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Keywords:

  • Developmental orthopedic disease;
  • Equine;
  • Neurologic disease;
  • Spinal ataxia

Abstract

  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. Statistical Analysis
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References

Background

Cervical vertebral malformation (CVM) is seen in young, rapidly growing horses, and is commonly associated with a poor prognosis for racing.

Hypothesis/Objective

To examine the records of a population of Thoroughbreds with a presumptive diagnosis of CVM and to determine which radiographic findings and neurologic exam findings have an effect on these horses achieving athletic function when managed conservatively.

Animals

One hundred and three thoroughbreds presumptively diagnosed with CVM and treated conservatively between 2002 and 2010.

Methods

Racing records were reviewed in this retrospective study to determine which horses raced after treatment. Horses were separated into groups based on whether or not they raced. Medical records were reviewed, and results of neurologic examination, radiographic and laboratory findings, treatments, and outcome were assessed and compared between groups.

Results

Sixteen horses were excluded because of insufficient information. Of the remaining horses, thirty-three were euthanized after diagnosis, while the remaining seventy were discharged for treatment. Twenty-one of 70 horses treated medically (30%) went on to race. Horses that went on to race had a significantly lower neurologic grade (= .0002), with a median of 1.0 in the thoracic limbs and 2.0 in the pelvic limbs. Euthanized horses and nonstarters were more likely to have kyphosis (= .041) or cranial stenosis (= .041) on standing lateral cervical radiographs.

Conclusions and Clinical Importance

Some horses can race after the diagnosis of CVM. Neurologic examination and radiographic findings can be helpful in predicting racing prognosis.

Abbreviations
CVM

cervical vertebral malformation

DMSO

dimethyl sulfoxide

EPM

equine protozoal myeloencephalitis

IFAT

indirect fluorescent antibody test

Cervical vertebral malformation (CVM) is a common cause of paresis and ataxia in horses caused by extradural compression of the cervical vertebral spinal cord.[1] This is most commonly seen in 2 groups of horses; the first consists of young horses demonstrating evidence of developmental orthopedic disease, and the 2nd group is comprised of older horses that develop compression secondary to osteoarthritis of caudal cervical articular process joints.[1] Multiple factors have been shown to lead to the development of these lesions, including breed, sex, age, osteochondrosis of the dorsal articular facets, and nutrition.[2-4]

Diagnosis of CVM is typically made based on neurologic exam findings and examination of plain lateral cervical radiographs or myelography in addition to ruling out other possible causes of inflammatory disease, such as equine protozoal myeloencephalitis (EPM), viral encephalidities, lameness caused by musculoskeletal injury, or equine degenerative myelopathy.[2, 3] Compressive lesions resulting in CVM are accurately identified using radiographic sagittal diameter ratios of ≤0.485; however, myelographic evidence of ≥50% obstruction of the dorsal contrast column or >20% reduction in the cord diameter, gross and histopatholgical postmortem examination findings of cord compression, or both have been considered the gold standard for lesion localization in cases where the site of cord compression cannot be identified based on plain radiographs.[2, 5-7]

There have been few published reports that have examined the outcome for horses with CVM following either medical or surgical treatment. Most recently, a multicenter case-control study reported that 173 of 263 (66%) of CVM cases were euthanized before discharge from the hospital, whereas 27 of the remaining 90 (30%) were treated surgically with the remainder treated medically.[8] However, long-term outcome of the horses treated in this study was not reported. In a report of 12 surgically managed triple level cervical cord compression cases, 5 of these horses were Thoroughbreds, and 1 of these horses (20%) went on to have at least 1 racing start.[9] Neurologic function was also improved in 56 of 73 horses (77%) that underwent either cervical vertebral interbody fusion (n = 63) or dorsal laminectomy (n = 10), and 17 of these (23%) went on to either train for or return to racing.[10] In addition, long-term outcome and race results were reported for a population of young Thoroughbreds with either radiographic evidence or clinical signs of spinal cord disease that were treated with a low-protein, low-energy diet and stall confinement.[11] In this study, 15 of 18 horses (83%) that met the criteria for the treatment groups went on to have at least 1 racing start.[11] However, this study population consisted only of foals less than 1 year of age, and inclusion in the treatment group was based on a presumptive diagnosis of CVM from a radiographic score established by these same authors in a previous study.[12]

Information concerning the prognosis for racing in horses with CVM treated conservatively has not been previously documented. Thus, the objective of this retrospective study was to examine the medical records of a population of Thoroughbreds with a presumptive diagnosis of CVM and to determine which neurologic exam findings and radiographic abnormalities can be used to predict the likelihood of these horses achieving athletic function when managed conservatively.

