Idiopathic Polyneuropathy in Alaskan Malamutes

Clinical and morphologic features of a progressive polyneuropathy in young mature Alaskan Malamutes are described. Clinical signs included progressive paraparesis, synchronous pelvic limb gait, exercise intolerance, hyperesthesia, hypore-flexia, muscle atrophy, and tetraplegia. Electromyographic testing revealed diffuse fibrillation potentials and positive sharp waves in limb muscles, especially in muscles below the elbow and stifle. Pathologic findings in skeletal muscles and peripheral nerves included neurogenic muscle atrophy, focal or diffuse loss of myelinated nerve fibers, myelinoaxonal necrosis, and variable demyelination or remyelination.
Ultrastructural changes included axonal degeneration, presence of numerous Büngner bands, and denervated Schwann cell subunits. The nature and distribution of abnormal electrophysiologic and pathologic findings were suggestive of a distal sensorimotor polyneuropathy, which we have termed idiopathic polyneuropathy of Alaskan Malamutes to distinguish this condition from hereditary polyneuropathy of Norwegian Alaskan Malamutes, last described in 1982.     

Distal peripheral polyneuropathy in a great dane

A spayed female five year old Great Dane dog was diagnosed as having a chronic, progressive, symmetrical distal polyneuropathy and concurrent hypothyroidism. Axonal degeneration and segmental demyelination were evident in teased nerve fiber preparations. Clinical signs included hindlimb weakness and muscle atrophy of the head and distal limbs. Diagnosis was based on clinical, electrophysiological, and nerve and muscle biopsy findings. Thyroxine supplementation for one month was of no benefit. The etiology of the polyneuropathy was not established but several causes were considered. The extent of demyelination in our case was of greater magnitude than described in a previous report of a similar idiopathic distal symmetrical polyneuropathy in a Great Dane.     

Insulinoma and Subclinical Peripheral Neuropathy in Two Dogs

Two dogs with diffuse, subclinical polyneuropathy associated with insulinoma are reported. Seizures were the dominant sign of central nervous system disease. One dog had clinical signs of facial nerve paralysis. Lesions in selected appendicular and cranial nerves included a mixture of demyelination, remyelination, and axonal degeneration. The incidence (range: 18-47%) of these changes far exceeded that of comparable nerves from six control dogs (range 0-11%). Myopathic and electrodiagnostic findings were compatible with the nerve changes.     

Peripheral neuropathy associated with malignant neoplasms in dogs

Common peroneal and ulnar nerves of 21 dogs between 2 and 15 years of age with malignant tumors were examined for possible paraneoplastic effects. Percent of abnormalities in single-teased fiber studies exceeded the confidence limits (P = 0.99) established for age-matched control dogs in 16 of 21 dogs (76%) with malignancies, none of which manifested clinical signs of polyneuropathy. The incidence of abnormalities was higher in common peroneal nerve (73%) than in ulnar nerve (57%). Lesions were characterized by a mixture of demyelination/remyelination and axonal degeneration; however, the former lesions predominated in most affected dogs. The severity of the neuropathy varied with different tumors, with the most severe lesions observed in a bronchogenic carcinoma (59%), a mammary adenocarcinoma (59%), a malignant melanoma (48%), and an insulinoma (47%).     

Prednisolone-responsive neuropathy in a cat

Chronic relapsing polyneuropathy was diagnosed in a 15-month-old cat with a 12-week history of limb weakness. The clinical course was punctuated by spontaneous remissions and relapse. There were two striking physical findings, weak withdrawal reflexes and atrophy of the proximal and distal limb muscles. Electrophysiological findings typical of a demyelinating motor neuropathy were present, namely small, dispersed compound muscle action potentials, markedly slow motor conduction and denervation potentials that were more prominent dis-tally. Muscle biopsies showed changes consistent with denervation and a paucity of myelinated axons in intramuscular nerve bundles. The neuropathy responded rapidly and completely to prednisolone administration, which was slowly tapered over several months.     

Vincristine-induced peripheral neuropathy in a dog.

A 12-year-old spayed Golden Retriever with mycosis fungoides was treated by use of a chemotherapy protocol that included vincristine. After 16 weekly vincristine injections, the dog began to have signs of peripheral neuropathy. Results of electromyographic examination were consistent with muscle denervation, and motor nerve conduction velocity was depressed. Histologic examination of a common peroneal nerve biopsy specimen revealed severe nerve fiber degeneration. Clinical response and pathologic evidence of improvement were observed after the drug had been discontinued for 2.5 months.     

