Hereditary encephalomyelopathy and polyneuropathy in an Alaskan husky

An Alaskan husky puppy was examined for a neurologic disease which began at six weeks of age with generalised paresis that progressed resulting in recumbency by 18 weeks. Thoracic limbs primarily exhibited lower motor neuron signs that included distal muscle atrophy and persistent elbow and carpal flexion that resisted manual extension. Pelvic limb signs primarily exhibited upper motor neuron and general proprioceptive deficits, but also included lower motor neuron signs. Abnormal vocalisation suggested a laryngeal paresis. Histopathologic lesions included a diffuse axonopathy and secondary demyelination in the nerves of the limbs and larynx and a similar bilaterally symmetrical degeneration in the spinal cord white matter suggestive of a dying back axonopathy. In addition, a degenerative process was present in nuclei in the brain stem and cerebellum. Recognition of this disease through clinical and pathologic examination in other related Alaskan Huskies suggested an autosomal recessive inherited disorder.     

Bromide toxicosis (bromism) in a dog treated with potassium bromide for refractory seizures.

A 4-year-old German Shepherd Dog was evaluated because of chronic hind limb lameness and recurrent seizures. Diagnostic evaluation of the dog confirmed rheumatoid arthritis and idiopathic epilepsy. The rheumatoid arthritis was treated with prednisone and piroxicam. The seizures were treated with phenobarbital plus clonazepam. The seizures were refractory and potassium bromide was substituted for clonazepam. The dog was reevaluated 4 months after initiation of potassium bromide treatment because of recurrence of arthritis signs. During hospitalization, the dog had neurologic signs, which progressed from depression to recumbency and stupor. Anisocoria, muscle pain, and hyporeflexia were noticed. Bromide toxicosis was diagnosed on the basis of toxic serum bromide concentration (2.7 mg/ml; therapeutic range, 1.0 to 2.0 mg/ml). Following cessation of potassium bromide treatment, the neurologic signs resolved. The seizures recurred 6 weeks after potassium bromide was discontinued. Bromide treatment was reinitiated at half the initial dosage. After 6 weeks, the serum bromide concentration was 1.9 mg/ml, and no seizures had been reported by the dog's owners. Therapeutic serum bromide concentrations in dogs has been reported to be 0.5 to 2.3 mg/ml. The serum bromide concentration at which toxic signs are expected is variable in human beings because individuals differ in their tolerance of the drug. Clinical trials are necessary to determine the toxic serum bromide concentrations in dogs. This case of bromism in a dog suggests that the dosage of potassium bromide should be based on serial measurement of serum bromide concentrations.     

Evaluation of glucose metabolism in three horses with lower motor neuron degeneration

OBJECTIVES: To determine whether increased glucose metabolism is the potential cause of the decreased plasma glucose curve determined after oral glucose tolerance testing in horses with lower motor neuron degeneration. ANIMALS: 3 horses with signs suggestive of lower motor neuron degeneration, 1 horse with malignant melanoma with multiple metastases, and an obese but otherwise healthy horse. Procedures-Glucose metabolism was assessed by use of the hyperglycemic clamp and euglycemic hyperinsulinemic clamp techniques. RESULTS: Mean rate of glucose metabolism of horses with lower motor neuron degeneration was significantly greater (mean, 3.7 times greater than control horses; range, 2.1 to 4.8 times greater) than that reported in 5 healthy control horses (41 +/- 13 micromol/kg/min vs 11 +/- 4.5 micromol/kg/min, respectively). In addition, one of the affected horses, an 8-year-old warmblood gelding, had a 5.6-times increased sensitivity to exogenously administered insulin, compared with that reported in 5 healthy control horses. Pancreatic insulin secretion was not insufficient in horses with lower motor neuron degeneration. Findings in the 2 diseased control horses were unremarkable. CONCLUSIONS AND CLINICAL RELEVANCE: Increased glucose metabolism in horses with lower motor neuron degeneration may be the cause of the decreased plasma glucose curve detected after oral glucose tolerance testing. This finding could aid in developing supportive treatments with respect to adequate glucose and vitamin E supplementation.     