Materials and Methods

  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. Statistical Analysis
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References

Electronic medical records from Peterson & Smith Equine Hospital between 2002 and 2010 were searched to identify Thoroughbreds with a diagnosis of CVM. All identified records were reviewed to satisfy criteria for either presumed or confirmed CVM. Confirmed CVM was defined as gross or microscopic evidence during necropsy examination of cervical spinal cord compression, as defined in the study by Levine et al, or myelographic evidence of spinal cord compression.[8] Presumptive diagnosis for this study was defined as having a history of neurologic deficits, neurologic examination findings consistent with lesion location in the cervical spinal cord and plain lateral cervical radiographs demonstrating the presence of bony abnormalities, narrow intravertebral sagittal ratios, or both. In some cases, additional laboratory diagnostics were performed to rule out other diseases. In addition, horses were excluded from this study if their radiographic reports were unavailable, their neurologic examination was not fully documented, or if they were positive for EPM on sampling of cerebrospinal fluid.

Signalment was recorded for all horses. Neurologic grade was reported for both the thoracic and pelvic limbs on a scale from 1 to 4 using the standardized system described by Mayhew et al.[13] Horses that were described as between 2 grades were given a score at the midpoint of the range provided (eg, a score of 2 to 3 was assigned as 2.5). Data concerning other clinical examination findings were obtained from the records, including cranial nerve exam findings, cervicofacial response, panniculus reflex response, any changes in musculature noted, changes in cervical range of motion, and the presence of increased hoof wear. Standing lateral cervical neck radiographs were examined by 1 of the 2 investigators (CJH or CKC), and intravertebral sagittal ratios were measured and recorded for all vertebrae from C4 to C7. When radiographs were unavailable, radiographic reports produced by other veterinarians at the practice were used for this information. Ratios were considered abnormal at C4, C5, and C6 when they were less than 0.5 and abnormal at C7 when less than 0.52.[14] Radiographs were also examined for kyphosis, caudal extension of the dorsal laminae, caudal epiphysitis, degenerative joint disease, cystic bone lesions, and cranial stenosis of the vertebral canal. These lesions and their location were recorded when present. Myelograms were only performed in cases where either surgical correction was being considered for treatment or when required by the insurance companies for confirmation of compression. Only 5 myelographic studies were available for this population, and results of myelography were used to confirm a diagnosis of CVM in these cases. Neuroanatomical localization was then recorded based on radiographic findings and neurologic examination findings.

Results of either serologic or cerebrospinal fluid indirect fluorescent antibody testing (IFAT) or western blot were recorded when available concerning antibodies for Sarcocystis neurona and Neospora hughesii. Horses were classified as either positive or negative for EPM based on the reference ranges provided by the respective testing laboratory. CSF cytology was also examined when available. Cases of EPM with a weak positive response on either serum IFAT or western blot were considered to be caused by exposure rather than an infection in the central nervous system, and not considered as a true positive as in previous studies.[8]

Records were reviewed for treatments administered after admission. Treatments were categorized as nonsteroidal anti-inflammatory administration, glucocorticoid administration, Vitamin E administration, administration of some type of pharmacologic EPM treatment, surgery (distraction and fusion of vertebral bodies), dimethyl sulfoxide (DMSO) administration, diet change, exercise restriction, and other osteoarthritis medication administration. Outcome was based on whether the horse was euthanized after diagnosis, survived to discharge but did not start in a race, or survived to discharge and went on to have at least one racing start. Racing status was determined from race and pedigree records from an online Jockey Club database. For each horse that went on to race, total number of starts and total career earnings were obtained.

Statistical Analysis

  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. Statistical Analysis
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References

Demographic data, neurologic examination findings, and radiographic findings were described using summary statistics such as mean or median, with either standard deviation or range, depending on whether data were continuous or ordinal. Normal distribution of data was determined by the Shapiro Wilk test for normality. Mann-Whitney or unpaired Student's t-test was used when appropriate to compare these data between groups. Categorical data were summarized with contingency tables. These were then individually compared between groups by a Fisher's exact test. For all analyses, a P value of <.05 was considered statistically significant. Statistical analyses were performed by commercially available computer software.1

Results

  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. Statistical Analysis
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References

