Association of clinical and magnetic resonance imaging findings with outcome in dogs suspected to have ischemic myelopathy: 50 cases (2000–2006)

Luisa De Risio The Centres for Small Animal Studies, Animal Health Trust, Newmarket, Suffolk, CB8 7UU, England.

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 DVM, PhD
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Vicki Adams Preventive Medicine, Animal Health Trust, Newmarket, Suffolk, CB8 7UU, England.

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 MA, DVM, PhD
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Ruth Dennis The Centres for Small Animal Studies, Animal Health Trust, Newmarket, Suffolk, CB8 7UU, England.

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 MA, VetMB
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Fraser J. McConnell Diagnostic Imaging Service, Faculty of Veterinary Science, University of Liverpool, Liverpool, England.

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Simon R. Platt Department of Small Animal Medicine, College of Veterinary Medicine, University of Georgia, Athens, GA 30602.

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Abstract

Objective—To determine whether clinical signs or magnetic resonance imaging findings were associated with outcome in dogs with presumptive ischemic myelopathy.

Design—Retrospective case series.

Animals—50 dogs.

Procedures—Medical records and magnetic resonance images were reviewed. A neurologic score from 1 (normal) to 5 (most severe degree of dysfunction) was assigned on the basis of neurologic signs at the time of initial examination. Follow-up information was obtained from the medical records and by means of a telephone questionnaire completed by owners and referring veterinarians.

Results—Median neurologic score at the time of initial examination was 3 (range, 2 to 5). Median follow-up time was 584 days (range, 4 to 2,090 days). Neurologic score at the time of initial examination and extent of the lesion seen on magnetic resonance images (quantified as the lesion length-to-vertebral length ratio and as the percentage cross-sectional area of the lesion) were significantly associated with outcome. Sensitivity of using a lesion length-to-vertebral length ratio > 2.0 or a percentage cross-sectional area of the lesion ≥ 67% to predict an unsuccessful outcome was 100%.

Conclusions and Clinical Relevance—Results suggested that severity of neurologic signs at the time of initial examination and extent of the lesions seen on magnetic resonance images were associated with outcome in dogs with ischemic myelopathy.

Abstract

Objective—To determine whether clinical signs or magnetic resonance imaging findings were associated with outcome in dogs with presumptive ischemic myelopathy.

Design—Retrospective case series.

Animals—50 dogs.

Procedures—Medical records and magnetic resonance images were reviewed. A neurologic score from 1 (normal) to 5 (most severe degree of dysfunction) was assigned on the basis of neurologic signs at the time of initial examination. Follow-up information was obtained from the medical records and by means of a telephone questionnaire completed by owners and referring veterinarians.

Results—Median neurologic score at the time of initial examination was 3 (range, 2 to 5). Median follow-up time was 584 days (range, 4 to 2,090 days). Neurologic score at the time of initial examination and extent of the lesion seen on magnetic resonance images (quantified as the lesion length-to-vertebral length ratio and as the percentage cross-sectional area of the lesion) were significantly associated with outcome. Sensitivity of using a lesion length-to-vertebral length ratio > 2.0 or a percentage cross-sectional area of the lesion ≥ 67% to predict an unsuccessful outcome was 100%.

Conclusions and Clinical Relevance—Results suggested that severity of neurologic signs at the time of initial examination and extent of the lesions seen on magnetic resonance images were associated with outcome in dogs with ischemic myelopathy.

Ischemic myelopathy has been identified frequently in dogs,1–13 with the most commonly reported cause of ischemic myelopathy being embolization of fibrocartilaginous material histochemically identical to the nucleus pulposus of the intervertebral disk.1,2,6–14 There have been several hypotheses as to how this fibrocartilaginous material accesses the spinal cord vasculature,14 but the true pathogenesis is still unclear.

Previous studies9–11,13 of ischemic myelopathy in dogs have suggested that loss of nociception, involvement of an intumescence, and symmetric signs are negative prognostic factors. However, the presumptive diagnosis of ischemic myelopathy was not supported by MRI in any of these studies, and conclusions were based on statistical analyses in only 1 report.13 Thus, questions remain as to the possible association between clinical signs and outcome in dogs with ischemic myelopathy. Similarly, although MRI has been reported to be useful in establishing a presumptive diagnosis of ischemic myelopathy,15–19 only limited information is available on the prognostic value of MRI findings.a

In a previous study19 involving 52 dogs with ischemic myelopathy, we found that severity of clinical signs at the time of initial examination was significantly associated with the likelihood that the lesion would be identified by means of MRI and with the extent of the lesion. However, no attempts were made in that study to determine whether clinical signs or MRI findings were associated with outcome. The purpose of the study reported here was to determine whether clinical signs or MRI findings were significantly associated with outcome in dogs with presumptive ischemic myelopathy.

