast, BNP plasma concentrations were significantly higher in GRMD dogs than in controls (mean +/- SD = 117 +/- 92 versus 46 +/- 22 pg/mL, respectively, P < .05). In dogs > or =12 months old, sensitivity and specificity of BNP for identifying GRMD with a cutoff of 65 pg/mL were 78 and 86%, respectively. For the same cutoff value, sensitivity dropped to 42%, whereas specificity reached 100% in dogs <12 months old. In conclusion, BNP may be a useful biochemical marker of asymptomatic cardiomyopathy. However, this peptide does not allow very early detection because its optimal discriminatory power was observed in adult dogs (ie, > or =12 months of age).     

Kinematic study of back movement in clinically sound malinois dogs with consideration of the effect of radiographic changes in the lumbosacral junction

Objective— To determine thoracolumbar spinal movement in dogs and the influence of subclinical radiographic changes involving the lumbosacral junction. Study Design— Experimental study. Animals— Clinically sound Malinois dogs (n=22). Methods— Kinematic analysis of markers on the spinal processes of C7, T6, T13, L3, L7, and S3 was performed while dogs were walking on a treadmill. Range of motion (ROM) in the transverse and vertical direction and the time of occurrence (TOO) of the maximal marker position were calculated. ROM and TOO of angulations formed by the corresponding markers were calculated. Initial kinematic analysis was performed without knowledge of the radiographic changes, and then data were reanalyzed to determine whether vertebral changes influenced back motion. Based on the results of radiographic analysis of the lumbosacral junction, dogs were divided into 3 groups: 1=no radiographic changes; 2=shortened L7 vertebra; and 3=transitional vertebrae, spondylosis, subluxations, and spondylarthrosis of the lumbosacral junction. ROM and TOO were compared using ANOVA for repeated measures and a Bonferroni's post hoc test; P<.05 was considered significant. Results— The highest transverse ROM was achieved by markers T6, T13, and L3, and in the vertical direction by S3; however, there were no significant differences in ROM in horizontal angulations. In the sagittal plane, T13–L3–L7 had a lower angulation than L3–L7–S3. In Group 3, transverse ROM for C7 was significantly higher than in Group 1; the horizontal angular maximum of T13–L3–L7 occurred significantly earlier. Conclusions— Significant kinematic changes were detected between clinically sound dogs with radiographic lumbosacral changes and dogs with no radiographic abnormalities. Clinical Relevance— Kinematic data from clinically sound dogs can be used for comparison with data from dogs with gait disturbances associated with orthopedic or neurologic disease or changes associated with therapy.     

Age-related thoracic radiographic changes in golden and labrador retriever muscular dystrophy

Golden retriever and Labrador retriever muscular dystrophy are inherited progressive degenerative myopathies that are used as models of Duchenne muscular dystrophy in man. Thoracic lesions were reported to be the most consistent radiographic finding in golden retriever dogs in a study where radiographs were performed at a single-time point. Muscular dystrophy worsens clinically over time and longitudinal studies in dogs are lacking. Thus our goal was to describe the thoracic abnormalities of golden retriever and Labrador retriever dogs, to determine the timing of first expression and their evolution with time. To this purpose, we retrospectively reviewed 390 monthly radiographic studies of 38 golden retrievers and six Labrador retrievers with muscular dystrophy. The same thoracic lesions were found in both golden and Labrador retrievers. They included, in decreasing frequency, flattened and/or scalloped diaphragmatic shape (43/44), pulmonary hyperinflation (34/44), hiatal hernia (34/44), cranial pectus excavatum (23/44), bronchopneumonia (22/44), and megaesophagus (14/44). The last three lesions were not reported in a previous radiographic study in golden retriever dogs. In all but two dogs the thoracic changes were detected between 4 and 10 months and were persistent or worsened over time. Clinically, muscular dystrophy should be included in the differential diagnosis of dogs with a combination of these thoracic radiographic findings.     

Muscular dystrophy in dogs: does the crossing of breeds influence disease phenotype?

