Scintigraphic evaluation of pulmonary perfusion in dogs experimentally infected with Dirofilaria immitis

Pulmonary arterial perfusion was evaluated by perfusion lung scans in ten dogs experimentally infected with heartworm. After larval inoculation, scans were done once a month for 11 months. In 8 of 10 dogs, pulmonary arterial perfusion deficits were detected. The perfusion deficits involved the left cranial, right cranial, and right caudal lung lobes. Generally, there was a poor correlation between vascular abnormalities detected on the survey thoracic radiographs and the perfusion deficits detected by lung scanning. The perfusion deficits did not produce clinical signs or pulmonary infarction.     

Asymmetrical focal neurological deficits in dogs and cats with naturally occurring tick paralysis (Ixodes holocyclus): 27 cases (1999-2006)

OBJECTIVE: To describe basic epidemiological features, clinical characteristics and outcomes of asymmetrical focal neurological deficits identified in dogs and cats with naturally occurring tick paralysis (Ixodes holocyclus). DESIGN: A retrospective study. PROCEDURE: Computer records were reviewed for all dogs and cats treated for tick paralysis between July 1999 and June 2006 at a suburban veterinary hospital in Newcastle, New South Wales. RESULTS: Neurological deficits were identified in 17/197 dogs and 10/89 cats and included unilateral facial paralysis (14 dogs; 2 cats), anisocoria (4 dogs; 7 cats), unilateral loss of the cutaneous trunci reflex (1 dog; 1 cat) and Horner's syndrome in 2 cats with anisocoria. Occurrence of deficits was not linked to season, severity of tick paralysis, breed, age, sex or body weight. With facial paralysis and anisocoria, the site of tick attachment was invariably on the head or neck and always ipsilateral to the facial paralysis. By contrast, with anisocoria alone, no consistent relationship was noted between any one pupillary dimension and the side of tick attachment. With cutaneous trunci deficits the site of tick attachment was the ipsilateral caudal axilla. Compared with recovery times from generalised signs of tick paralysis, those for facial paralysis were significantly longer (days to weeks; P < 0.001), those for anisocoria showed no significant difference (P = 0.25) and those for cutaneous trunci deficits lagged by 6 and 7 days. CONCLUSIONS: Asymmetrical focal neurological deficits are a consistent finding in a proportion of dogs and cats with naturally occurring tick paralysis due to I. holocylcus.     

Neurologic deficits associated with severe hyponatremia in 2 foals

Objective: To describe the neurologic deficits associated with profound hyponatremia in 2 critically ill foals. Series summary: A 4‐month‐old Thoroughbred colt and an 11‐day‐old Paint filly presented for acute diarrhea and depression. Severe neurologic deficits including blindness and head pressing were noted upon initial examination along with marked hyponatremia observed on biochemistry profile. Aggressive intravenous sodium replacement increased the serum sodium concentration to subnormal values with concurrent resolution of neurologic deficits. Intensive monitoring and fluid therapy were continued; the Thoroughbred colt was euthanized due to lack of response to the primary disease while the Paint filly was discharged clinically healthy without further complications. New or unique information provided: Mild hyponatremia (122–132 mEq/L) is a common clinicopathologic finding in equine medicine associated with a variety of diseases. The vast majority of horses with mild hyponatremia do not demonstrate direct clinical manifestations as a result of low serum sodium concentration. However, when severe acute hyponatremia occurs (<122 mEq/L), such as with acute enterocolitis, subtle to profound neurologic deficits may be observed and immediate and rapid treatment as well as serial evaluations of serum sodium concentration are warranted. Significant, and potentially permanent, neurologic deficits can occur if water balance and tonicity are not properly addressed. The cases presented here describe additional cases of a previously published disease in foals, acute hyponatremia and associated neurologic deficits, and describe the microscopic examination of the central nervous system in one foal that did not survive.     

Acquired idiopathic laryngeal paralysis as a prominent feature of generalised neuromuscular disease in 39 dogs

A retrospective evaluation of 17 dogs treated surgically for idiopathic acquired laryngeal paralysis demonstrated a marked variability in outcome, with many dogs continuing to exhibit weakness and exercise tolerance. In a subsequent prospective study, 22 consecutive affected dogs were tested for neurological deficits by neurological examination, electrodiagnostic evaluation, and blood analysis to measure thyroxine and thyroid-stimulating hormone and to detect any evidence of myasthenia gravis. Clinical neurological deficits and/or electrodiagnostic abnormalities were found in each case. There was limited evidence that specific neurological deficits were associated with a poor prognosis for full recovery of exercise tolerance. None of the dogs was positive for anti-acetylcholine receptor antibodies, and only three showed evidence of thyroid dysfunction.     

