MAGNETIC RESONANCE IMAGING FEATURES OF ORBITAL INFLAMMATION WITH INTRACRANIAL EXTENSION IN FOUR DOGS

This retrospective study describes the clinical and magnetic resonance (MR) imaging features of chronic orbital inflammation with intracranial extension in four dogs (two Dachshunds, one Labrador, one Swiss Mountain). Intracranial extension was observed through the optic canal (n=1), the orbital fissure (n=4), and the alar canal (n=1). On T1-weighted images structures within the affected skull foramina could not be clearly differentiated, but were all collectively isointense to hypointense compared with the contralateral, unaffected side, or compared with gray matter. On T2-, short tau inversion recovery (STIR)-, or fluid-attenuated inversion recovery (FLAIR)-weighted images structures within the affected skull foramina appeared hyperintense compared with gray matter, and extended with increased signal into the rostral cranial fossa (n=1) and middle cranial fossa (n=4). Contrast enhancement at the level of the affected skul foramina as well as at the skull base in continuity with the orbital fissure was observed in all patients. Brain edema or definite meningeal enhancement could not be observed, but a close anatomic relationship of the abnormal tissue to the cavernous sinus was seen in two patients. Diagnosis was confirmed in three dogs (one cytology, two biopsy, one necropsy) and was presumptive in one based on clinical improvement after treatment. This study is limited by its small sample size, but provides evidence for a potential risk of intracranial extension of chronic orbital inflammation. This condition can be identified best by abnormal signal increase at the orbital fissure on transverse T2-weighted images, on dorsal STIR images, or on postcontrast transverse or dorsal images.     

INCOMPLETE OSSIFICATION OF THE ATLAS IN DOGS WITH CERVICAL SIGNS

Osseous defects affecting the atlas were identified in computed tomography and magnetic resonance images of five dogs with cervical signs including pain, ataxia, tetraparesis, or tetraplegia. Osseous defects corresponded to normal positions of sutures between the halves of the neural arch and the intercentrum, and were compatible with incomplete ossification. Alignment between the portions of the atlas appeared relatively normal in four dogs. In these dogs the bone edges were smooth and rounded with a superficial layer of relatively compact cortical bone. Displacement compatible with unstable fracture was evident in one dog. Concurrent atlantoaxial subluxation, with dorsal displacement of the axis relative to the atlas, was evident in four dogs. Three dogs received surgical treatment and two dogs were treated conservatively. All dogs improved clinically. Incomplete ossification of the atlas, which may be associated with atlantoaxial subluxation, should be considered in the differential diagnosis of dogs with clinical signs localized to the cranial cervical region.     

COMPUTED TOMOGRAPHY VARIATIONS IN MORPHOLOGY OF THE CANINE ATLAS IN DOGS WITH AND WITHOUT ATLANTOAXIAL SUBLUXATION

Computed tomography images of 120 dogs were reviewed to characterize variations in atlas morphology, and to identify breed‐specific morphologic features. The neural arch of the atlas was thicker in large dogs and male dogs than in small dogs, having a layer of trabecular bone between the inner and outer layers of compact bone. The transverse processes of the atlas were relatively longer in large dogs than in small dogs. Twelve (10%) dogs had incomplete ossification of the atlas. Incomplete ossification of the atlas was associated with gun dogs. Eight dogs had atlantoaxial subluxation. All eight dogs with atlantoaxial subluxation had cervical signs, whereas none of the seven dogs with incomplete ossification of the atlas unaccompanied by atlantoaxial subluxation had clinical signs referable to that area. Of five dogs with both atlantoaxial subluxation and incomplete ossification of the atlas, four had osseous defects affecting both the intercentrum and neural arch, and one had only an osseous defect affecting the neural arch. There was a strong association between incomplete ossification of the atlas and atlantoaxial subluxation (odds ratio 35.0, 95% CI 7.0–175, P=0.00002), which supports the hypothesis that incomplete ossification of the atlas predisposes dogs to atlantoaxial subluxation.