Ataxia In Horses Research Articles

Evaluation of the diagnostic value of transcranial electrical stimulation (TES) to assess neuronal functional integrity in horses.

To evaluate the ability of the TES technique to assess neuronal functional integrity in ataxic horses by recording TES-induced muscular evoked potentials (MEPs) in three different muscles and to structurally involve multiple ancillary diagnostic techniques, such as clinical neurological examination, plain radiography (RX) with ratio assessment, contrast myelography, and post-mortem gross and histopathological examination. Nine ataxic horses, showing combined fore and hindlimb ataxia (grades 2-4), were involved, together with 12 healthy horses. TES-induced MEPs were recorded bilaterally at the level of the trapezius (TR), the extensor carpi radialis (ECR), and tibialis cranialis (TC) muscles. Two Board-certified radiologists evaluated intra- and inter-sagittal diameter ratios on RX, reductions of dorsal contrast columns, and dural diameters (range skull-T1). Post-mortem gross pathological and segmental histopathological examination was also performed by a Board-certified pathologist. TES-MEP latencies were significantly prolonged in both ECR and TC in all ataxic horses as opposed to the healthy horses. The TR showed a mixed pattern of normal and prolonged latency times. TES-MEP amplitudes were the least discriminative between healthy and ataxic horses. Youden's cutoff latencies for ataxic horses were 24.6 ms for the ECR and 45.5 ms for the TC (sensitivity and specificity of 100%). For healthy horses, maximum latency values were 22 and 37 ms, respectively. RX revealed spinal cord compression in 8 out of 9 involved ataxic horses with positive predictive values of 0-100%. All ataxic horses showed multi-segmental Wallerian degeneration. All pathological changes recorded in the white matter of the spinal cord were widely dispersed across all cervical segments, whereas gray matter damage was more localized at the specific segmental level. TES-MEP latencies are highly sensitive to detect impairment of spinal cord motor functions for mild-to-severe ataxia (grades 2-4).

Cerebrospinal fluid and serum proteomic profiles accurately distinguish neuroaxonal dystrophy from cervical vertebral compressive myelopathy in horses

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. Evaluate novel proteomic techniques and machine learning algorithms to predict biomarkers that can aid in the antemortem diagnosis of noninfectious spinal ataxia in horses. 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). . 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. 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%. Cross-species platform. Uneven sample size. 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.

Diagnostic imaging of the equine cervical spine – Are radiographs enough?

Diagnostic imaging of the equine cervical spine – Are radiographs enough?

Spinal ataxia in a 2‐year‐old colt caused by a compressive primary vertebral osteosarcoma

SummaryNeoplasia is a rare cause of ataxia in horses. This report describes a 2‐year‐old colt presented with sudden‐onset ataxia in which a cervical vertebral osteosarcoma causing severe compression of the spinal cord was diagnosed. Radiological changes included a large osteolytic lesion in the vertebral body, the vertebral arch, the right cranial articular process and the right transverse process of C4, interrupting the borders of the vertebral foramen and the right transverse foramen. Myelography revealed a marked spinal cord compression. Necropsy confirmed the presence of a well‐demarcated, invasive and firm mass protruding from the fourth cervical vertebral body that led to severe compression of the spinal cord. In spite of its strongly pleomorphic nature, the detection of osteoid confirmed the diagnosis of a central osteosarcoma of the combined type. To the best of our knowledge, a primary single vertebral osteosarcoma causing ataxia in a juvenile horse has not previously been reported, and findings of this case report could help in the diagnostic work‐up of similar cases.

Postmortem diagnoses of spinal ataxia in 316 horses in California.