Materials and Methods

Case selection criteria—Case selection criteria have been described previously.19 In brief, medical records of dogs examined at the Animal Health Trust between January 1, 2000, and June 30, 2006, were searched to identify dogs in which a presumptive diagnosis of ischemic myelopathy had been made on the basis of history, clinical signs, and results of CSF analysis and MRI. Dogs were included if they had had signs of an acute (< 24 hours onset), nonprogressive, nonpainful myelopathy; results of CSF analysis and MRI had been consistent with nontraumatic ischemic myelopathy; MRI of the vertebral column had been performed within 7 days of the onset of clinical signs; and a complete medical record and follow-up information were available. Dogs were excluded if they had MRI findings consistent with acute, noncompressive nucleus pulposus extrusion and spinal cord contusion, including focal hyperintensity in the spinal cord overlying an intervertebral disk with reduction in volume and signal intensity of the nucleus pulposus on T2-weighted images, reduced intervertebral disk space with evidence of rupture of the dorsal annulus on gradient-echo images or on T1-and T2-weighted images, or presence of epidural fat disruption and extraneous material within the vertebral canal dorsal to an abnormal disk with minimal to absent spinal cord compression.20 In addition, 2 dogs included in the previous study19 that were euthanatized during general anesthesia following MRI were excluded.

Medical records review—Information obtained from the medical records of dogs included in the study consisted of signalment (age, sex, and breed); history; results of general physical and neurologic examinations, clinicopathologic testing, MRI, and CSF analysis; treatment before and after referral; and duration of hospitalization. With regard to results of the initial neurologic examination, clinical neuroanatomic localization, the presence of upper motor neuron versus lower motor neuron signs, and lateralization of signs were specifically recorded.

To quantify severity of clinical signs, a neurologic score was assigned on the basis of results of neurologic examinations performed at the time of initial examination and, for dogs that were still hospitalized or were reexamined at these times, 2, 7, 15, 30, and 60 days after initial examination. For dogs with cervical or cervicothoracic lesions, a score of 1 (clinically normal), 2 (ambulatory hemiparesis or tetraparesis), 3 (nonambulatory hemiparesis, triparesis, or tetraparesis with or without monoplegia), 4 (tetraplegia, hemiplegia, or triplegia with minimal voluntary motor activity in the other limb or limbs), or 5 (tetraplegia with loss of nociception) was assigned. For dogs with thoracolumbar or lumbosacral lesions, a score of 1 (clinically normal), 2 (ambulatory monoparesis or paraparesis), 3 (nonambulatory paraparesis with or without monoplegia), 4 (paraplegia), or 5 (paraplegia with loss of nociception) was assigned.

With regard to results of MRI, site, lateralization, and extent of the hyperintense intramedullary lesion evident on midsagittal and transverse T2-weighted images were specifically recorded. Extent of the lesion was defined as the ratio between the length of the lesion (hyperintense area on sagittal T2-weighted images) and length of the vertebral body of C6 in dogs with cervical lesions or L2 in dogs with thoracolumbar lesions (lesion length-to-vertebral length ratio) and as the maximal cross-sectional area of the lesion (largest area of hyperintensity on transverse T2-weighted images) as a percentage of the cross-sectional area of the spinal cord at the same level (percentage cross-sectional area of the lesion).

Follow-up procedures and determination of outcome—Follow-up information was obtained by means of a telephone questionnaire completed by owners and referring veterinarians; all telephone conversations were conducted by a single author (LDR). In addition, reexamination at the Animal Health Trust was offered to owners of dogs that were still alive at the time of the present study.

Results of questionnaires completed by owners and referring veterinarians were combined with information obtained from the medical records and results of follow-up examinations to determine time to unassisted ambulation, time to maximal recovery, and outcome (successful vs unsuccessful). Time to recovery of voluntary motor activity was determined on the basis of information obtained from the medical records and was defined as the number of days from onset of clinical signs and number of days from initial examination until voluntary motor activity was evident in the involved limb or limbs. Time to unassisted ambulation was defined as the number of days from onset of clinical signs and number of days from initial examination until the dog was able to stand and take ≥ 10 steps without assistance and without falling. Time to maximal recovery was defined as the number of months until the dog reached its best degree of improvement. Outcome was defined as successful when the dog was clinically normal or had mild to moderate proprioceptive or motor deficits but was able to perform daily activities without extra care from the owner (eg, get up and walk unassisted, move around the house, eat, drink, go outside for walks, and play) and had urinary and fecal continence. Outcome was defined as unsuccessful if the dog had severe proprioceptive and motor deficits or episodic or persistent urinary or fecal incontinence or was euthanatized because of a lack of improvement.