Demographics

The study population was 119 Thoroughbreds diagnosed with CVM between 2002 and 2010. Horses that did not meet the inclusion criteria were excluded from further analysis. The remaining 103 horses were then split into 2 groups. Group 1 consisted of those horses that had at least 1 racing start, whereas group 2 contained those that had either been euthanized or had not raced. Group 2 was further broken down into those that had been euthanized (Group 2A) and those that were discharged, but nonstarters (2B). Group 1 contained 21 horses, whereas Group 2A was made up of 33 horses, which were euthanized shortly after diagnosis, and Group 2B had 49 horses that were discharged for medical treatment. No significant difference was found when comparing median age between groups (= .335). The median age of Group 1 was 1 year with a range of 0.25–2 years, whereas the median age of Group 2 was also 1 year with a range of 0.1–12 years. Group 1 consisted of 4 (19%) intact females, 2 (10%) neutered males, and 15 (71%) intact males, whereas Group 2 consisted of 18 (22%) intact females, 7 (8%) neutered males, and 57 (70%) intact males.

Neurologic Examination Findings

Neurologic grade was recorded as an average of the separate ataxia, paresis, conscious proprioception, and hypometria scores. The median thoracic limb neurologic grade for Group 1 was 1.0 (range, 0–2.25), which was significantly less (P = .026) than the median of Group 2 at 1.75 (range, 0–4). The median hind limb neurologic grade for Group 1 was 2.0 (range, 0.5–3), which was also significantly less (= .0002) than Group 2 at 2.5 (range, 0.5–4). Increased hoof wear was noted in 29 horses, with 3 from Group 1 and 26 from Group 2; however, this was not significantly different between groups (= .091). The presence of decreased range of motion in the neck, decreased cervicofacial response, decreased muscle mass, and decreased strength were compared between groups as well, and no significant differences were identified (Table 1).

Table 1. Neurologic examination abnormalities detected in horses with CVM––raced versus unraced/euthanized
 Raced (number affected/total)Unraced/Euthanized (number affected/total)P Value
Decreased range of motion5/2111/82.198
Absent cervicofacial response6/2117/82.309
Decreased muscle mass/tone3/2121/82.214
Decreased strength3/2125/82.109
Abnormal hoof wear3/2126/82.091

Radiographic Findings

Standing lateral cervical radiographs and radiographic reports were examined. Types of lesions observed included kyphosis between adjacent vertebrae, flaring of the caudal aspect of the vertebral epiphysis, caudal extension of the dorsal laminae, cystic lesions in the dorsal articular processes, degenerative joint disease of the articular processes, and stenosis of the cranial aspect of the vertebral canal (Table 2). The frequency of each lesion type was compared between groups. Horses with kyphosis (= .041) and cranial stenosis (= .041) were found to be less likely to return to racing. There was no significant difference between groups for caudal extension of the dorsal laminae, caudal epiphyseal flaring, cystic bone lesions, or degenerative joint disease, although the presence of cystic bone lesions approached significance at = .058 (Table 2).

Table 2. Radiographic abnormalities detected in horses with CVM––raced versus unraced/euthanized
LesionRaced (number affected/total)Unraced/Euthanized (number affected/total)P Value
Kyphosis3/2130/82.041
Caudal extension of dorsal laminae7/2134/82.337
Caudal epiphyseal flare15/2153/82.377
Cystic bone1/2118/82.058
Degenerative joint disease9/2148/82.148
Cranial stenosis3/2130/82.041

Intravertebral sagittal ratios were measured for the 4th cervical vertebrae through the 7th on all radiographs available for review. Sagittal diameter ratios of less than 0.5 were considered abnormal in this study for C4-C6, rather than the cut-off of 0.485 reported in the study by Hahn et al, to ensure that these cases were more closely inspected for neurologic examination abnormalities and other radiographic findings.[6] There were no significant differences between the mean intravertebral sagittal ratios at any location between groups (Table 3). The location of the lesions were identified as being between C1 and C5 or between C5 and T2 and then compared between groups. There was no significant difference between groups (= .383) for lesions located cranially versus caudally.

Table 3. Intravertebral sagittal ratio means in raced versus unraced/euthanized horses
VertebraeRaced (mean)Unraced/Euthanized (mean)P Value
C40.48760.489.451
C50.49240.4943.432
C60.48250.495.168
C70.53240.5391.334

The horses were then regrouped for analysis into those that were euthanized and those that survived to discharge. The frequency of specific lesions was then analyzed and compared between groups (Table 4). The only significant difference in lesions between these groups was horses with kyphosis were more likely to be euthanized than those with other lesions (= .039). There was no difference between these 2 groups in the neuroanatomical localization either (C1-C5 versus C5-T2), (= .56).