To determine period prevalences of postmortem diagnoses for spinal cord or vertebral column lesions as underlying causes of ataxia (spinal ataxia) in horses. 2,861 client-owned horses (316 with ataxia [ataxic group] and 2,545 without ataxia [control group]). The medical records database of the University of California-Davis Veterinary Medical Teaching Hospital was searched to identify horses necropsied between January 1, 2005, and December 31, 2017. Results were compared between the ataxic and control groups and between various groups of horses in the ataxic group. Period prevalences were determined for the most common causes of ataxia. 2,861 horses underwent full necropsy, and the period prevalences for the most common definitive diagnoses for ataxia were 2.7% (77/2,861) for cervical vertebral compressive myelopathy (CVCM), 1.3% (38/2,861) for equine neuroaxonal dystrophy or equine degenerative myeloencephalopathy (eNAD-EDM), and 0.9% (25/2,861) for trauma; the period prevalence of ataxia of unknown origin was 2.0% (56/2,861). Horses in the ataxic group (vs the control group) were more likely to have been warmblood horses (OR, 2.70) and less likely to have been Arabian horses (OR, 0.53). In the ataxic group, horses < 5 (vs ≥ 5) years of age had greater odds of CVCM (OR, 2.82) or eNAD-EDM (OR, 6.17) versus trauma or ataxia of unknown origin. Horses in the ataxic group with CVCM were more likely Thoroughbreds (OR, 2.54), whereas horses with eNAD-EDM were more likely American Quarter Horses (OR, 2.95) and less likely Thoroughbreds (OR, 0.11). Results indicated that breed distributions differed for horses with CVCM versus eNAD-EDM; therefore, breed should be considered in the clinical evaluation of spinal ataxia in horses.

Effect of Constant Rate Infusion of Xylazine &amp; Xylazine Morphine Combination on Sedation, Analgesia and Ataxia in Horses

In standing horses, notable sedation and analgesia may be attained by using α2-agonists/opioids combinations relative to α2-agonists alone. Therefore, this study aimed to evaluate the effect of a constant rate infusion (CRI) of xylazine (XYL) alone or in combination with morphine (XYL/ MOR) on sedation, analgesia and ataxia in horses.

Determination of magnetic motor evoked potential latency time cutoff values for detection of spinal cord dysfunction in horses.

BackgroundTranscranial 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.ObjectivesTo determine latency time cutoff for neurological dysfunction.AnimalsFive control horses and 17 horses with proprioceptive ataxia.MethodsCase‐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.ResultsDiagnostic 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 ImportanceMagnetic motor evoked potential analysis using these cutoff values is a promising diagnostic tool for spinal cord dysfunction diagnosis in horses.

Magnetic motor evoked potentials of cervical muscles in horses

BackgroundWhen surgical treatment of cervical vertebral malformation is considered, precise localization of compression sites is essential, but remains challenging. Magnetic motor evoked potentials (mMEP) from paravertebral muscles are useful in localizing spinal cord lesions, but no information about cervical muscle mMEP in horses is available yet. Therefore, the aim of this study was to determine the possibility, normal values, inter- and intra-observer agreement and factors that have an effect on cervical mMEP in healthy horses.MethodsTranscranial magnetic stimulation was performed on 50 normal horses and 4 (2 left, 2 right) muscle responses were recorded at the middle of each cervical vertebra (C1-C7) and additionally just caudal to C7 to evaluate cervical nerves (Cn) Cn1 to Cn8. Latency time and amplitude of the recorded mMEP were defined by both an experienced and an unexperienced operator.ResultsLatency increased gradually from 14.2 ± 1.38 ms for Cn3 to 17.7 ± 1.36 ms for Cn8, was significantly influenced by cervical nerve (P < 0.01), gender (P = 0.02) and height (P = 0.03) and had a good intra-observer agreement. The smallest mean amplitude (4.35 ± 2.37 mV) was found at Cn2, the largest (5.99 ± 2.53 mV) at Cn3. Amplitude was only significantly influenced by cervical nerve (P < 0.01) and had a low intra-observer agreement. No significant effect of observer on latency (P = 0.88) or amplitude (P = 0.99) measurements was found.ConclusionmMEP of cervical muscles in normal horses are easy to collect and to evaluate with limited intra- and inter-observer variation concerning amplitude and should be investigated in future studies in ataxic horses to evaluate its clinical value.