Statistical analysis—Continuous variables were summarized as median and range; categoric variables were summarized as frequency. Fisher exact tests were used to test for associations between outcome (successful vs unsuccessful) and neuroanatomic localization (C1-C5 vs C6-T2 vs T3-L3 vs L4-S3), type of neurologic signs (upper motor neuron vs lower motor neuron), symmetry of clinical signs (symmetric vs asymmetric), site of the lesion on magnetic resonance images (C1-C5 vs C6-T2 vs T3-L3 vs L4-S3), symmetry of lesions on magnetic resonance images (symmetric vs asymmetric), results of CSF analysis (normal vs abnormal), treatment prior to referral (methylprednisolone sodium succinate vs corticosteroids other than methylprednisolone vs carprofen or meloxicam vs corticosteroids other than methylprednisolone in combination with an NSAID vs no treatment and corticosteroid treatment vs other or no treatment), and whether physiotherapy was performed (yes vs no). The Wilcoxon rank sum test was used to test whether neurologic score at the time of initial examination was significantly different between dogs with a successful versus an unsuccessful outcome. The Fisher exact test was used to determine whether lesion length-to-vertebral length ratio or percentage cross-sectional area of the lesion was significantly associated with outcome. Receiver operating characteristic curve analysis was used to identify cutoff values for lesion length-to-vertebral length ratio and percentage cross-sectional area of the lesion that would maximize sensitivity when used to predict an unsuccessful outcome, and sensitivity and specificity for each cutoff were calculated. Multiple logistic regression and χ2 analysis were used to identify possible associations between outcome and neurologic score, lesion length-to-vertebral length ratio, and percentage cross-sectional area of the lesion. The Wilcoxon rank sum test was used to determine whether time to recovery of voluntary motor activity, time to unassisted ambulation, and time to maximal recovery differed significantly between dogs with upper motor neuron signs and dogs with lower motor neuron signs. The Kruskal-Wallis method was used to test for associations between recovery times and neurologic score at the time of initial examination, neuroanatomic localization (C1-C5 vs C6-T2 vs T3-L3 vs L4-S3), and site of the lesion on magnetic resonance images (C1-C5 vs C6-T2 vs T3-L3 vs L4-S3). The Spearman rank correlation method was used to test for associations between recovery times and lesion length-to-vertebral length ratio and percentage cross-sectional area of the lesion. Fisher exact tests were used to test for an association between treatment prior to referral and neurologic score at the time of initial examination, and the Kruskal-Wallis method was used to test for an association between treatment prior to referral and lesion length-to-vertebral length ratio and percentage cross-sectional area of the lesion. All analyses were performed with standard software.b,c The level of significance was set at P < 0.05 in all instances with exact P values reported where possible. Results are presented with 95% CIs where applicable.

Results

Fifty dogs met the criteria for inclusion in the study. Signalment, clinical and MRI findings, and results of CSF analyses have been reported previously.19

For dogs included in the study, median follow-up time was 584 days (range, 5 to 2,090 days). The follow-up questionnaire was answered by owners of all 50 dogs. In addition, information for 21 dogs was provided by the referring veterinarians, and 5 dogs were reexamined at the Animal Health Trust. In all instances, outcome assessments reported by the owners were consistent with information reported by referring veterinarians and were in agreement with findings obtained at the time of reexamination.

Median time from the onset of clinical signs to initial examination at the Animal Health Trust was 24 hours (range, ≤ 12 hours to 6 days). Median time from the onset of clinical signs to MRI was 24 hours (range, ≤ 12 hours to 7 days), with all but 6 dogs undergoing MRI within 72 hours after the onset of clinical signs. Median duration of hospitalization was 4 days (range, 0 to 36 days). Median time from the onset of clinical signs to recovery of voluntary motor activity was 6 days (range, 2.5 to 15 days), and median time from initial examination to recovery of voluntary motor activity was 5 days (range, 2 to 14 days). Median time from the onset of clinical signs to unassisted ambulation was 11 days (range, 4 to 136 days), and median time from initial examination to unassisted ambulation was 10 days (range, 3 to 135 days). Median time to maximal recovery was 3.75 months (range, 1 to 12 months).

Outcome was considered to be successful in 42 of the 50 (84%; 95% CI, 70% to 92%) dogs and unsuccessful in 8 (Table 1). Four of the 8 dogs with an unsuccessful outcome were euthanatized because of a lack of improvement; the other 4 had persistent severe neurologic dysfunction, including partial urinary and fecal incontinence in 3 of the 4.

Table 1—

Cross-tabulation of severity of neurologic abnormalities at the time of initial examination (neurologic score), neuroanatomic localization, and outcome in 50 dogs suspected to have ischemic myelopathy.

Neurologic scoreNeuroanatomic localizationOutcomeTotal
SuccessfulUnsuccessful
2C6-T2000
T3-L3606
L4-S3505
Total11011
3C6-T2516
T3-L3505
L4-S3707
Total17118
4C6-T2628
T3-L3303
L4-S3549
Total14620
5C6-T2000
T3-L3000
L4-S3011
Total011
All dogsNA42850

NA = Not applicable.

Neurologic scores at the time of initial examination ranged from 2 to 5 (Table 2); neurologic deficits were symmetric in 5 dogs and asymmetric in 45. The only dog with a neurologic score of 5 at the time of initial examination had symmetric neurologic deficits and a lesion localized to the L4-S3 region. The dog was euthanatized after 6 days because of a persistent lack of nociception in the hind limbs and tail, and the diagnosis of ischemic myelopathy secondary to fibrocartilaginous embolization was confirmed at necropsy. Two of the 20 dogs with a neurologic score of 4 at the time of initial examination were euthanatized 6 and 10 days after the onset of clinical signs because of a lack of clinical improvement. In 1 of these 2 dogs, the diagnosis of ischemic myelopathy secondary to fibrocartilaginous embolization was confirmed at necropsy. One of the 18 dogs with a neurologic score of 3 at the time of initial examination was euthanatized by the referring veterinarian because of a lack of clinical improvement 14 days after the onset of clinical signs.

