Background: Vestibular dysfunction is relatively common in dogs, with a prevalence of 0.08% reported in primary veterinary care in the UK. There are several studies investigating how to differentiate between peripheral and central vestibular disease but only limited information regarding the possible underlying causes for peripheral vestibular dysfunction in dogs. This study therefore aimed to describe the clinical signs, magnetic resonance imaging findings (MRI), underlying causes and outcome in a large population of dogs diagnosed with peripheral vestibular disease. Results: One hundred eighty-eight patients were included in the study with a median age of 6.9 years (range 3 months to 14.6 years). Neurological abnormalities included head tilt (n = 185), ataxia (n = 123), facial paralysis (n = 103), nystagmus (n = 97), positional strabismus (n = 93) and Horner syndrome (n = 7). The most prevalent diagnosis was idiopathic vestibular disease (n = 128), followed by otitis media and/or interna (n = 49), hypothyroidism (n = 7), suspected congenital vestibular disease (n = 2), neoplasia (n = 1) and cholesteatoma (n = 1). Long-term follow-up revealed persistence of head tilt (n = 50), facial paresis (n = 41) and ataxia (n = 6) in some cases. Recurrence of clinical signs was observed in 26 dogs. Increasing age was associated with a mild increased chance of diagnosis of idiopathic vestibular syndrome rather than otitis media and/or interna (P = 0.022, OR = 0.866; CI 0.765-0.980). History of previous vestibular episodes (P = 0.017, OR = 3.533; CI 1.251-9.981) was associated with an increased likelihood of resolution of the clinical signs whilst contrast enhancement of cranial nerves VII and/or VIII on MRI (P = 0.018, OR = 0.432; CI 0.251-0.868) was associated with a decreased chance of resolution of the clinical signs. Conclusions: Idiopathic vestibular disease is the most common cause of peripheral vestibular dysfunction in dogs and it is associated with advanced age. Incomplete recovery from peripheral vestibular disease is common, especially in dogs presenting with cranial nerve enhancement on MRI but less so if there is previous history of vestibular episodes.

Background Hypertensive or obstructive hydrocephalus is a common complication in dogs with tumors affecting the third ventricle for which few therapeutic options are available. Objectives To describe signalment, neurological status, and pre‐ and postsurgical findings, complications and survival time in 4 dogs with obstructive hydrocephalus caused by third ventricle tumors that were palliatively treated using ventriculoperitoneal shunting (VPS). Animals Four client‐owned dogs with obstructive hydrocephalus caused by tumors affecting the third ventricle. Methods Medical records were reviewed for dogs diagnosed with third ventricular tumors. Inclusion criteria were complete medical record, advanced diagnostic imaging for review, and VPS as sole surgical treatment. Results At the time of diagnosis, all patients displayed acute onset and rapidly progressive diffuse intracranial clinical signs. On advanced imaging, all dogs had a homogeneously enhancing mass occupying or collapsing the third ventricle as well as obstructive hydrocephalus. All of the dogs underwent VPS of the most dilated lateral ventricle. In 2 of the patients, intracranial hypertension followed by normotension after VPS placement was confirmed intraoperatively by means of direct intracranial pressure monitoring. Excellent clinical improvement was observed in all dogs immediately after surgery. Three patients required a second VPS in the contralateral lateral ventricle 3, 7 and 11 months after the first surgery, all of them with renewed improvement in clinical signs. Conclusion and Clinical Importance Ventriculoperitoneal shunting is a rapid and effective treatment for patients with obstructive (hypertensive) hydrocephalus caused by tumors located within the third ventricle.

Background Meningoencephalitis of unknown origin (MUO) comprises a group of debilitating inflammatory diseases affecting the central nervous system of dogs. Currently, no validated clinical scale is available for the objective assessment of MUO severity. Objectives Design a neurodisability scale (NDS) to grade clinical severity and determine its reliability and whether or not the score at presentation correlates with outcome. Animals One hundred dogs with MUO were included for retrospective review and 31 dogs were subsequently enrolled for prospective evaluation. Methods Medical records were retrospectively reviewed for 100 dogs diagnosed with MUO to identify the most frequent neurological examination findings. The NDS was designed based on these results and evaluated for prospective and retrospective use in a new population of MUO patients (n = 31) by different groups of independent blinded assessors, including calculation of interobserver agreement and association with outcome. Results The most common clinical signs in MUO patients were used to inform categories for scoring in the NDS: seizure activity, ambulatory status, posture and cerebral, cerebellar, brainstem, and visual functions. The intraclass correlation coefficient (ICC) for prospective use of the NDS was 0.83 (95% confidence interval [CI], 0.68‐0.91) indicating good agreement, and moderate agreement was found between prospective and retrospective assessors (ICC, 0.71; 95% CI, 0.56‐0.83). No association was found between NDS score and long‐term outcome. Conclusions and Clinical Importance The NDS is a novel clinical measure for objective assessment of neurological dysfunction and showed good reliability when used prospectively in MUO patients but, in this small population, no association with outcome could be identified.

A 5 mo old male golden retriever presented for evaluation of an acute onset, progressive neurologic disease. Although computed tomography (CT) was unremarkable, MRI identified an ill-defined mass located in the medulla, which was considered likely responsible for the clinical signs. The imaging features closely resembled the classic features of human brainstem gliomas in the pediatric population. Histopathologic examination confirmed the lesion to be an anaplastic oligodendroglioma.

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