Comparison between cerebrospinal fluid and serum lactate concentrations in neurologic dogs with and without structural intracranial disease.

The objectives of this study were to investigate the relationship between cerebrospinal fluid lactate and serum concentrations in dogs with clinical signs of central nervous system disease and to establish if cerebrospinal fluid lactate (CSF) concentrations are higher in dogs with structural intracranial disease (Group Pos-MRI) compared to dogs that have clinical signs of intracranial disease but no structural brain disease (Group Neg-MRI) based on magnetic resonance imaging (MRI) findings. Using a prospective study canine blood and cerebrospinal fluid were collected in 24 dogs with neurological signs after undergoing brain MRI. Dogs were divided in 2 groups. No significant difference between serum lactate (1.57 ± 0.9 mmol/L) and CSF lactate concentration (1.34 ± 0.3 mmol/L) was detected. There was a direct correlation between CSF and serum lactate concentration (R = 0.731; P = 0.01). No significant difference was found in CSF lactate concentration between the 2 groups of dogs (P = 0.13).

Les objectifs de la présente étude étaient d'examiner la relation entre les concentrations de lactate du liquide céphalo-rachidien (LCR) et du sérum chez des chiens présentant des signes cliniques de pathologie du système nerveux central et établir si les concentrations de lactate du LCR sont plus élevées chez les chiens avec une maladie intracrânienne structurale (Groupe Pos-IRM) comparativement à des chiens avec des signes cliniques de maladie intracrânienne mais sans maladie structurale du cerveau (Groupe Nég-IRM) sur la base des trouvailles en imagerie par résonnance magnétique (IRM). Utilisant une étude prospective, du sang canin et du LCR ont été prélevés chez 24 chiens avec des signes neurologiques après un examen par IRM du cerveau. Les chiens ont été séparés en deux groupes. Aucune différence significative ne fut détectée entre les concentrations de lactate sérique (1,57 ± 0,9 mmol/L) et de lactate du LCR (1,34 ± 0,3 mmol/L). Il y avait une corrélation directe entre les concentrations de lactate du LCR et du sérum (R = 0,731; P = 0,01). Aucune différence significative dans la concentration de lactate du LCR ne fut trouvée entre les deux groupes de chiens (P = 0,13).(Traduit par Docteur Serge Messier).

Evaluation of central vestibular syndrome in dogs using brainstem auditory evoked responses recorded with surface electrodes / Avaliação da síndrome vestibular central em cães usando respostas evocadas auditivas do tronco cerebral gravadas com eletrodos de superfície

The present study aimed to analyse the wave morphology, amplitude, latency, and intervals of the brainstem auditory evoked responses (BAERs) in dogs with central vestibular syndrome (CVS) recorded with surface electrodes. Ten dogs with CVS were examined by mono- and binaural stimulation, using the Neuropack electrodiagnostic system, with stimulus intensities of 90 dBSPL. BAERs examinations revealed morphological changes of waves I, II, III, and V and decreased amplitudes of all waves in 7/10 dogs. P values obtained were = 0.014 for wave I amplitude, 0.031 for II, and III and 0.032 for V. Comparing the latencies of waves I, II, III, and V generated by right and left monoaural stimulation in dogs with CVS, we did not observe significant differences (P > 0.05). No statistical differences were observed for BAERs latencies of the waves recorded after binaural and monaural stimulation (left or right). As far as we know, this is the first study of BAERs using surface electrodes, obtained from dogs with CVS.(AU)

Este estudo destina-se à análise da morfologia, da amplitude, da latência e do intervalo das ondas das respostas evocadas auditivas no tronco cerebral (BAERs) em cães com síndrome vestibular central (CVS) registrados com eletrodos de superfície. Dez cães com CVS foram examinados por estimulação mono e binaural usando um sistema de eletrodiagnóstico Neuropack, com intensidade do estímulo de 90 dBSPL. Os exames BAERs relevaram alterações morfológicas das ondas I, II, III e V, bem como baixas amplitudes para todas as ondas no caso dos 7/10 cães. Os valores de P obtidos foram = 0.014 para ampitude da onda I, 0.031 para a II e 0.032 para a V. Compararam-se as latências das ondas I, II, III e V geradas pelo estímulo monoaural direito e esquerdo em cães com CVS e não foram constatadas diferenças significativas (P > 0.05). Igualmente não foram observadas diferenças estatísticas no caso das latências BAERs no que diz respeito às ondas gravadas depois de estímulos binaural e monoaural (esquerdo ou direito). Pelo que é de conhecimento dos autores da presente pesquisa, este é o primeiro estudo sobre BAERs usando eletrodos de superfície obtidos em cães com CVS.(AU)

