Four Cases of the Melanotic Variant of Malignant Nerve Sheath Tumour: a Rare, Aggressive Neoplasm in Young Dogs with a Predilection for the Spinal Cord.

Four cases of a rare melanotic variant of malignant nerve sheath tumour (MNST) in dogs are described. All four cases presented with neurological clinical signs due to multicentric, intradural, intra- and extraparenchymal neoplasms that surrounded the spinal and cranial nerves and infiltrated the adjacent spinal cord and brain. The dogs were young (3 months to 3 years of age), all were female and four different breeds were represented. Characteristic histological features were interweaving fascicles of spindle-shaped cells, sometimes with an architecture reminiscent of Antoni A and B patterns. Some spindle cells showed prominent cytoplasmic melanin pigmentation and such cells were positive by Masson-Fontana stain. Immunohistochemistry performed in three cases was positive for S100 and vimentin, strongly positive for melan A in the melanized cells and negative for glial fibrillary acidic protein and periaxin. Non-melanized cells did not express melan A. Transmission electron microscopy findings in one case were consistent with a peripheral nerve sheath tumour and demonstrated cytoplasmic pre-melanosomes and melanosomes. Melanotic variants of MNSTs are rare in animals with only a solitary report of two previous canine cases in the literature.

Neuroendodermal cyst in the fourth ventricle of a dog.

CASE REPORT: We describe the MRI appearance and surgical outcome of a rare neuroendodermal cyst in the fourth ventricle of a German Shorthaired Pointer. The dog presented with uncoordinated gait and occasional falling that increased when she became excited. The MRI appearance is shown and the surgical treatment described. Recurrence occurred on two occasions and the dog was euthanased. CONCLUSION: Recurrence of these cysts is highly likely unless there is complete surgical resection.

Hemifacial Microsomia in a Cat.

A 7-month-old domestic medium hair cat presented with facial asymmetry affecting the bony and soft tissue structures of the right side of the head including the maxilla, nose, eye and pinna of the ear. Additionally, neurological dysfunction of the facial and vestibulocochlear nerves on the affected side was present. A congenital malformation affecting the first and second embryologic pharyngeal arches was suspected. This is the first case of hemifacial microsomia of likely congenital origin reported in a cat.

Unusual features in four canine meningiomas.

Several subtypes of canine meningioma are recognized. This report describes four canine meningiomas with previously unreported features. The four affected dogs were of different breeds. Three of the affected dogs were male and aged 7-10 years. In one dog, age and gender were not recorded. Meningiomas were located intracranially (three dogs) or within the vertebral canal (one dog). Two meningiomas resembled gemistocytic astrocytomas, while one had focal features of a rhabdoid tumour; these three meningiomas also contained amyloid deposits. The fourth tumour, a secretory meningioma, was rich in amianthoid fibres (i.e. unusual collagen deposits containing giant collagen fibres). All of these features are also described in human meningiomas.

Ventricular and extraventricular ependymal tumors in 18 cats.

Ependymal tumors are reported rarely in domestic animals. The aims of this study were to examine the clinical and pathologic features of ventricular and extraventricular ependymomas and subependymomas in 18 domestic cats examined between 1978 and 2011. Parameters examined included age, sex, breed, clinical signs, and macroscopic and histopathologic features. The mean age of affected cats was 9 years, 4 months; median age, 8.5 years. There were 8 female and 4 male cats, and 6 cats for which sex was not recorded. Breeds included 10 domestic shorthaired, 2 domestic longhaired, 1 Persian, and 1 Siamese. Clinical signs included altered mentation or behavior, seizures, circling, propulsive gait, generalized discomfort, and loss of condition. The tumors often formed intraventricular masses and usually arose from the lining of the lateral or third ventricles, followed by the fourth ventricle, mesencephalic aqueduct, and spinal cord central canal. Three tumors were extraventricular, forming masses within the cerebrum and adjacent subarachnoid space. Histologically, 15 tumors were classified as variants of ependymomas (classic, papillary, tanycytic, or clear cell) and 3 as subependymomas. Tumors were generally well demarcated; however, 6 ependymomas focally or extensively infiltrated the adjacent neural parenchyma. Characteristic perivascular pseudorosettes were observed in all ependymomas; true rosettes were less common. Some tumors had areas of necrosis, mineralization, cholesterol clefts, and/or hemorrhage. This cohort study of feline ependymal tumors includes subependymoma and primary extraventricular ependymoma, variants not previously described in the veterinary literature but well recognized in humans.

