Clinical, imaging and histopathological characterization of a series of three cats with cerebellar cortical degeneration.

BACKGROUND: Neurological inherited disorders are rare in domestic animals. Cerebellar cortical degeneration remains amongst the most common of these disorders. The condition is defined as the premature loss of fully differentiated cerebellar components due to genetic or metabolic defects. It has been studied in dogs and cats, and various genetic defects and diagnostic tests (including magnetic resonance imaging (MRI)) have been refined in these species. Cases in cats remain rare and mostly individual, and few diagnostic criteria, other than post-mortem exam, have been evaluated in reports with multiple cases. Here, we report three feline cases of cerebellar cortical degeneration with detailed clinical, diagnostic imaging and post-mortem findings. CASE PRESENTATION: The three cases were directly (siblings, case #1 and #2) or indirectly related (same farm, case #3) and showed early-onset of the disease, with clinical signs including cerebellar ataxia and tremors. Brain MRI was highly suggestive of cerebellar cortical degeneration on all three cases. The relative cerebrospinal fluid (CSF) space, relative cerebellum size, brainstem: cerebellum area ratio, and cerebellum: total brain area ratio, were measured and compared to a control group of cats and reference cut-offs for dogs in the literature. For the relative cerebellum size and cerebellum: total brain area ratio, all affected cases had a lower value than the control group. For the relative CSF space and brainstem: cerebellum area ratio, the more affected cases (#2 and #3) had higher values than the control group, while the least affected case (#3) had values within the ranges of the control group, but a progression was visible over time. Post-mortem examination confirmed the diagnosis of cerebellar cortical degeneration, with marked to complete loss of Purkinje cells and associated granular layer depletion and proliferation of Bergmann glia. One case also had Wallerian-like degeneration in the spinal cord, suggestive of spinocerebellar degeneration. CONCLUSION: Our report further supports a potential genetic component for the disease in cats. For the MRI examination, the relative cerebellum size and cerebellum: total brain area ratio seem promising, but further studies are needed to establish specific feline cut-offs. Post-mortem evaluation of the cerebellum remains the gold standard for the final diagnosis.

Iatrogenic adrenal atrophy following oral corticotherapy is not reliably identified ultrasonographically in cats.

Background: In dogs, corticosteroid administration is known to decrease adrenal gland height when measured ultrasonographically. However, comparable information is lacking in cats. Objectives: i) Validate that the adrenal height of our control population without corticosteroid administration was similar to previous data, ii) determine effects of dose and duration of oral corticosteroid therapy on adrenal height, and iii) determine an adrenal size threshold to differentiate cats receiving corticosteroids or not. Animals and procedures: Adult cats (N = 308) that received abdominal ultrasonographic examination(s) were retrospectively recruited and allocated into 2 groups: those with and without oral corticosteroid use. Cats receiving corticosteroids were subdivided into 6 subgroups by dose (supraphysiologic, anti-inflammatory, or immunosuppressive) and duration of therapy (≤ 1 mo or > 1 mo). Results: Adrenal height in cats without corticosteroid therapy was comparable to previous studies. An anti-inflammatory corticosteroid dose for > 1 mo caused a 21.4% decrease in adrenal height (mean difference of 0.8 mm; P = 0.009). However, no difference in adrenal height was noted in the other subgroups (P > 0.21), and no useful adrenal height threshold was established. Conclusion and clinical relevance: Feline iatrogenic adrenal atrophy may be difficult to establish with ultrasonography, as only cats receiving anti-inflammatory corticosteroid doses for > 1 mo had a modest (< 1 mm) decrease in adrenal height.

