[Electromyography and spinal evoked potentials in cauda equina syndrome of dogs]. / Elektromyographie und spinal evozierte Potentiale beim Cauda equina Syndrom des Hundes.

In order to investigate usefulness of electrodiagnostic methods in Cauda Equina-Compression, 26 dogs with this disease were subjected to electromyography and spinal evoked potentials. 16 normal dogs served as controls. It was found that--after stimulation of the Nn.tibialis, peronaeus, pudendus and coccygeales and recording at the lumbosacral junction--latencies and nerve-conduction velocities were largely normal. However the amplitudes were decreased and--depending on the severity of the compression--the morphology of the potentials was altered although considerable standard deviations were obtained. Electromyographically, increased spontaneous activity with fibrillations and positive sharp waves were found in the myotomes of the lumbosacral nerves. Their number increased according to the severity of the cauda equina compression and they had a centrifugal distribution pattern. Based on these results it appears indicated to perform an electromyographic exam before applying myelography. The technique of spinal evoked potentials will need more refinement and standardisation before being useful in a clinical situation.

Recording of visual-evoked potentials in dogs with scalp electrodes.

Following unsuccessful attempts to record visual-evoked potentials (VEPs) in dogs with scalp electrodes, adoption of a new stimulation technique seems to be beneficial. Previously, flashes of white light administered after dark adaptation induced relatively high amplitude electroretinograms (ERGs) covering any VEP activity over the surface of the skull. ERG amplitude, however, can be significantly reduced using flashes of red light after light adaptation (mostly cone stimulation). Simultaneous ERG and VEP recording allows identification of VEPs composed of three significantly different negative peaks (N1, N2, and N3) measured in dogs anesthetized with chloralose and halothane. No more than two of the three peaks were seen in one recording. Only the N1 and N3 waves were consistently recorded in dogs anesthetized with thiopental and thiopental combined with halothane. In 50% of all recordings, N1 was seen alone. The other VEPs consisted of N1 and N2, or N1 and N3 occurring concurrently. The simultaneous occurrence of N2 and N3 waves, however, was never seen. Among all recordings, N1 was most frequently recorded (85% of measurements), followed by N3 and N2 (38% and 31% of measurements, respectively). Peaks of less than 90 ms are highly reproducible. Anesthesia is necessary to eliminate frequent artifacts obtained in conscious and sedated dogs. Thiopental and/or halothane had no effect on measured latencies compared with chloralose.

Neurologic manifestations associated with hypothyroidism in four dogs.

Hypothyroidism was believed responsible for peripheral and central neurologic abnormalities in 4 dogs. Clinical signs consisted of abnormalities of gait and postural reactions and dysfunction of multiple cranial nerves in all 4 dogs. Circling, hypermetria, and spontaneous verticle nystagmus were observed in some of the dogs. Hypothyroidism was diagnosed in all 4 dogs on the basis of low resting serum thyroxine concentration and inadequate response to thyroid stimulating hormone. After thyroid hormone supplementation, resolution of neurologic abnormalities was complete in 2 dogs and partial in the other 2 dogs.

Chronic polyneuritis in a Rottweiler.

A 2-year-old male Rottweiler was examined because of progressive weakness and muscular atrophy in the 4 limbs. Neurologically, the disease was characterized by hypoactive segmental reflexes without ataxia. Function of the cranial nerves was maintained. Electromyographic findings, nerve conduction velocity measurements, recordings of somatosensory-evoked potentials, and results of histologic examination of nerve and muscle biopsy specimens indicated a peripheral neuropathy. Rapid progression of the disease over a 4.5-month period was observed before the dog was euthanatized. Necropsy was performed, and the histopathologic findings confirmed peripheral neuropathy, which appeared to involve the peripheral myelin. An immune-mediated process was suspected.

Cystometrography and urethral pressure profiles in healthy horse and pony mares.

Cystometrography and urethral pressure evaluations were performed in 7 horse mares and 5 pony mares before and after sedation with xylazine. Before sedation, mean (+/- SD) maximal bladder contraction pressure was 91.4 +/- 16.5 cm of H2O in horses and was 86.0 +/- 14.4 cm of H2O in ponies, and maximal urethral closure pressure was 49.1 +/- 19.4 cm of H2O in horses and 37.7 +/- 14.4 cm of H2O in ponies. A significant difference was not found between values of nonsedated vs sedated animals. Only values for threshold volume were significantly different (P less than 0.05) between nonsedated horses (1,982 +/- 1,241 ml) and ponies (825 +/- 412 ml).

Studies on the intrathecal humoral immune response in canine distemper encephalitis.

Albumin and IgG were quantitated in paired cerebrospinal fluid (CSF) and serum samples from dogs with demyelinating canine distemper virus (CDV) infection by means of rocket immunoelectrophoresis. The IgG index as indicator for intrathecal immunoglobulin synthesis was normal in animals with non-inflammatory demyelinating lesions and elevated in dogs with inflammatory myelin lesions. Specific antibodies against CDV and myelin were quantitated in CSF and serum from 8 dogs with an elevated IgG index. Eight of these dogs had significant amounts of antimyelin antibody and 4 dogs had neutralizing anti-CDV antibody in the CSF. Whereas the pathogenetic significance of antimyelin antibodies remains uncertain, the intrathecal antiviral immune response provides a plausible explanation for immunopathologic destruction of myelin in distemper.

