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L Poncelet

Publications and source records attributed to L Poncelet.

At least 19 recordsLinked to original sources
PubMed2006

N3 potentials in response to high intensity auditory stimuli in animals with suspected cochleo-saccular deafness.

We describe a previously un-reported vertex-negative potential evoked by high intensity click auditory stimuli in some dogs and cats with suspected cochleo-saccular deafness. Brainstem auditory evoked potential tracings from 24 unilaterally or bilaterally deaf animals, 22 dogs and 2 cats, among which 21 belonged to breeds with high prevalence of suspected or histologically confirmed cochleo-saccular deafness, were studied retrospectively. Values for latency, amplitude and threshold of this potential in dogs were 2.15+/-0.23 ms, 0.49+/-0.25 microV, and 91.9+/-4.7 dB NHL, respectively (mean+/-SD). Latency and threshold values in cats were in the mean+/-2 SD range of the dog values. Sensitivity to click stimulus polarity and to click stimulus delivery rate pointed towards a neural potential instead of a receptor potential. The vertex-negative wave observed in these animals shares all characteristics with the N3 potential described in some deaf humans with cochlear deafness, where it is presumed to arise from saccular stimulation. The combined degeneration of cochlea and sacculus usually reported in deaf white dogs and cats suggest that N3 may have a different origin in these species.

Acoustic Stimulation↗
PubMed2006

Focal canine tetanus: diagnostic value of electromyography.

A four-year-old, male Italian hound was presented with severe spasticity of both thoracic limbs that worsened with external stimuli. The remainder of the neurological and general physical examination was normal. Complete blood cell count, chemistry profile, and serology for protozoal diseases were within normal limits. Survey radiography of the cervicothoracic spine and abdominal ultrasonography showed no abnormalities. Electromyography of the thoracic limbs demonstrated the presence of "doublets" and simultaneous activity in both agonist and antagonist muscles. These abnormalities may be explained by a defective glycinergic inhibition at the spinal cord level. Together with the history, progression of signs, and clinical findings, electromyography supported a presumptive diagnosis of focal tetanus. The dog received tetanus antitoxin and antibiotic treatment and gradually improved over four months.

Animals↗
PubMed2006

Laryngeal paralysis-polyneuropathy complex in young related Pyrenean mountain dogs.

OBJECTIVES: To characterise clinical, electrophysiological and histopathological findings. To analyse pedigree information in six young related Pyrenean mountain dogs with laryngeal paralysis-polyneuropathy complex (LP-PNC). METHODS: A retrospective study of clinical records and pedigrees of six young related Pyrenean mountain dogs with LP-PNC was carried out. RESULTS: All dogs were presented with laryngeal paralysis and concurrent megaoesophagus. Electrodiagnostic testing was performed in three dogs and showed electrophysiological abnormalities in the distal appendicular muscles. Histopathological findings of peripheral nerve samples were dominated by distal axonal degeneration. Clinical, electrophysiological and histopathological findings were supportive of a diagnosis of degenerative, sensorimotor LP-PNC, similar to that reported in young dalmatians and rottweilers. All dogs died or were euthanased by two years of age. An autosomal recessive mode of inheritance was suspected based on pedigree analysis. CLINICAL SIGNIFICANCE: Congenital LP-PNC should be suspected in any young dog presenting with laryngeal dysfunction and other concurrent neurological abnormalities. The prognosis is usually poor.

Animals↗
PubMed2005

Brain stem auditory potentials evoked by clicks in the presence of high-pass filtered noise in dogs.