L'atrophie iatrogène des surrénales consécutive à une corticothérapie orale n'est pas identifiée de manière fiable par échographie chez le chat. Contexte: Chez le chien, l'administration de corticostéroïdes est connue pour diminuer la taille des glandes surrénales lorsqu'elle est mesurée par échographie. Cependant, des informations comparables manquent chez les chats. Objectifs: i) Valider que la taille des surrénales de notre population témoin sans administration de corticostéroïdes était similaire aux données précédentes, ii) déterminer les effets de la dose et de la durée de la corticothérapie orale sur la taille des surrénales, et iii) déterminer un seuil de taille des surrénales pour différencier les chats recevant des corticostéroïdes ou pas. Animaux et procédures: Des chats adultes (N = 308) qui ont subi un ou plusieurs examens échographiques abdominaux ont été recrutés rétrospectivement et répartis en 2 groupes : ceux avec et sans corticothérapie orale. Les chats recevant des corticostéroïdes ont été subdivisés en 6 sous-groupes selon la dose (supraphysiologique, anti-inflammatoire ou immunosuppresseur) et la durée du traitement (≤ 1 mois ou > 1 mois). Résultats: La taille des surrénales chez les chats sans corticothérapie était comparable à celle des études précédentes. Une dose de corticoïdes anti-inflammatoires pendant > 1 mois a entraîné une diminution de 21,4 % de la taille des surrénales (différence moyenne de 0,8 mm; P = 0,009). Cependant, aucune différence de taille surrénalienne n'a été notée dans les autres sous-groupes (P > 0,21) et aucun seuil de taille surrénalienne utile n'a été établi. Conclusion et pertinence clinique: L'atrophie surrénalienne iatrogène féline peut être difficile à établir par échographie, car seuls les chats recevant des doses de corticostéroïdes anti-inflammatoires pendant > 1 mois ont présenté une diminution modeste (< 1 mm) de la taille des surrénales.(Traduit par Dr Serge Messier).

Diffuse meningeal oligodendrogliomatosis characterized by spinal intra-parenchymal nodules on magnetic resonance imaging in a dog.

Meningeal oligodendrogliomatosis is a relatively rare neoplasm in dogs. Ante-mortem diagnosis is difficult due to nonspecific neurologic signs overlapping other conditions. The only reported consistent feature is a high level of protein in the cerebrospinal fluid. Veterinary literature offers only 1 case report with magnetic resonance imaging (MRI) of canine spinal meningeal oligodendrogliomatosis in a single dog. In contrast to the predominant diffuse meningeal enhancement shown in that report, we present the case of a young female cane corso dog with marked nodular invasion of the spinal cord on MRI, confirmed by histopathology to be consistent with diffuse meningeal oligodendrogliomatosis. Key clinical message: Meningeal oligodendrogliomatosis should be a differential diagnosis when marked nodular invasion of the spinal cord is seen on MRI, both with and without meningeal enhancement.

Oligodendrogliomatose méningée diffuse caractérisée par des nodules spinaux intraparenchymateux lors d'un examen d'imagerie par résonance magnétique chez un chien. L'oligodendrogliomatose méningée est un néoplasme relativement rare chez le chien. Son diagnostic ante-mortem est difficile en raison de signes neurologiques non spécifiques chevauchant d'autres conditions. La seule caractéristique fréquemment signalée est un niveau élevé de protéines dans le liquide céphalo-rachidien. La littérature vétérinaire ne propose qu'un seul rapport de cas illustrant des images obtenues suite à un examen d'imagerie par résonance magnétique (IRM) chez un seul chien diagnostiqué avec une oligodendrogliomatose méningée rachidienne. Contrairement au rehaussement méningé diffus prédominant montré chez ce chien, nous présentons le cas d'une jeune femelle Cane Corso avec une oligodendrogliomatose méningée diffuse confirmée à l'histopathologie, s'étant manifestée à l'IRM par une invasion nodulaire marquée de la moelle épinière.Message clinique clé:L'oligodendrogliomatose méningée doit être un diagnostic différentiel lorsqu'une invasion nodulaire marquée de la moelle épinière est observée à l'IRM, avec ou sans rehaussement méningé.(Traduit par Dre Isabelle Masseau).

Circadian and postprandial variation in plasma citrulline concentration in healthy dogs.

OBJECTIVE: To evaluate circadian and postprandial variations in plasma citrulline concentration in healthy dogs. ANIMALS: 8 healthy Beagles. PROCEDURES: Blood samples were collected from dogs after 12 hours of food withholding (0 hours; 8:00 am) and then every 2 hours for 12 hours (until 8:00 pm) and again at 24 hours (8:00 am the next day). The same protocol was repeated, with the only difference being that a meal was given immediately after the 0-hour sample collection point. Plasma citrulline concentration was measured by ion exchange chromatography. RESULTS: No significant difference in plasma citrulline concentration was identified among measurement points when food was withheld. Mean ± SD plasma citrulline concentration at 4 hours (72.2 ± 12.7 µmol/L) and 24 hours (56.1 ± 12.5 µmol/L) after dogs were fed was significantly different from that at 0 hours (64.4 ± 12.7 µmol/L). CONCLUSIONS AND CLINICAL RELEVANCE: Plasma citrulline concentration had no circadian variation in unfed dogs but increased significantly in fed dogs 4 hours after a meal. Therefore, food should be withheld from dogs for 8 to 12 hours before blood sample collection for measurement of citrulline concentration.