Equine herpesvirus type 1 (EHV-1) myeloencephalopathy: a case report

An outbreak of neurological disease occurred in a well-managed riding school. Ataxia and paresis were observed in several horses, five of which became recumbent and were euthanized. Post-mortem analysis revealed scattered haemorrhages along the spinal cord, that were reflected by multiple haemorrhagic foci on formalin-fixed sections, with the thoracic and lumbar segments being the most affected. Pathohistologically, perivascular mononuclear cuffing and axonal swelling, especially in the white matter, were evident. Parallel to the course of disease, alterations in myelin sheets and activation of astrocytes and microglial cells were also observed. Virological findings confirmed an acute equine herpesvirus type 1 infection and virus was isolated from the spinal cord of a 26-year-old mare.     

Leukoencephalomyelopathy in cats linked to abnormal fatty acid composition of the white matter of the spinal cord and of irradiated dry cat food

Four outbreaks of leukoencephalomyelopathy in colonies of SPF cats on a long‐term diet of irradiated dry cat food were observed in the Netherlands between 1989 and 2001. As a primary defect in myelin formation was suspected to be the cause of the disease and myelin consists mainly of lipids and their fatty acids, we investigated the fatty acid composition of the white matter of the spinal cord of affected and control cats and of irradiated and non‐irradiated food. The irradiated food had low levels of alpha‐linolenic acid compared to linoleic acid as well as a high total omega‐6:omega‐3 ratio of 7:1 in the irradiated and of 2:1 in the non‐irradiated food. The white matter of the spinal cord showed low levels of linoleic acid and absence of alpha‐linolenic acid in affected cats as well as absence of lignoceric and nervonic acid in both affected and control cats. These abnormalities in fatty acid composition of the white matter of the spinal cord may reflect an increased need for alpha‐linolenic acid as a substrate for longer chain omega‐3 fatty acids to compose myelin and thus indicate a particular species sensitivity to dietary deficiency in omega‐3 polyunsaturated fatty acids, particularly alpha‐linolenic acid in cats. Our findings indicate that abnormalities in fatty acid metabolism in myelin play an essential role in the pathogenesis of this acquired form of leukoencephalomyelopathy in cats.     

THE USE OF MAGNETIC RESONANCE IMAGING IN EVALUATING HORSES WITH SPINAL ATAXIA

To determine the accuracy of magnetic resonance imaging for diagnosing cervical stenotic myelopathy in horses, 39 horses with spinal ataxia and 20 control horses underwent clinical and neurologic examinations, cervical radiographs, euthanasia, magnetic resonance (MR) imaging of the cervical spine and necropsy. Twenty‐four horses were diagnosed with cervical stenotic myelopathy, 5 with cervical vertebral stenosis, 7 with idiopathic ataxia, 3 horses had other causes of ataxia, and 20 were controls. The MR images were assessed for spinal cord intensity changes, presence of spinal cord compression, spinal cord compression direction, shape of spinal cord, and the presence of synovial cysts, joint mice, and degenerative joint disease. The height, width, and area of the spinal cord, dural tube and vertebral canal were measured. The identification of spinal cord compression on MR images was significantly different in horses with cervical stenotic myelopathy (P < 0.02), but in the cervical stenotic myelopathy group the identification of spinal cord compression on MR images had poor to slight agreement with histopathologic evidence of compression (κ = 0.05). Horses with cervical stenotic myelopathy were more likely to have a T2 hyperintensity in the spinal cord (P < 0.05). Horses with cervical stenotic myelopathy or cervical vertebral stenosis were more likely to have degenerative joint disease than control horses or horses with other or idiopathic ataxia.     

Developmental delay in islet-1-positive motor neurons in chick spina bifida

Spina bifida aperta (SBA) is a congenital malformation of the spinal cord with complications such as spinal ataxia and bowel and bladder dysfunction. We have developed a chick model with surgery-induced SBA that shows spinal ataxia after hatching. In the present study, motor neurons in the early stages in chicks with and without SBA were observed by immunohistochemical staining with a monoclonal antibody against Islet-1, a motor neuron marker. Delay in migration and maturation of motor neurons was observed in SBA. Although the final numbers of Islet-1-positive neurons in these two groups were not different, a defect in the production and elimination of excess motor neurons in the early developmental stages in the SBA group may be involved in the pathological mechanism of the motor complications of this disease.     

