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Background: Cervical vertebral compressive myelopathy (CVCM) and equine neuroaxonal dystrophy/degenerative myeloencephalopathy (eNAD/EDM) are leading causes of spinal ataxia in horses. The conditions can be difficult to differentiate, and there is currently no diagnostic modality that offers a definitive antemortem diagnosis., Objective: Evaluate novel proteomic techniques and machine learning algorithms to predict biomarkers that can aid in the antemortem diagnosis of noninfectious spinal ataxia in horses., Animals: Banked serum and cerebrospinal fluid (CSF) samples from necropsy-confirmed adult eNAD/EDM (n = 47) and CVCM (n = 25) horses and neurologically normal adult horses (n = 45)., Methods: . A subset of serum and CSF samples from eNAD/EDM (n = 5) and normal (n = 5) horses was used to evaluate the proximity extension assay (PEA). All samples were assayed by PEA for 368 neurologically relevant proteins. Data were analyzed using machine learning algorithms to define potential diagnostic biomarkers., Results: Of the 368 proteins, 84 were detected in CSF and 146 in serum. Eighteen of 84 proteins in CSF and 30/146 in serum were differentially abundant among the 3 groups, after correction for multiple testing. Modeling indicated that a 2-protein test using CSF had the highest accuracy for discriminating among all 3 groups. Cerebrospinal fluid R-spondin 1 (RSPO1) and neurofilament-light (NEFL), in parallel, predicted normal horses with an accuracy of 87.18%, CVCM with 84.62%, and eNAD/EDM with 73.5%., Main Limitations: Cross-species platform. Uneven sample size., Conclusions and Clinical Importance: Proximity extension assay technology allows for rapid screening of equine biologic matrices for potential protein biomarkers. Machine learning analysis allows for unbiased selection of highly accurate biomarkers from high-dimensional data., (© 2023 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals LLC on behalf of American College of Veterinary Internal Medicine.)

A 2-y-old Brahman bull was presented with progressive hindlimb ataxia and paraparesis that led to recumbency. Postmortem examination revealed scattered pinpoint, red-brown foci within the brainstem and gray matter of the spinal cord, and a larger lesion within the spinal cord at the level of T13. Histology of the section of T13 contained cross-sections of nematodes consistent with Parelaphostrongylus tenuis . Evidence of inflammation was present in other affected areas of the spinal cord and brain. DNA extraction and nested PCR were performed, which demonstrated 98% identity and 100% coverage to both P. tenuis and P. andersoni . Our case highlights the utility of DNA sequencing in parasite identification.

Background: Transcranial magnetic stimulation (TMS) and recording of magnetic motor evoked potentials (MMEP) can detect neurological dysfunction in horses but cutoff values based on confirmed spinal cord dysfunction are lacking., Objectives: To determine latency time cutoff for neurological dysfunction., Animals: Five control horses and 17 horses with proprioceptive ataxia., Methods: Case-control study with receiver operating characteristic curve analysis, based on diagnostic imaging, TMS, and histopathological findings. Horses were included if all 3 examinations were performed., Results: Diagnostic imaging and histopathology did not show abnormalities in the control group but confirmed spinal cord compression in 14 of 17 ataxic horses. In the remaining 3 horses, histopathological lesions were mild to severe, but diagnostic imaging did not confirm spinal cord compression. In control horses, latency time values of thoracic and pelvic limbs were significantly lower than in ataxic horses (20 ± 1 vs 34 ± 16 milliseconds, P = .05; and 39 ± 1 vs 78 ± 26 milliseconds, P = .004). Optimal cutoff values to detect spinal cord dysfunction were 22 milliseconds (sensitivity [95% CI interval], 88% [73%-100%]; specificity, 100% [100%-100%]) in thoracic and 40 milliseconds (sensitivity, 94% [83%-100%]; specificity, 100% [100%-100%]) in pelvic limbs. To detect spinal cord dysfunction caused by compression, the optimal cutoff for thoracic limbs remained 22 milliseconds, while it increased to 43 milliseconds in pelvic limbs (sensitivity, 100% [100%-100%]; specificity, 100% [100%-100%] for thoracic and pelvic limbs)., Conclusions and Clinical Importance: Magnetic motor evoked potential analysis using these cutoff values is a promising diagnostic tool for spinal cord dysfunction diagnosis in horses., (© 2019 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine.)