Golden Retriever (GR) muscular dystrophy is an inherited degenerative muscle disease that provides an excellent model for Duchenne muscular dystrophy in humans. This study defined the histopathologic lesions, including the distribution of type I and II muscle fibers (FTI and FTII), in 12 dystrophic and 3 nondystrophic dogs between 7 and 15 months of age. The authors were interested in studying the influence on disease phenotype from crossing the base GR breed with Yellow Labrador Retrievers. The dystrophic dogs were divided according to breed: GRs and Golden Labrador Retrievers (GLRs). On hematoxylin and eosin staining, histopathologic lesions were more severe in GRs than GLRs. Six of eight GR muscles (75%) had a severe lesion grade (grade 3). In contrast, seven GLR muscles (87.5%) had mild lesions (grade 2), and only one had severe lesions (grade 3). Changes in fiber-type distribution were more pronounced in GRs versus GLRs. FTI:FTII ratio inversion was observed in three dystrophic GRs but only one GLR. The mean diameter of FTI and FTII was smaller in GRs and GLRs than in nondystrophic dogs (P < .01). The FTI of five GR muscles (62.5%) were larger than those of GLRs, whereas only one GLR muscle was larger (P < .05). The differential was less pronounced for FTII, with four GR muscles being larger and three GLR being larger. Observations indicate that crossing the base GR breed with Labrador Retrievers lessened the severity of the GR muscular dystrophy phenotype.     

Dystrophin‐deficient muscular dystrophy in two lurcher siblings

Two cases of dystrophin‐deficient muscular dystrophy in 16‐week‐old male lurcher siblings are reported. The myopathies were characterised by regurgitation, progressive weakness and muscle wastage. The dogs had generalised weakness in all four limbs, with more pronounced weakness in the pelvic limbs. Reduced withdrawal in all limbs, muscle contracture and lingual hypertrophy were noted. Serum creatine kinase activities were markedly elevated. Electromyographic abnormalities included fibrillation potentials. Histopathological and immunohistochemical staining were consistent with dystrophin‐deficient muscular dystrophy. Clinical improvement was noted in one of the cases with l ‐carnitine supplementation and supportive therapy. Genetic transmission of the disease was postulated as the dogs were siblings.     

Hypertrophic muscular dystrophy in a young dog

Hypertrophic muscular dystrophy was diagnosed in a 10-month-old male Rat Terrier with hypersalivation, dysphagia, gait abnormalities, and generalized weakness. Serum creatine kinase activity was high, and electromyography revealed myotonic discharges. Histologic examination of a muscle biopsy specimen revealed muscle fiber degeneration, clusters of basophilic regenerating fibers, and endomysial fibrosis. Staining for dystrophin, a sarcolemmal protein, was decreased, compared with that in muscle specimens from clinically normal dogs. Treatment with mexilitene hydrochloride and procainimide hydrochloride resulted in temporary improvement in clinical signs, but the disease became refractory to treatment, and the dog was euthanatized. Clinical and histologic characteristics of this dystrophin deficiency-related muscular dystrophy were similar to those of X-linked muscular dystrophy in dogs, hypertrophic muscular dystrophy in cats, and Duchenne muscular dystrophy in humans.     

RADIOGRAPHIC FEATURES OF GOLDEN RETRIEVER MUSCULAR DYSTROPHY

Golden Retriever muscular dystrophy is an inherited, degenerative myopathy due to the absence of dystrophin and is used as a model of Duchenne muscular dystrophy of young boys. This report describes the radiographic abnormalities of Golden Retriever muscular dystrophy in 26 dogs. The thoracic abnormalities included diaphragmatic asymmetry (18/26), diaphragmatic undulation (18/26), and gastro-esophageal hiatal hernia (6/26). Pelvic abnormalities included narrowing of the body of the ilia (14/19), ventral deviation and curvature of the tuber ischii (14/19), elongation of the obturator foramen with a decrease in opacity of the surrounding bone (12/19), and lateral flaring of the wings of the ilia (12/19). Abdominal abnormalities consisted of hepatomegaly (14/22) and poor serosal detail (12/22). The unique thoracic abnormalities were a consistent finding in affected Golden Retriever muscular dystrophy dogs. The diagnosis of muscular dystrophy should be included in the differential list if the combination of diaphragm undulation and asymmetry, and gastro-esophageal hiatal hernia are identified. These diaphragmatic abnormalities are related to hypertrophy and hyperplasia of the diaphragm. Additionally, the skeletal changes of pelvic tilt, elongation of the pelvis, widening of the obturator foramina and thinning of the ischiatic tables appear to be specific to Golden Retriever muscular dystrophy in dogs. These pelvic abnormalities are most likely secondary to bone remodeling associated with the progressive skeletal myopathy and subsequent contracture/fibrosis.     