Neurologic examination of the horse

Methodology for the neurologic examination in the equine species is described. Information is organized to assist the reader in defining neurologic deficits and in localizing lesions to the major subdivisions within the central or peripheral nervous system. Numerous examples of deficits are presented to assist the reader in recognition of common neurologic disease states.     

Presumed and confirmed striatocapsular brain infarctions in six dogs

OBJECTIVE: To describe the clinical and diagnostic features of the canine sensorimotor syndrome caused by striatocapsular brain infarctions (SCI). ANIMALS STUDIED: Six dogs with diagnostic imaging or postmortem evidence of SCI. PROCEDURES: Medical records of dogs with SCI were retrospectively reviewed and the signalment, history, clinical signs, antemortem clinicopathologic test results, diagnostic imaging findings, case outcomes, and pathologic findings recorded. RESULTS: All dogs had an acute onset of nonprogressive homonymous visual field deficits and contralateral general proprioceptive (GP) deficits. Contralateral hemiparesis and facial hypalgesia were noted in 5/6 dogs. CT scans were normal in 2/4 dogs, and revealed poorly defined hypoattenuating lesions in the subcortical white matter in two dogs. MRI exams were performed in 5/6 dogs and revealed unilateral, variably sized, striatocapsular lesions consistent with nonhemorrhagic infarctions. Diagnostic imaging (6/6) and postmortem examinations (2/6) suggested that SCI resulted from lesions in the vascular territories of the rostral choriodal (6/6) and lenticulostriate arteries (2/6). Diseases predisposing to infarction were not identified in 5/6 dogs. Improvements in mentation, behavior, proprioceptive deficits, and hemiparesis were seen in surviving dogs, but persistent, symptomatic sensory deficits were noted during the follow-up period. CONCLUSIONS: SCI should be considered as a differential diagnosis for dogs with acute onset, nonprogressive homonymous hemianopia, contralateral GP deficits or hemiparesis, and facial hypalgesia. MRI is the preferred modality for the antemortem imaging diagnosis of SCI. Although partial recovery occurred in all surviving dogs, visual and facial sensory disturbances persisted.     

Findings on low-field cranial MR images in epileptic dogs that lack interictal neurological deficits

Recurrent seizuring is a common neurological problem in dogs and can present diagnostic difficulties for the attending clinician. Associated interictal neurological deficits strongly suggest brain disease but the frequency of structural abnormalities in patients without such deficits is unknown. In this study the prevalence of clinically significant magnetic resonance imaging (MRI) abnormalities was determined in two groups of interictally normal dogs, those younger than 6 years and those older than 6 years of age. In the former group, only 1/46 dogs (2.2%) had significant MRI abnormalities, whereas in the latter group, 8/30 (26.7%) were abnormal. None of the dogs had an identifiable metabolic cause for the seizures. These findings suggest that the diagnostic yield of advanced neuroimaging techniques in young seizuring dogs without interictal neurological deficits is low, but reaffirms their value in similar older individuals.     

Potential central nervous system complications of von Willebrand's disease.

Three Doberman pinschers were presented on emergency referral for progressive neurological deficits. All three dogs had a similar onset of clinical signs associated with an apparently minor traumatic event. Each dog progressed to significant neurological dysfunction including paraplegia, tetraplegia, and/or loss of deep pain sensation. None of the animals was apparently affected by cervical vertebral instability ("Wobbler's Syndrome"). All were confirmed to have von Willebrand's disease. In all cases, significant epidural hemorrhage was identified. The etiology of each hemorrhage, however, was different for each animal. The cases presented here demonstrate a potential relationship between neurological deficits and the patient's ability to effectively coagulate blood. Hemostatic abnormalities, such as von Willebrand's disease, should be included as possible differential diagnoses or contributing factors in animals demonstrating neurological deficits. These abnormalities should especially be considered following trauma, intervertebral disk extrusion, or spinal surgery.     

Cauda equina neuritis: a chronic idiopathic polyneuritis in two horses

Two cases of cauda equina neuritis are compared and contrasted. Neurological deficits of the tail and perineum were noted and functional deficits were seen in gait, urination, defecation and cranial nerve function. Lesions consisted of nonsuppurative inflammation of the nerve trunks and proliferation of the perineurium of the cauda equina. Cranial nerve involvement in one case supported a diagnosis of polyneuritis equi rather than cauda equina neuritis. The possible etiologies and pathogenesis of this disease are discussed.     