Fatiga auditiva / Auditory fatigue

Introducción y objetivos: Ante posibles pérdidas de audición a causa de sobrecargas sonoras y la escasa referencia de procedimientos objetivos para su estudio, aportamos una técnica que suministra datos precisos sobre el perfil audiométrico y el factor reclutamiento. El objetivo del estudio es la determinación de la fatiga auditiva temporal a través de la respuesta microfónica coclear ante estímulos de sobrecarga de presión sonora y medida del tiempo de recuperación. Material y método: Instrumentación específica para el estudio de microfónicos cocleares, más un generador que nos proporciona estímulos sonoros de diversa intensidad y componente armónico. Utilizamos ratas Wistar. Medimos la respuesta microfónica normal y después el efecto que sobre ella ha ejercido la aportación de sobrecarga acústica. Resultados: Utilizando un tono puro a 60 dB obtenemos una respuesta microfónica. Fatigando de inmediato con 100 dB en la misma frecuencia, a los 15 min obtenemos una pérdida de 11 dB, a partir de los cuales el deterioro se lentifica y no supera los 15 dB. Mediante sonidos de banda compleja aleatoria o ruido blanco no se produce fatiga ni a niveles de 100 dB durante una hora de sobreestímulo. Conclusiones: No existe fatiga a nivel de los receptores sensoriales. El deterioro de la respuesta mediante intenso sobreestímulo posiblemente se deba a alteraciones bioquímicas de desensibilización por agotamiento. La fatiga auditiva en pruebas clínicas subjetivas afecta a tramos supracocleares. Las pruebas de fatiga auditiva encontradas no coinciden con las obtenidas subjetivamente en clínica ni en psicoacústica (AU)

Introduction and objectives: Given the relevance of possible hearing losses due to sound overloads and the short list of references of objective procedures for their study, we provide a technique that gives precise data about the audiometric profile and recruitment factor. Our objectives were to determine peripheral fatigue, through the cochlear microphonic response to sound pressure overload stimuli, as well as to measure recovery time, establishing parameters for differentiation with regard to current psychoacoustic and clinical studies. Material and method: We used specific instruments for the study of cochlear microphonic response, plus a function generator that provided us with stimuli of different intensities and harmonic components. In Wistar rats, we first measured the normal microphonic response and then the effect of auditory fatigue on it. Results: Using a 60 dB pure tone acoustic stimulation, we obtained a microphonic response at 20 dB. We then caused fatigue with 100 dB of the same frequency, reaching a loss of approximately 11 dB after 15 minutes; after that, the deterioration slowed and did not exceed 15 dB. By means of complex random tone maskers or white noise, no fatigue was caused to the sensory receptors, not even at levels of 100 dB and over an hour of overstimulation. Conclusions: No fatigue was observed in terms of sensory receptors. Deterioration of peripheral perception through intense overstimulation may be due to biochemical changes of desensitisation due to exhaustion. Auditory fatigue in subjective clinical trials presumably affects supracochlear sections. The auditory fatigue tests found are not in line with those obtained subjectively in clinical and psychoacoustic trials (AU)

Facial paralysis and vestibular syndrome in feedlot cattle in Argentina / Paralisia facial e síndrome vestibular de bovinos em confinamento