Spastic syndrome in a Holstein bull: a histologic study

A 4-year-old Canadian holstein bull developed the spastic syndrome, an episodic but progressive disorder causing pelvic limb muscular spasms. A post-mortem study, including morphometry of skeletal muscles and teased peripheral nerve fibers of the pelvic limb, revealed mild type II skeletal muscle fiber atrophy and minimal, focal segmental demyelination with remyelination, and axonal degeneration in peripheral nerves. Such alterations are probably incidental or age-associated. Idiopathic muscular cramps is the most probable explanation of the clinical disease and is consistent with the absence of significant morphologic pathologic lesions.     

Cholecystoenterostomy for treatment of extrahepatic biliary tract obstruction in cats: 22 cases (1994-2003)

OBJECTIVE: To identify factors associated with outcome in cats with extrahepatic biliary tract obstruction (EHBTO) that undergo biliary diversion surgery. DESIGN: Retrospective case series. ANIMALS: 22 cats. PROCEDURES: Medical records of cats with surgically confirmed EHBTO that underwent cholecystoenterostomy were reviewed. RESULTS: Clinical signs and physical examination findings included vomiting, anorexia, icterus, lethargy, weakness, and weight loss. Common clinicopathologic abnormalities included high serum hepatic enzyme activities and serum bilirubin concentration. Abdominal ultrasonography was performed in 21 cats, and all 21 had findings consistent with EHBTO. Eleven of 15 cats in which blood pressure was monitored had intraoperative hypotension. Eighteen cats had anemia following surgery, and 14 cats had persistent hypotension. Extrahepatic biliary tract obstruction was a result of neoplasia in 9 cats and chronic inflammatory disease in 13. Fourteen cats survived long enough to be discharged from the hospital, but only 6 survived > 6 months after surgery, all of which had chronic inflammatory disease. Median survival time for cats with neoplasia (14 days) was significantly shorter than that for cats with inflammatory disease (255 days). No other variable was associated with outcome. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that cats with EHBTO secondary to neoplasia have a poorer prognosis than cats with EHBTO secondary to chronic inflammatory disease. However, the overall prognosis for cats with EHBTO undergoing cholecystoenterostomy must be considered guarded to poor, and the incidence of perioperative complications is high.     

Ultrasonographic and histopathological features in 8 cats with fibrotic small intestinal stricture

Benign stricture is an uncommon cause of chronic small intestinal obstruction in the cat. The purpose of this retrospective case series was to describe the ultrasonographic features, histopathological findings, and clinical presentation in a group of cats with benign small intestinal stricture. Inclusion criteria were cats presenting during the period 2010‐2017, and that had ultrasonography and small intestinal stricture confirmed at surgery. For each cat, clinical data and ultrasonographic findings were retrieved from the medical record, and histopathology, where available, was reviewed. Eight cats met the inclusion criteria. The location of strictures was duodenum (1/8), mid‐ to distal jejunum (4/8), and ileum (3/8). Ultrasonographic findings included gastric distension (8/8) and generalized (3/8) or segmental (5/8) intestinal dilation consistent with mechanical obstruction. Ingesta did not propagate beyond the strictured segment. Wall thickening was mild to moderate (3‐6 mm). Normal wall layering was disrupted in all cats. Strictures were predominantly hypoechoic (7/8) and associated with hyperechoic peri‐intestinal mesentery (6/8). Annular strictures (5/8) were less than 15 mm in length whereas long‐segment strictures (3/8) were greater than 15 mm in length. Histopathology showed transmural disease with fibrosis and inflammation (8/8), often (6/8) extending into the bordering mesentery. The mucosa was the most severely affected layer and epithelial injury accompanied the mucosal fibrosis/inflammation. Clinical presentation reflected delayed diagnosis of chronic bowel obstruction with debilitation (8/8), marked weight loss (8/8), and prerenal azotemia (5/8). Benign fibrostenotic stricture should be considered a differential diagnosis in debilitated young cats presenting with chronic bowel disease and ultrasonographic features of intestinal obstruction.     

