Brain neoplasia is diagnosed in an increasing number of dogs. Consequently, there is a higher need for an effective treatment. Chemotherapy is considered in cases where surgery or radiation is not optional. The objective of this retrospective study was to evaluate the difference in median survival time (MST) of dogs with intracranial masses, treated symptomatically with corticosteroids and anti-epileptic drugs, compared with the same symptomatic treatment supplemented with lomustine. The records of 71 dogs with intracranial masses were retrospectively evaluated. Fifteen dogs were treated symptomatically with corticosteroids and anti-epileptics, and 56 dogs received additional therapy with lomustine. There was no statistically significant difference in MST between both groups, being 60 and 93 days, respectively. Age, duration of symptoms, intracranial localization of the mass and intra- or extra-axial localization had no influence on survival time. However, female dogs survived significantly longer than male dogs.

Feline hippocampal and piriform lobe necrosis (FHN) has been reported from several countries worldwide and is considered an important aetiology for feline epileptic seizures. The aetiology of FHN remains unclear, however it is suspected that FHN might occur secondary to intense epileptic activity as described in humans and dogs although this has not yet been documented in cats. The purpose of our report is to describe the first cases of FHN in Finland diagnosed by magnetic resonance imaging (MRI) and histopathology. The two cases we describe had a well documented history of pre-existing seizures with normal brain MRI at the onset of cluster seizures but MRI done when the cats exhibited clinical deterioration secondary to severe seizure activity, revealed lesions in the hippocampus and piriform lobes typical of FHN. Our report confirms that feline hippocampus and piriform lobe necrosis does occur in the Finnish cat population and should therefore be considered as a differential diagnosis in cats with seizures. In addition, the presentation, clinical findings, results of MRI and/or histopathology shows that cats may develop FHN secondary to severe seizure activity.

Background Naso-ethmoidal meningoencephalocele is usually a congenital anomaly consisting of a protrusion of cerebral tissue and meninges into the ethmoidal labyrinth. The condition is a rare cause of structural epilepsy in dogs. We report the clinical presentation, surgical intervention, postoperative complications and outcome in a dog with drug resistant epilepsy secondary to a meningoencephalocele. Case presentation A 3.3-year-old male neutered Tamaskan Dog was referred for assessment of epileptic seizures secondary to a previously diagnosed left-sided naso-ethmoidal meningoencephalocele. The dog was drug resistant to medical management with phenobarbital, potassium bromide and levetiracetam. Surgical intervention was performed by a transfrontal craniotomy with resection of the meningoencephalocele and closure of the dural defect. Twenty-four hours after surgery the dog demonstrated progressive cervical hyperaesthesia caused by tension pneumocephalus and pneumorrhachis. Replacement of the fascial graft resulted in immediate resolution of the dog’s neurological signs. Within 5 months after surgery the dog progressively developed sneezing and haemorrhagic nasal discharge, caused by sinonasal aspergillosis. Systemic medical management with oral itraconazole (7 mg/kg orally q12h) was well-tolerated and resulted in resolution of the clinical signs. The itraconazole was tapered with no relapsing upper airway signs. The dog’s frequency of epileptic seizures was not affected by surgical resection of the meningoencephalocele. No treatment adjustments of the anti-epileptic medication have been necessary during the follow-up period of 15 months. Conclusions Surgical resection of the meningoencephalocele did not affect the seizure frequency of the dog. Further research on prognostic factors associated with surgical treatment of meningoencephaloceles in dogs is necessary. Careful monitoring for postsurgical complications allows prompt initiation of appropriate treatment.

BackgroundNeurodegenerative diseases are a heterogeneous group of disorders characterized by loss of neurons and are commonly associated with a genetic mutation.Hypothesis/ObjectivesTo characterize the clinical and histopathological features of a novel degenerative neurological disease affecting the brain of young adult Nova Scotia Duck Tolling Retrievers (NSDTRs).AnimalsNine, young adult, related NSDTRs were evaluated for neurological dysfunction and rapid eye movement sleep behavior disorder.MethodsCase series review.ResultsClinical signs of neurological dysfunction began between 2 months and 5 years of age and were progressive in nature. They were characterized by episodes of marked movements during sleep, increased anxiety, noise phobia, and gait abnormalities. Magnetic resonance imaging documented symmetrical, progressively increasing, T2‐weighted image intensity, predominantly within the caudate nuclei, consistent with necrosis secondary to gray matter degeneration. Abnormalities were not detected on clinicopathological analysis of blood and cerebrospinal fluid, infectious disease screening or urine metabolite screening in most cases. Postmortem examination of brain tissue identified symmetrical malacia of the caudate nuclei and axonal dystrophy within the brainstem and spinal cord. Genealogical analysis supports an autosomal recessive mode of inheritance.Conclusions and Clinical ImportanceA degenerative encephalopathy was identified in young adult NSDTRs consistent with a hereditary disease. The prognosis is guarded due to the progressive nature of the disease, which is minimally responsive to empirical treatment.