Development of a snapback method of single-strand conformation polymorphism analysis for genotyping Golden Retrievers for the X-linked muscular dystrophy allele.

OBJECTIVE: To develop a snapback method of single-strand conformation polymorphism (SSCP) analysis for genotyping Golden Retrievers for the X-linked muscular dystrophy allele. ANIMALS: 20 Golden Retriever puppies from a colony with X-linked muscular dystrophy. PROCEDURE: DNA spanning the canine dystrophin mutation was amplified by means of a polymerase chain reaction (PCR), using a primer modified to have an additional sequence at the 5' terminus. The primer was designed so that 1 terminus of the single-stranded PCR product could anneal to the normal sequence flanking the region of the mutation in the allele but not in the mutant allele. True disease status of the dogs was determined by means of a PCR and restriction digest protocol. RESULTS: Snapback SSCP analysis allowed for accurate and unambiguous genotyping of unaffected, carrier, and affected dogs, whereas conventional SSCP analysis, using the unmodified primer, did not. Creatine kinase activities measured within 24 hours after birth were not consistent with genotype. CONCLUSION AND CLINICAL RELEVANCE: Snapback SSCP analysis provided a simple, fast, and accurate method for genotyping Golden Retrievers for the mutation known to cause X-linked muscular dystrophy.     

Clinical electromyographic studies of canine X-linked muscular dystrophy

Clinical electromyographic studies were performed in dogs (6 weeks to 5.5 years old) with a degenerative myopathy analogous to Duchenne muscular dystrophy. Spontaneous activity, consisting primarily of complex repetitive discharges (pseudomyotonic discharges), was found in all dogs tested, but was most prominent in dogs greater than or equal to 10 weeks old. Myotonic discharges also were found, but were less frequent. Motor unit potentials were generally abnormally brief and frequently polyphasic. Ulnar nerve conduction velocities determined in two 4-month-old dogs were similar to those of unaffected littermates. It was concluded that canine X-linked muscular dystrophy is a primary myopathic process in which complex repetitive discharges and myotonic discharges are a prominent feature. The basis for this spontaneous activity is not known.     

Muscular dystrophy in female dogs

The most common form of muscular dystrophy in dogs and humans is caused by mutations in the dystrophin gene. The dystrophin gene is located on the X chromosome, and, therefore, disease-causing mutations in dystrophin occur most often in males. Therefore, females with dystrophin deficiency or other forms of muscular dystrophy may be undiagnosed or misdiagnosed. Immunohistochemistry was used to analyze dystrophin and a number of other muscle proteins associated with muscular dystrophy in humans, including sarcoglycans and laminin alpha2, in muscle biopsy specimens from 5 female dogs with pathologic changes consistent with muscular dystrophy. The female dogs were presented with a variety of clinical signs including generalized weakness, muscle wasting, tremors, exercise intolerance, gait abnormalities, and limb deformity. Serum creatine kinase activity was variably high. One dog had no detectable dystrophin in the muscle; another was mosaic, with some fibers normal and others partly dystrophin-deficient. A 3rd dog had normal dystrophin but no detectable laminin alpha2. Two dogs could not be classified. This study demonstrates the occurrence of dystrophin- and laminin alpha2-associated muscular dystrophy and the difficulty in clinical diagnosis of these disorders in female dogs.     

Effect of RA233 on metastasis in dogs with osteosarcomas

The influence of RA233, an inhibitor of platelet function, on the occurrence of metastasis in 18 dogs with osteosarcomas was evaluated. At least 24 hours before surgical removal of the primary tumor, dogs were given RA233 orally (20 mg/kg of body weight divided into 3 equal doses). Original sites of the osteosarcoma included humerus, 6 dogs; radius, 5 dogs; tibia, 3 dogs; femur, 2 dogs; maxilla, 1 dog; and mandible, 1 dog. Survival time for 13 dogs euthanatized for progression of neoplastic disease ranged from 3 months to 10 months, with a mean survival time of 5.5 months. Medication was discontinued in 1 dog because of possible adverse reaction. One dog died of disease unrelated to the tumor, and one dog was euthanatized after the surgery. Two dogs were tumor free 9 and 17 months after surgery. Seemingly, the metastasis potential was not diminished in dogs given 20 mg of RA233/kg/day.     