IMAGING DIAGNOSIS—PULMONARY ALVEOLAR PROTEINOSIS IN A DOG

A young dog was presented for cyanosis and right heart failure. Radiographic and CT characteristics included right heart/pulmonary artery enlargement, hepatomegaly, abdominal effusion, and severe, generalized air‐space filling. Focal increased opacities were present in the peripheral lung, as were multiple pulmonary blebs and bullae. Echocardiographic findings were consistent with cor pulmonale and pulmonary hypertension. Bronchoscopic findings were consistent with chronic inflammation. Pulmonary alveolar proteinosis (PAP) was confirmed at necropsy. Pulmonary alveolar proteinosis is an interstitial lung disease that results in accumulation of phospholipoproteinaceous material and should be included as a differential diagnosis for dogs with these clinical and imaging characteristics.     

Facial neuropathy in dogs and cats: 95 cases (1975-1985)

The medical records of 79 dogs and 16 cats admitted to the New York State College of Veterinary Medicine between January 1975 and October 1985 with facial nerve dysfunction were reviewed. In 31 dogs and 8 cats, facial neuropathy was the only abnormal finding. In 48 dogs and 8 cats, the clinical findings most often noted in the records in addition to facial neuropathy were vestibular signs. Facial neuropathy appeared unassociated with gender or right vs left sides in both dogs and cats, or with hypothyroidism in dogs. Facial neuropathy was associated with increased age, with certain breeds in both dogs and cats, and with otitis media/interna and keratoconjunctivitis sicca in dogs. Causes of facial nerve dysfunction in dogs and cats included surgical and nonsurgical trauma, neoplasia, and otitis media/interna. Facial neuropathy was judged to be idiopathic in 74.7% of dogs and 25% of cats.     

Assessment of the neurologic effects of dietary deficiencies of phenylalanine and tyrosine in cats

OBJECTIVE: To determine the neurologic effects of reduced intake of phenylalanine and tyrosine in black-haired cats. ANIMALS: 53 specific pathogen-free black domestic shorthair cats. PROCEDURE: Cats were fed purified diets containing various concentrations of phenylalanine and tyrosine for < or = 9 months. Blood samples were obtained every 2 months for evaluation of serum aromatic amino acid concentrations. Cats were monitored for changes in hair color and neurologic or behavioral abnormalities. Three cats with neurologic deficits underwent clinical and electrophysiologic investigation; muscle and nerve biopsy specimens were also obtained from these cats. RESULTS: After 6 months, neurologic and behavioral abnormalities including vocalization and abnormal posture and gait were observed in cats that had received diets containing < 16 g of total aromatic amino acid/kg of diet. Electrophysiologic data and results of microscopic examination of muscle and nerve biopsy specimens from 3 cats with neurologic signs were consistent with sensory neuropathy with primary axonal degeneration. Changes in hair color were detected in cats from all groups receiving < 16 g of phenylalanine plus tyrosine/kg of diet. CONCLUSIONS AND CLINICAL RELEVANCE: Findings suggested that chronic dietary restriction of phenylalanine and tyrosine in cats may result in a predominantly sensory neuropathy. In cats, the long-term nutritional requirement for phenylalanine and tyrosine appears to be greater for normal neurologic function than that required in short-term growth experiments. Official present-day recommendations for dietary phenylalanine and tyrosine in cats may be insufficient to support normal long-term neurologic function.     

Histological and ultrastructural evidence that recurrent laryngeal neuropathy is a bilateral mononeuropathy limited to recurrent laryngeal nerves

Reasons for performing study: Recurrent laryngeal neuropathy (RLN) is a common and debilitating peripheral nerve disease of horses, but it remains unclear if this disease is a mono‐ or polyneuropathy. An understanding of the distribution of the neuropathological lesions in RLN affected horses is fundamental to studying the aetiology of this very significant disease of tall horses. Objective: To determine whether RLN should be classified as a mono‐ or polyneuropathy. Methods: Multiple long peripheral nerves and their innervated muscles were examined systematically in 3 clinically affected RLN horses Results: Severe lesions were evident in the left as well as right recurrent laryngeal nerves in all horses, both distally and, in one case, also proximally. No primary axonal lesions were evident in other nerves nor were changes found in their innervated muscles. Conclusions: RLN is not a polyneuropathy but should be classified as a bilateral mononeuropathy. Potential relevance: Genetic and local factors specifically affecting the recurrent laryngeal nerves in RLN‐affected horses should now be investigated further.     