Pathophysiology,Clinical Importance,and Management of Neurogenic Lower Urinary Tract Dysfunction Caused by Suprasacral Spinal Cord Injury

Management of persistent lower urinary tract dysfunction resulting from severe thoracolumbar spinal cord injury can be challenging. Severe suprasacral spinal cord injury releases the spinal cord segmental micturition reflex from supraspinal modulation and increases nerve growth factor concentration in the bladder wall, lumbosacral spinal cord, and dorsal root ganglion, which subsequently activates hypermechanosensitive C‐fiber bladder wall afferents. Hyperexcitability of bladder afferents and detrusor overactivity can cause urine leaking during the storage phase. During urine voiding, the loss of supraspinal control that normally coordinates detrusor contraction with sphincter relaxation can lead to spinal cord segmental reflex‐mediated simultaneous detrusor and sphincter contractions or detrusor‐sphincter dyssynergia, resulting in inefficient urine voiding and high residual volume. These disease‐associated changes can impact on the quality of life and life expectancy of spinal‐injured animals. Here, we discuss the pathophysiology and management considerations of lower urinary tract dysfunction as the result of severe, acute, suprasacral spinal cord injury. In addition, drawing from experimental, preclinical, and clinical medicine, we introduce some treatment options for neurogenic lower urinary tract dysfunction that are designed to: (1) prevent urine leakage arising because of detrusor overactivity during bladder filling, (2) preserve upper urinary tract integrity and function by reducing intravesical pressure and subsequent vesicoureteral reflux, and (3) prevent urinary tract and systemic complications by treating and preventing urinary tract infections.     

Fluorine‐18 fluorodeoxyglucose positron emission tomography imaging exhibits increased SUVmax at the level of the spinal intumescence in normal dogs

Positron emission tomography (PET) imaging utilizing fluorine‐18 labeled fluorodeoxyglucose is a relatively new imaging modality in veterinary medicine that is becoming more common for oncological staging and for musculoskeletal imaging. Thus, it is important to identify the normal variations on PET imaging that may be mistaken for pathology. Variation in standardized uptake values (SUVmax) have been anecdotally identified in the spinal cord of dogs undergoing fluorodeoxyglucose (FDG) PET–CT examinations for oncological staging, with notable increase in SUVmax values identified in the region of the cervical and lumbar spinal intumescences. The aim of this retrospective, analytical study was to compare the SUVmax values at four different locations throughout the spinal cord (C3, C5‐T1, T13, and L3‐S1) of a group of dogs with no evidence of neurologic disease and compare those findings to histologic specimens from dogs euthanized for unrelated disease. SUVmax values were significantly higher at the cervical and lumbar intumescences in comparison to the control regions (P < .0001 and P < .0001, respectively). Neuronal count and spinal cord gray matter area were also significantly greater at the cervical and lumbar intumescences (neuronal count P = .0025 and P = .0001; area P = .0004 and P = .0009, respectively) while overall neuronal density was lower (P = .003 and P = .028, respectively). We presume the increased SUVmax values at the spinal cord intumescences are the result of overall increased neuron count, increased proportion of gray matter, and increased spinal cord gray matter area. These findings will aid in the interpretation of future PET–CT studies and hopefully prevent the misdiagnosis of spinal cord disease in normal canines.     

MAGNETIC RESONANCE IMAGING FINDINGS IN THE SPINE OF SIX DOGS DIAGNOSED WITH LYMPHOMA

Lymphoma is one of the most common neoplasms in the dog. Despite its prevalence and the increasing use of advanced diagnostic imaging in veterinary patients only few reports of magnetic resonance imaging (MRI) findings in spinal lymphoma have been published to date. The purpose of this retrospective case series study was to describe the MRI findings in dogs with confirmed lymphoma affecting the spine and/or paraspinal soft tissues. Medical records were searched for patients that had MRI of the spine and a diagnosis of lymphoma during the period of 2005–2015. Data recorded from retrieved MRI studies were presence of focal or multifocal disease, structures involved, and signal characteristics on T2‐W, short tau inversion recovery (STIR), and T1‐W sequences prior to and following intravenous contrast medium administration. Six dogs met the inclusion criteria. Common findings included multifocal disease (4/6), vertebral involvement (5/6), spinal cord compression (4/6), and involvement of more than one spinal compartment (medullary cavity, vertebral canal, paraspinal soft tissues) (6/6). Vertebral changes were confined to the medullary cavity without evidence of cortical osteolysis. There was questionable involvement of the spinal cord in one case. All spinal and paraspinal lesions identified were T2‐W isointense to hyperintense, STIR hyperintense, T1‐W hypointense to isointense, and showed variable moderate to strong contrast enhancement. Additional lesions identified were enlarged intraabdominal lymph nodes, hepatomegaly, splenomegaly, and a splenic nodule. The STIR and T1‐W postcontrast sequences were subjectively the most useful in identification of the spinal and paraspinal lesions.     

