@article{licht_lin_luo_hyson_licht_harper_sullivan_fernandez_johnston_2007, title={Clinical characteristics and mode of inheritance of familial focal seizures in Standard Poodles}, volume={231}, ISSN={["1943-569X"]}, DOI={10.2460/javma.231.10.1520}, abstractNote={Abstract
Objective—To determine clinical characteristics and mode of inheritance of seizures in a family of Standard Poodles.
Design—Case series.
Animals—90 Standard Poodles descended from the same maternal bloodline (30 with probable idiopathic epilepsy [PIE] and 60 without any history of seizures).
Procedures—Researchers contacted owners to determine whether dogs had ever had any seizures and, if so, the nature of any such seizures and any potential underlying causes. Dogs were considered to have PIE if they were between 6 months and 7.5 years old at the time of seizure onset and had no evidence of any underlying cause. To determine the mode of inheritance, segregation analyses were designed to allow the family to be analyzed as a whole, as opposed to as nuclear families. Competing models of inheritance were compared statistically for their ability to explain the data.
Results—Of the dogs with PIE, 28 (93%) had focal onset seizures with or without secondary generalization. Median age of onset was 3.7 years; 6 dogs were > 5 years old at the onset of seizures. Segregation analyses strongly suggested that PIE was inherited as a simple recessive autosomal trait with complete or almost complete penetrance.
Conclusions and Clinical Relevance—Results suggested that in this family of Standard Poodles, PIE was inherited as a simple recessive autosomal trait with complete or almost complete penetrance. Seizures often had focal, as opposed to generalized, onsets, and it was not uncommon for seizures to begin after 5 years of age.}, number={10}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Licht, Barbara G. and Lin, Shili and Luo, Yuqun and Hyson, Linda L. and Licht, Mark H. and Harper, Kathleen M. and Sullivan, Stacey A. and Fernandez, Soledad A. and Johnston, Eric V.}, year={2007}, month={Nov}, pages={1520–1528} }
 @article{pease_sullivan_olby_galano_cerda-gonzalez_robertson_gavin_thrall_2006, title={Value of a single-shot turbo spin-echo pulse sequence for assessing the architecture of the subarachnoid space and the constitutive nature of cerebrospinal fluid}, volume={47}, ISSN={["1740-8261"]}, DOI={10.1111/j.1740-8261.2006.00136.x}, abstractNote={Three case history reports are presented to illustrate the value of the single‐shot turbo spin‐echo pulse sequence for assessment of the subarachnoid space. The use of the single‐shot turbo spin‐echo pulse sequence, which is a heavily T2‐weighted sequence, allows for a rapid, noninvasive evaluation of the subarachnoid space by using the high signal from cerebrospinal fluid. This sequence can be completed in seconds rather than the several minutes required for a T2‐fast spin‐echo sequence. Unlike the standard T2‐fast spin‐echo sequence, a single‐shot turbo spin‐echo pulse sequence also provides qualitative information about the protein and the cellular content of the cerebrospinal fluid, such as in patients with inflammatory debris or hemorrhage in the cerebrospinal fluid. Although the resolution of the single‐shot turbo spin‐echo pulse sequence images is relatively poor compared with more conventional sequences, the qualitative information about the subarachnoid space and cerebrospinal fluid and the rapid acquisition time, make it a useful sequence to include in standard protocols of spinal magnetic resonance imaging.}, number={3}, journal={VETERINARY RADIOLOGY & ULTRASOUND}, author={Pease, A and Sullivan, S and Olby, N and Galano, H and Cerda-Gonzalez, S and Robertson, ID and Gavin, P and Thrall, D}, year={2006}, pages={254–259} }
 @article{sullivan_harmon_purinton_greene_glerum_2003, title={Lobar holoprosencephaly in a Miniature Schnauzer with hypodipsic hypernatremia}, volume={223}, DOI={10.2460/javma.2003.223.1783}, abstractNote={A 9-month-old male Miniature Schnauzer was examined because of a lifelong history of behavioral abnormalities, including hypodipsia. Diagnostic evaluation revealed marked hypernatremia and a single forebrain ventricle. The behavioral abnormalities did not resolve with correction of the hypernatremia, and the dog was euthanatized. At necropsy, midline forebrain structures were absent or reduced in size, and normally paired forebrain structures were incompletely separated. Findings were diagnostic for holoprosencephaly, a potentially genetic disorder and the likely cause of the hypodipsia. Similar evaluation of affected Miniature Schnauzer dogs may reveal whether holoprosencephaly routinely underlies the thirst deficiency that may be seen in dogs of this breed.}, number={12}, journal={JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Sullivan, SA and Harmon, BG and Purinton, PT and Greene, CE and Glerum, LE}, year={2003}, month={Dec}, pages={1783–1787} }