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.     

Sensory neuropathy in a Border Collie puppy

The clinical, electrophysiological and pathological features of a purely sensory polyneuropathy in a Bordie Collie puppy are described. It was found to be ataxic, with a loss of proprioception and of pain sensation. Electrophysiological testing confirmed that the neuropathy was restricted to sensory function. Examination of nerve biopsy material revealed an axonopathy.     

Lesions in the cat spinal cord following local injections of 6-aminonicotinamide.

Lesions were made in the spinal cord of cats by means of local injections of 6-aminonicotinamide. The concentration needed to induce primary demyelination also caused extensive axonal death. In the early stages following injection there was evidence of astrocyte and oligodendrocyte destruction and with longer survival times most of the surviving demyelinated axons were remyelinated by Schwann cells. This experimental system indicates that Schwann cell remyelination of central axons follows astrocyte destruction, but it was not considered a suitable model system for the study of cellular relationships in remyelination because of the extensive concomitant axonal damage.     

CASE REPORT: Bilateral vision loss in a captive cheetah (Acinonyx jubatus)

The following case report describes a 1‐year‐old female cheetah (Acinonyx jubatus) with bilateral blindness and unresponsive pupils. For comparison, a second healthy 2.5‐year‐old male cheetah without visual deficits was also examined. Clinical examination of both animals included biomicroscopy, indirect ophthalmoscopy, tonometry, and electroretinography. The young female cheetah showed no menace response, no direct or indirect pupillary light reflex, and no dazzle reflex in either eye. Fundus lesions, as detected by indirect ophthalmoscopy, are described for the female animal. In both eyes, the fundus color was green/turquoise/yellow with multiple hyperpigmented linear lesions in the tapetal area around the optic nerve. The optic nerve head was dark gray and about half the normal size suggesting bilateral optic nerve hypoplasia and retinal dysplasia or differentially optic nerve atrophy and chorioretinal scarring. The ERG had low amplitudes in the right eye but appeared normal in the left eye compared with the male cheetah. Blood levels did not suggest current taurine deficiency. This is addressed to some degree in the discussion. Bilateral optic nerve hypoplasia or optic nerve atrophy is a rare anomaly in cats and has not yet been described in a cheetah.     

Peripheral neuropathy associated with dietary riboflavin deficiency in the chicken. I. Light microscopic study

Chickens fed a riboflavin-deficient diet from hatching had leg weakness and paralysis as early as 12 days of age. Signs worsened through day 16; after 35 days, recovery was evident. Sciatic nerves from affected chickens were enlarged. Significant microscopic lesions were confined to peripheral nerves and included tissue separation (suggesting interstitial edema), Schwann cell swelling, perivascular leukocytic infiltration, and segmental demyelination accompanied by accumulation of osmiophilic debris in Schwann cell cytoplasm. Axon degeneration was present, but was not a primary lesion. Acid phosphatase enzyme activity of Schwann cells was increased in affected nerves. These results demonstrate that dietary riboflavin deficiency causes a demyelinating peripheral neuropathy in young, rapidly growing chickens.     

Intravenous administration of docetaxel to cats with cancer

Background: The safety of IV administration of docetaxel to cats with cancer has not been reported. Objectives: Document adverse effects of IV administration of docetaxel to cats. Animals: Twenty‐one client‐owned cats with any confirmed malignancy. Methods: Cats received up to 5 docetaxel treatments, administered IV every 3 weeks. The initial dosage was 1.0 mg/kg, and dosages were increased by increments of 0.25 mg/kg in cohorts of 3 cats. Adverse events were determined by a CBC at days 7 and 21, serum chemistry and urine specific gravity at day 21, and medical histories provided by the owners. Results: Cats received docetaxel dosages ranging from 1.0 to 2.5 mg/kg, for a median of 2 treatments. Dose‐limiting toxicoses included fever, neutropenia, and vomiting, seen in 2 of the 4 cats treated at 2.5 mg/kg. Hypersensitivity reactions were infrequent (4 of the 21 cats) and mild. The maximum tolerated dosage was 2.25 mg/kg. Conclusions and Clinical Importance: Docetaxel can be administered IV to cats with a low incidence of adverse effects.