IMAGING DIAGNOSIS—SPINAL CORD HISTIOCYTIC SARCOMA IN A DOG

A 12‐year‐old mixed breed dog was presented for evaluation of progressive paraparesis and ataxia. Magnetic resonance (MR) imaging was performed and identified multifocal intradural spinal cord mass lesions. The lesions were hyperintense in T2‐weighted sequences, isointense to mildly hyperintense in T1‐weighted sequences with strong contrast enhancement of the intradural lesions and spinal cord meninges. Spinal cord neoplasia was suspected. A diagnosis of intramedullary spinal cord histiocytic sarcoma, confined to the central nervous system, was confirmed histopathologically. Spinal cord histiocytic sarcoma is a rare neoplasm, but should be included in the differential diagnosis for dogs with clinical signs of myelopathy.     

Evaluation of osseous‐associated cervical spondylomyelopathy in dogs using kinematic magnetic resonance imaging

Osseous‐associated cervical spondylomyelopathy in dogs is characterized by both static and dynamic spinal cord compression; however, standard MRI methods only assess static compression. In humans with cervical spondylotic myelopathy, kinematic MRI is commonly used to diagnose dynamic spinal cord compressions. The purpose of this prospective, analytical study was to evaluate kinematic MRI as a method for characterizing the dynamic component of osseous‐associated cervical spondylomyelopathy in dogs. We hypothesized that kinematic MRI would allow visualization of spinal cord compressions that were not identified with standard imaging. Twelve client‐owned dogs with osseous‐associated cervical spondylomyelopathy were enrolled. After standard MRI confirmed a diagnosis of osseous‐associated cervical spondylomyelopathy, a positioning device was used to perform additional MRI sequences with the cervical vertebral column flexed and extended. Morphologic and morphometric (spinal cord height, intervertebral disc width, spinal cord width, vertebral canal height, and spinal cord area) assessments were recorded for images acquired with neutral, flexion, and extension imaging. A total of 25 compressions were seen with neutral positioning, while extension identified 32 compressions. There was a significant association between extension positioning and presence of a compressive lesion at C4‐C5 (p = 0.02). Extension was also associated with a change in the most severe site of compression in four out of 12 (33%) dogs. None of the patients deteriorated neurologically after kinematic imaging. We concluded that kinematic MRI is a feasible method for evaluating dogs with osseous‐associated cervical spondylomyelopathy, and can reveal new compressions not seen with neutral positioning.     

Experimental classical bovine spongiform encephalopathy: definition and progression of neural PrP immunolabeling in relation to diagnosis and disease controls

Tissues from sequential-kill time course studies of bovine spongiform encephalopathy (BSE) were examined to define PrP immunohistochemical labeling forms and map disease-specific labeling over the disease course after oral exposure to the BSE agent at two dose levels. Study was confined to brainstem, spinal cord, and certain peripheral nervous system ganglia-tissues implicated in pathogenesis and diagnosis or disease control strategies. Disease-specific labeling in the brainstem in 39 of 220 test animals showed the forms and patterns observed in natural disease and invariably preceded spongiform changes. A precise temporal pattern of increase in labeling was not apparent, but labeling was generally most widespread in clinical cases, and it always involved neuroanatomic locations in the medulla oblongata. In two cases, sparse labeling was confined to one or more neuroanatomic nuclei of the medulla oblongata. When involved, the spinal cord was affected at all levels, providing no indication of temporal spread within the cord axis or relative to the brainstem. Where minimal PrP labeling occurred in the thoracic spinal cord, it was consistent with initial involvement of general visceral efferent neurons. Labeling of ganglia involved only sensory ganglia and only when PrP was present in the brainstem and spinal cord. These experimental transmissions mimicked the neuropathologic findings in BSE-C field cases, independent of dose of agent or stage of disease. The model supports current diagnostic sampling approaches and control measures for the removal and destruction of nervous system tissues in slaughtered cattle.     