Antemortem diagnosis of canine neural angiostrongylosis using ELISA

A 5-month-old female Kelpie developed paraparesis, hind limb ataxia and spinal hyperaesthesia 4 days after ovariohysterectomy. Neurological examination demonstrated upper motor neuron signs in the pelvic limbs with lower motor neuron signs in the tail. Cerebrospinal fluid analysis demonstrated an increased protein concentration and marked eosinophilic pleocytosis. The dog was known to have eaten rats, snails and slugs. A tentative diagnosis of neural angiostrongylosis was made and later confirmed using an ELISA based on soluble antigens obtained from larval 4 Angiostrongylus cantonensis. Antibody titres from the patient's serum and CSF were 800 and 6400, respectively. The dog was treated successfully with prednisolone. ELISA testing of serum may provide a non-invasive means for diagnosing neural angiostrongylosis in dogs.     

Neurological Manifestations of Hypothyroidism: A Retrospective Study of 29 Dogs

Neuromuscular signs in association with hypothyroidism are described in 29 dogs. Eleven dogs had lower motor neuron signs, 9 had peripheral vestibular deficits, 4 had megaesophagus, and 5 had laryngeal paralysis. Primarily older (mean = 9.5 years), large-breed dogs were affected, and there was no sex or breed predisposition. Duration of clinical signs before presentation ranged from 2 to 8 weeks (mean = 5 weeks). The diagnosis was based on (1) results of neurological examination (29 dogs); (2) electromyographic abnormalities (18 dogs), including fibrillation potentials (n = 18), positive sharp waves (n = 15), and complex repetitive discharges (n = 4); (3) high serum cholesterol concentration (10 dogs; mean = 335 mg/dL); (4) low response to thyroid-stimulating hormone (29 dogs; mean T₄ prestimulation concentration = 0.8 μg/dL; mean T₄ poststimulation = 1.2 μg/dL); and (5) good response to thyroxine supplementation (26 dogs). Dogs with vestibular deficits had abnormal brainstem auditory-evoked responses (BAER), including increased latencies of P₁-P₆ and decreased amplitude of P_4,5-N₅. Seven other dogs had similar BAER abnormalities without manifesting clinical signs of vestibular involvement. Three dogs with vestibular signs had fibrillation potentials and positive sharp waves without exhibiting lower motor neuron signs. All dogs were supplemented with levothyroxine (0.02 mg/kg P0 bid). The follow-up period ranged between 6 and 30 months (mean, 14 months). Serum T₄ concentrations were measured at least 3 times for each dog every 2 months (mean T₄ concentration = 2.6 μg/dL). All but 1 dog with lower motor neuron signs and 1 dog with vestibular signs recovered after 2 months (mean, 57 days). Signs of megaesophagus became progressively less severe over 4 months. Dogs with laryngeal paralysis improved partially after 5 months. We suggest that either vestibular or lower motor neuron signs, megaesophagus, or laryngeal paralysis may be the only clinical signs of an underlying, more generalized polyneuropathy associated with hypothyroidism. Electro-diagnostic abnormalities may be detected before clinical disease develops.     

Syringohydromyelia in Cavalier King Charles spaniels

Syringohydromyelia secondary to foramen magnum overcrowding is described in seven Cavalier King Charles spaniels. Clinical signs were consistent with a central spinal cord lesion. The most common signs were persistent scratching at the shoulder region with apparent neck, thoracic limb, or ear pain and thoracic limb lower motor neuron deficits. The diagnosis was made by magnetic resonance imaging. The syringohydromyelia is postulated to be a consequence of an occipital bone malformation resulting in a small caudal fossa and cerebellar herniation. Clinical signs improved but did not completely resolve when the dogs received treatment with corticosteroids or nonsteroidal anti-inflammatory drugs.     

Fibrocartilaginous emboli.

Fibrocartilaginous embolism (FCE) is an acute ischemic myelopathy, primarily of large or giant breed dogs, which results from occlusion of blood vessels within the spinal cord parenchyma or the adjacent leptomeninges by masses of fibrocartilage. Lateralizing and asymmetric neurologic deficits are very suggestive of spinal cord infarction. The diagnosis of FCE is made by eliminating causes of acute compressive myelopathy such as trauma and intervertebral disc herniation. Patients with lower motor neuron deficits secondary to FCE have a more guarded prognosis than those with upper motor neuron deficits. In most instances, if recovery is to occur, improvement will be evident within the first 10 days after the onset of clinical signs.     