Background: Cervical vertebral stenotic myelopathy (CVSM) remains one of the most important abnormalities of the cervical spine resulting in neurological deficits in horses. The aim of the following study was to compare the results of the clinical and neurological examination, the results of myelography and the post mortem anatomical and histological appearance of the spinal cord and cervical vertebrae in a horse with CVSM., Case Presentation: The following study describes a clinical case of an eight-month-old stallion with ataxia. Plain cervical radiographs indicated narrowing of the spinal canal. Conservative therapy using NSAIDs did not result in any improvement in the gait of the horse. Due to economic constraints, surgical intervention was excluded. The owner chose to humanely euthanise the horse. Immediately after euthanasia, post mortem myelography was performed, and measurements of the myelographic dye column were taken. They revealed a 67% DMC reduction and a 64% DD reduction at the C3/C4 level. Afterwards, an anatomical dissection was performed. The cervical vertebrae and vertebral canal were macroscopically inspected and measured and indicated a 44% narrowing of the canal at the C3/C4 level. The spinal cord was removed and underwent histological evaluation after staining. Microscopic lesions were visible at the level of the compression and included axonal degeneration with partial or complete loss of myelin in the white matter of the lateral and dorsal funiculi as well as the formation of dysfunctional so-called "spongy structures". An increase in the number of microglial cells and collagen was also observed. The formation of glial scars was excluded. Immunohistochemical studies revealed a negative transmembrane glycoprotein CD68(-) - monocyte response and a negative tumor necrosis alpha TNFα (-) reaction., Conclusions: CVSM may be difficult to diagnose, even for experienced veterinary surgeons. Currently, an ex vivo histopathologic examination of the spinal cord is thought to be the gold standard in the diagnosis of CVSM. Our histological examination revealed no CVSM-specific glial scar formation and a CD68(-) negative and TNF-α negative reaction, which have not been previously reported. Histological lesions in CVSM may vary depending show inter-individual variability and on the treatment, which further hinders ex-vivo diagnostics.

Equine degenerative myeloencephalopathy (EDM) is characterized by a symmetric general proprioceptive ataxia in young horses, and is likely underdiagnosed for 2 reasons: first, clinical signs overlap those of cervical vertebral compressive myelopathy; second, histologic lesions--including axonal spheroids in specific tracts of the somatosensory and motor systems--may be subtle. The purpose of this study was (1) to utilize immunohistochemical (IHC) markers to trace axons in the spinocuneocerebellar, dorsal column-medial lemniscal, and dorsospinocerebellar tracts in healthy horses and (2) to determine the IHC staining characteristics of the neurons and degenerated axons along the somatosensory tracts in EDM-affected horses. Examination of brain, spinal cord, and nerves was performed on 2 age-matched control horses, 3 EDM-affected horses, and 2 age-matched disease-control horses via IHC for calbindin, vesicular glutamate transporter 2, parvalbumin, calretinin, glutamic acid decarboxylase, and glial fibrillary acidic protein. Primary afferent axons of the spinocuneocerebellar, dorsal column-medial lemniscal, and dorsospinocerebellar tracts were successfully traced with calretinin. Calretinin-positive cell bodies were identified in a subset of neurons in the dorsal root ganglia, suggesting that calretinin IHC could be used to trace axonal projections from these cell bodies. Calretinin-immunoreactive spheroids were present in EDM-affected horses within the nuclei cuneatus medialis, cuneatus lateralis, and thoracicus. Neurons within those nuclei were calretinin negative. Cell bodies of degenerated axons in EDM-affected horses are likely located in the dorsal root ganglia. These findings support the role of sensory axonal degeneration in the pathogenesis of EDM and provide a method to highlight tracts with axonal spheroids to aid in the diagnosis of this neurodegenerative disease., (© The Author(s) 2015.)