Skeletal and neurological malformations in pigs congenitally infected with Menangle virus

OBJECTIVE: To describe the pathological findings in stillborn piglets and fetuses delivered by sows naturally infected with Menangle virus, a recently recognised Paramyxovirus. DESIGN: Observations of the gross and microscopic pathology of natural disease. PROCEDURE: Postmortem examinations were performed on 49 stillborn piglets, 35 mummified or semi-mummified full-term fetuses and 6 aborted fetuses from 20 litters at a 2600-sow intensive piggery in New South Wales during an outbreak of reproductive disease from June to September 1997. Body weights, crown-rump lengths and gross pathological changes were recorded. Tissues, including brain and spinal cord, were processed for histopathological examination. RESULTS: Litters with reduced numbers of live born piglets had mummified fetuses and stillborn piglets. Affected stillborn and aborted piglets frequently had arthrogryposis, craniofacial and spinal deformities, pulmonary hypoplasia and degeneration of the brain and spinal cord. Intranuclear and intracytoplasmic inclusion bodies were observed in neurones and other cells in the brain and spinal cord in association with extensive degeneration, necrosis, infiltration of macrophages and gliosis. CONCLUSIONS: In utero infection of piglets with Menangle virus is associated with severe skeletal and neurological malformations.     

Prevalence of diseases of the spinal cord of cats

A retrospective review of records of 205 cats with histologically confirmed disease of the spinal cord was performed to identify the prevalence of disease in this nonrandomly selected population of cats. Clinical records were reviewed, and age, duration of neurologic illness, and clinical and histopathologic findings in cats with spinal cord disease were abstracted. Disease processes were classified into 7 categories and 23 groups. The most common diseases affecting the spinal cord of cats were feline infectious peritonitis (FIP), lymphosarcoma (LSA), and neoplasia of the vertebral column secondarily affecting the spinal cord. Information on age, onset and duration of clinical signs, and lesion localization at the postmortem examination in cats belonging to the 7 categories of disease were analyzed to create a practical list of differential diagnoses. Cats were also subcategorized into 3 groups based on their age at death. FIP was the most common disease of cats younger than 2 years of age. LSA and vertebral column neoplasia were the most common diseases affecting cats between 2 and 8 years of age. Vertebral column neoplasia was the most common disease affecting cats older than 8 years of age. Results of this histopathologic study showed that FIP and LSA were the most common disease processes affecting the spinal cord of cats. However, at least 21 other groups of diseases and their relative prevalence were identified.     

Fibrocartilaginous embolism of the spinal cord (FCE) in juvenile Irish Wolfhounds

Summary

This study describes the occurrence of fibrocartilaginous embolism of the spinal cord (FCE) in eight juvenile Irish Wolfhounds that were presented within a period of 16 months (1996–1997). The dogs, seven males and one female between eight and 13 weeks of age, were presented because of an acute onset of abnormal locomotion. Five dogs were euthanized and FCE was diagnosed by the histomorphological presence of focal myelomalacia and Alcian blue‐positive‐nucleus‐pulposus material in the spinal cord vasculature. Three dogs, which were thought to have FCE because of their clinical symptoms, improved with partial or almost complete return to normal locomotion. Although the observed high incidence may be a coincidence, oral information from breeders and lay reports of similar cases in journals for dog breeders from various countries suggest that FCE is a common disorder in young Irish Wolfhounds.     

Diaphragmatic dysfunction in dogs with cervical spinal disorders before and after surgery using fluoroscopy,motion‐mode ultrasound and radiography was not different than a group of control dogs

Cervical spinal disorders can lead to life‐threatening respiratory complications. Diaphragmatic dysfunction is attributed to spinal cord morbidity secondary to cervical myelopathy or decompressive surgical intervention. The purpose of this observational case‐control study was to determine the frequency of diaphragmatic dysfunction in dogs with cervical spinal disorders and a control group, the strength of association between cervical myelopathies and decompressive surgery with diaphragm paresis, and the agreement between and clinical usefulness of fluoroscopy, motion‐mode ultrasonography, and radiography for diagnosing diaphragmatic dysfunction. Thirty‐five client‐owned dogs were recruited with 14 control dogs and 21 test dogs. Dogs were evaluated for the presence of diaphragmatic dysfunction using radiography, M‐mode ultrasonography, and fluoroscopy before and after an anesthetic or surgical event. Diaphragmatic dysfunction was observed more frequently in dogs with cervical spinal disease prior to surgery (8/21; 38.1%) compared to control dogs (3/14; 21.4%) but was not statistically significant (P = .30). The occurrence of diaphragmatic dysfunction did not significantly increase following surgical decompression in either group. There was no to slight agreement between all imaging modalities. Most dogs with diaphragmatic dysfunction were asymptomatic. Diaphragmatic dysfunction was not statistically associated with cervical myelopathy or decompressive surgery. Ultrasonography and radiography were not useful diagnostic tests for determining diaphragmatic dysfunction in asymptomatic dogs when compared to fluoroscopy.     

