Magnetic resonance imaging (MRI) was performed on 50 dogs with intracranial neoplasia. The following tumor features were assessed: axial origin, location, shape, growth pattern, MRI signal intensity, evidence for edema, and paramagnetic contrast enhancement. Histologic diagnoses included 5 intracranially invading nasal tumors, 7 pituitary tumors, 22 meningiomas, 6 choroid plexus tumors, 7 astrocytomas, 1 ependymoma, and 2 oligodendrogliomas. Axial origin, site, shape, and growth pattern were important diagnostic characteristics for tumor type. Signal intensity Magnetic resonance imaging (MRI) is the preferred imaging method for human beings with central nervous system disease, and it has become increasingly available and affordable for use in veterinary medicine. The MRI features of canine neurologic disease have been described, but histologic diagnoses have not been available in all instance^.'.^ In this study, MRI scans of 50 histologically diagnosed canine intracranial tumors were evaluated retrospectively to identify distinguishing characteristics.
Materials and Methods
Selection CriteriaDogs with clinical signs of intracranial disease were referred to Washington State University Veterinary Teaching Hospital. The dogs were evaluated using a standard diagnostic protocol as part of a phase I clinical trial for boron neutron capture therapy, which was conducted with approval from the Animal Care and Use Committee.4.' Most dogs in the study had been treated with corticosteroids at the time of imaging. All patients had a complete MRI brain scan and histologic diagnosis of intracranial tumor. Patients with potential metastatic intracranial neoplasia were not included in the study.
From the
Magnetic Resonance Scan ProtocolDetails of the MRI protocol have been described previously.' Briefly, MRI was performed with a 1.5 T magnet (General Electric Signa, Milwaukee, WI). Under general anesthesia, dogs were placed in sternal recumbency, and a sagittal localizer series (time of relaxation or TR = 400 msec/time to echo or TE = 20 msec) was performed to delineate subsequent transverse images. Transverse proton density-weighted images (PDWI) and TZ-weighted images (TZWI) were obtained with a multiple spin echo series at TR = 2000 msec with TE = 20 to 30 and 80 to 90 msec. Transverse and sagittal precontrast and postcontrast T1-weighted images (T1 WI) were performed using TR = 800 msec and TE = 20 msec. Three to 5 mm slices with an interslice gap of 0 to 1.5 mm were obtained from the foramen magnum rostrally through the cribriform plate.
Magnetic resonance imaging (MRI) examinations from 18 dogs with a histologically confirmed peripheral nerve sheath tumor (PNST) of the brachial plexus were assessed retrospectively. Almost half (8/18) had a diffuse thickening of the brachial plexus nerve(s), six of which extended into the vertebral canal. The other 10/18 dogs had a nodule or mass in the axilla (1.2-338 cm3). Seven of those 10 masses also had diffuse nerve sheath thickening, three of which extended into the vertebral canal. The majority of tumors were hyperintense to muscle on T2-weighted images and isointense on T1-weighted images. Eight of 18 PNSTs had only minimal to mild contrast enhancement and many (13/18) enhanced heterogeneously following gadolinium DTPA administration. Transverse plane images with a large enough field of view (FOV) to include both axillae and the vertebral canal were essential, allowing in-slice comparison to detect lesions by asymmetry of structures. Higher resolution, smaller FOV, multiplanar examination of the cervicothoracic spine was important for appreciating nerve root and foraminal involvement. Short tau inversion recovery, T2-weighted, pre and postcontrast T1-weighted pulse sequences were all useful. Contrast enhancement was critical to detecting subtle diffuse nerve sheath involvement or small isointense nodules, and for accurately identifying the full extent of disease. Some canine brachial plexus tumors can be challenging to detect, requiring a rigorous multiplanar multi-pulse sequence MRI examination.
The clinical findings and computed tomographic and magnetic resonance images from four dogs with nasal tumors that invaded the central nervous system were revlewed. There were minimal or no clinical signs related to nasal disease. Brain imaging with magnetic resonance or computed tomography demonstrated antemortem involvement of brain and nasal structures. Magnetic resonance imaging was optimal for demonstrating this involvement and showed more detailed anatomic features of the mass and secondary pathologies attributed to the mass.
Borocaptate sodium (Na2B12HjjSH) is a boron-carrying compound under consideration for use in boron neutron capture therapy. The biodistribution of boron from borocaptate sodium adminition will partly determine boron neutron capture therapy efficacy and normal tissue radiation tolerance. The biodistribution of boron was determined in 30 dogs with spontaneous intracranial tumors at 2, 6, or 12 hr after intravenous borocaptate sodium infusion. Blood and tissue boron concentrations were measured using inductively coupled plasma atomic emission spectroscopy. Mean tumor boron concentration (mean ± standard error) was 35.9 ± 4.6 (n = 15), 22.5 ± 6.0 (n = 9), and 7.0 ± 1.1 jpg of boron per g (a = 6) at 2, 6, and 12 hr, respectively, after borocaptate sodium infusion. Peritumor boron concentrations were elevated above that of normal brain in half of the dogs. Normal brain boron concentration (mean ± standard error) was 4.0 1 0.5, 2.0 ± 0.4, and 2.0 ± 0.3 jg of boron per g at 2, 6, and 12 hr after infusion, respectively. Some cranial and systemic tissues, and blood, had high boron concentration relative to tumor tissue. Geometric dose sparing should partly offset these relatively high normal tissue and blood concentrations. Borocaptate sodium biodistribution is favorable because tumor boron concentrations of recommended magnitude for boron neutron capture therapy were obtained and there was a high tumor-to-normal brain boron concentration ratio.Boron neutron capture therapy (BNCT) is an experimental form of radiation therapy for cancer that results in targeted high linear energy transfer (LET) radiation. BNCT has a number oftheoretical advantages over conventional low LET radiation therapy and has recently been reviewed (1, 2). The localization of a boronated compound within tumor tissue is critical to the success of BNCT, and multiple compounds are under development as potential boron carriers. Promising biodistribution results were obtained with the administration of borocaptate sodium (BSH) in rodents with experimental tumors (3). BSH has low relative toxicity, is available in a standardized form, and has produced favorable results during Japanese clinical trials in humans with malignant brain tumors (4). However, few data are available on biodistribution and pharmacokinetics of BSH, and data are needed prior to approval of human pharmacokinetic trials in the United States. Studies using dogs with spontaneous brain tumors were performed to evaluate the relative biodistribution of BSH and potential implications for use of BSH for BNCT are discussed.MATERIALS AND METHODS Dogs with spontaneous intracranial tumors were referred by regional veterinary practitioners. Diagnosis of intracranial tumors was based on results of pre-and post-contrast magnetic resonance imaging and computed tomography of the brain. BSH (natural isotopic ratio: 80% 11B, 20% 10B; Callery Chemical, Pittsburgh) was administered intravenously at 55 mg of boron per kg of body weight dissolved in 11 ml of physiological saline per kg ofbody weight ...
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