Table 4. Radiographic abnormalities detected in horses with CVM––euthanized versus treated horses
LesionEuthanized (number affected/total)Treated (number affected/total)P Value
Kyphosis18/3315/70.039
Caudal extension of dorsal laminae14/3327/70.436
Caudal epiphyseal flaring20/3348/70.281
Cystic bone8/3311/70.219
Degenerative joint disease19/3338/70.461
Cranial vertebral body stenosis14/3319/70.094

Laboratory Results

Seventeen of the 96 horses who were either euthanized or nonstarters were tested for EPM, using either serum or CSF IFAT or a Western blot on CSF, while 8 of the 23 that raced were tested. CSF cytology was reported as normal in all but 2 cases, which were negative for EPM, but showed a nonspecific subtle increase in protein. There was 1 horse that tested positive on serum that did not go on to race, that had normal intravertebral sagittal ratios on cervical radiographs, but had caudal epiphyseal flare from C4-C5, and a dorsal overriding arch at C3-C4 and C4-C5. Three of the horses that raced tested positive for EPM, 1 on serum and 2 on CSF samples. Of these horses, the one that tested positive on serum had caudal epiphyseal flaring from C3 to C6 and degenerative joint disease at C6-C7 with no abnormalities of its intravertebral sagittal ratios. One of the horses that tested positive on CSF had narrow intravertebral sagittal ratios at C4-C6 and caudal epiphyseal flaring at C5. The last horse had a radiographic report indicating caudal epiphyseal flaring at C4 and C6 as well as degenerative joint disease at C6-C7. To decrease confounding factors, the horses that tested positive or EPM on CSF were excluded from further analysis.

Treatments

Medications used to decrease inflammation around the spinal cord included nonsteroidal anti-inflammatories, corticosteroids, and DMSO. Additional treatments used included Vitamin E supplementation, diet changes, exercise restriction, and osteoarthritis medications. There were no significant differences between groups for any of the above-listed interventions.

Discussion

  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. Statistical Analysis
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References

Cervical vertebral malformation is a commonly recognized cause of spinal ataxia, typically encountered in young, rapidly growing horses.[11, 15] In this study, 30% of horses with a presumptive diagnosis of CVM that were managed conservatively were able to have at least one racing start. Horses were more likely to race if they had a neurologic grade of ≤1.0 in the thoracic limbs and ≤2.0 in the pelvic limbs. In addition, horses that were euthanized or nonstarters were more likely to have evidence of kyphosis or cranial stenosis on standing lateral cervical radiographs. Although there have been a few previous reports that examined outcome of horses with this condition, there has been limited investigation into the racing prognosis, possible prognostic indicators from neurologic examination or radiograph findings, or the efficacy of conservative management in horses with a presumptive diagnosis of CVM.

For this study, the horses were divided into 2 groups based on racing status. The median age at presentation for both groups was 1 year, which corresponds to previous studies, which conclude that CVM is more commonly seen in horses ≤4 years of age.[8] Previous authors have attributed this to the presence of nutritional imbalances during development leading to osteochondrosis and congenital malformation-malarticulation.[1, 10, 11, 13, 16-19] However, in older horses, CVM can also develop as a result of degenerative joint disease causing extradural compression of the spinal cord.[16] Horses over 4 years of age were seen in Group 2 of this study population and typically had degenerative joint disease of the caudal cervical spine.

Neurologic examination findings revealed a median thoracic limb neurologic grade of 1.75 in Group 2 compared to 1.0 in Group 1 and a median pelvic limb neurologic grade of 2.5 in Group 2 compared to 2.0 in Group 1. This corresponds with the findings of the study by Levine et al, which showed that horses with lower grades of both thoracic and pelvic limb ataxia (median 1.0 and 2.5, respectively) had a significantly higher likelihood of surviving to discharge.[8] Previous studies in other species have shown that the severity of physical examination-based assessments are linked to neurologic outcome after spinal cord injury; thus, these values may be useful as a marker for the cases that may be more likely to respond favorably to conservative management.[20-23] Although the rest of the examination findings were not significantly different between groups, additional deficits such as a lack of cervicofacial response, abnormal hoof wear, or decreased muscle tone in the neck should also be considered when managing cases of CVM.