Table 2—

Neurologic score at the time of initial examination and at various times after initial examination in 50 dogs suspected to have ischemic myelopathy.

Neurologic scoreTime after initial examination (d)
0*27153060
2111123272214
3182615631
420125000
5110000
Total505043332515

Day of initial examination.

Results of MRI were considered normal in 11 of the 50 dogs. The remaining 39 dogs had a focal, relatively sharply demarcated intramedullary lesion that was hyperintense on T2-weighted images and hypointense or isointense on T1-weighted images; MRI lesions were symmetric in 8 of the 39 dogs and asymmetric in 31. Median lesion length-to-vertebral length ratio was 1.8 (range, 0.5 to 5.0) in the 14 dogs with a cervical or cervicothoracic lesion and 2.2 (range, 0.6 to 6.7) in the 25 dogs with a thoracolumbar or lumbosacral lesion. For all 39 dogs with MRI lesions, median percentage cross-sectional area of the lesion was 74% (range, 20% to 100%). Outcome was successful in all 11 dogs with normal MRI findings and in 31 of the 39 dogs with abnormal MRI findings.

Neurologic score at the time of initial examination was significantly (P = 0.02) associated with outcome (successful vs unsuccessful). However, outcome was not significantly associated with clinical neuroanatomic localization (C1-C5 vs C6-T2 vs T3-L3 vs L4-S3; P = 0.3), type of neurologic signs (upper motor neuron vs lower motor neuron; P = 0.09), symmetry of clinical signs (symmetric vs asymmetric; P = 0.2), site of the lesion on magnetic resonance images (C1-C5 vs C6-T2 vs T3-L3 vs L4-S3; P = 0.1), or symmetry of lesions on magnetic resonance images (symmetric vs asymmetric; P = 0.3).

For the 39 dogs with an MRI lesion, both lesion length-to-vertebral length ratio (P = 0.001) and percentage cross-sectional area of the lesion (P = 0.008) were significantly associated with outcome. Receiver operating characteristic curve analysis revealed that for the lesion length-to-vertebral length ratio, a cutoff value of 2.0 would maximize sensitivity when used to predict an unsuccessful outcome. Lesion length-to-vertebral length ratio was > 2.0 in 19 dogs, including all 8 dogs with an unsuccessful outcome, whereas in 20 of the 31 dogs with a successful outcome and abnormal MRI findings, lesion length-to-vertebral length ratio was ≤ 2.0. Therefore, sensitivity of using a ratio > 2.0 to predict an unsuccessful outcome was 100% (95% CI, 60% to 100%) and specificity was 65% (95% CI, 48% to 81%). Alternatively, all 20 dogs with a lesion length-to-vertebral length ratio ≤ 2.0 had a successful outcome, but only 11 of the 19 (58%) dogs with a ratio > 2.0 had a successful outcome.

Similarly, receiver operating characteristic curve analysis revealed that for percentage cross-sectional area of the lesion, a cutoff value of 67% would maximize sensitivity when used to predict an unsuccessful outcome. Percentage cross-sectional area was ≥ 67% in 23 dogs, including all 8 dogs with an unsuccessful outcome, whereas in 16 of the 31 dogs with a successful outcome and abnormal MRI, percentage cross-sectional area was < 67%. Therefore, sensitivity of using a percentage cross-sectional area ≥ 67% to predict an unsuccessful outcome was 100% (95% CI, 60% to 100%) and specificity was 52% (95% CI, 34% to 69%). Alternatively, all 16 dogs with a percentage cross-sectional area < 67% had a successful outcome, but only 15 of the 23 (65%) dogs with a percentage cross-sectional area ≥ 67% had a successful outcome.

Although neurologic score at the time of initial examination, lesion length-to-vertebral length ratio, and percentage cross-sectional area of the lesion were all significantly associated with outcome in univariate analyses, it was not possible to build a multiple logistic regression model examining the association of these factors with outcome because of quasi-complete data separation (ie, a value of 0 in 1 of the 4 cells of a 2 × 2 contingency table).

Neurologic score at the time of initial examination was not significantly associated with time from onset of clinical signs to recovery of voluntary motor activity (P = 0.8), time from initial examination to recovery of voluntary motor activity (P = 0.7), time from onset of clinical signs to unassisted ambulation (P = 0.4), time from initial examination to unassisted ambulation (P = 0.7), or time to maximal recovery (P = 0.3). Recovery times were not significantly associated with neuroanatomic localization, type of neurologic signs (upper motor neuron vs lower motor neuron), site of the lesion on magnetic resonance images, lesion length-to-vertebral length ratio, or percentage cross-sectional area of the lesion (all P values ≥ 0.2).

Gradient-echo magnetic resonance images were obtained in 26 dogs. The area corresponding with the area of intramedullary hyperintensity seen on T2-weighted images was isointense, compared with normal spinal cord gray matter, in 17 dogs and hyperintense in 9. In 3 of the 9 dogs with hyperintense lesions on gradient-echo images, patchy areas of decreased signal suggestive of parenchymal hemorrhage were also seen. The outcome was unsuccessful in 2 of these 3 dogs and successful in 1.

