Transcranial photobiomodulation therapy improves cognitive test scores in dogs with presumptive canine cognitive dysfunction: A case series of five dogs.

Background: Canine cognitive dysfunction (CCD) is considered the canine version of human Alzheimer's disease (AD). As with AD, CCD is a multifactorial and progressive neurodegenerative disorder for which effective treatment options are continuously being sought. Transcranial photobiomodulation (tPBMT) or transcranial laser therapy has shown promise as a treatment for cognitive impairment in rodent AD investigations and several human AD clinical trials. Aim: The purpose of this prospective case series was to evaluate the effect of tPBMT on cognitive scores when applied to senior dogs with CCD over a 60-day period. Methods: Five senior (>9-year-old) dogs with moderate (16-33) to severe (>33) cognitive scores were enrolled. Owners were instructed on the use of a Class IM laser device and administered a specific dose of laser energy transcranially to both sides of the patient's head, three times per week for one month and two times per week for a second month. No additional therapeutic measures aimed at enhancing cognitive ability were permitted during the 60-day evaluation time. Baseline cognitive scores were compared with scores obtained at 30- and 60-days post-treatment. Results: Cognitive scores showed improvement in 4/5 dogs at 30 days (27.6% reduction) and all dogs at 60 days (43.4% reduction). There were no adverse effects attributable to tPBMT. Conclusion: Results of our small case series suggest that tPBMT may improve cognitive scores in dogs with moderate to severe CCD by 30 days of application and the improvement is sustained at 60 days. Further studies are needed to ascertain optimal tPBMT protocols for CCD.

Oral administration of an integrative supplement (CogniCaps®) improves cognitive scores in aging dogs with canine cognitive dysfunction for at least two months: An open-label investigation in 10 dogs.

Background: Canine cognitive dysfunction (CCD), the dog analog of human Alzheimer's disease (AD), is a progressive neurodegenerative condition that presents many treatment challenges. There are few effective drugs with acceptable side effects for AD/CCD, which has prompted investigation into non-drug options, collectively termed nutraceuticals. Nutraceutical supplements are conceptually divided into conventional (Western) and non-conventional (Eastern) ingredients. Many of these individual supplements have shown in vitro and/or in vivo efficacy in ameliorating neuronal damage in rodent models, and some have demonstrated positive effects on cognition in rodent models and clinical trials in dogs and humans with cognitive impairment. Aim: The purpose of this open-label clinical trial was to investigate the effect of an oral integrative (combination of conventional nutraceuticals and Chinese herbals) supplement (CogniCaps®) on cognitive scores when administered to aging dogs with CCD over a 2-month period. Methods: Ten aging (>9-year-old) dogs with moderate (16-33) cognitive scores were recruited and administered oral CogniCaps® for two months. No additional drugs or nutraceuticals directed at improving cognitive function were allowed during the study period. Baseline cognitive scores were compared with those procured at 30 and 60 days. Cognitive scores for baseline, 30- and 60-days post-treatment were compared. Results: Cognitive scores improved at 30 days (38% reduction) and 60 days (41% reduction) post-treatment (p = 0.002). Scores did not differ between 30- and 60-day assessments (p = 0.7). Conclusion: The results of this small preliminary study suggest that the integrative supplement CogniCaps® might improve cognitive scores in dogs with CCD within the first 30 days of administration and that this improvement is sustained at 60-day follow up.

Felbamate as an oral add-on therapy in six dogs with presumptive idiopathic epilepsy and generalized seizures resistant to drug therapy.