Ultrasonographic intestinal muscularis thickening in dogs with histologically confirmed inflammatory bowel disease: 13 cases (2010–2021)

Ultrasonographic intestinal muscularis thickening has not been described as an imaging feature of canine inflammatory bowel disease. In this retrospective case series, patients were identified by searching sonographic reports for “muscularis” and/or “muscular layer.” Patients were included if small intestinal muscularis thickening was reported, and sonographic images and histopathological samples of the small intestine were available for review. Cases with small intestines nodules, masses, or complete loss of wall layering were excluded. Sonographic images were retrospectively evaluated for jejunal muscularis layer thickness, and ratios of intestinal layer measurements were performed. Histological samples were retrospectively reviewed. Thirteen dogs met inclusion criteria: all dogs had sonographic intestinal muscularis thickening relative to the submucosa (>1.0, range of 1.3–2.5), and most dogs had muscular layer thickness above normal published ranges (11/13; all 13/13 above the weight-specific mean). More than half of the patients had overall normal wall thickness (11/13) and several had normal mucosal echogenicity (6/13). Therefore, in some dogs, the only sonographic abnormality in the small intestine was muscularis thickening. No dogs had lymphadenomegaly. Endoscopic partial-thickness (n = 11, duodenum and/or ileum) or surgical full-thickness (n = 2) samples confirmed inflammatory bowel disease. Direct comparison between jejunum sonographic characteristics and histology features was limited due to both partial thickness biopsies and lack of direct comparison between anatomical locations of ultrasonographic assessment and biopsy site. However, no cases that met the inclusion criteria had normal small intestinal histology. Comparable to cats, dogs with ultrasonographic intestinal muscularis thickening may have inflammatory bowel disease, and further workup for enteropathy is indicated.     

Dysphagia in Bouviers associated with muscular dystrophy; evaluation of 24 cases

Twenty-four Bouviers with dysphagia were examined between October 1986 and October 1988. The type of dysphagia was characterised by the results from the clinical examination, the videofluorographic examination and the electromyographic recordings from the oral, pharyngeal, and esophageal muscles. Electromyography indicated neurogenic as well as myogenic causes of dysphagia. Tissues from 10 dogs were available for histopathologic examination. In nine dogs there was a progressive muscular degeneration of the pharyngeal and/or esophageal muscles, resembling muscular dystrophy. In two of these dogs the same abnormalities were also noticed in the masseter and temporalis muscles and in the intrinsic laryngeal muscles. In one dog small areas with hyalin degeneration and fragmentation of muscle fibres were found in the cricopharyngeal muscle. No abnormalities in nerve tissue were found. Muscular dystrophy is a hereditary disease. The mode of transmission in these Bouviers is not yet known.     

Clinical and Radiographic Evaluation of Intertrochanteric Osteotomy in Dogs: A Retrospective Study of 18 Dogs

Objective- To determine whether intertrochanteric osteotomy (ITO) can prevent the progression of degenerative joint disease (DJD) in dysplastic hip joints.
Study Design- The results of ITO were assessed retrospectively by using owner questionnaires, physical examination, and radiographic evaluation.
Animals- Eighteen client-owned dogs (29 coxofemoral joints were evaluated).
Methods- Lameness was scored according to a grading system. A scoring system was also developed to assess radiographically evident osteoarthritis on a ventrodorsal projection of the coxofemoral joints in extension.
Results- Twenty-nine ITO were performed in 18 dogs with varying degrees of hip dysplasia. The dogs were lame on 19 of 29 rear limbs on physical examination before surgery. In 22 of the 29 hip joints, palpation caused signs of pain. The median age at the first and second surgical procedure was 14.5 months and 18 months, respectively. Follow-up evaluation was performed on average at 9.77 (FU I), 22.52 (FU II), and 47.50 months (FU in) after surgery. Based on the owners' evaluation, there was a tendency toward improvement after surgery. The results of the physical examination at the preoperative examination and at the three follow-up examinations did not differ significantly. The follow-up radiographic scores showed significantly worse DJD than the preoperative scores.
Conclusions- ITO does not prevent progression of DJD in the dysplastic hip.
Clinical Relevance- Knowledge of the long-term effects of ITO is essential for surgeons trying to achieve improvement in dogs with hip dysplasia.     