Cerebrospinal fluid analysis was performed in 32 dogs, and results were abnormal (high total protein concentration with or without pleocytosis) in 14 (1 dog was excluded because of blood contamination of the CSF sample). Results of CSF analysis were normal in all 11 dogs in which results of MRI were normal and abnormal in 14 of the 39 dogs in which results of MRI were abnormal. Outcome was not significantly (P = 1.0) associated with results of CSF analysis.

Treatment prior to referral was classified as administration of methylprednisolone sodium succinate (12 dogs), administration of corticosteroids other than methylprednisolone (12 dogs), administration of carprofen or meloxicam (12 dogs), administration of corticosteroids other than methylprednisolone in combination with an NSAID (6 dogs), and no treatment (8 dogs). Thus, 30 dogs received corticosteroids and 20 did not. Ten of the 12 dogs treated with methylprednisolone received a single dose (30 mg/kg [13.6 mg/lb], IV), and 2 received 2 doses (30 mg/kg each, IV) 6 hours apart. Time between onset of clinical signs and administration of methylprednisolone by the referring veterinarian was not available; however, it was < 24 hours in all 12 dogs. Of the 12 dogs treated with a corticosteroid other than methylprednisolone, 8 received a single dose of dexamethasone IV or IM, 2 received a single dose of betamethasone IV, and 2 received prednisolone at anti-inflammatory dosages for 3 days. Treatment prior to referral was not significantly (P= 0.4) associated with outcome. Whether dogs received corticosteroids prior to referral was also not significantly (P = 0.12) associated with outcome.

Treatment prior to referral was not associated with neurologic score at the time of initial examination (P = 0.6) or with lesion length-to-vertebral length ratio or percentage cross-sectional area of the lesion (P > 0.2). In addition, whether dogs received corticosteroids prior to referral was not associated with neurologic score at the time of initial examination (P = 0.9) or with the lesion length-to-vertebral length ratio or percentage cross-sectional area of the lesion (P = 0.6).

Thirty-five dogs received physiotherapy consisting of passive and active range-of-motion exercises, stretching, massage, standing exercises, assisted walking, and hydrotherapy. Type and duration of the physiotherapy program varied on the basis of severity of neurologic dysfunction and owner-related circumstances. Dogs with a neurologic score ≥ 3 at the time of initial examination were significantly (P = 0.03) more likely to undergo physiotherapy than were dogs with a score ≤ 2. However, whether dogs received physiotherapy was not significantly (P = 0.4) associated with outcome (Table 3).

Table 3—

Cross-tabulation of severity of neurologic abnormalities at the time of initial examination (neurologic score), use of physiotherapy, and outcome in 50 dogs suspected to have ischemic myelopathy.

Neurologic scorePhysiotherapyOutcome
SuccessfulUnsuccessful
2No70
Yes40
3No51
Yes120
4No20
Yes126
5No00
Yes0 

Discussion

Results of the present study suggested that neurologic score at the time of initial examination and extent of the lesion seen on magnetic resonance images (quantified as the lesion length-to-vertebral length ratio and as the percentage cross-sectional area of the lesion) were significantly associated with outcome in dogs with presumptive ischemic myelopathy. Sensitivity of using a lesion length-to-vertebral length ratio > 2.0 or a percentage cross-sectional area of the lesion ≥ 67% to predict an unsuccessful outcome was 100%. In a previous study19 involving the same dogs, we found that neurologic score at the time of initial examination was significantly associated with the extent of lesions seen on magnetic resonance images.

The cutoff for percentage cross-sectional area of the lesion identified in the present study was in agreement with preliminary results of another studya involving 25 dogs with ischemic myelopathy. In that study, dogs with a lesion occupying < 50% of the cross-sectional area of the spinal cord were reportedly more likely to recover than were dogs with lesions involving a higher percentage of the spinal cord. Comparisons between the 2 studies are limited, however, because longitudinal extent of the lesions was not evaluated in the previous study and the time interval between the onset of clinical signs and MRI was not mentioned.

Timing of MRI may affect whether spinal cord lesions are seen in people and dogs with ischemic myelopathy.19,21–24,d In the present study, all 50 dogs underwent MRI within 7 days after the onset of clinical signs, with 44 (88%) undergoing MRI within 3 days of the onset, limiting variability associated with the timing of MRI. Eleven of the dogs in the present study, all of which underwent MRI within 3 days after the onset of clinical signs, did not have any MRI abnormalities. Similarly, in people, results of conventional MRI may be normal during the acute phase of ischemic myelopathy,22–24 and a recent reportd described normal MRI findings in dogs with histologically confirmed ischemic myelopathy. Thus, the earliest time at which abnormal findings can be detected by means of MRI remains to be determined.23 Nevertheless, our findings indicated that in dogs suspected to have ischemic myelopathy in which MRI lesions were seen, the extent of those lesions could be used to help predict the eventual outcome.

In people, whether MRI lesions are seen during the acute phase of ischemic myelopathy depends both on the size of the affected area and the degree of the ischemia.23 Therefore, patients without evidence of MRI lesions would be expected to be more likely to have a favorable outcome, and as expected, all 11 dogs in the present study without MRI lesions had a successful outcome. Similarly, a preliminary reportd involving 26 dogs with ischemic myelopathy stated that dogs without MRI lesions had a more favorable outcome.