Background: Idiopathic or genetic epilepsy commonly affects dogs; affected dogs are often refractory to anti-seizure drug therapy. Felbamate is an anti-seizure drug with established pharmacokinetic and safety data for dogs, but little published evidence of efficacy for managing generalized seizures in this species. Aim: The purpose of this retrospective case series was to evaluate the clinical efficacy and tolerability of oral felbamate in six presumptive epileptic dogs experiencing generalized seizures. Methods: Medical records from six dogs with presumptive idiopathic/genetic epilepsy manifesting as generalized seizure activity, for which oral felbamate was used as an add-on treatment, were reviewed. The number of seizures recorded for the 3-month period immediately before instituting felbamate was recorded for each dog. Short-term (3 months) and long-term (6 months or greater) seizure frequency post-felbamate therapy was recorded for each dog and compared with baseline. Results: Overall, dogs experienced a reduction (82%) in seizures after adding felbamate in the short term, with 5/6 dogs (83%) classified as responders (50% or greater reduction in seizures) and 3/6 dogs (50%) attaining seizure-free status. Mean and median long-term follow-up times were 13 and 11 months, respectively (range: 6 to 23 months). Four of the 6 dogs (67%) remained drug responders at final follow-up, with an average seizure reduction of 98%, 2 of which remained seizure-free at 8 and 21 months. Two dogs (33%) experienced increased seizure activity during long-term follow-up (12 and 23 months) and were considered non-responders. The non-responder dogs had an average long-term seizure reduction of 33%. No dog experienced any obvious adverse effects associated with felbamate administration. However, one dog not included in the analysis because of insufficient (<3 month) post-felbamate follow-up, was weaned off felbamate because of suspected hepatotoxicity. Conclusion: Our small case series suggests that oral felbamate might show promise as an add-on drug for epileptic dogs experiencing generalized seizures resistant to drug therapy. These results warrant a more controlled, prospective investigation into felbamate as a therapeutic agent for canine epilepsy.

Transcranial photobiomodulation (laser) therapy for cognitive impairment: A review of molecular mechanisms and potential application to canine cognitive dysfunction (CCD).

Alzheimer's disease (AD) is a common degenerative brain disorder of aging people which shares many clinical and pathological features with canine cognitive dysfunction (CCD). CCD is considered a naturally occurring model of human AD. Transcranial photobiomodulation therapy (tPBMT), also known as transcranial laser therapy, entails delivering photons of near infrared to infrared light from the skin surface of the scalp to the underlying brain. Specific molecular cellular receptors, called chromophores, absorb this energy, and use it to initiate biological reactions with potential therapeutic benefit. Improvement in cognitive ability using tPBMT has been documented in rodent AD models and human clinical trials. The purposes of this review are to provide an overview of the suspected molecular mechanisms of action of tPBMT for the treatment of cognitive decline and to propose potential application of this treatment modality for dogs affected by CCD.

The scientific basis of acupuncture for veterinary pain management: A review based on relevant literature from the last two decades.

The practice of acupuncture is becoming increasingly popular in veterinary medicine, especially as a method of providing pain relief. Originally based on principles derived from centuries of observation, conventional scientific mechanisms of action for acupuncture as a pain-relieving modality have recently been elucidated. Acupuncture points allow access to multiple regions of the body via the peripheral nervous system and its connection with the central nervous system. Local, segmental (spinal), and suprasegmental (brain) effects of acupuncture involve enhanced release of pain-relieving endogenous substances (e.g., opioids) and mitigated release of pain-inducing substances (e.g., inflammatory cytokines). In addition, there is evidence that acupuncture can induce positive neurochemical and cytoarchitectural change in the central nervous system via the phenomenon of neuroplasticity. Electroacupuncture is considered the most effective type of acupuncture delivery, allowing for more potent and long-lasting pain relief than is achieved via other methods (e.g., dry needling). The purpose of this review article is to summarize the relevant scientific literature from the last two decades relating to the physiological mechanisms of action of acupuncture as a pain-relieving modality.

Periodontal disease is associated with cognitive dysfunction in aging dogs: A blinded prospective comparison of visual periodontal and cognitive questionnaire scores.