This paper reports 6 outbreaks of neurological disease associated with paralysis of the facial and vestibulocochlear nerves caused by intracranial space occupying lesions in feedlot cattle. The clinical signs observed were characterized by head tilt, uni or bilateral drooping and paralysis of the ears, eyelid ptosis, keratoconjunctivitis, and different degrees of ataxia. Morbidity and mortality rates ranged from 1.1 to 50 percent and 0 to 1 percent, respectively. Gross lesions observed included yellow, thickened leptomeninges, and marked enlargement of the roots of cranial nerves VII (facial) and VIII (vestibulocochlear). Histopathologically, there was severe, chronic, granulomatous meningitis and, in one case, chronic, granulomatous neuritis of the VII and VIII cranial nerves. Attempts to identify bacterial, viral, or parasitic agents were unsuccessful. Based on the morphologic lesions, the clinical condition was diagnosed as facial paralysis and vestibular syndrome associated with space occupying lesions in the meninges and the cranial nerves VII and VIII. Feedlot is a practice of growing diffusion in our country and this is a first report of outbreaks of facial paralysis and vestibular disease associated with space occupying lesions in Argentina.

Descrevem-se 6 surtos de uma doença neurológica com paralisia dos nervos facial e vestibulo-coclear causada por lesões intracraniais que ocupam espaço em bovinos em confinamento. Os sinais clínicos foram desvio da cabeça, queda e paralisia das orelhas, ptose palpebral, ceratoconjuntivite e diferentes graus de ataxia. As taxas de morbidade e mortalidade foram de 1.1 por cento-50 por cento e de 0-1 por cento, respectivamente. As lesões macroscópicas incluíram engrossamento das meninges, que se apresentavam amareladas, e marcado engrossamento das raízes dos nervos cranianos VII (facial) e VIII (vestíbulo-coclear). Histologicamente observaram-se meningite crônica granulomatosa e, em um caso, neurite granulomatosa crônica do VII e VIII pares cranianos. Cultivos para bactérias ou vírus resultaram negativos. De acordo com as lesões observadas o quadro clínico foi diagnosticado como paralisia facial e síndrome vestibular associadas a lesões que ocupam espaço nas meninges e nervos cranianos VII e VIII. O confinamento é uma prática em expansão na Argentina e este é o primeiro relato, neste país, de surtos de paralisia facial e síndrome vestibular associados com lesões que ocupam espaço.

[Unilateral facial paralysis and keratitis sicca, signs of temporohyoid osteoarthropathy in the horse]. / Eenzijdige facialis-paralyse en keratitis sicca bij een paard met temporohyoïd-osteoartropathie.

A 9-year-old Dutch Warmblood mare was presented with a history of abnormal behaviour and acute facial nerve paralysis on the left side. Clinical examination revealed a slight head tilt and a corneal ulcer of the left eye. The base of the left ear was warm and painful. Endoscopic examination of the left guttural pouch showed thickening of the proximal part of the stylohyoid bone. Computer tomography revealed a left-sided prominent bony enlargement of the middle and proximal part of the stylohyoid bone and the tympanic bulla, fusion of the temporrhoid joint, and osseous proliferation of the pars petrosa of the temporal bone. The diagnosis was confirmed postmortem. The literature concerning the anatomy, clinical signs, and therapy of temporrhoid osteoarthropathy is discussed.

Temporohyoid osteoarthropathy in 33 horses (1993-2000).

A retrospective study of the medical records of 33 horses was performed to determine the clinical and diagnostic abnormalities associated with temporohyoid osteoarthropathy. Data collected from medical records included signalment, presenting complaints, history, physical examination findings, laboratory data, results of diagnostic imaging studies, and treatments. Follow-up information was obtained from a review of case records; by telephone conversation with the owner, veterinarian, or trainer; or by both methods. Of 33 horses with temporohyoid osteoarthropathy, 29 presented with facial nerve (cranial nerve VII) deficits and 23 presented with vestibulocochlear nerve (cranial nerve VIII) deficits. Guttural pouch endoscopy was more reliable than radiography for diagnosis. Of horses with unilateral clinical signs, 22.6% actually had bilateral disease. Magnetic resonance imaging and computed tomography identified the lesions in all horses in which these tests were performed. Of 30 horses for which follow-up information was obtained, 20 (67%) were alive. Eight horses were euthanized and 1 died because of problems associated with temporohyoid osteoarthropathy. Nineteen of 20 surviving horses (95%) were considered by the owner or trainer to be suitable for athletic use. Twelve surviving horses (60%) had residual facial nerve deficits; 11 horses (55%) had residual vestibulocochlear nerve deficits. Horses with temporohyoid osteoarthropathy have a fair prognosis for return to some type of athletic function, but there is risk of acute death. The majority of horses would be expected to have some residual cranial nerve dysfunction, and it could take a year or longer for maximal improvement to occur.

