Magnetic resonance imaging features and clinical signs associated with presumptive and confirmed progressive myelomalacia in dogs: 12 cases (1997-2008)

Midori Okada Veterinary Research Center, Nihon University 1866 Kameino, Fujisawa, Kanagawa 252-0880, Japan.
Pet Clinic ANIHOS, 1-14-11 Minamitokiwadai, Itabashi, Tokyo 174-0072, Japan.

Search for other papers by Midori Okada in
Current site
Google Scholar
PubMed Close
 DVM
,
Masato Kitagawa School of Veterinary Medicine, Nihon University 1866 Kameino, Fujisawa, Kanagawa 252-0880, Japan.

Search for other papers by Masato Kitagawa in
Current site
Google Scholar
PubMed Close
 DVM, PhD
,
Daisuke Ito School of Veterinary Medicine, Nihon University 1866 Kameino, Fujisawa, Kanagawa 252-0880, Japan.

Search for other papers by Daisuke Ito in
Current site
Google Scholar
PubMed Close
 DVM, PhD
,
Takuya Itou Veterinary Research Center, Nihon University 1866 Kameino, Fujisawa, Kanagawa 252-0880, Japan.

Search for other papers by Takuya Itou in
Current site
Google Scholar
PubMed Close
 DVM, PhD
,
Kiichi Kanayama School of Veterinary Medicine, Nihon University 1866 Kameino, Fujisawa, Kanagawa 252-0880, Japan.

Search for other papers by Kiichi Kanayama in
Current site
Google Scholar
PubMed Close
 DVM, PhD
, and
Takeo Sakai Veterinary Research Center, Nihon University 1866 Kameino, Fujisawa, Kanagawa 252-0880, Japan.

Search for other papers by Takeo Sakai in
Current site
Google Scholar
PubMed Close
 DVM, PhD
DOI:
https://doi.org/10.2460/javma.237.10.1160
Volume/Issue:
Volume 237: Issue 10
Online Publication Date:
15 Nov 2010
Full access
Sign In Reprints and Permissions

Abstract

Objective—To characterize clinical signs and findings from magnetic resonance imaging (MRI) and CSF analysis for dogs with progressive myelomalacia (PM) diagnosed on the basis of clinical and histologic features.

Design—Retrospective case series.

Animals—5 dogs with confirmed PM and 7 with presumptive PM evaluated from 1997 through 2008.

Procedures—Medical records of study dogs were reviewed, and clinical signs and MRI and CSF findings were evaluated. A clinical diagnosis of PM was made on the basis of detection of disk-associated spinal cord compression via MRI and progression of clinical signs from initial paraparesis or paraplegia to thoracic limb lower motor neuron paresis to tetraplegia associated with cranial migration of the extent of cutaneous trunci reflex extinction and analgesia, terminating in death due to respiratory paralysis.

Results—All dogs were paraplegic and had signs of lower motor neuron lesions. As revealed by MRI of the vertebral column, the length of abnormal signal intensity was more than 6-fold, compared with the body length of L2. In some dogs, these abnormal MRI findings were observed before PM was clinically diagnosed. The CSF examination revealed hemorrhagic xanthochromia.

Conclusions and Clinical Relevance—A hyperintense region of the spinal cord > 6 times the length of L2 on T2-weighted imaging might be a characteristic MRI finding of PM. In some dogs, such MRI findings were observed before PM was clinically diagnosed. Progressive myelomalacia may thus be diagnosable at the early stage through MRI and CSF examination before signs of PM develop.

Abstract

Objective—To characterize clinical signs and findings from magnetic resonance imaging (MRI) and CSF analysis for dogs with progressive myelomalacia (PM) diagnosed on the basis of clinical and histologic features.

Design—Retrospective case series.

Animals—5 dogs with confirmed PM and 7 with presumptive PM evaluated from 1997 through 2008.

Procedures—Medical records of study dogs were reviewed, and clinical signs and MRI and CSF findings were evaluated. A clinical diagnosis of PM was made on the basis of detection of disk-associated spinal cord compression via MRI and progression of clinical signs from initial paraparesis or paraplegia to thoracic limb lower motor neuron paresis to tetraplegia associated with cranial migration of the extent of cutaneous trunci reflex extinction and analgesia, terminating in death due to respiratory paralysis.