Kinematic discrimination of ataxia in horses is facilitated by blindfolding.

Agreement among experienced clinicians is poor when assessing the presence and severity of ataxia, especially when signs are mild. Consequently, objective gait measurements might be beneficial for assessment of horses with neurological diseases. To assess diagnostic criteria using motion capture to measure variability in spatial gait-characteristics and swing duration derived from ataxic and non-ataxic horses, and to assess if variability increases with blindfolding. Cross-sectional. A total of 21 horses underwent measurements in a gait laboratory and live neurological grading by multiple raters. In the gait laboratory, the horses were made to walk across a runway surrounded by a 12-camera motion capture system with a sample frequency of 240Hz. They were made to walk normally and with a blindfold in at least three trials each. Displacements of reflective markers on head, fetlock, hoof, fourth lumbar vertebra, tuber coxae and sacrum derived from three to four consecutive strides were processed and descriptive statistics, receiver operator characteristics (ROC) to determine the diagnostic sensitivity, specificity and area under the curve (AUC), and correlation between median ataxia grade and gait parameters were determined. For horses with a median ataxia grade ≥2, coefficient of variation for the location of maximum vertical displacement of pelvic and thoracic distal limbs generated good diagnostic yield. The hoofs of the thoracic limbs yielded an AUC of 0.81 with 64% sensitivity and 90% specificity. Blindfolding exacerbated the variation for ataxic horses compared to non-ataxic horses with the hoof marker having an AUC of 0.89 with 82% sensitivity and 90% specificity. The low number of consecutive strides per horse obtained with motion capture could decrease diagnostic utility. Motion capture can objectively aid the assessment of horses with ataxia. Furthermore, blindfolding increases variation in distal pelvic limb kinematics making it a useful clinical tool.

Pigment retinopathy in warmblood horses with equine degenerative myeloencephalopathy and equine motor neuron disease.

A pigment retinopathy has been reported in adult horses with equine motor neuron disease (EMND) arising from chronic α-tocopherol (α-TP) deficiency. A pigment retinopathy has not been identified in horses with neuroaxonal dystrophy/equine degenerative myeloencephalopathy (NAD/EDM) that affects genetically susceptible young horses with α-TP deficiency. The objective of this report is to describe, for the first time, a pigment retinopathy in a family of α-TP-deficient Warmbloods (WB) with clinically apparent NAD/EDM or EMND. Twenty-five WB horses from one farm underwent complete neurologic and ophthalmic examinations and serum α-TP concentrations were assessed. Two of the most severely ataxic horses were euthanized and postmortem examinations performed. Alpha-TP deficiency was widespread on this farm (22 of 25 horses). Eleven of 25 horses were clinically normal (age range 2-12 years), one had signs of EMND (6 years of age), 10 had signs of ataxia consistent with NAD/EDM (1-10 years), and two of these were postmortem confirmed concurrent NAD/EDM and EMND. A pigment retinopathy characterized by varying amounts of granular dark pigment in the tapetal retina was observed in four clinically apparent NAD/EDM horses (two postmortem confirmed concurrent NAD/EDM and EMND) and one horse with clinical signs of EMND. A pigment retinopathy can be present in young α-TP-deficient Warmblood horses with clinical signs of EMND as well as those with signs of NAD/EDM.

Objective assessment of gait in xylazine-induced ataxic horses.