Acute paraplegia associated with vasculitis in a dog with leishmaniasis

A 14-month-old female crossbreed dog with leishmaniasis, receiving allopurinol, was presented with acute paraplegia. A diagnosis of renal failure with pelvic limb lower motor neuron signs was made and the dog was euthanased. Histopathological examination demonstrated leukocytoclastic vasculitis in multiple organs. Malacia and haemorrhage affecting the spinal cord was associated with multiple foci of vasculitis within the nervous tissue. Rupture and thrombosis of inflamed vessels caused haemorrhage in the spinal cord and subsequent paralysis.     

Fibrocartilaginous embolism

Fibrocartilaginous embolism (FCE) is an acute myelopathy that affects primarily dogs and human beings, and occasionally other mammalian species. It is frequently associated with trauma or vigorous exercise; in dogs it tends to affect mature non-chondrodystrophoid and giant breeds. Signs are acute and frequently indicate a very lateralized or focal lesion within the spinal cord, with resultant disparities in sensory and motor function. Lower motor neuron disease is common and hyperesthesia is unusual. The primary differential diagnoses are concussive trauma and intervertebral disc herniation, but the acute onset of strongly lateralizing spinal cord deficits without hyperesthesia in a breed at risk is strongly suggestive of the FCE syndrome. Attention must be given to other systemic diseases that might also give rise to emboli in the absence of FCE. Diagnosis is based on history, clinical signs, and elimination of other differential diagnoses. Treatment is largely supportive, although high doses of methylprednisolone may be beneficial early in the course of the disease. Affected patients may make a functional recovery if deep pain sensation is preserved and there are not complete lower motor neuron signs in affected limbs or sphincters.     

Delayed swayback in goat kids, a study of 23 cases

The results of a retrospective study of 23 goat kids with delayed swayback are reported. Principal clinical signs were ataxia, loss of postural control, spasticity of the hindlimbs, and muscular weakness, often progressing to permanent recumbency. Denervation of skeletal muscles was demonstrated by electromyography in 2 kids. Three kids slowly recovered during hospitalisation. Histopathological changes were characterized by degeneration of selected neuronal populations with their processes within the central and the peripheral nervous system. Affected systems included upper motor neuron, vestibular, general proprioceptive, and lower motor neuron pathways, with additional involvement of the cerebellar cortex in some animals. Our findings, including limited ultrastructural observations, support the notion that the neuraxon rather than the myelin sheath is the prime target of disease in delayed swayback. The available copper values of affected kids and their unaffected herd mates were significantly lower than those of random control goats, which provides further support for a role of copper deficiency in the aetiology of this disease in the goat.     

Intraoperative use of ultrasonography during continuous dorsal laminectomy in two dogs with caudal cervical vertebral instability and malformation ("Wobbler syndrome")

OBJECTIVE: To describe an intraoperative ultrasound imaging technique during dorsal laminectomy in 2 dogs with caudal cervical vertebral instability and malformation (CCVIM, "Wobbler syndrome"). STUDY DESIGN: Clinical case report. SAMPLE POPULATION: Two dogs with CCVIM. RESULTS: On neurologic examination there was tetraparesis with upper motor neuron signs in the thoracic limbs and lower motor neuron signs in the pelvic limbs in dog 1, and hyperreflexia of the rear limbs, normoreflexia of the right front limb, and hyporeflexia of the left front limb of dog 2. Both dogs had signs of marked cervical pain and radiographic signs of cervical spinal cord compression. Intraoperative ultrasonography of the spinal cord revealed protruding intervertebral disc at C5-6 (dog 1) and C6-7 (dog 2), and the parallel borders of the spinal cord and central canal after decompression. Continuous dorsal laminectomy (CDL) resulted in improvement over 16 months (dog 1) and 20 months (dog 2). CONCLUSIONS: Intraoperative ultrasonographic imaging of the cervical spinal cord after CDL was helpful in determining adequate decompression (postlaminectomy) of the spinal cord in relation to the ventral and lateral compressive component(s) and to image the protruding intervertebral disc. CLINICAL RELEVANCE: Intraoperative ultrasonography can be used to provide valuable information on the spinal cord and surrounding soft tissues for the neurosurgeon.     