TRUNCATION ARTIFACT IN MAGNETIC RESONANCE IMAGES OF THE CANINE SPINAL CORD

The truncation artifact in magnetic resonance (MR) images is a line of abnormal signal intensity that occurs parallel to an interface between tissues of markedly different signal intensity. In order to demonstrate the truncation artifact in sagittal images of the canine spinal cord and the effect of changing spatial resolution, we conducted an experimental in vitro study. A section of fixed canine spinal cord was imaged using a 1.5T magnet. Spatial resolution was increased by increasing the acquisition matrix and reconstruction matrix, producing series of T2‐weighted (T2w) images with the following pixel sizes: A, 1.6 (vertical) × 2.2 mm² (horizontal); B, 1.2 × 1.7 mm²; C, 0.8 × 1.1 mm²; D, 0.4 × 0. 6 mm². Plots of mean pixel value across the cord showed variations in signal intensity compatible with truncation artifact, which appeared as a single, wide central hyperintense zone in low‐resolution images and as multiple narrower zones in high spatial resolution images. Even in images obtained using the highest spatial resolution available for the MR system, the edge of the spinal cord was not accurately defined and the central canal was not visible. The experiment was repeated using an unfixed spinal cord specimen with focal compression applied to mimic a pathologic lesion. Slight hyperintensity was observed within the spinal cord at the site of compression although the cord was normal histologically. Results of this study suggest that caution should be applied when interpreting hyperintensity affecting the spinal cord in T2w sagittal images of clinical patients because of the possibility that the abnormal signal could represent a truncation artifact.     

Association of spinal cord compression seen on magnetic resonance imaging with clinical outcome in 67 dogs with thoracolumbar intervertebral disc extrusion

OBJECTIVES: To determine whether there is an association between the degree of transverse spinal cord compression detected by magnetic resonance imaging following thoracolumbar Hansen type 1 intervertebral disc disease in dogs and their presenting and postsurgical neurological status. METHODS: Medical records of 67 dogs with surgically confirmed Hansen type 1 intervertebral disc disease (2000 to 2004) were reviewed to obtain the rate of onset of disease, duration of clinical signs and presurgical and postsurgical neurological grade. Percentage of spinal cord compression was determined on transverse T2-weighted magnetic resonance images. Linear regression was used to examine the association between spinal cord compression and each of the above variables. Chi-squared tests were used to examine associations among postsurgical outcome and presurgical variables. RESULTS: Eighty-five per cent (57 of 67) of dogs were chondrodystrophoid. Mean spinal cord compression was 53 per cent (sd=219.7, range 14.3 to 84.9 per cent). There was no association between the degree of spinal cord compression and the neurological grade at presentation, rate of onset of disease, duration of clinical signs or postsurgical outcome, with no difference between chondrodystrophoid and non-chondrodystrophoid dogs. CLINICAL SIGNIFICANCE: The degree of spinal cord compression documented with magnetic resonance imaging in dogs with thoracolumbar Hansen type 1 intervertebral disc disease was not associated with the severity of neurological signs and was not a prognostic indicator in this study.     

Long-term survival of a dog with Alexander disease

A 1-year- and 11-month-old spayed female toy poodle had showed progressive ataxia and paresis in the hindlimbs since 11 months old. Magnetic resonance imaging revealed high signal intensity on T2-weighted and fluid-attenuated inversion recovery images at the thoracic and lumbar spinal cord. The dog’s neurological condition slowly deteriorated and flaccid tetraparesis was exhibited. At 4 years and 11 months old, the dog died of respiratory failure. On postmortem examination, eosinophilic corkscrew bundles (Rosenthal fibers) were observed mainly in the thoracic and lumbar spinal cord. Histological features were comparable to previously reported cases with Alexander disease. This is a first case report to describe the clinical course and long-term prognosis of a dog with Alexander disease.     