This study evaluates the effects of a high-frequency hearing loss simulated by the high-pass-noise masking method, on the click-evoked brain stem-evoked potentials (BAEP) characteristics in dogs. BAEP were obtained in response to rarefaction and condensation click stimuli from 60 dB normal hearing level (NHL, corresponding to 89 dB sound pressure level) to wave V threshold, using steps of 5 dB in eleven 58 to 80-day-old Beagle puppies. Responses were added, providing an equivalent to alternate polarity clicks, and subtracted, providing the rarefaction-condensation potential (RCDP). The procedure was repeated while constant level, high-pass filtered (HPF) noise was superposed to the click. Cut-off frequencies of the successively used filters were 8, 4, 2 and 1 kHz. For each condition, wave V and RCDP thresholds, and slope of the wave V latency-intensity curve (LIC) were collected. The intensity range at which RCDP could not be recorded (pre-RCDP range) was calculated. Compared with the no noise condition, the pre-RCDP range significantly diminished and the wave V threshold significantly increased when the superposed HPF noise reached the 4 kHz area. Wave V LIC slope became significantly steeper with the 2 kHz HPF noise. In this non-invasive model of high-frequency hearing loss, impaired hearing of frequencies from 8 kHz and above escaped detection through click BAEP study in dogs. Frequencies above 13 kHz were however not specifically addressed in this study.

Acoustic Stimulation↗
PubMed2004

Olivopontocerebellar atrophy in two adult cats, sporadic cases or new genetic entity.

Two otherwise healthy adult cats were presented with progressive cerebellar signs of different severity. Owners requested euthanasia. Necropsy disclosed whole cerebellum and pontine atrophy, with a severity paralleling the neurologic dysfunction. We used cell type-specific immunolabelings to characterize the lesions. The severity of the cerebellar cortex atrophy followed a general gradient from the midvermis toward the hemispheres and a local gradient from the depth of the folia toward their tip. Along these gradients, Purkinje cells were the first to disappear, followed by basket, Golgi, and stellate cells, and eventually by granule cells. Bergmann glia cells and unipolar brush cells were preserved. Pontine nuclei and the olivary complex were also severely depopulated. Neurons in the cerebellar nuclei, vestibular nuclei, and other cerebellar system-associated structures were preserved, as well as substantia nigra. Olivopontocerebellar atrophy (OPCA) in a domestic animal species was rarely reported. Some features allow tentative linking to either familial or sporadic OPCA of humans. However, the ordered disappearance of all cortical neuronal types has never been described before. Either this entity is cat specific or it might pinpoint the need for increased knowledge about differential gene expression depending on genetic background, i.e., among different species. It also would open prospects about gene product interactions within neurons.

Animals↗
PubMed2004

Dark-cell areas in the dog vestibular endorgans: an immunohistochemical study.

The stria vascularis in the cochlea and the dark-cell areas in the vestibular endorgans are structures involved in the production of endolymphatic fluid. This study investigated the dark-cell areas in the vestibular endorgans of the dog by classical staining and by immunohistochemistry (anti-Na,K-ATPase beta2 isoform, anti-cytokeratins (against cytokeratins 5 and 8), anti-vimentin and anti-S100A6) from birth to 110 postnatal days. Using classical staining, it was not possible to discriminate dark cells from other epithelial cells lining the vestibular endolymphatic spaces. From birth, the Na,K-ATPase beta2 isoform was expressed in the lateral and basal cell membranes of a subset of cells located in the utricular wall, at the base of the cristae ampullaris and was identified as dark cells. From birth, anti-cytokeratins labelled all the cells forming the epithelial lining, including the dark cells, while anti-vimentin labelled the underlying mesenchymal cells. From postnatal day 10, anti-S100A6 labelled subepithelial cells exclusively located underneath the dark-cell areas and were identified as vestibular melanocyte-like cells. From birth, Fontana staining evidenced fine melanin granules in the subepithelial layer. The amount of melanin granules increased during the first month. Melanin distribution was closely associated with the region where S100A6-positive cells were located. The cell-specific antigen expression in the dog dark-cell areas was clearly comparable to that of the dog stria vascularis previously described. The present investigation also suggested an earlier histological and immunohistological maturity in the dark-cell areas than in the stria vascularis of dogs. This preliminary morphological description of the normal dark-cell areas in dogs by means of immunomarkers may be instrumental in studying pathological processes involving the fluid-secreting structures in vestibular endorgans.

Animals↗
PubMed2003

Inner ear morphology in a bilaterally deaf Dogo Argentino pup.

