Background: Magnetic resonance imaging (MRI) is a correlate to physical examination in various myelopathies and a predictor of functional outcome.Objectives: To describe associations among MRI features, neurological dysfunction before MRI, and functional outcome in dogs with disk herniation.Animals: One hundred and fifty-nine dogs with acute thoracolumbar disk herniation. Methods: Retrospective case series. Signalment, initial neurological function as assessed by a modified Frankel score (MFS), and ambulatory outcome at hospital discharge and 43 months (long-term) follow-up were recorded from medical records and telephone interview of owners. Associations were estimated between these parameters and MRI signal and morphometric data.Results: Dogs with intramedullary T2W hyperintensity had more severe pre-MRI MFS (median 2, range 0-4) and lower ambulatory proportion at long-term follow-up (0.76) than those dogs lacking hyperintensity (median MFS 3, range 0-5; ambulatory proportion, 0.93) (P5.001 and .013, respectively). Each unit of T2W length ratio was associated with a 1.9 times lower odds of long-term ambulation when adjusted for pre-MRI MFS (95% confidence interval 1.0-3.52, P5.05). Dogs with a compressive length ratio 41.31 (which was the median ratio within this population) had more severe pre-MRI MFS (median 3, range 0-5) compared with those with ratios 1.31 (median MFS 3, range 0-4; P5.006).Conclusions and Clinical Importance: MRI features were associated with initial injury severity in dogs with thoracolumbar disk herniation. Based on results of this study, the T2W length ratio and presence of T2W intramedullary hyperintensity appear to be predictive of long-term ambulatory status.
Twenty-one dogs with confirmed tumors of the spinal cord or paraspinal tissues were imaged with magnetic resonance (MR) imaging. Anatomical location, location in relation to the dura and the medulla (spinal cord), and bone infiltration were assessed on the MR images and compared to findings at surgery or necropsy. Localization of tumors in the intradural-extramedullary compartment was not always possible. Bone infiltration was correctly assessed in all but one dog, and the anatomical locations involved were accurately determined in all dogs. Sagittal T2-weighted images were helpful to determine the anatomical location. Transverse T1-weighted images pre and post Gd-DTPA administration were helpful for additional localization and definition of tumor extension.
A stereotactic brain biopsy system that is magnetic resonance (MR) imaging-guided has not been validated in dogs. Our purpose was to determine the mean needle placement error in the caudate nucleus, thalamus, and midbrain of a canine cadaver brain using the modified Brainsight stereotactic system. Relocatable reference markers (fiducial markers) were attached to the cadaver head using a dental bite block. A T1-weighted gradient echo three-dimensional (3D) sequence was acquired using set parameters. Fiducial markers were used to register the head to the acquired MR images in reference to a 3D position sensor. This allowed the planning of trajectory path to brain targets in real time. Coordinates (X, Y, Z) were established for each target and 0.5 microl of diluted gadolinium was injected at each target using a 26-gauge needle to create a lesion. The center of the gadolinium deposition was identified on the postoperative MR images and coordinates (X', Y', Z') were established. The precision of this system in bringing the needle to target (needle placement error) was calculated. Seventeen sites were targeted in the brain. The mean needle placement error for all target sites was 1.79 +/- 0.87 mm. The upper bound of error for this stereotactic system was 3.31 mm. There was no statistically significant relationship between needle placement error and target depth (P = 0.23). The ease of use and precision of this stereotactic system support its development for clinical use in dogs with brain lesions > 3.31 mm.
Nerve-sheath tumor was diagnosed in 10 dogs with clinical signs of unilateral trigeminal nerve dysfunction. Unilateral temporalis and masseter muscle atrophy were present in all cases. An enlarged foramen and distorted rostral petrous temporal bone were seen with computed tomography imaging in one case. Magnetic resonance imaging was used to identify the lesion accurately in seven cases. Surgery was performed for biopsy and lesion removal in three cases. Cases not treated had a progressive course eventually resulting in euthanasia or death. Of the cases treated surgically, one case is alive without disease progression 27 months after surgery. Survival times of the nontreated cases ranged from five to 21 months.
Clinical outcomes and complications of a technique used for atlantoaxial stabilization were evaluated in a group of 12 dogs. At surgery, the atlantoaxial joint was realigned and rigidly fixated using cortical bone screws, K-wire, and polymethyl methacrylate. Results in nine dogs were graded as excellent. Results in two dogs were judged as good. One dog was euthanized 17 months after surgery for recurrent cervical pain. Eight dogs had no postoperative complications. The surgical technique described provided an adaptable method for the correction of atlantoaxial instability.
The medical records and magnetic resonance (MR) images of dogs with an acquired trigeminal nerve disorder were reviewed retrospectively. Trigeminal nerve dysfunction was present in six dogs with histologic confirmation of etiology. A histopathologic diagnosis of neuritis (n=2) or nerve sheath tumor (n=4) was made. Dogs with trigeminal neuritis had diffuse enlargement of the nerve without a mass lesion. These nerves were isointense to brain parenchyma on T1-weighted (T1W) precontrast images and proton-density-weighted (PDW) images and either isointense or hyperintense on T2-weighted (T2W) images. Dogs with a nerve sheath tumor had a solitary or lobulated mass with displacement of adjacent neuropil. Nerve sheath tumors were isointense to the brain parenchyma on T1W, T2W, and PDW images. All trigeminal nerve lesions enhanced following contrast medium administration. Atrophy of the temporalis and masseter muscles, with a characteristic increase in signal intensity on T1W images, were present in all dogs.
ABSTRACT:P-glycoprotein is considered to be a major factor impeding effective drug therapy for many diseases of the central nervous system (CNS). Thus, efforts are being made to gain a better understanding of P-glycoprotein's role in drug distribution to brain parenchyma and cerebrospinal fluid (CSF). The goal of this study was to validate and introduce a novel P-glycoprotein-deficient (ABCB1-1⌬) canine model for studying P-glycoprotein-mediated effects of drug distribution to brain tissue and CSF. CSF concentrations of drug are often used to correlate efficacy of CNS drug therapy as a surrogate for determining drug concentration in brain tissue. A secondary goal of this study was to investigate the validity of using CSF concentrations of P-glycoprotein substrates to predict brain tissue concentrations. Loperamide, an opioid that is excluded from the brain by P-glycoprotein, was used to confirm a P-glycoprotein-null phenotype in the dog model. ABCB1-1⌬ dogs experienced CNS depression following loperamide administration, whereas ABCB1 wild-type dogs experienced no CNS depression. In summary, we have validated a novel P-glycoprotein-deficient canine model and have used the model to investigate transport of the P-glycoprotein substrate 99m Tc-sestamibi at the blood-brain barrier and blood-CSF barrier.
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