Delayed swayback in goat kids,a study of 23 cases

Summary

The results of a retrospective study of 23 goat kids with delayed swayback are reported. Principal clinical signs were ataxia, loss of postural control, spasticity of the hindlimbs, and muscular weakness, often progressing to permanent recumbency. Denervation of skeletal muscles was demonstrated by electromyography in 2 kids. Three kids slowly recovered during hospitalisation.

Histopathological changes were characterized by degeneration of selected neuronal populations with their processes within the central and the peripheral nervous system. Affected systems included upper motor neuron, vestibular, general proprioceptive, and lower motor neuron pathways, with additional involvement of the cerebellar cortex in some animals. Our findings, including limited ultrastructural observations, support the notion that the neuraxon rather than the myelin sheath is the prime target of disease in delayed swayback. The available copper values of affected kids and their unaffected herd mates were significantly lower than those of random control goats, which provides furt her support for a role of copper deficiency in the aetiology of this disease in the goat.     

Neospora caninum infection in three dogs

Infection with Neospora caninum in three young dogs is described. The predominant clinical signs were lower motor neuron deficits of the pelvic limbs, bladder and rectum. In two cases there was liver infection and dysfunction. The younger dogs had an acute onset rapidly progressive syndrome. The older dog had a similar but more chronic course. The diagnosis was confirmed by an immunofluorescence antibody test. The parasite is sensitive to clindamycin and trimethoprim/sulphonamide preparations, however the prognosis for return to function is poor especially if muscle contracture has occurred.     

Bromide intoxication in a 3-year-old Thoroughbred filly

A 3-year-old Thoroughbred filly presented with a several-month history of weight loss, polydipsia and polyuria, intermittent diarrhoea and behavioural changes and intermittently uncoordinated gait. Neurological examination revealed hyperexcitability, bilaterally reduced pupillary light reflexes and quadrilateral ataxia with proprioceptive deficits more obvious in the forelimbs than in the hindlimbs. A multifocal neurological lesion was suspected. The laboratory finding of a persistent hyperchloraemia and an apparent negative anion gap prompted measurement of serum bromide concentration and subsequently confirmed bromide intoxication. Further questioning of the trainer revealed that the filly had been administered oral potassium bromide for behavioural modification over several months. Clinical signs of bromide intoxication resolved within 20 days following the last bromide administration, without specific medical intervention. This case report describes the risk of inadvertent bromide overdosing in horses and highlights the need for control of bromide use in the equine industry.     

What is your diagnosis? Marked hyperchloremia in a dog

Abstract: A 5‐year‐old neutered male Cavalier King Charles Spaniel was evaluated for a 3‐week history of progressive paresis. The dog had been receiving potassium citrate capsules to acidify urine for the past 2 years because of an earlier history of urolithiasis. Results of neurologic examination, spinal cord radiography, and magnetic resonance imaging of the skull and spinal cord revealed no lesions that could have accounted for the neurologic signs. The main abnormalities on a clinical chemistry profile were marked hyperchloremia (179 mmol/L, reference interval 108–122 mmol/L) and an anion gap of ?50.4 mmol/L (reference interval 16.3–28.6 mmol/L). Because of the severe hyperchloremia, serum bromide concentration was measured (400 mg/dL; toxic concentration >150 mg/dL; some dogs may tolerate up to 300 mg/dL). Analysis of the potassium citrate capsules, which had been compounded at a local pharmacy, yielded a mean bromide concentration of 239 mg/capsule. Administration of the capsules was discontinued and there was rapid resolution of the dog's neurologic signs. This case of extreme bromide toxicity, which apparently resulted from inadvertent use of bromide instead of citrate at the pharmacy, illustrates the importance of knowing common interferents with analyte methodologies and of pursing logical additional diagnostic tests based on clinical and laboratory evidence, even when a patient's history appears to rule out a potential etiology.     