Gradient-echo magnetic resonance images are the most sensitive for detecting hemorrhage in the CNS, with areas of hemorrhage appearing hypointense on gradient-echo images at all stages,25 and the presence of hypointense lesions on gradient-echo images has been associated with a poor outcome in human patients with traumatic spinal cord injury.26,27 In the present study, only 3 dogs had intramedullary hypointense lesions on gradient-echo images and outcome was unsuccessful in 2 and successful in 1. Therefore, the prognostic value of this MRI finding could not be assessed.

Previous studies9–11,13 of the prognostic value of clinical findings in dogs with ischemic myelopathy did not use a grading system to quantify the severity of neurologic signs, as was done in the present study. The significant association between neurologic score at the time of initial examination and outcome in the present study was in agreement with results of studies24,28 involving human patients with ischemic myelopathy.

Previous studies9–11,13 have suggested that loss of nociception, involvement of an intumescence, and symmetric signs are negative prognostic factors in dogs with ischemic myelopathy. In the present study, only 1 dog had loss of nociception. Therefore, the prognostic value of this clinical finding could not be investigated. All of the dogs with an unsuccessful outcome in the present study had a lesion localized to the C6-T2 or L4-S3 region. However, we did not identify significant associations between outcome and neuroanatomic localization, type of neurologic signs (upper motor neuron vs lower motor neuron), symmetry of clinical signs, site of the lesion on magnetic resonance images, or symmetry of lesions on magnetic resonance images. This lack of associations was most likely attributable to the low number of cases and subsequent low statistical power to detect associations.

A previous study13 involving dogs suspected to have ischemic myelopathy did not identify any significant associations between time to recovery (defined as spontaneous, physiologic paw positioning while standing and walking) and clinical localization of the lesion, involvement of an intumescence, or severity of motor dysfunction. Similarly, in the present study, we did not identify any significant associations between recovery times (ie, time to recovery of voluntary motor activity, unassisted ambulation, and maximal recovery) and neuroanatomic localization, type of neurologic signs, neurologic score at the time of initial examination, site of the lesion on magnetic resonance images, or extent of the lesion on magnetic resonance images. This lack of association between variables, however, was most likely attributable to the low number and uneven distribution of cases, which resulted in low statistical power.

Previous studies11,13 of dogs with ischemic myelopathy have suggested that CSF abnormalities may be associated with a poorer outcome. In our previous study,19 we found that dogs with CSF abnormalities were more likely to have MRI abnormalities; however, detection of CSF abnormalities was not associated with extent of the lesion on magnetic resonance images. Similarly, in the present study, we did not identify an association between CSF abnormalities and outcome.

Treatment of dogs with ischemic myelopathy is controversial. Previous studies9,10 have suggested that administration of corticosteroids, particular methylprednisolone, during the acute phase may result in a better outcome in dogs with ischemic myelopathy. Similarly, administration of methylprednisolone within the first few hours after injury have been reported to produce small, but clinically detectable, benefits in human patients with acute spinal cord injury.29,30 However, the role of methylprednisolone in human patients with acute spinal cord injury is still controversial,31 and it is uncertain whether treatment with methylprednisolone is of any benefit in dogs with spontaneous spinal cord injury.32 In the present study, we did not identify any significant association between treatment prior to referral and outcome, regardless of whether dogs were grouped on the basis of specific treatment (methylprednisolone, corticosteroids other than methylprednisolone, NSAIDs, corticosteroids and an NSAID, or no treatment) or simply on the basis of having received or not received corticosteroids. These results, however, should be interpreted cautiously because of the wide range of protocols and timing of treatment prior to referral. Prospective randomized controlled trials involving standardized treatment protocols are needed to investigate the role of methylprednisolone in the treatment of dogs with ischemic myelopathy. In addition, in the present study, we did not identify any significant association between treatment prior to referral and neurologic score at the time of initial examination or extent of the lesion on MRI (quantified as the lesion length-to-vertebral length ratio and as the percentage cross-sectional area of the lesion). Therefore, it is unlikely that treatment prior to referral could have influenced our results regarding associations between these clinical and MRI variables and outcome.

Physiotherapy is thought to have a role in stimulating neuronal plasticity, and its benefits in dogs with ischemic myelopathy have been described.13,33 In the present study, we did not identify a significant association between whether dogs received physiotherapy and outcome. However, dogs with more severe neurologic dysfunction were more likely to undergo physiotherapy than were dogs with milder deficits, which likely limited our ability to identify an association. In addition, the variability in physiotherapy protocols used and in the duration and frequency of physiotherapy likely limited our ability to identify an association with outcome.

ABBREVIATIONS

CI

Confidence interval

MRI

Magnetic resonance imaging

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    Cauzinille L, Kornegay JN. Fibrocartilaginous embolism of the spinal cord in dogs: review of 36 histologically confirmed cases and retrospective study of 26 suspected cases. J Vet Intern Med 1996;10:241245.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12.

    Hawthorne JC, Wallace LJ, Fenner WR, et al. Fibrocartilaginous embolic myelopathy in miniature schnauzers. J Am Anim Hosp Assoc 2001;37:374383.

  • 13.