There is poor agreement between observers of equine neurological gait abnormalities using the modified Mayhew grading scale. To stimulate a dose-dependent ataxia in horses through xylazine administration and identify quantifiable relevant gait parameters. Balanced, randomised, 2-way crossover design. Eight horses were assessed before and after administration of xylazine (low dose and high dose). Gait analyses performed before and after xylazine administration included: 1) kinematic data collected on an equine high-speed treadmill (flat and 10% decline) and from accelerometers placed on head and sacrum; and 2) kinetic data collected on a force plate. All horses developed dose-dependent ataxia. Horses developed a dose-dependent increased stride time, stride length, and time of contact (P<0.0001), and a decreased stride frequency (P<0.0002) after administration of xylazine. Although pelvic acceleration increased in the mediolateral direction (P<0.05) in horses walked on the treadmill, this movement decreased when walking over ground after administration of xylazine (P<0.05). Furthermore, centre of pressure and path length indices changed significantly in horses following administration of xylazine (P<0.05). This study examined one breed of horse (Arabian), all of similar height and weight. Accelerometers were attached to skin, not bone; no correction was made for artefacts from skin displacement. The sedative drug effect is of certain duration, limiting the data collection period. Administration of xylazine induced a dose-dependent ataxia in horses and resulted in significant changes of gait parameters, pelvic accelerations, and stabilographic variables, some of which changed in a dose-dependent fashion. Some of the altered gait parameters in this model were probably a result of overall slowing down of the stride cycle secondary to the sedative effect. Continued efforts to discover and evaluate quantifiable gait parameters that are susceptible to change following development of clinical neurological disease in horses is warranted.

Cervical Vertebral Compressive Myelopathy Associated with Articular Processes Osteoarthritis in Horses: Report of Three Cases

Cervical Vertebral Compressive Myelopathy Associated with Articular Processes Osteoarthritis in Horses: Report of Three Cases Cervical vertebral compressive myelopathy is a neuropathy resulting in ataxia in horses. Three horses with different signs of incoordination were presented for further evaluation. A fiveyear-old gelding with a long history of abnormal head and neck carriage, a six-year-old gelding with a history of previous neurological episodes and a two-day history of acute episodes of walking difficulties, and a sixteen-year-old mare with a onemonth history of left fore-limb ataxia were diagnosed with osteoarthritis of the facet joints of the caudal cervical vertebrae. Lateral radiographs of caudal cervical vertebrae confirmed osteoarthritis of the articular processes. Radiographic changes, such as enlargement of the articular process joint, periarticular new bone growth and reduction or narrowing of the intervertebral foramen, were observed in all three cases. Cervical vertebral compressive myelopathy should be considered in ataxic horses with normal laboratory findings.

Rater Agreement on Gait Assessment during Neurologic Examination of Horses

BackgroundReproducible and accurate recognition of presence and severity of ataxia in horses with neurologic disease is important when establishing a diagnosis, assessing response to treatment, and making recommendations that might influence rider safety or a decision for euthanasia.ObjectivesTo determine the reproducibility and validity of the gait assessment component in the neurologic examination of horses.AnimalsTwenty‐five horses referred to the Royal Veterinary College Equine Referral Hospital for neurological assessment (n = 15), purchased (without a history of gait abnormalities) for an unrelated study (n = 5), or donated because of perceived ataxia (n = 5).MethodsUtilizing a prospective study design; a group of board‐certified medicine (n = 2) and surgery (n = 2) clinicians and residents (n = 2) assessed components of the equine neurologic examination (live and video recorded) and assigned individual and overall neurologic gait deficit grades (0–4). Inter‐rater agreement and assessment‐reassessment reliability were quantified using intraclass correlation coefficients (ICC).ResultsThe ICCs of the selected components of the neurologic examination ranged from 0 to 0.69. “Backing up” and “recognition of mistakes over obstacle” were the only components with an ICC > 0.6. Assessment‐reassessment agreement was poor to fair. The agreement on gait grading was good overall (ICC = 0.74), but poor for grades ≤ 1 (ICC = 0.08) and fair for ataxia grades ≥ 2 (ICC = 0.43). Clinicians with prior knowledge of a possible gait abnormality were more likely to assign a grade higher than the median grade.Conclusion and Clinical ImportanceClinicians should be aware of poor agreement even between skilled observers of equine gait abnormalities, especially when the clinical signs are subtle.