Background: Periodontal disease has been linked to the development of Alzheimer's disease in people. It is theorized that the chronic inflammatory condition characteristic of oral dysbiosis in patients with periodontal disease leads to disruption of the blood-brain barrier, cytotoxin- and pathogen-induced brain damage, and accumulation of neurotoxic ß-amyloid. In this inflammatory theory of Alzheimer's disease, ß-amyloid-a known antimicrobial protein-accumulates in response to oral pathogens. Canine cognitive dysfunction (CCD) is considered a naturally occurring animal model of human Alzheimer's disease. Like humans, periodontal disease is quite common in dogs; however, a link between periodontal disease and cognitive dysfunction has not been identified in this species. Aim: The purpose of this prospective investigation was to compare visual periodontal scores (from digital oral photographs) with numerical (0-54) cognitive assessment questionnaire forms in aging dogs with and without a clinical diagnosis of CCD. Methods: A visual analogue scale (0-4) was used to score the severity of periodontal disease in 21 aging dogs: 11 dogs with a clinical diagnosis of presumptive CCD and 10 dogs without a clinical history of cognitive decline. Individuals scoring the dental photographs were blinded to all case information, including cognitive assessment scores. Cognitive assessment scores were compared with periodontal disease scores for all dogs. Results: There was a significant (p < 0.05) association between periodontal and cognitive scores, with higher cognitive impairment scores being more likely in dogs with more severe periodontal disease and vice versa. No associations were identified between age and either periodontal disease or cognitive impairment. Conclusion: Although a cause-and-effect relationship between periodontal disease and cognitive impairment cannot be ascertained from this preliminary study, we established a link between these two disorders that warrants further investigation using more stringent criteria for evaluating both periodontal disease and cognitive dysfunction.

Pharmacokinetics of zonisamide after oral single dosing and multiple-dose escalation administration in domestic chickens (Gallus gallus).

BACKGROUND: There are few effective drugs for treatment of seizures in avian species. OBJECTIVES: To investigate the pharmacokinetics and safety of zonisamide in chickens. METHODS: Phase 1: chickens (n = 4) received a single oral dose of zonisamide at 20 mg/kg. Blood samples were collected intermittently for 36 hr after dosing. Phase 2: chickens (n = 8) received zonisamide in a dose escalation protocol (20, 30, 60 and 80 mg/kg orally every 12 hr). The dose was increased weekly, and peak and trough blood samples were collected on Days 1, 3, and 7 each week. Two birds were randomly euthanized at the end of each week. Plasma zonisamide concentrations were analysed using a commercial immunoassay. Drug concentration vs. time data were subjected to non-compartmental pharmacokinetic analysis. RESULTS: For Phase 1, peak plasma zonisamide (Cmax ) was 15 ± 3 µg/ml at 2 ± 1 hr (Tmax ). The disappearance half-life was 6.5 ± 1 hr. Mean plasma concentrations remained within the (human) therapeutic range (10-40 µg/ml) for 6 hr. For Phase 2 of the study, plasma concentrations of zonisamide remained within or close to the recommended mammalian therapeutic range for birds in the 20 and 30 mg/kg dose. Area under the curve (AUC) and Cmax were dose dependent. Two birds developed immune-mediated haemolytic anaemia. CONCLUSIONS: Zonisamide appears to be a viable drug for use in chickens at a dose of 20 mg/kg orally every 12 hr.

Little brainiacs and big dummies: Are we selecting for stupid, stout, or small dogs?

Background: Brain size has been associated with intelligence of various orders and families of animals, leading to the concept of encephalization. Brain size scales with body weight between species within mammals to approximately the 0.67 power. However, within species, this scaling exponent appears to be much smaller (approximately 0.27 power). Aim: We examined whether this relationship has persisted in dogs over the 120 years since this was originally observed. Methods: Comparative cross-sectional study of magnetic resonance imaging (MRI) data obtained from 127 dogs, compared to historical data from 157 dogs and 24 non-dog canid species. Results: Brain size in dogs measured by MRI had a scaling exponent virtually identical to that observed previously (0.24 vs. 0.26). However, the proportionality constant was smaller, suggesting that dogs in the study cohort had relatively smaller brains than the historical cohort. Absolute brain size appeared to have both a lower and upper limit in dogs. When compared to non-dogs canids, the most appropriate "representative" size for a "typical dog" when examining allometric scaling across Canidae appeared to be approximately 10-15 kg. Conclusions: We interpreted the slight reduction in relative brain size to be a function of increased obesity in the study cohort compared to dogs examined 120 years ago. Further, we suggest that dog brains have a finite lower size limit. Finally, concepts of encephalization should not be applied to dogs.

Intravenous Ketamine Bolus(es) for the Treatment of Status Epilepticus, Refractory Status Epilepticus, and Cluster Seizures: A Retrospective Study of 15 Dogs.