Results—All dogs were paraplegic and had signs of lower motor neuron lesions. As revealed by MRI of the vertebral column, the length of abnormal signal intensity was more than 6-fold, compared with the body length of L2. In some dogs, these abnormal MRI findings were observed before PM was clinically diagnosed. The CSF examination revealed hemorrhagic xanthochromia.

Conclusions and Clinical Relevance—A hyperintense region of the spinal cord > 6 times the length of L2 on T2-weighted imaging might be a characteristic MRI finding of PM. In some dogs, such MRI findings were observed before PM was clinically diagnosed. Progressive myelomalacia may thus be diagnosable at the early stage through MRI and CSF examination before signs of PM develop.

Myelomalacia is defined as gross softening of the spinal cord resulting from hemorrhagic necrosis and most commonly occurs as a sequel to acute spinal cord injury associated with IVDH.1–8 Myelomalacia may manifest as a focal lesion associated with the point of contusion or may spread cranially and caudally from the initial lesion. The latter is called ascending hemorrhagic myelomalacia, diffuse myelomalacia, PM, ascending syndrome, ascending myelomalacia, or ascending-descending myelomalacia.1–10 Although the precise pathophysiologic mechanisms are not known, PM might develop following primary and secondary injury of the spinal cord (ie, vascular damage, ischemia, or free-radical production).2 The disease affects < 10% of dogs with severe neurologic deficits associated with thoracolumbar IVDH.1,4,6,7

Progressive myelomalacia is believed to develop within hours after the onset of primary injury, resulting in paraplegia with loss of nociception. Following thoracolumbar disk herniation, progressive ischemic necrosis or spinal cord hemorrhage will cause dogs with PM to have cranial migration of the extent of cutaneous trunci reflex extinction and analgesia, a shift from signs of upper motor neuron lesions to signs of LMN lesions in the pelvic limbs, and neurologic deficits progressing to involve the thoracic limbs. This change will often cause death within several days due to respiratory failure.2,11

No treatment is available for PM, so informing the owner of the diagnosis and prognosis is of primary importance. Another problem is that PM sometimes develops after surgery in dogs with paraplegia with no deep nociception. Veterinarians must therefore explain this risk to owners before performing spinal surgery

Diagnosis of PM is achieved through detection of the aforementioned signs following the development of acute paraplegia. When an affected dog is brought in for evaluation immediately after the acute onset of paraplegia and pelvic limb analgesia, it is not possible to clinically recognize that PM has developed. The lack of accurate diagnostic methods in the early stage of PM causes challenges when advising owners about the possible benefits of surgical intervention. The purpose of the study reported here was to investigate relationships among clinical signs, MRI findings, and CSF characteristics in 12 dogs with presumptive or confirmed PM.

Materials and Methods

Case selection—Study subjects were selected from dogs that were evaluated at the Nihon University Animal Medical Center or Pet Clinic ANIHOS for acute paraplegia and that underwent MRI there from 1997 through 2008. A presumptive diagnosis of PM was made on the basis of evidence of vertebral disk-associated spinal cord compression on MRI and progression of clinical signs from initial paraparesis or paraplegia to thoracic limb LMN paresis to tetraplegia associated with cranial migration of the extent of cutaneous trunci reflex extinction and analgesia, terminating in death due to respiratory paralysis. A confirmed diagnosis of PM was made through necropsy or gross surgical inspection. Whenever PM was strongly suspected before MRI was performed, the investigators recommended euthanasia because of the poor prognosis.

Medical record review—When reviewing the medical record for each dog, the following data were recorded: breed, age, sex, body weight, clinical findings from neurologic examination, existence of pelvic limb nociception prior to MRI examination, existence of vertebral column hyperesthesia, interval between onset of clinical signs and signs of LMN lesions in the pelvic limbs or cranial migration of neurologic deficits, interval between onset of clinical signs and MRI examination, existence of Horner syndrome, and interval from onset of clinical signs to death.