Cervical extradural haematoma in an ataxic horse

SummaryAs neurological diseases in horses share many overlapping clinical signs, the veterinarian is required to know how to perform a focused evaluation of this system as well as how to carry out complementary examinations to establish an aetiological diagnosis. This is a case report of an ataxic horse presenting with an extradural haematoma in the region of the 7th cervical vertebra. The 7‐year‐old Criollo mare presented with clinical signs of ataxia grade 3 (scale 1–5) in all limbs and a proprioceptive deficit. Radiological evaluation did not show bone changes or narrowing of the cervical canal. Samples of blood, serum and cerebrospinal fluid were collected and tested negative for antibodies to equine herpes virus type 1–4, Trypanosoma evansi and Sarcocystis neurona. The disease evolution was followed over a 4‐week period, after which the animal showed worsening overall clinical signs, and thus euthanasia was performed. A necropsy did not reveal macroscopic changes in any organs, except for an extradural haematoma in the region of the 7th cervical vertebra causing spinal cord compression. Histological examinations showed that the nodular lesion consisted of fibrovascular tissue, granulation tissue at different stages of maturation, red blood cells, cellular debris, fibrin and macrophages. The white matter of the ventral horn of the spinal cord contained degenerative lesions. In addition, the brain tested negative for rabies virus encephalitis. Based on the history, the laboratory test results, anamnesis and the lesion observed at necropsy, it was concluded that the ataxia was due to spinal cord compression, which was caused by an extradural haematoma in the region of the 7th cervical vertebra. Evaluation of the equine neurological system is highly important in localising the area of lesions, and complementary examinations are useful in differentiating between diseases affecting this system. Spinal cord compression injuries, such as extradural haematomas, are rarely reported in the literature, and their pathophysiology is difficult to understand. Nevertheless, they should be included in the differential diagnosis of ataxia in horses.

Ultrasound-guided atlanto-occipital puncture for cerebrospinal fluid analysis on the standing horse

The atlanto-occipital site (AO) is convenient for retrieving an adequate volume and quality of cerebrospinal fluid (CSF) in the diagnosis of neurological disease in horses. However, general anaesthesia is not...

Ataxia due to vertebral hemangiosarcoma with evidence of disseminated disease in a 20-year old Swiss Warmblood mare

A 20-year old Swiss Warmblood mare was referred to the Swiss Institute of Equine Medicine with a history of poor performance, coughing and ataxia and hindlimb weakness which progressed to recumbency. Lung auscultation revealed pronounced wheezing, blood work showed signs of chronic inflammation and increased bone turnover and thoracic ultrasound indicated patchy pulmonary consolidation. Cerebrospinal fluid revealed only mild, unspecific changes allowing exclusion of meningoencephalomyelitis and clinically relevant bleeding. Despite medical treatment and support in a sling the mare did not improve and was euthanized. Necropsy revealed a poorly demarcated, non-encapsulated and invasively growing mass dorsally in the musculature at the level of the forth cervical vertebra (C4) infiltrating the vertebral body and the spinal canal at the level of C1–C2. Multiple nodular, firm masses were present in all lobes of the lung and appeared to be mainly located in vessels. Histologically the masses were composed of spindle cells with marked anisocytosis, anisocaryosis, a high mitotic activity and showed invasive growth. These neoplastic cells stained positive for CD31, an endothelial cell marker, which confirmed diagnosis of a hemangiosarcoma. Definite ante mortem diagnosis of hemangiosarcoma, which is rare in horses, is challenging. Besides the vertebral localization, disseminated, locally invasive and cutaneous forms of hemangiosarcoma exist and can be either acquired or congenital. Prognosis for equine hemangiosarcoma and response to treatment are usually poor and progression of clinical signs is rapid. Vertebral hemangiosarcoma is an uncommon cause of spinal ataxia in horses.