Encephalomyelopathy and polyneuropathy associated with neuronal vacuolation in two Boxer littermates.

Neuronal vacuolation and spinocerebellar degeneration is a rare, presumably inherited condition that is reported only in Rottweilers and in crossbred dogs with known or potential Rottweiler heritage. Gross and histopathologic findings include laryngeal muscle atrophy, neuronal vacuolation, and a combined central and peripheral axonopathy. Two 6-month-old Boxer puppies from the same litter were referred for evaluation of progressive pelvic limb paresis and ataxia, upper airway stridor, and visual deficits. Examination of each dog suggested a combined myelopathy and peripheral neuropathy, as well as congenital ocular disease. Gross lesions were limited to atrophy of the intrinsic laryngeal muscles. Histopathologically, there was diffuse loss of axons and myelin in the dorsolateral and ventral funiculi throughout the spinal cord and extending into the caudal aspect of the brain stem. Vacuolation of scattered neuronal cell bodies was present in the spinal cord and selected brain stem nuclei. Multifocal axonal degeneration and demyelination was observed in the recurrent laryngeal nerve, sciatic nerve, and brachial plexus and was most severe in the recurrent laryngeal nerve. Ocular abnormalities included microphthalmia, cataracts, and retinal dysplasia. The findings in these Boxer dogs, unrelated to the Rottweiler breed, are analogous to the syndrome of neuronal vacuolation and spinocerebellar degeneration reported in Rottweilers.

Verminous encephalitis in a horse produced by nematodes in the family protostrongylidae.

Parasitic granulomatous eosinophilic inflammation was observed in the central nervous system (CNS) of a 6-month-old Arabian colt from New York state. Inflammation was associated with eggs, larvae, and adult nematodes in the cerebellum. Nematodes had histological characteristics of the superfamily Metastrongyloidea. The presence of dorsal-spined larvae in the CNS was further indicative of infection with a nematode in the family Protostrongylidae. Infections were most compatible with Parelaphostrongylus tenuis but specific diagnosis was not possible. This is the first definitive report of a protostrongylid nematode infection in a horse.

Oligodendroglial dysplasia in two bullmastiff dogs.

Leukodystrophies are inherited neurological disorders involving central nervous system white matter. They are uncommon in animals but a few, breed-specific entities have been described. In 2002, two young-adult, purebred Bullmastiff dogs from central New York State presented to their referring veterinarians displaying moderate to severe ataxia of all limbs, spastic tetraparesis that was worse in the pelvic limbs, and a diffuse, action-related, whole-body tremor. Clinical signs were insidious in onset and slowly progressive. Anatomic diagnoses considered were a C1-C5 lesion or, based on the whole-body tremor, a diffuse central nervous system disorder. No gross lesions were apparent in the brain or spinal cord. Histopathologically, numerous, multifocal, sharply demarcated, small, ovoid to angular areas of myelin pallor (plaques) were present throughout the major white matter tracts of the brainstem and spinal cord. These plaques, which often were traversed by axons, did not stain with luxol fast blue for myelin and were associated with minimal astrocytosis. Ultrastructural findings include occasional hypertrophic glia in white matter, rare unmyelinated segments of axons, and focal proliferation of tubule-containing cytoplasmic glial cell processes (oligodendroglial). The described clinical and morphological findings and age of onset are similar to the well-characterized, presumably hereditary, bovine syndrome known as Charolais ataxia or oligodendroglial dysplasia. This article presents the first description of a leukodystrophy in the Bullmastiff breed and the first report of oligodendroglial dysplasia in animals other than Charolais cattle.

Gliomatosis cerebri in six dogs.