Sensory neuropathy in a Jack Russell terrier

A six-year-old male Jack Russell terrier was referred for investigation of an abnormal hindlimb stance and unresolving lesion on the dorsum of the right hindfoot. Clinical examination revealed cutaneous sensory and proprioceptive deficits affecting predominantly the hindlimbs. However, no motor deficits were evident. A sensory abnormality was confirmed by histological examination of a biopsy of a lateral branch of the superficial peroneal nerve, which contained only a single myelinated fibre. The condition was diagnosed as a sensory neuropathy, a disorder previously unrecognised in this breed.     

Solitary plasmacytoma of bone in two successfully treated cats

This is the first report of feline solitary plasmacytoma of bone. We describe the clinical, clinico-pathological, radiographic and pathological findings of two successfully treated cats with long-term follow-up. The first case presented with spinal pain and neurological deficits. Radiographs demonstrated sclerosis of lumbar vertebra L6 and a myelogram confirmed interference to flow of contrast in the L4-7 region. A biopsy of L6 revealed neoplastic plasma cell infiltration. There was no evidence of paraproteinaemia on serum protein electrophoresis. The cat underwent hypofractionated megavoltage radiotherapy. Clinical signs resolved completely and 4 years after diagnosis the cat remains well and has no electrophoretically detectable paraproteinaemia. The second case presented with neurological deficits of the tail and spinal radiographs revealed extensive osteolysis of the sacrum. A biopsy of sacral bone demonstrated neoplastic plasma cell infiltration. The animal was normoglobulinaemic. The cat improved clinically with induction chemotherapy (melphalan and methylprednisolone). The same chemotherapeutics were continued at maintenance doses for 4.3 years, at which time there was recurrence of neurological deficits and a palpable sacral mass. Cytological examination of a fine needle aspirate confirmed recurrence of plasma cell neoplasia. A low concentration monoclonal paraproteinaemia was detected. Vincristine was administered resulting in resolution of neurological deficits and a palpably smaller sacral mass. Eighteen months into vincristine therapy, there was recurrence of clinical signs and the cat was euthanased, more than 6 years after the initial diagnosis.     

Listeriosis

The signs of bovine listeriosis include depression and variable cranial nerve deficits indicative of brain stem inflammation. Because a wide range of cranial nerve deficits exists in bovine listeriosis patients, a thorough neurologic examination and cerebrospinal fluid analysis are essential to accurate diagnosis. Treatment should consist of intensive antibiotic therapy owing to the intracellular location of the causative organisms and should also address metabolic acidosis in those patients with loss of buffer because of excessive salivation. The public health implications of bovine listeriosis require the veterinarian to protect all persons attending the bovine patient affected with listeriosis.     

Iatrogenic brainstem injury during cerebellomedullary cistern puncture

Cerebrospinal fluid collection is fundamental to the investigation of central nervous system disorders although it carries potential risks. Herein we report the clinical signs and magnetic resonance (MR) imaging findings associated with needle injury to the brainstem during cerebellomedullary cistern puncture in four dogs. Three dogs were nonambulatory tetraparetic with cranial nerve deficits and one dog had unexplained left thoracic limb paresis. In MR images, there were conspicuous T2 hyperintensities in the myelencephalon in all dogs. In T2* gradient echo images, the lesions were hypointense in two dogs with multiple cranial nerve deficits, and hyperintense in another dog. One dog was euthanized due to sudden neurologic deterioration 12 days later, one died shortly after MR imaging, and a third was euthanized due to concurrent cervical spondylomyelopathy. The fourth dog recovered gradually. Diagnosis was confirmed histopathologically in one dog and was presumptive based on clinical signs and MR findings in three dogs. None of the dogs with cranial nerve deficits recovered, only the one dog with left thoracic limb paresis and concurrent syringomyelia.     