Two bilaterally deaf and three unilaterally deaf pups were identified from a litter of 10 Dogo Argentino pups presented for hearing evaluation by electrophysiological investigation. One pup, a bilaterally deaf female aged 43 days, was available for histopathology. Examination of both inner ears revealed bilateral cochlear degeneration with atrophy of the stria vascularis, collapse of the cochlear duct, degeneration of the organ of Corti, and abnormal tectorial membrane. The left vestibule, including the sacculus, was normal. The spiral and vestibular ganglia were essentially normal. This is the first histopathological description of lesions associated with deafness in a Dogo Argentino, but abnormalities were similar to those previously described in deaf Dalmatian pups and in other white hair-coated breeds. The defect was classified as a cochleosaccular degeneration. It was probably congenital and genetic causes were suspected.

Animals↗
PubMed2003

Laminin alpha2 deficiency-associated muscular dystrophy in a Maine coon cat.

A European case of laminin alpha2 deficiency-associated muscular dystrophy in a 12-month-old, female Maine coon pedigree cat is reported. The history and eventual clinical presentation of this cat differed from those of two cats reported in the USA. In this case, the myopathy was characterised by progressively worsening weakness, muscle atrophy and joint contracture. Tendon reflexes were diminished, and motor nerve conduction velocities were slowed. Muscle biopsy demonstrated a dystrophic phenotype with endomysial fibrosis. Occasional thinly myelinated nerve fibres were present within a peripheral nerve specimen. Poorly myelinated fibres were also found at the root level on necropsy specimens. Immunohistochemical staining revealed the absence of laminin alpha2. The cat's family history did not indicate genetic transmission of the disease.

Animals↗
PubMed2001

Immunolocalization of the calcium binding S100A1, S100A5 and S100A6 proteins in the dog cochlea during postnatal development.

The immunolocalization of three members of the S100 calcium-binding protein family was investigated in the dog cochlea during normal postnatal development. Sections of decalcified and paraffin-embedded cochleae from 16 beagle puppies aged from birth to 3 months were treated with polyclonal antisera raised against the human recombinant S100A1, S100A5, and S100A6 proteins. At birth, in the dog cochlea, S100A1 was expressed in the immature Deiter's cells, and slightly in the pillar cells. From the second week, S100A1 was detected in the supporting structures of the organ of Corti, i.e. the Deiter's, the pillar, the border, and the Hensen's cells, and in the reticular membrane. From birth onwards, S100A5 remained a neuronal-specific protein, only located in a subpopulation of neurons in the spiral ganglion. S100A6 was not expressed at birth. From the second week of life, the Schwann cells and nerve sheaths in the modiolus, in the spiral ganglion, and running in the direction of the organ of Corti exhibited S100A6-labeling. From the 12th postnatal day, some scattered intermediate cells started to express S100A6 protein in the stria vascularis. The number of labeled intermediate cells increased during the third week. At adult stage, the intermediate cells were S100A6-stained with cytoplasmic labeling throughout the stria vascularis from the base to the apex of the cochlea. None of the other cochlear structures expressed the S100 proteins under study during the postnatal development of the dog cochlea. The S100A1, S100A5, S100A6 immunostaining was limited to specific cell types in dog cochlea. These S100 proteins were useful markers in the study of supporting cells, neurons, nerve fibers sheaths and stria vascularis (S100A6) during the normal postnatal development of the dog cochlea.

Animals↗
PubMed2001

An original inner ear neuroepithelial degeneration in a deaf Rottweiler puppy.

Histopathological investigation was conducted on both inner ears from a 4.5-month-old Rottweiler puppy with electrophysiologically confirmed bilateral deafness. The lesions were restricted to the organ of Corti and spiral ganglion that both displayed severe degenerative changes. The outer hair cells were less affected than the inner hair cells. The number of spiral ganglion neurons was reduced, and remaining neurons were altered. The basal and middle cochlear turns were more affected than the apical one. The vestibules were normal. Immunostaining with calbindin, calretinin, S100A1 and S100A6 polyclonal antisera was helpful in identifying different cell-types in the degenerated cochlea. The early and severe spiral ganglion cell degeneration is an uncommon finding no matter the species. Such lesions bear significance within the frame of cochlear implants technology for deaf infants.

Animals↗
PubMed2000

Immunolocalization of calbindin D28k and calretinin in the dog cochlea during postnatal development.