All MRI examinations were performed while dogs were anesthestized by use of a 0.4-T, a 0.5-T,b or 1.5-Tc MRI unit. Sagittal and transverse T1W (TR, 232 to 800 milliseconds; TE, 13 to 22 milliseconds) and also sagittal and transverse T2W (TR, 1,900 to 4,000 milliseconds; TE, 105 to 120 milliseconds) were performed. Findings were reviewed by 3 veterinarians who reached an agreement on interpretations of the MRIs, including site and side of IVDH and location and abnormal signal intensities of the spinal cord. Abnormal signal intensities of the spinal cord were characterized as hyperintense, isointense, or hypointense, compared with healthy spinal cord parenchyma on sagittal and transverse TlWs and T2WIs. Lengths of abnormal signal intensity were measured in comparison to the body length of L2. In some dogs, a CSF sample was obtained from the lumbar subarachnoid space or cerebellomedullary cistern. Total protein concentration, total cell count, cell differential, and appearance of the CSF were evaluated. In 1 dog, protein concentration was measured by use of a urine dipstick test.d In some dogs, the gross appearance of the spinal cord during decompressive surgery was examined.

Statistical analysis—Correlations were calculated among the area of abnormal signal intensity of the spinal cord, the interval between onset of clinical signs and MRI, and the interval between onset of clinical signs and LMN signs in the pelvic limbs or cranial migration of cutaneous trunci reflex extinction and analgesia. Pearson correlation coefficients were calculated to determine correlations between area of abnormal signal intensity of the spinal cord and interval between onset of clinical signs and performance of an MRI or interval between onset of clinical signs and LMN signs or cranial migration of neurologic signs. Continuous values are reported as mean ± SD. A value of P < 0.05 was considered significant for correlation analyses.

Results

Dogs—Twelve dogs met the criteria for inclusion in this study: 9 miniature Dachshunds, 1 Toy Poodle, 1 Beagle, and 1 Toy Poodle-Miniature Dachshund cross (Table 1). Six dogs were male, and 6 were female. Mean ± SD age of dogs was 4.5 ± 1.9 years, and mean body weight was 6.2 ± 2.0 kg (13.6 ± 4.4 lb).

Table 1—

Signalment and neurologic signs of dogs with confirmed or presumptive PM.
Dog No.BreedAge (y)SexBody weight* (kg)NociceptionHyperesthesiaHorner syndromeSurvival duration (d)Diagnosis status
1Miniature Dachshund3M6.4−+NR10P
2Toy Poodle2M4.5−+NR7P
3Beagle7M11.0−−−7†C
4Miniature Dachshund5F4.4−−+7P
5Miniature Dachshund5F5.7±−+7C
6Miniature Dachshund4M8.9−−+7C
7Miniature Dachshund2M4.7−−+5P
8Miniature Dachshund5M6.6−−+9C
9Miniature Dachshund—Toy Poodle cross3F6.7−−NRUnknownP
10Miniature Dachshund8F6.7−−NR9P
11Miniature Dachshund6F4.0−+−6‡C
12Miniature Dachshund4F5.0−−NR12P

*To convert kilograms to pounds, multiply value by 2.2.

†Died when anesthetized.

‡Euthanatized at the owner's request on day 6 after onset of clinical signs once MRI results were obtained.

C = Confirmed (via necropsy or gross surgical inspection). F = Female. M = Male. NR = Not recorded. P = Presumptive (via characteristic clinical signs of PM).

− = Absent. + = Present. ± = Reduced.

Clinical signs—The chief complaint in all dogs was sudden onset of paraplegia. Eleven of the 12 dogs developed paraplegia within 12 hours after onset of discomfort, anorexia, or paraparesis at the owner's house, and the remaining dog developed paraplegia 48 hours after onset of paraparesis. According to clinical histories, each dog lacked nociception in the pelvic limbs at the time it was referred for evaluation. Three of 12 dogs had profound vertebral column hyperesthesia, which was determined in the portion of the body innervated by the still intact spinal cord close to the cranial extent of cutaneous trunci reflex extinction and analgesia. Areas of the body innervated by the affected spinal cord segments lacked sensation. Six of the 12 dogs had signs of LMN lesions (defined as a loss of all motor activity including motor tone and reflexes) in the pelvic limbs or cranial migration of lesion progression on the day of referral. In the other 6 dogs, MRI was performed before onset of signs of LMN lesions in the pelvic limbs or cranial migration of neurologic deficits. All dogs eventually developed LMN signs in the pelvic limbs, cranial migration of neurologic deficits, or both.