Gliomatosis cerebri is a well-recognized entity in human medicine characterized by unusually widespread infiltration of the neuraxis by neoplastic glial cells with relative preservation of brain architecture. This report describes the pathologic features of the disease in six dogs. The dogs ranged from 3 to 9 years of age (mean 6.1 years) without evidence of breed predilection; five of the six dogs were neutered or intact males. The clinical findings were mixed (including depression, circling, cranial nerve deficits), reflecting the diffuse nature of the disease. Histologically, there was remarkably diffuse infiltration of the white and gray matter of the brain by small numbers of elongated neoplastic cells. Areas of greater cellularity formed grossly visible lesions in four cases. Anisocytosis and pleomorphism were greater in areas of higher cellularity. Other features of tumor growth included subpial accumulation, neuronal satellitosis, perivascular cuffing, and tropism for cranial nerve and brain stem nuclei. Neoplastic cells were negative on immunohistochemical stains for glial fibrillary acid protein (GFAP) and leukocyte markers, reflecting the uncertain histogenesis of these unusual neoplasms.

Postanaesthetic cerebral necrosis in five horses.

After being anaesthetised for between one hour 40 minutes and seven hours, five adult horses developed acute neurological signs and extensive cerebrocortical necrosis. Four of them had had abdominal surgery for colic and one had had repeated orthopaedic interventions. Between five hours and seven days after the surgery, all five horses suddenly developed severe signs of a predominantly prosencephalic disturbance: bilateral blindness with normal pupillary light responses, abnormal behaviour varying from propulsive pacing to head pressing profound lethargy and generalised seizures. They were euthanased between 24 hours and three weeks after the onset of these signs. In three of the cases a gross examination of the brain revealed patchy malacia of the cerebral grey matter and some discolouration of the adjacent white matter. Microscopical examination revealed lesions that varied from laminar neuronal necrosis in the grey matter of the cerebral cortex to more diffuse necrosis of the cortex and underlying white matter. Four of the five cases had had a period of hypercapnea while anaesthetised, and two of them (and possibly a third) had also had hypoxaemia.

Marginal siderosis and degenerative myelopathy: a manifestation of chronic subarachnoid hemorrhage in a horse with a myxopapillary ependymoma.

Marginal siderosis is recognized in humans as an uncommon clinicopathologic entity characterized by degeneration of neural tissue at the surface of the brain and spinal cord, in association with the accumulation of hemosiderin, and resulting from chronic subarachnoid hemorrhage. The sources of hemorrhage are various and include neoplasms, malformations, cysts, and vasculopathy. Marginal siderosis of the spinal cord due to a myxopapillary ependymoma was diagnosed in a 19-year-old Dutch Warm Blood horse with clinical signs of myelopathy. There is only one previous report of marginal siderosis in the veterinary literature, also in a horse with clinical myelopathy.

Possible intraspinal metastasis of a canine spinal cord nephroblastoma.

A 2-year-old Basset Hound was admitted to the University of Florida Veterinary Medical Teaching Hospital with progressive spastic paraparesis. At necropsy, intradural extramedullary tumors produced areas of spinal cord swelling and softening in spinal cord segments T11-T12 and L4-L6. Histologic examination of the masses revealed sheets of polygonal blastemal cells, epithelial cells forming tubules and rosettes, and embryonal glomeruloid-like structures in the thoracic mass. Cells in the lumbar mass were less differentiated, forming rare tubules and no glomeruloid-like structures. The occurrence of two tumors in the spinal cord along with the less differentiated appearance of the lumbar tumor raises the possibility that the lumbar mass arose as a result of intraspinal metastasis. To our knowledge, this is the first report of multifocal or metastatic canine spinal nephroblastoma. In addition, the vimentin and cytokeratin immunohistochemical staining characteristics of these spinal cord nephroblastomas are described.

Spinal accessory nerve biopsy as an ante mortem diagnostic test for equine motor neuron disease.

The effectiveness of spinal accessory nerve branch biopsy evaluation as a means to confirm the diagnosis of equine motor neuron disease (EMND) was investigated. Sixteen horses with histories and clinical signs suggestive of EMND and 16 control horses with neither histories nor clinical signs of any neurological disorder, were subjects of the study. Biopsy samples of the ventral branch of the spinal accessory nerve were obtained either surgically, under general anaesthesia or post mortem immediately after euthanasia. Evaluation was done on the spinal cord of all horses to serve as the definitive diagnostic indicator of EMND. Results indicate that biopsy of the ventral branch of the spinal accessory nerve is a reliable ante mortem diagnostic test for EMND. Histological evidence of the degeneration of myelinated axons is present in both acute and arrested cases. The ventral branch of the spinal accessory nerve is easy to approach surgically and biopsy of the nerve causes no disfigurement of the sternocephalicus muscle. The use of semi-thin Epon sections is an excellent method of sample preparation. Formalin fixation and routine paraffin embedment may prove more accessible and provide good quality preparations for reliable interpretation. In the hands of an experienced pathologist, the sensitivity and specificity reliability coefficients for spinal accessory nerve branch biopsy are 94%, making this technique an extremely valuable diagnostic tool for the ante mortem diagnosis of EMND.