    Gandini G, Cizinauskas S, Lang J, et al. Fibrocartilaginous embolism in 75 dogs: clinical findings and factors influencing the recovery rate. J Small Anim Pract 2003;44:7680.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14.

    Cauzinille L. Fibrocartilaginous embolism in dogs. Vet Clin North Am Small Anim Pract 2000;30:155167.

  • 15.

    MacKay AD, Rusbridge C, Sparkes AH, et al. MRI characteristics of suspected acute spinal cord infarction in two cats, and a review of the literature. J Feline Med Surg 2005;7:101107.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 16.

    Mikszewski JS, Van Winkle TJ, Troxel MT. Fibrocartilaginous embolic myelopathy in five cats. J Am Anim Hosp Assoc 2006;42:226233.

  • 17.

    Grunenfelder FI, Weishaupt D, Green R, et al. Magnetic resonance imaging findings in spinal cord infarction in three small breed dogs. Vet Radiol Ultrasound 2005;46:9196.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 18.

    Abramson CJ, Garosi L, Platt SR, et al. Magnetic resonance imaging appearance of suspected ischemic myelopathy in dogs. Vet Radiol Ultrasound 2005;46:225229.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 19.

    De Risio L, Adams V, Dennis R, et al. Magnetic resonance imaging findings and clinical associations in 52 dogs with suspected ischemic myelopathy. J Vet Intern Med 2007;21:12901298.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 20.

    Chang Y, Dennis R, Platt S, et al. Magnetic resonance imaging features of traumatic intervertebral disc extrusion in dogs. Vet Rec 2007;160:795799.

  • 21.

    Fortuna A, Ferrante L, Acqui M, et al. Spinal cord ischemia diagnosed by MRI. J Neuroradiol 1995;22:115122.

  • 22.

    Weidauer S, Nichtweiss M, Lanfermann H, et al. Spinal cord infarction: MR imaging and clinical features in cases. Neuroradiology 2002;44:851857.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 23.

    Luo CB, Chang FC, Teng MM, et al. Magnetic resonance imaging as a guide in the diagnosis and follow-up of spinal cord infarction. J Chin Med Assoc 2003;66:8995.

    • Search Google Scholar
    • Export Citation
  • 24.

    Masson C, Pruvo JF, Cordonneir C, et al. Spinal cord infarction: clinical and magnetic resonance imaging findings and short term outcome. J Neurol Neurosurg Psychiatry 2004;75:14311435.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 25.

    Weingarten K, Zimmerman RD, Deo-Narine V, et al. MR imaging of acute intracranial hemorrhage: findings on sequential spin-echo and gradient echo images in a dog model. Am J Neuroradiol 1991;12:457467.

    • Search Google Scholar
    • Export Citation
  • 26.

    Flanders AE, Spettell AM, Friedman DP, et al. The relationship between the functional abilities of patients with cervical spinal cord injury and the severity of damage revealed by MR imaging. Am J Neuroradiol 1999;20:926934.

    • Search Google Scholar
    • Export Citation
  • 27.

    Flanders AE, Spettell CM, Tartaglino LM, et al. Forecasting motor recovery following cervical spinal cord injury: value of MR imaging. Radiology 1996;201:649655.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 28.

    Salvador de la Barrera S, Barca-Buyo A, Montoto-Marques A, et al. Spinal cord infarction: prognosis and recovery in a series of 36 patients. Spinal Cord 2001;39:520525.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 29.

    Bracken MB, Holford TR. Effects of timing of methylprednisolone or naloxone administration on recovery of segmental and long tract neurological function in NASCIS 2. J Neurosurg 1993;79:500507.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 30.

    Bracken MB, Shepard MJ, Holford TR, et al. Methylprednisolone or trilazide mesylate administration after acute spinal cord injury: 1-year follow up. Results of the third National Acute Spinal Cord Injury randomized controlled trial. J Neurosurg 1998;89:699706.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 31.

    Sayer FT, Kronvall E, Nilsson OG. Methylprednisolone treatment in acute spinal cord injury: the myth challenged through a structured analysis of published literature. Spine J 2006;6:335343.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 32.

    Olby N. Current concepts in the management of acute spinal cord injury. J Vet Intern Med 1999;13:399407.

  • 33.

    Olby N, Halling KB, Glick TR. Rehabilitation for the neurologic patient. Vet Clin North Am Small Anim Pract 2005;35:13891409.

a.

Davies ESS, Cherubini GB, Brodbelt DC, et al. Prognostic value of magnetic resonance imaging in dogs with presumptive ischaemic myelopathy (abstr), in Proceedings. 19th Annu Symp Eur Soc Vet Neurol 2006;61.

b.

SPSS, version 14.0.1, SPSS Inc, Chicago, Ill.

c.

Stata, version 9.2, StataCorp, College Station, Tex.

d.

Stein VM, Wagner F, Bull C, et al. Findings of magnetic resonance imaging in suspected canine fibro-cartilaginous embolization (abstr), in Proceedings. 19th Annu Symp Eur Soc Vet Neurol 2006;157.

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    Griffiths IR. Spinal cord infarction due to emboli arising from the intervertebral disc in the dog. J Comp Pathol 1973;83:225232.