Histopathology of eighth cranial nerve of mass stranded dolphins at Goto Islands, Japan.

We examined four dolphins (Grampus griseus) of 582 mass-stranded. Almost no contents were found in the alimentary canal. Nasitrema gondo and Crassicauda grampicola were found in the tympanic cavity. Severe degeneration of the eighth cranial nerve was observed microscopically in all animals and an egg of Nasitrema was found in a tissue crevice of the nerve. We propose that the nerves were damaged directly by Nasitrema.

A degenerative disorder of the central auditory system of the gerbil.

A previously unidentified disorder which affects primarily the cochlear nucleus was observed in two species of gerbils, Meriones unguiculatus and M. libycus. Unusual lesions were observed in the cochlear nucleus bilaterally in all animals examined. In light and electron microscopic specimens these lesions were characterized by the presence of microcysts and vacuolar neuronal degeneration. The microcysts resembled large holes, containing trabeculae, organelles and cellular remnants. Also observed were light and dark degeneration of neuronal perikarya and degenerated axons, dendrites, and synapses, accompanied by phagocytosis. Astrocytosis was not conspicuous. In the one cochlea examined, no microcysts were observed. In young animals the microcysts were prevalent in the cochlear nerve root region and the posteroventral cochlear nucleus. In older animals the microcysts increased in number and area. In the oldest animals, the microcysts had spread to other central auditory structures, including the superior olivary complex, the nuclei of the lateral lemniscus, and the inferior colliculus. Other regions of the brain were largely free of microcysts. The etiology and behavioral manifestations of this disorder are unknown, although it is clearly neurodegenerative and perhaps genetically determined.

Mass stranding of Odontoceti caused by parasitogenic eighth cranial neuropathy.

Hearing organs of the Odontoceti from two mass strandings in 1983 and 1986 were examined histopathologically. In the 1983 stranding, two of three pilot whales (Globicephala macrorhynchus) were necropsied and numerous Nasitrema sp. were found close to the eighth cranial nerve (nervus vistibulo cochlearis) in both animals. Patchy degeneration of the eighth cranial nerve in and out of the modiolus of the cochlea was observed. In the 1986 stranding, five of 125 false killer whales (Pseudorca crassiclens) were examined and numerous trematodes (Nasitrema gondo) were found in the tympanic cavities. Severe degeneration of the eighth cranial nerve was discovered and there were many trematode eggs in the nervous and surrounding tissues. Parasitogenic eighth neuropathy is proposed again as the cause of mass stranding of the Odontoceti.

Review of idiopathic feline vestibular syndrome in 75 cats.

Idiopathic feline vestibular syndrome, a peripheral vestibular deficit of unknown cause, was diagnosed in 75 cats at the New York State College of Veterinary Medicine Teaching Hospital from July 1975 to October 1984. Review of the medical records of these cats indicated that the syndrome was seen in more cats in July and August (P less than 0.001) than in other months. Clinical signs included head tilt, ataxia, rolling, rotatory or horizontal nystagmus, and occasional vomiting.

Vestibular syndrome associated with temporohyoid joint fusion and temporal bone fracture in three horses.

Acute onset of vestibulocochlear and facial nerve dysfunction due to a stress fracture of the petrous part of the temporal bone was diagnosed in 3 horses. The fracture was secondary to chronic inflammatory changes in the petrous part of the temporal bone and the proximal stylohyoid bone, with fusion of the temporohyoid joint. Bacterial meningoencephalitis was a complicating factor. Treatment resulted in reduction of severity of clinical signs in 2 of the 3 cases, but residual compensated vestibular deficits persisted.

Facial and vestibulocochlear nerve disease in six horses.

In 6 horses, clinical signs of illness implicated a lesion involving the facial and vestibulocochlear nerves. One horse had signs of otitis externa. Five horses had radiographic changes primarily involving periosteal bony proliferation of the stylohyoid bone at its articulation with the temporal bone. Five horses improved with antibiotic therapy. Otitis media-interna was found at necropsy of one horse.