Clinical and neurological characteristics of aortic thromboembolism in dogs

OBJECTIVES: To characterise the clinical presentation and neurological abnormalities in dogs affected by aortic thromboembolism. METHODS: The medical records of 13 dogs diagnosed with aortic thromboembolism as the cause of the clinical signs, and where a complete neurological examination was performed, were reviewed retrospectively. RESULTS: The onset was acute in only four dogs, chronic in five dogs (with all of these presenting as exercise intolerance) or chronic with acute deterioration in four dogs. Dogs with an acute onset of clinical signs were more severely affected exhibiting neurological deficits, while dogs with a chronic onset of disease predominantly presented with the exercise intolerance and minimal deficits. The locomotor deficits included exercise intolerance with pelvic limb weakness (five of 13), pelvic limb ataxia (one of 13), monoparesis (two of 13), paraparesis (two of 13), non-ambulatory paraparesis (two of 13) and paraplegia (one of 13). There was an apparent male predisposition and the cavalier King charles spaniel was overrepresented. CLINICAL SIGNIFICANCE: The rate of onset of clinical signs appears to segregate dogs affected by aortic thromboembolism into two groups, with different clinical characteristics and outcomes. Dogs with an acute onset of the clinical signs tend to be more severely affected, while dogs with a chronic onset predominantly present with exercise intolerance. It is therefore important to consider aortic thromboembolism as a differential diagnosis in dogs with an acute onset of pelvic limb neurological deficits and in dogs with longer standing exercise intolerance.     

Pancarpal Arthrodesis in the Dog: A Review of Forty-five Cases

This report describes an open surgical technique for pancarpal arthrodesis and its efficacy in 45 canine cases. Indications for carpal arthrodesis include hyperextension injuries, severe fracture/luxations, end-stage arthritis, and selected neurologic deficits. Chronic joint instability was the major indication for surgery (76%). Degenerative joint disease (18%) and neurologic deficits (6%) accounted for the other cases. In a subjective owner survey, 97% of the owners reported that their animals' gait improved following arthrodesis, and 74% stated that their animals walked and ran normally.     

Temporohyoid osteoarthropathy in 33 horses (1993-2000)

A retrospective study of the medical records of 33 horses was performed to determine the clinical and diagnostic abnormalities associated with temporohyoid osteoarthropathy. Data collected from medical records included signalment, presenting complaints, history, physical examination findings, laboratory data, results of diagnostic imaging studies, and treatments. Follow-up information was obtained from a review of case records; by telephone conversation with the owner, veterinarian, or trainer; or by both methods. Of 33 horses with temporohyoid osteoarthropathy, 29 presented with facial nerve (cranial nerve VII) deficits and 23 presented with vestibulocochlear nerve (cranial nerve VIII) deficits. Guttural pouch endoscopy was more reliable than radiography for diagnosis. Of horses with unilateral clinical signs, 22.6% actually had bilateral disease. Magnetic resonance imaging and computed tomography identified the lesions in all horses in which these tests were performed. Of 30 horses for which follow-up information was obtained, 20 (67%) were alive. Eight horses were euthanized and 1 died because of problems associated with temporohyoid osteoarthropathy. Nineteen of 20 surviving horses (95%) were considered by the owner or trainer to be suitable for athletic use. Twelve surviving horses (60%) had residual facial nerve deficits; 11 horses (55%) had residual vestibulocochlear nerve deficits. Horses with temporohyoid osteoarthropathy have a fair prognosis for return to some type of athletic function, but there is risk of acute death. The majority of horses would be expected to have some residual cranial nerve dysfunction, and it could take a year or longer for maximal improvement to occur.     

Suspect novel adverse drug reactions to trimethoprim-sulphonamide combinations in horses: a case series

Adverse drug reactions to trimethoprim-sulphonamide combinations are common in many species, manifesting as gastrointestinal tract disorders, dermatopathies and blood dyscrasias. In this case series, neurological abnormalities in 4 horses being treated with trimethoprim-sulphonamide combinations at normal dosages and in one foal that received an overdose are described. The horses developed hypermetric gait, agitation and erratic behaviour. All signs resolved once medication was withdrawn, and no horse had residual deficits. No other cause for observed neurological deficits could be determined. These clinical signs appear to represent a novel adverse drug reaction to some commonly used antimicrobial combinations.     

Clinical and pathological features of a cerebellar oligodendroglioma in a cat

A cerebellar oligodendroglioma was responsible for the progressive development of neurological deficits in a six-year-old castrated male domestic longhaired cat. These abnormalities included a head tilt and loss of balance, nystagmus, proprioceptive deficits and eventually a fine head tremor and hypermetria of the forelimbs. The tumour was found to have destroyed most of the cerebellar grey matter, the flocculus, and the cerebellar roof nuclei on the right hand side. Increased peri-axonal space and axonal vacuolation were visible in fibre tracts which connected to the cerebellum. The clinical signs and location of the tumour are related to the functional anatomy of the cerebellum.