Trypanosoma cruzi infection in Walker hounds from Virginia.

Trypanosomiasis has been reported in dogs from Texas, Oklahoma, Louisiana, and South Carolina. We describe the first isolation and characterization of Trypanosoma cruzi from a Walker Hound pup in Virginia that also had postvaccinal distemper. The mother of the pup and 7 of its 8 siblings also were found to be infected with T cruzi, suggesting that the parasite had been transmitted transplacentally or through lactation. Parasitologic, serologic, histologic, and molecular methods were used to establish the diagnosis of T cruzi infection in these dogs. In a serologic survey of 12 dogs (including the sire of the pups) from the area in which the index case occurred, none were found to have antibodies to T cruzi. However, 2 of a further 52 dogs from different areas (to the index case), but in the same county, were seropositive to T cruzi. These findings indicate that canine trypanosomiasis is present in an area of the United States not previously known to be enzootic.

Motor neuron degeneration in a horse.

A 9-year-old Quarter Horse mare was examined because of progressive weight loss, weakness, muscle atrophy and tremors, and behavioral change. Selenium and glutathione peroxidase assays, blood lead analysis, erythrocyte transketolase analysis, pseudorabies and Borrelia burgdorferi serology, electromyography, and CSF analysis were performed. Motor neuron degeneration was diagnosed by microscopic examination of neural tissues. The cause of the disease was not substantiated, but several possibilities were excluded via diagnostic testing. Diagnosis of motor neuron degeneration in horses may be made from an accurate history, thorough neurologic examination, and ancillary testing. In particular, antemortem diagnosis may be based on finding scattered angular atrophy of predominantly type-1 or of type-1 and -2 skeletal muscle fibers in frozen sections of muscle biopsy specimens.

Cervical fibrotic stenosis in a young Rottweiler.

An 18-month-old neutered male Rottweiler was examined because of slowly progressive spastic tetraparesis and ataxia. Signalment and clinical signs were suggestive of 2 neuronal degenerative diseases presumed to be inherited in young Rottweilers: leukoencephalomyelopathy and neuroaxonal dystrophy. Myelography revealed an extradural compression at the articulation of the second and third cervical vertebrae. At surgery, focal hypertrophy of the yellow ligament was observed to compress the spinal cord ventrally at that site.

Multisystemic chromatolytic neuronal degeneration in Cairn terriers. A case with generalized cataplectic episodes.

Multisystemic chromatolytic neuronal degeneration, a newly recognized disease of Cairn Terriers, is described in a second affected North American puppy. In this puppy, the early onset of hind limb weakness at 11 weeks and rapid development of signs of diffuse CNS involvement were distinctive. Signs of cerebellar dysfunction were prominent, but bouts of cataplectic collapse in this puppy constituted the most distinguishing clinical feature. Although electroencephalograph (EEG) recordings lacked a true rapid eye movement (REM) pattern during cataplectic episodes, cervical electromyograph (EMG) potentials ceased or diminished, and imipramine injection was associated with arousal. Postmortem studies revealed that chromatolytic degeneration was very widespread, affecting many neuronal populations in the brain and spinal cord as well as neurons in sensory ganglia. Although the pattern of chromatolysis varied among affected perikarya, chromatolysis was consistently related to dispersion and loss of ribosomes. In this puppy, as opposed to six studied previously, thoracolumbar myelomalacia also occurred symmetrically in the dorsal horns and adjoining funicular white matter. The metabolic derangement underlying this chromatolytic neuronal degeneration and myelomalacia remains unknown.

Neuromuscular disease in a dog.

Diffuse neuromuscular disease occurs sporadically in dogs. The most commonly reported diffuse neuromuscular diseases are polyradiculoneuritis (coonhound paralysis), tick paralysis, botulism, and myasthenia gravis (1,2,12). This clinical report describes an atypical presentation of a diffuse neuromuscular disease in a dog.