Five days before referral, a 12-year-old male neutered domestic shorthair had developed an acute onset of paraplegia. The cat lived strictly indoors and no known history of trauma or intoxication was reported by the owner. The cat had never displayed similar complaints before and he seemed to be in good general condition. The blood work and thoracic and abdominal radiographs showed no significant abnormalities, except for the narrowing of the intervertebral disk (IVD) space between T9T10 and T10T11. Treatment with dexamethasone (Rapidexon; Eurovet; 0,1 mg/kg, IM) was initiated. No improvement was observed, and in fact the condition even worsened somewhat. For this reason, the cat was referred to the Neurology Department of the Faculty of Veterinary Medicine at Ghent University.No abnormalities were detected on general physical examination. During neurological examination, the cat appeared alert, but showed severe paraparesis. The cat was unable to stand up, but it was able to walk with the support of a sling, although it had an extremely ataxic, stilted gait in de pelvic limbs. Conscious proprioceptive deficits were noted in the pelvic limbs, with diminished hopping, which were worse on the left side than on the right side. The patellar reflexes were normal, while the withdrawal reflexes in the pelvic limbs were exaggerated. A crossed extensor reflex was found in the pelvic limbs. Nociception was normal in all four limbs. No neck or back pain could be elicited. The bladder function was doubtful, as the bladder was quite small but could easily be expressed manually and the cat had not urinated spontaneously. The clinical signs were ascribed to a thoracolumbar spinal cord lesion. Differential diagnoses included fibrocartilaginous embolism, myelitis caused by Feline Infectious Peritonitis (FIP) virus, neoplasia (e.g. lymphoma) of the spinal cord, spinal trauma and disk herniation.Plain and contrast radiographs were performed under general anesthesia. The patient was preme dicated with methadone (Mephenon; Federa; 0,1 mg/kg, IV). After ten minutes, the induction of anesthesia was performed with midazolam (Dormicum; Roche; 0,2 mg/kg, IV), immediately followed by propofol (Propovet; Abbott Animal Health; 3 mg/kg, IV). The cat was intubated with a 3.5 mm internal diameter endotracheal tube after 0.2 ml of lidocaine (Xylocaine 2%; AstraZeneca) was sprayed on the laryngeal mucosa to prevent the occurrence of laryngeal spasms. Anesthesia was further maintained with isoflurane in 100 oxygen, delivered by a semi-closed anesthetic rebreathing circuit.Radiographic examination of the thoracolumbar Favorable outcome of conservative treatment in a cat with T9T10 intervertebral disk diseaseSuccesvolle conservatieve behandeling van discus hernia ter hoogte van T9T10 bij een kat

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Tick-borne encephalitis (TBE) is caused by the neurotropic tick-borne encephalitis virus (TBEV). In dogs, this virus may affect the central nervous system (CNS), causing meningoencephalitis, meningomyelitis, radiculitis or any combination of these. Diagnosis of TBE relies on a combination of clinical signs of CNS disease and laboratory findings, including CSF pleocytosis and serum TBEV antibody titers. Exposure to TBEV does not necessarily cause clinical disease, and seroprevalence has been reported as high as 40% in endemic areas. This causes concerns of over-diagnosing TBE in dogs with CNS disease. By examining TBEV antibodies in dogs with and without neurological disease in a TBEV endemic area, this study aimed to evaluate the diagnostic value of TBEV antibodies in the cerebrospinal fluid (CSF) in dogs. Eighty-nine dogs were included in the study, 56 with neurological disease and 33 neurologically normal control dogs. A positive TBEV CSF and serum IgG antibody titer (> 126 U/mL) was found in 3/89 dogs (3.4%). A positive serum TBEV antibody titer was found in 11 of the 89 dogs (12.4%). None of the control dogs showed a positive CSF antibody titer, whilst two showed positive serum concentrations. A positive CSF IgG antibody titer supports a clinical diagnosis of TBE in patients with acute onset of CNS disease and may help reduce the risk of over-diagnosis.

Objectives The primary objective of this study was to investigate the prevalence of epileptic seizures and of presumed idiopathic epilepsy (PIE, describing epilepsy of unknown origin) in a cohort of British Shorthair (BSH) cats in Sweden. The secondary objective was to describe epileptic seizure characteristics and outcome for cats with PIE. Methods Owners of BSH cats born between 2006 and 2016 and registered with SVERAK (the Swedish Cat Clubs’ National Association) were invited to reply to a questionnaire about their cat’s general health. Owners who indicated that their cat had experienced epileptic seizures were invited to participate in an in-depth telephone interview about the epileptic seizures. The clinical characteristics of epileptic seizures in BSH cats were determined from the results of the interview. Results In this population comprising 1645 BSH cats (representing 28% of registered BSHs), the prevalence of epileptic seizures was 0.9% and for PIE it was 0.7%. BSH cats with PIE presented with infrequent but consistent epileptic seizures. Twenty-seven percent of BSH cats with epileptic seizures had cluster seizures but none presented with status epilepticus. None of the BSH cats was treated with antiepileptic drugs, and none of the owners reported epileptic seizure remission in their cat. Conclusions and relevance The prevalence of PIE in this population of BSH cats was 0.7%. The prevalence of epileptic seizures was 0.9%. In general, PIE in the BSH cat displayed a relatively benign phenotype where progression of epileptic seizures was uncommon.