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    Gilmore DR, de Lahunta A. Necrotizing myelopathy secondary to presumed or confirmed fibrocartilaginous embolism in 24 dogs. J Am Anim Hosp Assoc 1986;23:373376.

    • Search Google Scholar
    • Export Citation
  • 10.

    Dyce J, Houlton JEF. Fibrocartilaginous embolism in the dog. J Small Anim Pract 1993;34:332336.

  • 11.

    Cauzinille L, Kornegay JN. Fibrocartilaginous embolism of the spinal cord in dogs: review of 36 histologically confirmed cases and retrospective study of 26 suspected cases. J Vet Intern Med 1996;10:241245.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12.

    Hawthorne JC, Wallace LJ, Fenner WR, et al. Fibrocartilaginous embolic myelopathy in miniature schnauzers. J Am Anim Hosp Assoc 2001;37:374383.

  • 13.

    Gandini G, Cizinauskas S, Lang J, et al. Fibrocartilaginous embolism in 75 dogs: clinical findings and factors influencing the recovery rate. J Small Anim Pract 2003;44:7680.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14.

    Cauzinille L. Fibrocartilaginous embolism in dogs. Vet Clin North Am Small Anim Pract 2000;30:155167.

  • 15.

    MacKay AD, Rusbridge C, Sparkes AH, et al. MRI characteristics of suspected acute spinal cord infarction in two cats, and a review of the literature. J Feline Med Surg 2005;7:101107.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 16.

    Mikszewski JS, Van Winkle TJ, Troxel MT. Fibrocartilaginous embolic myelopathy in five cats. J Am Anim Hosp Assoc 2006;42:226233.

  • 17.

    Grunenfelder FI, Weishaupt D, Green R, et al. Magnetic resonance imaging findings in spinal cord infarction in three small breed dogs. Vet Radiol Ultrasound 2005;46:9196.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 18.

    Abramson CJ, Garosi L, Platt SR, et al. Magnetic resonance imaging appearance of suspected ischemic myelopathy in dogs. Vet Radiol Ultrasound 2005;46:225229.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 19.

    De Risio L, Adams V, Dennis R, et al. Magnetic resonance imaging findings and clinical associations in 52 dogs with suspected ischemic myelopathy. J Vet Intern Med 2007;21:12901298.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 20.

    Chang Y, Dennis R, Platt S, et al. Magnetic resonance imaging features of traumatic intervertebral disc extrusion in dogs. Vet Rec 2007;160:795799.

  • 21.

    Fortuna A, Ferrante L, Acqui M, et al. Spinal cord ischemia diagnosed by MRI. J Neuroradiol 1995;22:115122.

  • 22.

    Weidauer S, Nichtweiss M, Lanfermann H, et al. Spinal cord infarction: MR imaging and clinical features in cases. Neuroradiology 2002;44:851857.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 23.

    Luo CB, Chang FC, Teng MM, et al. Magnetic resonance imaging as a guide in the diagnosis and follow-up of spinal cord infarction. J Chin Med Assoc 2003;66:8995.

    • Search Google Scholar
    • Export Citation
  • 24.

    Masson C, Pruvo JF, Cordonneir C, et al. Spinal cord infarction: clinical and magnetic resonance imaging findings and short term outcome. J Neurol Neurosurg Psychiatry 2004;75:14311435.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 25.

    Weingarten K, Zimmerman RD, Deo-Narine V, et al. MR imaging of acute intracranial hemorrhage: findings on sequential spin-echo and gradient echo images in a dog model. Am J Neuroradiol 1991;12:457467.

    • Search Google Scholar
    • Export Citation
  • 26.

    Flanders AE, Spettell AM, Friedman DP, et al. The relationship between the functional abilities of patients with cervical spinal cord injury and the severity of damage revealed by MR imaging. Am J Neuroradiol 1999;20:926934.

    • Search Google Scholar
    • Export Citation
  • 27.

    Flanders AE, Spettell CM, Tartaglino LM, et al. Forecasting motor recovery following cervical spinal cord injury: value of MR imaging. Radiology 1996;201:649655.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 28.

    Salvador de la Barrera S, Barca-Buyo A, Montoto-Marques A, et al. Spinal cord infarction: prognosis and recovery in a series of 36 patients. Spinal Cord 2001;39:520525.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 29.

    Bracken MB, Holford TR. Effects of timing of methylprednisolone or naloxone administration on recovery of segmental and long tract neurological function in NASCIS 2. J Neurosurg 1993;79:500507.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 30.

    Bracken MB, Shepard MJ, Holford TR, et al. Methylprednisolone or trilazide mesylate administration after acute spinal cord injury: 1-year follow up. Results of the third National Acute Spinal Cord Injury randomized controlled trial. J Neurosurg 1998;89:699706.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 31.

    Sayer FT, Kronvall E, Nilsson OG. Methylprednisolone treatment in acute spinal cord injury: the myth challenged through a structured analysis of published literature. Spine J 2006;6:335343.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 32.

    Olby N. Current concepts in the management of acute spinal cord injury. J Vet Intern Med 1999;13:399407.

  • 33.

    Olby N, Halling KB, Glick TR. Rehabilitation for the neurologic patient. Vet Clin North Am Small Anim Pract 2005;35:13891409.

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