Status epilepticus (SE) and cluster seizures (CS) are common occurrences in veterinary neurology and frequent reasons of admission to veterinary hospitals. With prolonged seizure activity, gamma amino-butyric acid (GABA) receptors (GABAa receptors) become inactive, leading to a state of pharmacoresistance to benzodiazepines and other GABAergic medications, which is called refractory status epilepticus (RSE). Prolonged seizure activity is also associated with overexpression of N-methyl-D-aspartic (NMDA) receptors. Rodent models have shown the efficacy of ketamine (KET) in treating RSE, and its use has been reported in one canine case of RSE. Boluses of KET 5 mg/kg IV have become the preferred treatment for RSE in our hospital. A retrospective study was performed to evaluate and report our experience with KET IV bolus to treat prolonged and/or repeated seizure activity in cases of canine CS, SE, and RSE. A total of 15 dogs were retrieved, for 20 hospitalizations and 28 KET IV injections over 3 years. KET IV boluses were used 12 times for RSE (9 generalized seizures, 3 focal seizures) and KET terminated the episode of RSE 12/12 times (100%); however, seizures recurred 4/12 times (33%) within ≤6 h of KET IV bolus. When used for CS apart from episodes of RSE, KET IV bolus was associated with termination of the CS episode only 4/14 times (29%). Only 4/28 (14%) KET IV boluses were associated with adverse effects imputable only to the use of KET. One dog experienced a short, self-limited seizure activity during administration of KET IV, which was most likely related to a pre-mature use of KET IV (i.e., before GABAergic resistance and NMDA receptor overexpression had taken place). This study indicates that KET 5 mg/kg IV bolus may be successful for the treatment of RSE in dogs.

Canine cognitive dysfunction patients have reduced total hippocampal volume compared with aging control dogs: A comparative magnetic resonance imaging study.

Background: Hippocampal atrophy is a key pathologic and magnetic resonance imaging (MRI) feature of human Alzheimer's disease (AD). Hippocampal atrophy has not been documented via MRI in canine cognitive dysfunction (CCD), which is considered as the dog model of human AD. Aim: The purpose of this retrospective comparative volumetric MRI study was to compare total hippocampal volumes between successfully aging (control) dogs and dogs diagnosed with CCD. Methods: Mimics® software was used to derive total hippocampal volumes and total brain volumes from the MRI studies of 42 aging dogs (≥ 9 years): 16 dogs diagnosed with CCD and 26 successfully aging controls. Hippocampal volumes were normalized to total brain volume and these values were compared between groups using Mann-Whitney U tests. Results: Total hippocampal volume normalized to total brain volume was significantly less for CCD patients compared with control dogs (p = 0.04). Conclusion: The results of this study suggest that - similar to human AD - hippocampal atrophy is a pathological feature of CCD. This finding has potential importance for both investigating disease mechanisms related to dementia as well as future hippocampal-targeted therapies.

In vivo detection of microstructural spinal cord lesions in dogs with degenerative myelopathy using diffusion tensor imaging.

BACKGROUND: Degenerative myelopathy (DM) in dogs is a progressive neurodegenerative condition that causes white matter spinal cord lesions. These lesions are undetectable on standard magnetic resonance imaging (MRI), limiting diagnosis and monitoring of the disease. Spinal cord lesions cause disruption to the structural integrity of the axons causing water diffusion to become more random and less anisotropic. These changes are detectable by the technique of diffusion tensor imaging (DTI) which is highly sensitive to diffusion alterations secondary to white matter lesion development. OBJECTIVE: Perform spinal DTI on cohorts of dogs with and without DM to identify if lesions caused by DM will cause a detectable alteration in spinal cord diffusivity that correlates with neurological status. ANIMALS: Thirteen dogs with DM and 13 aged-matched controls. METHODS: All animals underwent MRI with DTI of the entire spine. Diffusivity parameters fractional anisotropy (FA) and mean diffusivity (MD) were measured at each vertebral level and statistically compared between groups. RESULTS: Dogs with DM had significant decreases in FA within the regions of the spinal cord that had high expected lesion load. Decreases in FA were most significant in dogs with severe forms of the disease and correlated with neurological grade. CONCLUSIONS AND CLINICAL IMPORTANCE: Findings suggest that FA has the potential to be a biomarker for spinal cord lesion development in DM and could play an important role in improving diagnosis and monitoring of this condition.