Acute and Long‐Term Cardiomyopathy and Delayed Neurotoxicity after Accidental Lasalocid Poisoning in Horses

Horses are extremely susceptible to ionophore intoxication. Although numerous reports are available regarding monensin, little is known about lasalocid toxicity. To describe accidental lasalocid poisoning on a farm in Belgium. Eighty-one horses, of which 14 demonstrated clinical signs from day 0-21 after being fed a new concentrate batch. One horse died on day 20 and another on day 27. The most severe cases (n=7), admitted to the clinic on day 29-46, underwent cardiac examination and blood biochemical analysis, including determination of plasma cardiac troponin I (cTnI) at admission and during follow-up. On day 57-70, cardiac examination, cTnI determination or both were undertaken on 72 remaining horses. Short-term effects of lasalocid intoxication included inappetance, lethargy, sweating, and muscular weakness. All 7 horses admitted to the clinic demonstrated signs of myocardial degeneration such as increased cTnI, dysrhythmia and reduced myocardial contractility. Four horses developed ataxia on day 40-50. Five horses died or were euthanized on day 30-370, 2 horses recovered fully and returned to previous athletic use. None of the 72 remaining horses exhibited clinical signs between day 57-70, but 34 had dysrhythmia and 13 had increased cTnI concentrations. After a period of rest, all horses returned to their previous work. Lasalocid was detected in hepatic tissue of 2 necropsied horses. Lasalocid intoxication induced myocardial and neurological damage. Although uncommon, this should be included as differential diagnosis for unexplained inappetance, signs of depression, cardiomyopathy, and ataxia in horses.

Is a single force plate adequate for stabilographic analysis in horses?

Postural balance can be quantified using stabilographic variables derived from force plate data that describe movements of the horse's centre of pressure (COP) in the horizontal plane. Most force plates are not large enough to accommodate all 4 limbs of a standing horse, so the study was designed to assess whether representative stabilographic data could be collected from the forelimbs or hindlimbs. To determine whether stabilographic data from either the forelimbs or the hindlimbs were representative of data for the total body. Stabilographic data (960 Hz) were collected from 17 sound horses standing with the forelimbs and the hindlimbs on separate force plates. To increase variability in the data, horses were of different sizes, the recording duration was varied (15-60 s) and data were collected under sighted and blindfolded conditions. Correlation matrices indicated that total body stabilographic variables were highly significantly correlated with both forelimb and hindlimb data but correlation coefficients were higher for forelimb data. Forward stepwise regression selected forelimb data for inclusion in the model for 15/16 variables, the exception being mean absolute mediolateral velocity. Ground reaction force data from a pair of limbs, preferably the forelimbs, can be used to measure variables that represent total body postural balance in sound standing horses. Stabilographic data from either the forelimbs or hindlimbs may be useful for detecting and quantifying deficiencies in postural balance in ataxic horses.

Qualitative assessment of corticosteroid cervical articular facet injection in symptomatic horses

SummaryCervical stenotic myelopathy (CSM) is the most common cause of noninfectious spinal cord ataxia in horses. Intra‐articular injection of corticosteroids into the facet joints of horses with CSM may relieve clinical signs of the disease process. However, there is a paucity of literature regarding the efficacy of facet injection therapy in horses with CSM. This retrospective study describes the return to normal function or improvement in performance of horses after ultrasound‐guided cervical facet injection that had previously shown signs of ataxia, obscure lameness or neck pain, prior to injection.

Diagnosis and surgical treatment of epidural neoplasms in two ataxic horses

SummaryTwo cases of ataxia caused by epidural neoplasia diagnosed with myelography and histopathology are presented in this report. One horse was diagnosed with lymphohistiocytic lymphosarcoma and the other with haemangiosarcoma. In both cases, subtotal dorsal decompression was performed as part of their treatment protocol. One horse was subjected to euthanasia immediately after surgery; however, the other horse recovered well, with no gait abnormalities and a normal myelographic dye column seen at 6 months post surgery. Although both horses were ultimately subjected to euthanasia, subtotal dorsal decompression provides a potential surgical treatment for epidural neoplasia.