Immunoelectrophoretic determination of albumin and IgG in serum and cerebrospinal fluid in dogs with neurological diseases.

Albumin and IgG concentrations were determined in the cerebrospinal fluid (CSF) and serum from 21 normal dogs and 79 dogs with neurological disease, using rocket immunoelectrophoresis. A qualitative protein reaction, cell count and cytological examination were also performed on most CSF samples. The values obtained in normal dogs were used to establish baseline data. Those obtained in neurologically ill dogs were divided into five groups according to the clinical and pathological findings; infectious inflammatory diseases, tumours, degenerative conditions, spinal cord compression and vascular disorders. The absolute CSF albumin content was used as an indicator for blood-brain barrier disturbance and the IgG index for the detection of intrathecal IgG synthesis. Four categories of findings were distinguished; normal CSF, blood-brain barrier disturbance (increased transudation), intrathecal IgG synthesis, combined barrier disturbance and IgG synthesis. The results correlated largely with the pathological findings although in some cases the CSF values could not be explained by the morphological data. It was concluded that rocket immunoelectrophoresis, although it is an elaborate technique, is a useful addition to other CSF examination methods.

Degenerative myelopathy in a family of Siberian Husky dogs.

Three closely related, Siberian Husky dogs had chronic progressive paresis and ataxia with muscle atrophy in the hindlimbs. Radiologic and myelographic examination of the spine revealed no abnormalities. On histologic examination, disseminated degeneration of the white matter, particularly in the thoracic segments, was seen. The clinical and pathological findings were similar to those described in aging large dogs with so-called degenerative myelopathy. The cause of this disease is unknown but the fact that these 3 Huskies were closely related suggest that hereditary factors may play a role.

Lymphocyte responsiveness to lectin and myelin antigens in canine distemper infection in relation to the development of demyelinating lesions.

Eleven dogs were experimentally infected with canine distemper virus and studied for periods of up to 63 days post-inoculation. The responsiveness of lymphocytes in vitro toward phytohemagglutinin, myelin basic protein and galactocerebroside was tested at regular intervals during the course of infection by means of [3H]thymidine incorporation and flow cytometry. All dogs developed a marked decrease of lymphocyte responsiveness toward phytohemagglutinin. Four dogs recovered rapidly from the immunosuppression and did not develop demyelination or had only mild lesions, while two others failed to recover at all and developed severe non-inflammatory demyelinating lesions. The remaining dogs exhibited a slow or partial immune recovery and had various degrees of inflammatory demyelination. Lymphocytes from 2 dogs with demyelination and 2 dogs without myelin lesions responded to myelin antigens. The findings indicate that the degree of immunosuppression in canine distemper virus infection may determine the type of demyelination and autoimmune reactions that occur during the inflammatory stage of demyelination may be epiphenomena.

Glial proteins in canine distemper virus-induced demyelination. A sequential immunocytochemical study.

A temporal series of demyelinating lesions in experimental canine distemper virus (CDV) infection was examined with immunohistological techniques demonstrating myelin basic protein (MBP), myelin-associated glycoprotein (MAG), and glial fibrillary acidic protein (GFAP) on serial sections. The earliest lesions were characterized by decreased MBP and MAG and increased GFAP. During the further progression of the disease, MBP and MAG losses continued to match each other. There was no indication of MAG loss preceding the disappearance of MBP. In the more advanced lesions there was a marked decrease of GFAP positive cells. Since these findings differed considerably from similar immunohistochemical studies in progressive multifocal leukoencephalopathy (PML) where demyelination results from oligodendroglial infection, it was concluded that the oligodendroglial cell body is not the primary target of CDV. The marked astroglial changes were also considered to contribute to demyelination in CDV infection but the mechanism by which this happens remains unknown.

Hereditary neurovisceral mannosidosis associated with alpha-mannosidase deficiency in a family of Persian cats.

Several kittens in a family of Persian cats had a metabolic storage disease. Clinically the disorder was characterized by hepatomegaly, neurological signs and early death. The microscopic lesions consisted of widespread vacuolation of neurons and glial cells in the central nervous system and in liver cells. Electronmicroscopically the lesions consisted of intracytoplasmic accumulation of membrane-bound "empty" vacuoles. In addition to the storage disease, poor myelination of the cerebral white matter was found. The defect was reproduced in breeding trials. On biochemical analysis of brain tissue, deficient function of the enzyme alpha-mannosidase was detected. The clinical and pathological features of mannosidosis in Persian cats were compared to similar defects in other species.

Oral immunization of foxes against rabies. Laboratory and field studies.

A short description is given of the laboratory experience gained in oral immunization of foxes against rabies, and its application in a limited field trial in Switzerland with an attempt to control two outbreaks of fox rabies.