OBJECTIVE To estimate reliability of interpretation of neurologic examination findings for localization of vestibular dysfunction in dogs.
DESIGN Cross-sectional study.
ANIMALS 496 dogs that underwent MRI of the head for diagnosis of a neurologic problem between September 2011 and September 2015.
PROCEDURES Medical records were reviewed and data collected regarding signalment and neurologic examination, MRI, and CSF findings. Independent observers interpreted the findings, and agreement was assessed for a subset of dogs. Distributions of variables were compared between dogs with and without a neurologic findings–based interpretation of vestibular disease.
RESULTS 37% (185/496) of dogs had signs of vestibular dysfunction, of which 82% (151/185) had MRI abnormalities. In 73% (110/151) of dogs with MRI abnormalities, lesions involved central vestibular structures, and in 19% (29/151), lesions involved peripheral vestibular structures. On the basis of neurologic findings interpretation, 86% (160/185) of dogs were classified as having central vestibular dysfunction, and 61% (98/160) of these had an MRI-identified central vestibular lesion. Agreement among 3 independent observers was good (κ = 0.72) regarding use of neurologic examination findings to diagnose central versus peripheral vestibular dysfunction and very good (κ = 0.85) regarding use of MRI to diagnose peripheral vestibular lesions. Despite this agreement, only 29% (7/24) of dogs with a consensus clinical interpretation of peripheral vestibular dysfunction had MRI-identified peripheral lesions.
CONCLUSIONS AND CLINICAL RELEVANCE Although interobserver agreement was good for distinguishing central from peripheral vestibular dysfunction in dogs through interpretation of neurologic examination findings, this interpretation did not agree with the MRI-based diagnosis.
To investigate the time course of circulating neutrophil priming and activity in dogs with spinal cord injury secondary to intervertebral disk herniation that undergo decompressive surgery.
9 dogs with spinal cord injury and 9 healthy dogs (controls).
For dogs with spinal cord injury, blood samples were collected on the day of hospital admission and 3, 7, 30, and 90 days after injury and decompressive surgery. A single blood sample was collected from the control dogs. Flow cytometry analysis was performed on isolated neutrophils incubated with antibody against CD11b and nonfluorescent dihydrorhodamine 123, which was converted to fluorescent rhodamine 123 to measure oxidative burst activity.
Expression of CD11b was increased in dogs with spinal cord injury 3 days after injury and decompressive surgery, relative to day 7 expression. Neutrophils expressed high oxidative burst activity both 3 and 7 days after injury and decompressive surgery, compared with activity in healthy dogs.
For dogs with spinal cord injury, high CD11b expression 3 days after injury and decompressive surgery was consistent with findings for rodents with experimentally induced spinal cord injury. However, the high oxidative burst activity 3 and 7 days after injury and decompressive surgery was not consistent with data from other species, and additional studies on inflammatory events in dogs with naturally occurring spinal cord injury are needed.