Five of 12 dogs developed bilateral Horner syndrome the day before death (Table 1). Median survival duration for 10 of the 12 dogs (excluding data for 1 dog euthanatized on day 6 after onset of clinical signs and 1 dog for which date of death could not be determined) was 8 days from onset of clinical signs. Ten dogs had a spontaneous death, 1 dog died while anesthetized, and the remaining dog was euthanatized.

Diagnosis—A diagnosis of PM was confirmed in 5 dogs, which all had a similar progression of clinical signs from the initial paraparesis or paraplegia to thoracic limb LMN paresis to tetraplegia associated with cranial migration of neurologic deficits, terminating in death due to respiratory paralysis. Progressive myelomalacia was confirmed at necropsy in 2 of these 5 dogs (Figure 1). The remaining 7 dogs were presumed to have PM in accordance with the case definition. Six of 12 dogs were strongly suspected as having PM on the basis of the clinical signs that were evident before MRI was performed. However, the owners of 11 of the 12 dogs did not elect euthanasia, so the dogs were treated empirically with corticosteroids, antimicrobials, and IV fluid administration. As previously mentioned, the other dog was euthanatized at the owner's request after MRI was performed.

Figure 1—
Figure 1—

Photograph of the thoracolumbar portion of the spinal cord in the cadaver of a 6-year-old Miniature Dachshund with suspected PM. Red to dark coloration is evident in the caudal region. The junction of healthy and diseased spinal cord segments is indicated (arrow).

Citation: Journal of the American Veterinary Medical Association 237, 10; 10.2460/javma.237.10.1160

Hemilaminectomy was performed in 3 of the 12 dogs, and in all 3, a large amount of intervertebral disk material was present within the vertebral canal. After removal of disk material, a dark red coloration of the spinal cord was revealed.

MRI—Median interval from onset of clinical signs to MRI examination was 3.7 days (range, 2 to 7 days). In all dogs, IVDH was detected (Table 2) and diffuse abnormal signal intensities were evident in the spinal cord at the site of IVDH. The T1WI scans of the affected areas had an isointense signal, compared with that of healthy spinal cord, whereas hyperintense signals were detected via T2WI scans (Figure 2). In 1 dog, transverse T1WI scans had evidence of isointensity of the spinal cord relative to that of healthy spinal cord, and transverse T2WI scans had hypointensity in the center of the spinal cord and hyperintensity surrounding the hypointense area between T1 and T7 (Figure 3). The other area of spinal cord from T7 to L5 in that dog had isointensity on transverse T1WI scans and hyperintensity on transverse T2WI scans. The length of abnormal hyperintensity of the spinal cord on sagittal T2WI scans ranged from approximately 6 to 20 times the length of the L2 vertebral body. No significant correlations were identified between length of abnormal signal intensity and interval from onset of clinical signs to MRI examination or between interval from onset of clinical signs to detection of LMN deficits in the pelvic limbs or cranial migration of the neurologic deficits.

Table 2—

Findings of MRI in dogs with confirmed or presumptive PM.
Dog No.Magnetic field intensity used in imaging (T)Site of IVDHLength of signal hyperintensity*Interval between onset of clinical signs and MRI (d)Interval between onset of clincal signs and LMN deficits in pelvic limbs (d)
10.5T13-L17.036
20.5T11-127.545
30.5L3-410.144†
40.5T11-1211.066†
50.4T12-138.324
60.4T12-136.424
70.4T11-1214.223
80.4L5-66.722†
90.4T11-1215.322
101.5T12-1319.766†
110.5T12-1310.144†
120.5T11-1211.477†

*Expressed as multiples of the length of the body of L2 at the site of IVDH.

†Indicated dog had signs of LMN deficits in the pelvic limbs on the day of referral to the hospital.