Case Description: An 11-year-old male breeding alpaca was evaluated for a 2-day history of lowered head carriage and lethargy., Clinical Findings: On initial examination, the alpaca had signs of lethargy and lowered carriage of the head and neck, but no specific neurologic deficits. Medical management improved the clinical signs, but 8 months later, the alpaca developed acute, progressive general proprioceptive ataxia affecting all 4 limbs and was referred for further evaluation and treatment. Magnetic resonance imaging and CT identified disruption of the normal osseous architecture of C7 and T1. Medical management was attempted, but because of a lack of improvement, the patient underwent surgery 14 months after initial examination., Treatment and Outcome: A dorsal laminectomy of C7 and T1 via a dorsal midline approach was performed, and the spinous processes of both vertebrae were removed prior to removal of the overlying lamina. Free dorsal expansion of the spinal cord was ensured by resection of the ligamentum flavum. Six months after surgery, the alpaca had returned to successful breeding with 7 hembra bred in the first year after surgery, producing 6 crias, and 4 crias in the second year. The patient was eventually euthanized 28 months after surgery because of neurologic deterioration but was still ambulatory at that time., Conclusions and Clinical Relevance: A good outcome with adequate alleviation of clinical signs and breeding soundness for > 2 years following dorsal laminectomy was achieved in this camelid patient. The surgical approach was similar to that in other species and was associated with mild postoperative morbidity. Veterinarians treating camelids should be aware of the initial clinical signs and treatment options for cervical vertebral stenotic myelopathy. In acute cases, the signs of reduced cervical mobility and pain on manipulation should prompt investigation including appropriate diagnostic imaging. Timely surgical intervention should be considered in patients that respond poorly to medical treatment to avoid irreversible spinal cord injury and optimize outcome.

Background: Leukoencephalomyelopathy is an inherited neurodegenerative disorder that affects the white matter of the spinal cord and brain and is known to occur in the Rottweiler breed. Due to the lack of a genetic test for this disorder, post mortem neuropathological examinations are required to confirm the diagnosis. Leukoencephalopathy with brain stem and spinal cord involvement and elevated lactate levels is a rare, autosomal recessive disorder in humans that was recently described to have clinical features and magnetic resonance imaging (MRI) findings that are similar to the histopathologic lesions that define leukoencephalomyelopathy in Rottweilers. Leukoencephalopathy with brain stem and spinal cord involvement is caused by mutations in the DARS2 gene, which encodes a mitochondrial aspartyl-tRNA synthetase. The objective of this case report is to present the results of MRI and candidate gene analysis of a case of Rottweiler leukoencephalomyelopathy to investigate the hypothesis that leukoencephalomyelopathy in Rottweilers could serve as an animal model of human leukoencephalopathy with brain stem and spinal cord involvement., Case Presentation: A two-and-a-half-year-old male purebred Rottweiler was evaluated for generalised progressive ataxia with hypermetria that was most evident in the thoracic limbs. MRI (T2-weighted) demonstrated well-circumscribed hyperintense signals within both lateral funiculi that extended from the level of the first to the sixth cervical vertebral body. A neurodegenerative disorder was suspected based on the progressive clinical course and MRI findings, and Rottweiler leukoencephalomyelopathy was subsequently confirmed via histopathology. The DARS2 gene was investigated as a causative candidate, but a sequence analysis failed to identify any disease-associated variants in the DNA sequence., Conclusion: It was concluded that MRI may aid in the pre-mortem diagnosis of suspected cases of leukoencephalomyelopathy. Genes other than DARS2 may be involved in Rottweiler leukoencephalomyelopathy and may also be relevant in human leukoencephalopathy with brain stem and spinal cord involvement.