Review of standing lateral cervical radiographs revealed that horses with kyphosis and cranial stenosis were less likely to return to racing with conservative management, and that horses with kyphosis were more likely to be euthanized. Cranial stenosis and kyphosis were also 2 of the 3 most commonly detected lesions on postmortem examination in the study by Levine et al, with degenerative joint disease being the third.[8] These types of lesions represent permanent changes of the skeletal structure that are more likely to cause repeated compression of the spinal cord, and thus more permanent neurologic deficits. On the other hand, caudal epiphyseal flaring and caudal extension of the dorsal laminae seem to remodel more successfully when the growth rate of the animal is managed compared with the aforementioned lesions. In addition, some of the horses that went on to race in this study might have had acute trauma to their spinal cord because of subtle spinal canal narrowing that may not have been appreciated using intravertebral sagittal ratios. Cervical canal stenosis occurs over a wide spectrum of severity in the population. In humans, minor decreases in sagittal diameter, whether congenital or acquired, can lead to an increased incidence of acute transient neurapraxia or “stingers” in these individuals, characterized by a sensation of burning pain, numbness, tingling, loss of sensation, and motor changes consisting of paresis or complete paralysis.[24-26] Therefore, some of these horses with apparently normal radiographs might have been uniquely susceptible to external trauma, causing transient neurologic impairment. Myelography would be a more sensitive test to detect mild narrowing of the spinal canal; however, only 5 horses in this study had myelograms performed.

Although the presence of bone cysts did not have a statistically significant effect on racing status in this study, this type of lesion had a tendency to occur more commonly in Group 2 horses (= .058). Similar lesions in other parts of the appendicular skeleton are typically associated with lameness and require correction via either surgical debridement or injection. While these types of lesions do not always lead to compression of the spinal cord, their presence may cause enough discomfort to the animal to prevent optimal athletic performance.[27, 28] Likewise, degenerative joint disease was found to have no significant effect on racing status in this study. This might be attributable to the fact that up to 50% of horses with radiographic changes consistent with degenerative joint disease show no clinical signs.[29] Thus, some of the horses in this study had evidence of osteoarthritis on their radiographs, but no clinical signs, and vice versa. In addition, osteoarthritis of articular processes tends to occur in older horses, and represents a protracted response to repeated injury.[28] The median age of the horses in this study was 1 year old, thus this study population might not have been old enough for degenerative joint disease to have a significant effect on their outcome. Finally, no significant difference was found when comparing the intravertebral sagittal ratios between groups. This finding suggests that sagittal ratios should not solely be used to determine racing prognosis.

Four of the horses in this study before exclusion were positive for EPM on the IFA test of either serum or CSF in addition to having radiographic lesions suggestive of CVM. In addition, a smaller proportion of the euthanized and unraced horses were tested for EPM compared with the horses that went on to race, most likely attributable to the more pronounced radiographic abnormalities observed in the euthanized/unraced group compared with the raced group. Likewise, very few horses had a myelogram performed to determine if their radiographic lesions were definitively compressive. Previous studies have shown that standing lateral cervical radiographs are less accurate than myelography for diagnosing compressive spinal cord lesions, and can lead to a false positive diagnosis of up to 50% at all sites except C3-4, where the false positive rate is 15%.[7] Therefore, additional diagnostics, including a myelogram and CSF analysis, are an important part in the diagnostic workup of any young ataxic horse with subtle or inconclusive radiographic changes. Collection of spinal fluid for cytology and immunodiagnostics, as well as serum, is preferred over serum EPM tests alone.[23, 30]

Treatment in conservatively managed cases was geared at decreasing inflammation, decreasing concussion to the spinal cord, and when possible, regulating the growth rate to prevent continued progression of developmental orthopedic disease. For this particular population, specific dietary recommendations for horses less than 12–14 months of age included feeding only grass hay or pasture with no grain and supplemented with a ration balancer to ensure adequate protein and mineral intake. However, dietary changes had no significant effect on whether or not horses with CVM returned to racing in this study (= .16). In the study by Donawick et al, a diet formulated to meet 65–75% of the 1978 National Research Council recommendations for crude protein and energy was fed to foals with neurologic signs of spinal cord disease or radiographic evidence of spinal cord compression, and adjustments were made at 3–4 months intervals through their 1st year of life.[11] All animals treated in the Donawick study were reported to have improvement in their neurologic or radiographic signs, indicating that dietary management from an early age may play an important role in preventing CVM. However, the horses in this study typically presented as older yearlings or 2 year olds that had just entered into race training, so the window for which dietary modification may have had an impact on changing the rate of growth may have been missed.[11, 17]