A progressive neuronopathy in the young cairn terrier

The clinical signs and neuropathological changes of a nervous disease of pedigree cairn terriers are described. Three animals, of both sexes, between five and seven months of age showed hind leg weakness, quadriparesis, ataxia, loss of superficial and deep reflexes and tremor of the head. Pathologically there was chromatolysis of neurons in the spinal cord and brain stem. Although Wallerian-type degeneration was present in the spinal cord and peripheral nerves, its severity did not correlate with the intensity of the neuronal changes. This suggests that the chromatolysis observed may reflect a primary neuronal abnormality rather than represent a secondary change resulting from a primary degeneration of peripheral axons. Although the age of onset and some of the clinical signs are similar to those seen with globoid cell leucodystrophy (an inherited disease which also affects cairn terriers), the presence of lower motor neuron paralysis and the absence of signs of severe brain involvement in progressive neuronopathy should enable the conditions to be distinguished clinically.     

Reduced tongue tone associated with degeneration of the hypoglossal nerve nucleus in a horse with equine motor neuron disease

Equine motor neuron disease (EMND) is a condition characterised by generalised weakness and muscle atrophy associated with degeneration of motor neurons in the ventral horns of the spinal cord. Despite the frequent detection of cranial nerve nuclei pathology during post mortem examination, associated clinical signs are rarely reported. This report describes a case of EMND in a pony gelding that presented with clinical signs of diffuse neuromuscular weakness associated with marked flaccidity of the tongue, making differentiation from similar neuromuscular conditions, particularly botulism, extremely challenging.     

Spinal cord medulloepithelioma in a dog

Medulloepithelioma, an embryonal neural tumor, was diagnosed in a 6-month-old Bullmastiff. Clinical signs of incomplete, upper motor neuron, transverse myelopathy involving the hindlimbs were observed on examination. Myelography was required to identify the cause of clinical abnormality. The tumor involved the L1 spinal cord segment.     

Coral Snake (Micrurus Fulvius Fulvius) Envenomation In Five Dogs: Present And Earlier Findings

The purpose of this study is to report on five cases of coral snake envenomation in the dog to substantiate earlier findings in four dogs reported previously, and to describe any additional clinical features that have not yet been noted. The combined results from both studies allow for a more accurate projection of the frequency of certain clinical signs. Both groups showed signs of lethargy, lower motor neuron weakness (8 of 9 dogs) and varying hematologic changes with hemolysis and hemoglobinuria occurring most commonly (7 of 9 dogs). Cardiac dysrhythmias were recorded infrequently (2 of 9 dogs). Not reported previously was the presence of a subtle bite wound located on the upper or lower lip of three dogs in the present series. An unexpected finding in this second series was the occurrence of an anaphylactoid reaction in one dog presumably attributed to the antivenin. Close examination of the lip might reveal the site of envenomation (as found in 4 of 9 dogs from both studies). Treatment with coral snake antivenin should be given as early as possible and followed by close observation for signs of anaphylaxis. The results of this study substantiate earlier findings and provide for a larger data base for further reference.     

Functional outcome in dogs after surgical treatment of caudal lumbar intervertebral disk herniation.

Caudal lumbar disk herniations (i.e., third lumbar [L3] to seventh lumbar [L7] intervertebral spaces) represent approximately 15% of surgically treated thoracolumbar disk herniations in dogs. A retrospective case-control study was conducted to determine the postoperative outcome of this subset of dogs in the authors' neurosurgical practice. Medical records (1985 through 1996) were reviewed for dogs with caudal lumbar disk herniation confirmed at surgery. Thirty-six cases were identified. For each case, two dogs that underwent surgical treatment for upper motor neuron thoracolumbar disk herniation (tenth thoracic [T10] to L3 intervertebral spaces) were selected as controls. Probabilities of functional recovery for cases and controls were 81% and 85%, respectively (p value of 0.49). In dogs with caudal lumbar disk herniation, complete sensorimotor loss was the only significant predictor of functional recovery (p value of 0.005). Disk herniations that occur at the thoracolumbar junction and those that occur in the caudal lumbar region should not be considered to be different in terms of surgical treatment and postoperative outcome. The lower motor neuron signs that often accompany caudal lumbar disk herniation reflect the site of spinal cord injury and do not necessarily predict a poor prognosis.