The cervical spinal cords of 2 horses with equine degenerative myeloencephalopathy (EDM) were evaluated for evidence of oxidative damage to the central nervous system (CNS) using immunohistochemical staining for 3-nitrotyrosine (3-NT) and 4-hydroxynonenol (4-HNE). Neurons of the CNS from horses with EDM had positive immunohistochemical staining, whereas control samples did not, thus supporting the theory that oxidative damage is a potential underlying factor in horses with EDM. In addition, serum vitamin E concentration was low in both EDM-affected horses, and vitamin E concentration was also deficient in the cerebrospinal fluid in 1 EDM horse, further supporting the association between low vitamin E concentrations and oxidative damage to the CNS. Continued research is necessary to further define the pathophysiologic mechanisms of EDM.

Ten rottweilers presenting with spinal arachnoid pseudocysts were investigated. In six dogs, the lesions were localised dorsally at C2-C3; in three dogs, dorsally and ventrally at C5-C6; and, in one dog, dorsally and ventrally at C6-C7. Clinical signs were consistent with focal compression of the affected spinal cord segments. The animals showed ataxia of all four limbs, with truncal ataxia and marked hypermetria in cases of C2-C3 involvement, or ambulatory tetraparesis in cases of C5-C6 or C6-C7 involvement. Other than signs indicative of spina bifida in one dog, no abnormalities could be detected on plain radiographs. Myelography was used to define the localisation and extent of the pseudocysts. Additional information was obtained using magnetic resonance imaging in five dogs. Five dogs underwent a dorsal laminectomy; in three cases, the pseudocyst was treated by marsupialisation and, in two, by durectomy.

Fifteen English cocker spaniels with confirmed vitamin E deficiency were examined physically, ophthalmologically and neurologically. Eleven of them had clinical signs of neurological dysfunction which included ataxia, proprioceptive deficits, abnormal spinal reflexes and muscle weakness. In the two dogs examined histopathologically there was central neuronal fibre degeneration with prominent neuroaxonal dystrophy, particularly within the sensory relay nuclei of the brainstem, and one of the dogs had severe intestinal lipofuscinosis.

Numerous cases of ataxia, hind limb paresis, and paralysis have occurred in cheetah (Acinonyx jubatus) cubs over the past 10 yr within the European Endangered Species Program population, including 12 in mainland Europe, two in the British Isles, one in Namibia, and one in Dubai. The condition is the most important medical factor limiting European cheetah population growth. Eight cubs at the Salzburg Zoo, Austria, were affected. They demonstrated upper motor neuron lesions when alive and bilateral, symmetrical myelin degeneration of the spinal cord on necropsy. Ballooning of myelin sheaths surrounded mostly preserved axons, and no spheroids, characteristic of acute axonal degeneration, were found. Myelin loss markedly exceeded axonal degeneration. The syndrome's etiology is unclear, although viral, bacterial, parasitic, genetic, nutritional-metabolic, toxic, and physical causes have been considered.

Spinal cord dysfunction secondary to spinal arachnoid cysts (SACs) has been reported previously in dogs. This retrospective study reviews the clinical signs, radiographic findings, and outcome after surgical resection of SACs in 14 dogs. Plain vertebral column radiographs and myelography were done in all dogs. Computed tomography (CT) was done in 7 dogs and magnetic resonance (MR) imaging in 3 dogs. Affected dogs were between 1 and 12 years of age, and 8 of 14 were Rottweilers. Abnormalities detected on neurological examination depended on the location of the SAC. Five dogs had bilobed or multiple SACs. SACs were located in the cervical vertebral column in 11 dogs and in the thoracic vertebral column in 4 dogs. All dogs had dorsally or dorsolaterally located SACs. Two dogs also had additional ventrally located SACs. Spinal cord compression secondary to intervertebral disc extrusion or protrusion was demonstrated at the site of the SACs in 2 dogs. Surgical resection of the SACs was completed in all dogs. Eleven dogs were available for follow-up. Five weeks postoperatively, 7 dogs improved in neurological function, with some residual ataxia and paresis in 6 of these dogs. Neurological function had deteriorated in 4 dogs. It was concluded from this study that Rottweilers have a higher incidence of SACs than other breeds of dog. Furthermore, bilobed or multiple SACs can occur commonly, and myelography effectively localized SACs in dogs. Surgical resection of SACs resulted in improvement in neurological function in the majority of treated dogs.