Interthalamic adhesion size in aging dogs with presumptive spontaneous brain microhemorrhages: a comparative retrospective MRI study of dogs with and without evidence of canine cognitive dysfunction.

OBJECTIVE: Spontaneous brain microhemorrhages in elderly people are present to some degree in Alzheimer's disease patients but have been linked to brain atrophy in the absence of obvious cognitive decline. Brain microhemorrhages have recently been described in older dogs, but it is unclear whether these are associated with brain atrophy. Diminution of interthalamic adhesion size-as measured on MRI or CT-has been shown to be a reliable indicator of brain atrophy in dogs with canine cognitive dysfunction (CCD) in comparison with successfully aging dogs. We hypothesized that aging dogs with brain microhemorrhages presenting for neurologic dysfunction but without obvious features of cognitive decline would have small interthalamic adhesion measurements, like dogs with CCD, compared with control dogs. The objective of this study was to compare interthalamic adhesion size between three groups of aging (>9 years) dogs: (1) neurologically impaired dogs with presumptive spontaneous brain microhemorrhages and no clinical evidence of cognitive dysfunction (2) dogs with CCD (3) dogs without clinical evidence of encephalopathy on neurologic examination (control dogs). MR images from 52 aging dogs were reviewed and measurements were obtained of interthalamic adhesion height (thickness) and mid-sagittal interthalamic adhesion area for all dogs, in addition to total brain volume. Interthalamic adhesion measurements, either absolute or normalized to total brain volume were compared between groups. Signalment (age, breed, sex), body weight, presence and number of SBMs, as well as other abnormal MRI findings were recorded for all dogs. RESULTS: All interthalamic adhesion measurement parameters were significantly (P < 0.05) different between control dogs and affected dogs. Both dogs with cognitive dysfunction (12/15; 80%) and dogs with isolated brain microhemorrhages had more microhemorrhages than control dogs (3/25; 12%). Affected dogs without cognitive dysfunction had significantly more microhemorrhages than dogs with cognitive dysfunction. In addition to signs of cognitive impairment for the CCD group, main clinical complaints for SBM and CCD dogs were referable to central vestibular dysfunction, recent-onset seizure activity, or both. Geriatric dogs with spontaneous brain microhemorrhages without cognitive dysfunction have similar MRI abnormalities as dogs with cognitive dysfunction but may represent a distinct disease category.

Efficacy of frameless stereotactic radiotherapy for the treatment of presumptive canine intracranial gliomas: A retrospective analysis (2014-2017).

The use of conventional multi-fractionated radiotherapy for the treatment of glial tumours is well documented in the literature. Recently, stereotactic radiotherapy (SRT) has become more widely available allowing for hypo-fractionated protocols; however, its usefulness in the treatment of canine intracranial gliomas is largely undetermined. We conducted a retrospective analysis, including 21 dogs diagnosed with presumptive intracranial gliomas treated with one or more courses of three fractions of 8 to 10 Gy CyberKnife SRT. The objective of this study was to evaluate the efficacy, safety and prognostic factors associated with the use of SRT for the treatment of canine intracranial gliomas. Overall MST for all dogs was 636 days (d). Dogs treated with one course of the described SRT protocol had a MST of 258 days while those treated with >1 course had a MST of 865 days (P = .0077 log rank, 0.0139 Wilcoxon). Dogs treated with one course of SRT who received adjuvant chemotherapy had a MST of >658 days and lived significantly longer than those who did not receive chemotherapy (MST, 230 days) (P = .0414 log rank, 0.0453 Wilcoxon). The most common adverse event included presumptive transient demyelination in 3/21 dogs, which was treated successfully with corticosteroids in all patients. This study provides evidence that SRT is effective in prolonging survival in dogs with intracranial gliomas, and may provide similar results to conventional fractionated protocols, while decreasing the number of hospital visits and anaesthetic episodes. Additionally, it appears that patients can be safely treated with multiple rounds of SRT resulting in improved survival times.