Subclinical exocrine pancreatic insufficiency in dogs

OBJECTIVE: To study progression of autoimmune-mediated atrophic lymphocytic pancreatitis from the subclinical to the clinical phase (exocrine pancreatic insufficiency [EPI]) and determine whether progression of the disease could be halted by treatment with immunosuppressive drugs. DESIGN: Randomized controlled trial. ANIMALS: 20 dogs with subclinical EPI. PROCEDURE: Diagnosis of subclinical EPI was determined on the basis of repeatedly low serum trypsin like-immunoreactivity (TLI) in dogs with no signs of EPI. Laparotomy was performed on 12 dogs with partial acinar atrophy and atrophic lymphocytic pancreatitis. A treatment group (7 dogs) received an immunosuppressive drug (azathioprine) for 9 to 18 months, and a nontreatment group (13) received no medication. RESULTS: During the subclinical phase, serum TLI was repeatedly low (< 5.0 microg/L). Although a few dogs had nonspecific gastrointestinal tract signs, they did not need diet supplementation with enzymes. While receiving immunosuppressive medication, treated dogs had no clinical signs of EPI, but within 2 to 6 months after treatment was stopped, 2 dogs had signs of EPI, and diet supplementation with enzymes was started. Five of the 13 untreated dogs needed diet supplementation with enzymes within 6 to 46 months. During follow-up of 1 to 6 years, 3 of the 7 treated dogs and 8 of the 13 untreated dogs did not need continuous diet supplementation with enzymes. CONCLUSIONS AND CLINICAL RELEVANCE: Progression of atrophic lymphocytic pancreatitis varied widely. The subclinical phase may last for years and sometimes for life. The value of early treatment with an immunosuppressive drug was questionable and, because of the slow natural progression of the disease, cannot be recommended.     

Evaluation of the 6-minute walk test in pet dogs

Background: The 6‐minute walk test (6MWT) is widely used in human medicine to objectively assess the degree of impairment, and to provide objective evidence of disease progression or response to therapy. Hypothesis/Objectives: The 6MWT will be easy to perform and well‐tolerated in pet dogs. Dogs with pulmonary disease will walk shorter distances than healthy dogs. Animals: Sixty‐nine healthy dogs were recruited from the hospital community. Six dogs with mild to moderate pulmonary disease were recruited from animals presented for evaluation at the teaching hospital. Methods: Prospective study. Dogs walked for 6 minutes in a hallway and the distance covered was measured. Pulse oximetry and heart rate were recorded before and after walking. Physical characteristics of the dogs, including age, leg length, body condition score, and weight, were recorded. Healthy dogs were compared with affected dogs by a Student's t‐test (P < .05). Correlations were calculated between the age, physical characteristics, and distances walked in the healthy dogs. Results: Healthy dogs walked 522.7 ± 52.4 m, while sick dogs (n = 6) walked 384.8 ± 41.0 m (P < .001). There was low (r= 0.13) to moderate (r= 0.27) correlation in the healthy dogs between physical characteristics and distances walked. Conclusions and Clinical Importance: The 6MWT was easy to perform and discriminated between healthy dogs and dogs with pulmonary disease.     

Kinematic analysis of the hind limb during swimming and walking in healthy dogs and dogs with surgically corrected cranial cruciate ligament rupture

OBJECTIVE: To determine hip, stifle, and tarsal joint ranges of motion (ROM) and angular velocities during swimming and walking in healthy dogs and dogs with surgically corrected cranial cruciate ligament (CCL) rupture. DESIGN: Prospective clinical study. ANIMALS: 13 healthy dogs and 7 dogs with CCL rupture. PROCEDURE: Dogs with CCL rupture were enrolled in a postoperative aquatic rehabilitation program and evaluated 21 to 35 days after surgery. Dogs were filmed while swimming in a pool and while walking at a fast (1.3 m/s) or slow (0.9 m/s) pace on a treadmill. Maximal angles of extension and flexion, ROM, and angular velocities were calculated. RESULTS: In healthy dogs, swimming resulted in a significantly greater ROM in the hip joint than did walking, but in dogs with CCL rupture, ROM of the hip joint did not vary with swimming versus walking. For dogs in both groups, swimming resulted in significantly greater ROM of the stifle and tarsal joints than did walking, primarily because of greater joint flexion. Stifle joint ROM was significantly lower in dogs with CCL rupture than in healthy dogs, regardless of whether dogs were swimming or walking. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that following surgical management of a ruptured CCL in dogs, swimming resulted in greater ROM of the stifle and tarsal joints than did walking. This suggests that if ROM is a factor in the rate or extent of return to function in these dogs, then aquatic rehabilitation would likely result in a better overall outcome than walking alone.