The calbindin (CB) and the calretinin (CR) immunoreactivities were studied in the dog cochlea during its postnatal maturation from birth to the 33rd postnatal day. At birth, CB was expressed in the Kölliker's organ, in the immature inner (IHC) and outer hair cells (OHC), in neurons of the spiral ganglion, and in nerve fibers running in the basilar membrane of the apical turn. During the cochlear maturation, non-sensorineuronal structures, such as the Kölliker's organ, the rods of Corti, and the inner sulcus cells, displayed a transient CB-staining. In the adult-like dog cochlea, CB was found in the cytoplasm, the cuticular plate, and the stereocilia of the IHC and OHC. All the neurons of the spiral ganglion and some nerves fibers in the modulius were CB-positive. At birth, CR exhibited a neuronal distribution: about 75% of the spiral ganglion neurons, some nerve fibers in the modulius and nerve fibers running in the basilar membrane were CR-labeled. During the postnatal maturation, a CR-immunostaining appeared around the IHC body and CR was expressed transiently in the OHC. In the adult-like dog cochlea, a CR-positive network surrounded the unlabeled IHC. The neuronal CR-labeling remained unchanged from birth.

Aging↗
PubMed1999

Use of midlatency auditory-evoked potentials as indicator of unconsciousness in the dog: characterisation of the effects of acepromazine-thiopentone, medetomidine-thiopentone and medetomidine-butorphanol-midazolam combinations.

Middle latency auditory-evoked potentials were measured in sedated and anaestetised dogs to determine their possible usefulness in monitoring of unconsciousness during anaesthesia and to compare the effects of anaesthetic protocols. There were three groups of five dogs: group I received acepromazine; groups 2 and 3 received medetomidine; 30 minutes later, groups 1 and 2 received thiopentone and group 3 received midazolam and butorphanol. Groups 2 and 3 received atipamezole 60 minutes after medetomidine was administered. Auditory-evoked potentials were recorded at time 15, 40 and 75 minutes. Thiopentone administration resulted in a profound modification of the pattern of response, and several peaks were no longer identified. In group 3, the administration of midazolam-butorphanol tended to increase the latency of the different peaks, but lesser than thiopentone did. Middle latency-evoked potentials appeared to be potentially useful in the monitoring of unconsciousness in the dog.

Acepromazine↗
PubMed1998

Effect of stimulus intensity on spine recorded somatosensory evoked potential in dogs.

OBJECTIVE: To investigate the effect of stimulus intensity on the characteristics of the spine recorded somatosensory evoked potentials (SEP) in dogs. ANIMALS: 11 healthy Beagles, 1 to 2 years old. DESIGN AND PROCEDURE: In 10 dogs, square-wave stimuli (0.1-ms duration, 4 Hz) were delivered through needle electrodes inserted close to the right tibial nerve at the tibiotarsal joint. A standard stimulus strength (reference effective stimulus [RS]) was established for each dog by determining the stimulus necessary to induce a maximal M wave (muscle evoked potential) in the plantar interosseus muscles. The polarity of the stimulating electrodes was then reversed, and an SEP was recorded at the level of the T13-L1 interarcuate ligament. Subsequently, stimuli at fractions (1/4x, 1/2x) and multiples (2x, 4x) of RS were delivered. Recordings, using 10x RS stimuli, also were obtained in 2 dogs; in 1 of them, the recordings were obtained before and after curarization. In each instance, the latencies and the amplitudes of the first 3 reproducible deflections were measured and evaluated. RESULTS: The SEP waveform recorded at the T13-L1 level using RS was similar in all dogs; at least 3 deflections were recognized. Altering stimulus intensity did not significantly change latency of the first 3 peaks; conversely, amplitudes of the first 3 peaks increased (P < 0.01) when the stimulus intensity was increased from 1/4x RS to 1x RS. Stimulation at 10x RS induced the recording of a large potential, which was suppressed by the curarization. CONCLUSION: Only slight variations affect latency data through a wide range of stimulus intensities; latency measurement can be considered a robust tool in the vicinity of RS. Slight variations in the electrode position during an SEP session should not invalidate the results. Differences in the definition of the stimulus intensity among laboratories should not preclude the comparison of the results.