CLINICAL,IMAGING, AND PATHOLOGIC CHARACTERISTICS OF GURLTIA PARALYSANS MYELOPATHY IN DOMESTIC CATS FROM CHILE

Gurltia paralysans is a rare metastrongylid nematode of domestic cats that is found mainly in the veins of the spinal cord subarachnoid space and parenchyma. Endemic regions for G. paralysans mainly include Chile and Argentina. The ante mortem diagnosis of gurltiosis is difficult and based primarily on neurological signs, epidemiological factors, and the exclusion of other causes of feline myelopathies. The purpose of this retrospective case series was to describe clinical, imaging, and pathologic characteristics in nine domestic cats naturally infected with G. paralysans. Imaging tests included radiography, myelography, computed tomographic myelography (myelo‐CT), and magnetic resonance imaging (MRI). Neurological signs included paraparesis, paraplegia, pelvic limb ataxia and proprioceptive deficits, pelvic limb tremors, lumbosacral hyperesthesia, and tail trembling or atony. Complete blood count findings included a decrease in the mean corpuscular hemoglobin concentration value in eight cats. Eosinophilia in peripheral blood was observed in three cats, and thrombocytopenia was observed in three cats. Cerebrospinal fluid analysis revealed mononuclear pleocytosis in five cases. Myelo‐CT showed diffuse enlargement of the spinal cord at the midthoracic, lumbar, and sacral regions in all cats. Magnetic resonance image findings in the thoracic and lumbar region demonstrated multiple small nodular areas of T2 hyperintensity in the periphery of the spinal cord parenchyma. Localized intraparenchymal areas of increased T2 intensity were also observed in the thoracolumbar spinal cord and lumbosacral conus medullaris. In conclusion, G. paralysans should be considered as a differential diagnosis for domestic cats in endemic regions that have this combination of clinical and imaging characteristics.     

Concentrations of trace minerals in the spinal cord of horses with equine motor neuron disease

OBJECTIVE: To compare concentrations of trace minerals in the spinal cord of horses with equine motor neuron disease (EMND) with those of horses without neurologic disease (control horses). ANIMALS: 24 horses with EMND and 22 control horses. PROCEDURE: Spinal cord trace mineral concentrations in horses with EMND and control horses were analyzed by use of inductively coupled plasma atomic emission spectroscopy (calcium, phosphorus, sodium, potassium, magnesium, copper, iron, manganese, nickel, zinc, aluminum, cobalt, and chromium), atomic absorption spectrophotometry (lead and cadmium), flameless atomic absorption (mercury), and fluorometry (selenium). RESULTS: Copper concentration was significantly higher in the spinal cord of horses with EMND, compared with control horses; spinal cord concentrations of all other trace minerals were similar between groups. CONCLUSION AND CLINICAL RELEVANCE: Among spinal cord trace minerals investigated in the study, only copper concentrations were significantly different between horses with EMND and horses without neurologic disease, which suggests that copper may be involved in the pathogenesis of EMND. An hypothesis of oxidative injury in this disease is supported by the finding of increased copper concentrations in the spinal cord and by low vitamin E concentrations reported by other researchers.     

Evaluation of magnetic resonance imaging for the differentiation of inflammatory,neoplastic, and vascular intradural spinal cord diseases in the dog

Magnetic resonance imaging (MRI) is a common test for dogs with suspected intradural spinal cord lesions, however studies on diagnostic performance for this test are lacking. Objectives of this multi‐institutional, retrospective, case‐control study were to estimate sensitivity and specificity of MRI for (1) distinguishing between histopathologically confirmed intradural spinal cord disease versus degenerative myelopathy in dogs, (2) categorizing intradural spinal cord diseases as neoplastic, inflammatory, or vascular; and (3) determining tumor type within the etiologic category of neoplasia. Additional aims were to (1) determine whether knowledge of clinical data affects sensitivity and specificity of MRI diagnoses; and (2) report interrater agreement for MRI classification of intradural spinal lesions. Cases were recruited from participating hospital databases over a 7‐year period. Three reviewers independently evaluated each MRI study prior to and after provision of clinical information. A total of 87 cases were sampled (17 degenerative myelopathy, 53 neoplasia, nine inflammatory, and eight vascular). Magnetic resonance imaging had excellent (>97.6%) sensitivity for diagnosis of intradural spinal cord lesions but specificity varied before and after provision of clinical data (68.6% vs. 82.4%, P = 0.023). Magnetic resonance imaging had good sensitivity (86.8%) and moderate specificity (64.7–72.5%) for diagnosing neoplasia. Sensitivity was lower for classifying inflammatory lesions but improved with provision of clinical data (48.1% vs. 81.5%, P = 0.015). Magnetic resonance imaging was insensitive for diagnosing vascular lesions (25.0%). Interrater agreement was very good for correctly diagnosing dogs with intradural lesions (? = 0.882–0.833), and good (? = 0.726–0.671) for diagnosing dogs with neoplasia.