Histological, electrophysiological and clinical effects of thermal radiofrequency therapy of the saphenous nerve and pulsed radiofrequency therapy of the sciatic nerve in dogs.

OBJECTIVE: Thermal radiofrequency (TRF) of the saphenous nerve (a sensory nerve) combined with pulsed radiofrequency (PRF) of the sciatic nerve (a sensory and motor nerve) might relieve intractable stifle osteoarthritis (OA) pain in dogs. The objective was to determine if saphenous nerve TRF induces Wallerian degeneration and if sciatic nerve PRF induces degeneration or dysfunction. STUDY DESIGN: Blinded, controlled, randomized, preclinical study. ANIMALS: A group of six intact, female Beagle dogs aged 14-16 months. METHODS: In each dog, one pelvic limb was assigned randomly to the control group and the other to the treatment group. Dogs were anesthetized and, using ultrasonography, radiofrequency electrodes were positioned adjacent to saphenous and sciatic nerves bilaterally; TRF and PRF were performed only in the treatment limb. Motor nerve conduction velocity (MNCV) was measured in both sciatic nerves 2 weeks later, and the dogs were euthanized. Hematoxylin and eosin-stained sections of saphenous and sciatic nerves were examined using light microscopy. Degeneration and inflammation were scored 0 (none) to 3 (severe). A one-tailed, paired Wilcoxon signed-rank test was used to test for differences in scores and MNCV between control and treatment nerves. RESULTS: Degeneration and inflammation scores were higher in treatment saphenous nerves in 5/6 dogs [83%; 95% confidence interval (CI), 36%, 99%]; however, after Bonferroni correction only degeneration score was higher (p = 0.0313). Degeneration, inflammation or decreased MNCV were not observed in sciatic nerves (each outcome: 0/6 nerves, 0%; 95% CI, 0%, 48%). No dogs experienced postprocedural pain or neurological deficits. CONCLUSIONS AND CLINICAL RELEVANCE: The degeneration in TRF-treated saphenous nerves appears sufficient to impair transmission. Sciatic nerve PRF did not cause degeneration with attendant motor deficits, consistent with a proposed neuromodulatory mechanism. A clinical trial is needed to confirm the combined techniques produce analgesia without motor deficits in dogs with stifle OA.

Canine Cognitive Dysfunction: Pathophysiology, Diagnosis, and Treatment.

Canine cognitive dysfunction (CCD) is the canine analog of human Alzheimer disease (AD). The pathophysiology of CCD/AD is multifaceted. CCD is common in aged (>8 years) dogs, affecting between 14% and 35% of the pet dog population. Apparent confusion, anxiety, disturbance of the sleep/wake cycle, and decreased interaction with owners are all common clinical signs of CCD. Although there is no cure for CCD, several proven effective therapeutic approaches are available for improving cognitive ability and maintaining a good quality of life; instituting such therapies early in the disease course is likely to have the greatest positive clinical effect.

Pharmacokinetics of Single-Dose Oral Pregabalin Administration in Normal Cats.

Objective: To describe the pharmacokinetic parameters of oral pregabalin in normal cats after single oral dosing. Animals: Six healthy adult research cats. Procedures: Following sedation and indwelling catheter placement, one oral (4 mg/kg) dose of pregabalin was administered. Blood samples were collected at 0, 15 and 30 min and 1, 1.5, 2, 3, 4, 6, 8, 12, 24, and 36 h after administration. Plasma pregabalin concentrations were measured by high-performance liquid chromatography and subjected to pharmacokinetic analysis using commercial software. Results: Four of six cats developed moderate sedation after pregabalin administration. The peak pregabalin concentration was 8.3 ± 1.6 µg/ml which occurred at 2.9 ± 1.2 h. Elimination half-life was 10.4 ± 2.6 h and area under the curve was 133.9 ± 71.5 µg-h/ml. Time above the minimum therapeutic concentration for seizure control in dogs and people (2.8 µg/ml) was 17.6 ± 6.2 h. Using these data, predicted minimum, maximum and average steady state concentrations were calculated for 12 and 24 h dosing intervals. Conclusions and Clinical Relevance: Pregabalin (4 mg/kg) administered orally to cats results in plasma concentrations within the range considered to be efficacious for seizure control in dogs and humans between 1.5 and at least 12 h. Because of moderate sedative side effects in the majority of cats at this dose and high calculated maximum steady state concentrations, a lower dose, given more frequently (1-2 mg/kg q 12 h), should be evaluated in prospective clinical studies.