Analysis of Variance↗
PubMed1998

Study of spinal cord evoked injury potential by use of computer modeling and in dogs with naturally acquired thoracolumbar spinal cord compression.

OBJECTIVE: To add objective measurements of the characteristics of evoked injury potentials (EIP) and their relations to clinical severity in dogs with thoracolumbar spinal cord damage. ANIMALS: 25 dogs with naturally acquired spinal cord compression attributable to disk extrusion or vertebral fracture at the level of the thoracolumbar junction and with various degrees of paresis/paralysis. PROCEDURE: Spinal cord potentials evoked by tibial nerve stimulation were recorded every 5 to 10 mm at the lamina level in the vicinity of the cord compression. This allowed an EIP to be recorded even in the least handicapped dogs. A computer model yielded information about the waveform changes of the EIP in the vicinity of conduction blocks. RESULTS: The EIP waveform changed from biphasic to monophasic a short distance caudad to the location of spinal cord compression. Location of a maximal conduction block was measured in relation to position of the electrodes recording this waveform change. The distance between the assumed conduction block and the actual spinal cord compression was larger in the most affected dogs. The amplitude of the EIP was not related to severity of the clinical picture; however, the proximity of the recording electrode to the spine influenced the amplitude and the waveform of the EIP. CONCLUSION AND CLINICAL RELEVANCE: Change in the EIP waveform from biphasic to monophasic makes it possible to estimate the conduction block location along the spinal cord. A large distance between the assumed conduction block and site of actual cord compression could be an objective argument to confirm severity of a lesion.

Animals↗
PubMed1995

Motor evoked potentials induced by electrical stimulation of the spine in dogs: which structures are involved?

A minimally invasive method for the stimulation of the spinal cord in dogs was developed. Electrical stimuli were delivered to the spine at the T8 vertebral level through partially insulated needles and under ketamine anesthesia. This allowed the recording of reproducible responses in hind limb muscles of intact dogs. Chronic unilateral deafferentation suppressed the muscle responses on the operated side. A cordotomy sparing the dorsal columns at the L1 level did not completely suppress the muscle responses. It was concluded that motoneuron activation through antidromic conduction in first-order sensory neurons was possible with thoracic spine stimulation and that the recording of muscle responses did not necessarily assess central motor pathways.

Animals↗
PubMed1994

Acute polymyopathy after carbamate poisoning in a dog.

The acute polymyopathy in a seven-year-old German shepherd dog was attributed to the muscular hypertonia, tremors and seizures which developed during the acute phase of carbamate poisoning. After two days of generalised muscular rigidity, the dog adopted a characteristic fetal position which could be explained by the imbalance between the injuries to the extensor and flexor muscles. The polymyopathy resolved gradually over the course of a week.

Acute Disease↗
PubMed1993

Somatosensory potentials in dogs with naturally acquired thoracolumbar spinal cord disease.

Somatosensory evoked potentials (SEP) were recorded at the scalp and at various levels along the lumbar and caudal thoracic parts of the spine in response to tibial nerve stimulations. The SEP were observed in 24 diseased dogs, 2 with a vertebral fracture, 1 with a spinal cord tumor, 1 with a vertebral tumor, and 20 with disk herniation. Cord compression location was confirmed by myelography, laminectomy, or both. The clinical state had significant (P < 0.0001) influence on SEP characteristics. The scalp-recorded SEP latency changed only in association with the most severe lesions; spine-recorded SEP conduction velocity was lower in association with mild lesions; scalp-recorded SEP amplitude changed with lesions of intermediary severity. Because these 3 electrophysiologic variables were influenced differently by cord damage, it was possible to discriminate the various clinical grades by use of these techniques. However, dogs with signs of pain only could not be differentiated from clinically normal dogs. The evoked injury potential was observed in all but 4 diseased dogs, and its maximal amplitude corresponded, in all cases, with cord damage location. Increased duration (P < 0.05) of the spine-recorded SEP was associated with long-standing problems, but not necessarily with clinically detectable malfunction. Use of SEP and evoked injury potential for identifying lateralized cord damage may be of value.

Animals↗