Lesions in four captive pronghorn antelope (Antilocapra americana) naturally infected with Parelaphostrongylus tenuis in eastern Nebraska (USA) are described in this report. Animals were bright and alert with hind limb ataxia that progressed to sternal or lateral recumbency between July 28 and October 17, 1998. Animals were euthanized due to disease progression despite therapy. Multifocal decubital ulcers over bony prominences occurred in two animals and chronic unilateral otitis media was present in one animal. Histopathologic examination revealed severe Wallerian degeneration randomly scattered throughout the spinal cords of all four animals. Spinal cord sections from two animals contained adult nematode parasites consistent with P. tenuis. This is the first report of naturally occurring P. tenuis infection in pronghorn antelope. Pronghorn antelope should be considered susceptible to P. tenuis infection and contact with infected white-tailed deer as well as intermediate gastropod hosts of P. tenuis should be prevented in endemic areas.

Objective: To evaluate use of transcranial magnetic motor evoked potentials for assessment of the functional integrity of the cervical spinal cord in large-breed dogs with cervical spinal cord disease., Design: Randomized, controlled, masked study., Animals: 10 healthy large-breed control dogs and 25 large-breed dogs with cervical spinal cord diseases., Procedure: Affected dogs were allocated to 3 groups on the basis of neurologic status: signs of neck pain alone, ambulatory with ataxia in all limbs, or nonambulatory. Transcranial magnetic stimulation was performed on each dog with the same standard technique. Motor evoked potentials (MEP) were recorded from electrodes inserted in the tibialis cranialis muscle. Following the procedure, each dog was anesthetized and cervical radiography, CSF analysis, and cervical myelography were performed. The MEP latencies and amplitudes were correlated with neurologic status of the dogs after correction for neuronal path length., Results: Mean MEP latencies and amplitudes were significantly different between control dogs and dogs in each of the 3 neurologic categories, but were not significantly different among dogs in the 3 neurologic categories. A linear association was evident between MEP latencies and amplitudes and severity of neurologic deficits; the more severe the neurologic deficits, the more prolonged the latencies and the more decreased the amplitudes., Conclusions and Clinical Relevance: Transcranial magnetic MEP are useful to assess severity of cervical spinal cord disease in large-breed dogs. Impairment of the functional integrity of the cervical spinal cord was found even in dogs with neck pain alone.

The aim of this study was to investigate the use of magnetic motor evoked potentials as an ancillary diagnostic test in horses with cervical cord lesions. Transcranial magnetic stimulation was performed in 12 ataxic horses and the results of the evoked responses were compared to those found in normal horses. The latency and peak-to-peak amplitude of the potentials in the 12 ataxic horses were significantly different from those measured in normal horses. The configuration of the abnormal potentials was also polyphasic. Normalisation of the evoked potentials occurred in none of the horses, presented after a period of clinical improvement. These findings demonstrate that the technique is also able to detect lesions in horses with subtle clinical signs of incoordination. Magnetic transcranial stimulation is a valuable ancillary test to assess the integrity of the motor tracts. The technique is painless and safe and shows good sensitivity to detect lesions along the descending motor pathways.

Seventy-three fattening calves ranging from 6 to 15 months old on a farm were affected by ataxia over a period of four months. About 10 ataxic animals recovered after the administration of various kinds of vitamins and needle puncture therapy. The principal lesions in 14 ataxic animals examined were characterized by bilateral vacuolation with axonal degeneration confined to the spinal white matter. Ultrastructurally, the vacuoles were present in the periaxonal areas and bounded by dissociated myelin lamellae. No pathogen was isolated from the visceral organs of the animals. The serum copper remained within the normal range. Possible etiological factors remain unknown in the ataxic disease.