Histopathologic characteristics of biopsies from dogs undergoing surgery with concurrent gross splenic and hepatic masses: 125 cases (2012-2016).

OBJECTIVE: To investigate the histopathologic characteristics of concurrent splenic and liver masses in dogs undergoing splenectomy and liver mass biopsy/resection. Medical records of 125 client-owned dogs found to have splenic mass or masses and a liver mass or masses during surgery were examined. Signalment (age, sex, breed), body weight, and results of histopathology were recorded for all dogs. RESULTS: Twenty-seven percent (34/125) of the dogs in this study had no evidence of malignancy in either the liver or the spleen. Sixty of 125 dogs (48.0%) had malignancy in the spleen and liver, and 56 (56/60, 93.3%) of those dogs had the same malignancy in both organs. Signalment was similar to that in other reports of splenic pathology. In this clinical population of dogs, 27% of dogs with concurrent gross splenic and liver masses discovered intraoperatively had benign lesions in both locations and therefore had a favorable prognosis.

A Subset of Dogs with Presumptive Idiopathic Epilepsy Show Hippocampal Asymmetry: A Volumetric Comparison with Non-Epileptic Dogs Using MRI.

MRI-acquired volumetric measurements from 100 dogs with presumptive idiopathic epilepsy (IE) and 41 non-epileptic (non-IE) dogs were used to determine if hippocampal asymmetry exists in the IE as compared to the non-IE dogs. MRI databases from three institutions were searched for dogs that underwent MRI of the brain and were determined to have IE and those that were considered non-IE dogs. Volumes of the right and left hippocampi were measured using Mimics® software. Median hippocampal volumes of IE and non-IE dogs were 0.47 and 0.53 cm3, respectively. There was no significant difference in overall hippocampal volume between IE and non-IE dogs; however, IE dogs had greater hippocampal asymmetry than non-IE dogs (P < 0.012). A threshold value of 1.16 from the hippocampal ratio had an 85% specificity for identifying IE-associated asymmetry. Thirty five percent of IE dogs had a hippocampal ratio >1.16. Asymmetry was not associated with any particular hemisphere (P = 0.67). Our study indicates that hippocampal asymmetry occurs in a subset of dogs with presumptive idiopathic/genetic epilepsy, suggesting a structural etiology to some cases of IE.

Transnasal, Endoscopically Guided Skull-Based Surgery by Pharyngotomy for Mass Removal from the Sphenopalatine Sinus in a Horse.

OBJECTIVE: To report a transnasal, endoscopically guided ventral surgical approach for accessing the cranial and caudal segments of the sphenopalatine sinus for mass removal in a horse. STUDY DESIGN: Case report. ANIMAL: Adult horse with acute onset blindness referable to a soft tissue mass within the sphenopalatine sinus. CLINICAL REPORT: A 7-year-old Warmblood gelding presented with a history of running into a fence and falling. No neurologic signs were identified at initial examination but acute blindness was noted 3 weeks later. On computed tomography (CT) the sphenopalatine sinus was filled with a large homogeneous mass with poor contrast enhancement that extended dorsally with thinning to the dorsal cortex of the sphenoid bone, just rostral to the entrance of the optic canals into the cranial cavity. Surgical access to the sphenopalatine sinus was achieved using a transnasal, endoscopically guided ventral pharyngotomy approach and the mass lesion was removed. A presumptive diagnosis of chondroma was made based on histopathology. The horse recovered well from surgery, and although it has not regained vision as of 6.5 years postoperatively, the disease has not progressed. CONCLUSION: Transnasal, endoscopically-guided ventral surgical access to the sphenopalatine sinus is possible in horses and may improve access in horses with disease extending caudally beyond the palatine portion of the sinus. Use of smaller diameter or specialized instruments, such as various endoscopic bone cutting instruments, and CT image guidance may improve sinus access by this route.