Another management recommendation for horses in this study population included small paddock turnout, without other horses if possible, to allow light exercise while minimizing trauma. This is based on treatment recommendations for degenerative joint disease in other locations of the equine skeleton. Although stall rest is beneficial during episodes of acute pain or joint instability, light to moderate exercise can help to stimulate articular chondrocyte metabolism and may improve range of motion and muscle strength.[31] In addition, it has been shown that regular submaximal loading of joints, as with regular paddock turnout, in horses from 5 to 11 months of age, is best for the optimal development of musculoskeletal tissues compared with stall rest or stall rest with intermittent exercise.[32]

For horses in this study with evidence of caudal epiphyseal flare on standing lateral cervical radiographs, recommendations were made for treatment with a low level of anti-inflammatory medication such as 1 mg/kg of flunixin meglumine PO every other day alternated with dexamethasone at 0.02 mg/kg PO every other day for 30 days. In addition, supplementation with at least 5000 IU/day of a water-soluble form of Vitamin E was recommended for all conservatively managed cases. Nonsteroidal anti-inflammatory medications are used in the treatment of acute physitis in the appendicular skeleton, and corticosteroids are indicated for the treatment of acute spinal cord trauma associated with compressive lesions.[1, 33] Vitamin E supplementation is recommended because this is the treatment for equine degenerative myelopathy, which is an important differential diagnosis in any young neurologic horse.[1] Horses in this study were typically sent home for treatment and management at the farm, and reevaluated 3–6 months later for improvement in their neurologic deficits or radiographs. If no neurologic deficits were appreciated on recheck examination, then a gradual return to exercise and training was recommended based on the horse's response to increased exercise. However, this recommendation was made with an understanding among the owner, trainer, and riders that these horses may be more susceptible to a repeated episode of cervical trauma and that riding should be discontinued if neurologic signs recur. If the horse continued to demonstrate mild neurologic deficits, then another period of paddock turnout with continued management changes, or using the horse for purposes other than racing, was then recommended. If the horse's neurologic deficits worsened during the treatment period, then further diagnostics and treatments may be required.

There are several limitations with this study, the most important of which is its retrospective design. This study design made it was difficult to obtain a standardized amount of information about the neurologic examination findings and radiographic findings because of the varied record keeping practices among clinicians, although the authors tried to compensate for this by excluding cases that did not have a full set of data. In addition, although EPM status was often reported in the file, laboratory work completed by veterinarians outside this practice was often not included in the patient file. In all but 5 of these cases, a presumptive diagnosis of CVM was made; therefore, it is possible that the ataxia attributed to CVM in these cases may have been attributable to another cause. Finally, although racing records from the Jockey Club could be reviewed to determine racing prognosis, it would have been beneficial to have more in-depth follow-up on the horses that did not race, but were sent home for treatment to determine if these horses were successful in another career. Likewise, information on how closely treatment recommendations were followed after discharge might have allowed determination of the efficacy of specific treatments or management changes.

This study reviewed the medical records of horses with a presumptive or confirmed diagnosis of CVM to determine which specific radiographic or neurologic examination findings were useful as prognostic indicators in conservative management of these cases. Horses that raced were more likely to have a neurologic grade of ≤1.0 in the thoracic limbs and ≤2.0 in the pelvic limbs. Likewise, euthanized horses and nonstarters were more likely to have evidence of kyphosis or cranial stenosis on standing lateral cervical radiographs. Specific types of treatment were not shown to have an effect on prognosis. However, decreasing inflammation associated with sudden onset of ataxia was an important aspect of conservatively managed cases, followed by small paddock turnout. Approximately 30% (21/70) of cases in this study population were able to have at least 1 racing start with conservative management. Further studies are needed to better characterize the associations of neurologic examination findings, radiographic findings, and conservative management with the outcome of CVM. A prospective study that allows the accrual of specific information during the diagnostic process as well as an interactive follow-up with trainers and owners after discharge would help to more accurately identify response to specific treatment options as well as identifying the types of cases that would best respond to conservative treatment.

Acknowledgments

  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. Statistical Analysis
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References

Conflict of Interest Declaration: Authors disclose no conflict of interest.

Footnote
  1. 1

    GraphPad Prism Version 5.03 for Windows, GraphPad Software, San Diego, CA

References

  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. Statistical Analysis
  5. Results
  6. Discussion
  7. Acknowledgments
  8. References
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