Neuroaxonal dystrophy and minimal diffuse degenerative myelopathy was diagnosed in two female full sibling, 1- and 2-year-old, Haflinger horses. Both animals developed slowly progressive ataxia from the age of 4 months. Clinical signs, which were more prominent in the hind legs, included hypermetria and dysmetria. Histological examination revealed neuroaxonal dystrophy characterized by spheroid formation, vacuolation, astrogliosis and lipofuscin pigment deposition in macrophages and neuronal perikarya. These changes were restricted to the gracilis and cuneate nuclei, nucleus of the solitary tract, nucleus intermediomedialis in the sacral and the seventh segment of the cervical spinal cord and Stilling-Clarke's column in both horses and the medial vestibular nucleus in the older horse. Both diseased Haflingers had significantly reduced serum alpha- and gamma-tocopherol values. No significant alteration in serum total lipid concentrations and serum selenium values were observed. It is likely that the condition has a familial hereditary basis. It is unclear whether there is a link between the observed neuroaxonal dystrophy and vitamin E deficiency and further investigations are warranted.

The paper describes the assessment and practical implications of a laryngeal adductory reflex in a series of 30 ataxic and 64 non-ataxic horses. The reflex was evoked by slapping the saddle region just caudal to the withers. In normal horses this produced a flickering adductory movement of the contralateral arytenoid cartilage which was observed endoscopically. Abolition of the laryngeal response was encountered in in 3 situations:--(1) Disruption of the afferent impulse occurred in those horses in which there was significant spinal cord pathology affecting the pathway from the cranial thoracic region to the medulla. (2) Disruption of the efferent impulse was manifest when damage to the adductory component of the recurrrent laryngeal nerve prevented normal adduction. (3) The reflex was abolished in tense or frightened horses, possibly due to interference from higher centres. The laryngeal adductory reflex was considered to be a useful diagnostic and prognostic aid in the assessment of ataxia and spinal cord lesions in the horse.

The purpose of this communication is to report the first diagnosed case of spinal ataxia in the horse in Finland. The horse was atactic and had a wobbling gait. Especially in turning and backing the rear legs tended to swing outwards. Macroscopical studies revealed malformation of the cervical vertebral articular facets and narrowing of the cervical vertebral canal. The vertebral malformation caused the degeneration of the spinal cord, through the compression of the cord. In this paper the macroscopial and microscopical findings are discussed and compared with the findings of other authors.

A 4-year-old male Great Dane with a history of progressive ataxia and associated bilateral atrophy of the muscles of the shoulder was found to have severe osseous metaplasia of the spinal dura mater. These dural ossifications were directly associated with underlying spinal cord degeneration. No other condition could be identified that would account for the pathologic changes in the spinal cord. The lower motor neuron (LMN) type weakness was in contrast to the upper motor neuron (UMN) type weakness said to occur with this disease and recently reported to be due to primary degenerative myelopathy.

Clinical and pathological findings from instances of ataxia in a group of wildebeeste (Connochaetes taurinus), two llamas (Llama glama) and one Arabian camel (Camelus dromedarius) are presented. Clinically, all the affected animals showed a non-febrile, progressive ataxia. Neuropathologically, Wallerian degeneration was diffuse in the spinal cord of the camel and llamas but was focal in the wildebeeste. Degeneration was present in the cervical dorsal roots in the wildebeeste and in the ventral nerve roots at all levels of the cord in the llamas. Peripheral nerve were affected in all the species. The possible roles of copper deficiency and plant poisons in the aetiology of the condition are discussed.

Two horse farms, on which there was a high incidence of proven and suspected equine degenerative myeloencephalopathy (EDM), were studied. Symmetric ataxia and paresis, along with laryngeal adductor, cervicofacial, local cervical, and cutaneous trunci hyporeflexia, characterized the syndrome. Serum vitamin E concentration reflected a deficient state in affected and unaffected horses on both farms when compared with selected reference groups and with published values. A high incidence of the disease was evident in offspring of two particular sires on one farm. Vitamin E supplementation resulted in correction of the deficient state in most horses and was associated with a drastic reduction in the incidence of EDM on one farm from 40% to less than 10% the year following vitamin E supplementation. In addition, during the last year, the severity of signs in the few cases was dramatically reduced. This information substantiates the hypothesis that EDM is a vitamin E-responsive disorder of Equidae with a possible familial predisposition.