*See Table 1 for remainder of key.

Figure 2—
Figure 2—

Sagittal T1WI (A) andT2WI (B) and transverseT2WI (C and D) views of portions of the spinal cord in the same dog as in Figure 1. In panels A and B, compression of the spinal cord is evident betweenT12 andT13 (short arrow). The spinal cord appears isointense relative to the healthy spinal cord on the T1WI view, and abnormal hyperintensity of the spinal cord extends from T9 to L3 on the T2WI view. The length of signal hyperintensity was calculated as the length of the area of hyperintensity (long double-headed arrow) divided by length of the L2 vertebral body (short double-headed arrow) and equalled 10.1. In panel C, abnormal hyperintensity of the spinal cord is detectable on the transverse section, which reveals slight compression of the spinal cord and extruded intervertebral disk material (arrow). Panel D shows the continuation of L1-2 to the caudal aspect of the spinal cord.

Citation: Journal of the American Veterinary Medical Association 237, 10; 10.2460/javma.237.10.1160

Figure 3—
Figure 3—

Two adjacent sagittal images from T2WI (A and B) and transverse T2WI (C and D) views for an 8-year-old Miniture Dachshund with suspected PM. Compression of the spinal cord is seen between T12 and T13 (A and B; short arrow). L2 ratio = Length of the area of hyperintensity (long double-headed arrow) divided by length of the L2 vertebral body (short double-headed arrow). Transverse T2WI of the spinal cord from T1 to T7 showed hypointensity in the center of the spinal cord and surrounded by a hyperintense area (C;T2-3). Transverse T2WI of the spinal cord from T7 to L5 showed hyperintensity of the spinal cord without hypointensity in the center of the spinal cord (D;T12-13). See Figure 3C for different signal intensity in the center of the spinal cord.

Citation: Journal of the American Veterinary Medical Association 237, 10; 10.2460/javma.237.10.1160

CSF analysis—Samples of CSF from 6 dogs were collected and analyzed after MRI was performed (Table 3). All samples had evidence of hemorrhagic xanthochromia. In addition, a high protein concentration and neutrophilic pleocytosis were evident in 5 of the 6 dogs.

Table 3—

Characteristics of CSF samples obtained from dogs with confirmed or presumptive PM.
Dog No.Day of CSF collectionApproach to CSF collectionNo. of nucleated cells/μLCell differential (L:N)*Protein (mg/dL)Xanthochromia
24Lumbar531:656Present
34Lumbar431:4126Present
46Cisternal651:838Present
92Cisternal881:1.142Present
106Cisternal1001:2.3100†Present
114Cisternal401:3.632Present

*On day after MRI examination.

†Protein was measured in CSF by use of a urine dipstick test.

L:N = Ratio of lymphocytic to neutrophilic cells.

Discussion

The purpose of the present study was to characterize clinical signs, MRI findings, and CSF features associated with PM in dogs. Diagnosis of PM was based on characteristic clinical signs. These were associated with images of extensive hyperintensity involving ≥ 6 lengths of the L2 vertebral body on T2WI scans. In 5 dogs, the diagnosis was confirmed via necropsy or gross surgical inspection. Although descriptions of PM in dogs have been published,2–7,10 little clinical research has been conducted to evaluate MRI findings of PM in dogs, and the few studies1,9 that have been performed included only small numbers of dogs.

In dogs with PM, MRI of the spinal cord typically reveals hyperintensity on T2W1 scans.1,9 Similar to findings of other studies,1,9 abnormal hyperintense areas of spinal cord on T2W1 were seen in all dogs in the present study. Moreover, signal void within the spinal cord on gradient echo images has been reported,1 suggesting intraparenchymal hemorrhage. However, no dogs underwent gradient echo imaging in our study. Rather, our study revealed that the length of the hyperintense area of spinal cord on T2WI scans was from 6 to 20 times the length of L2. The most important point is that detection of a long abnormality of the spinal cord on MRI might be indicative of PM. Other researchers have reported that abnormal hyperintensity of the spinal cord on T2WI scans was related to poor prognosis of paraplegic dogs without nociception when IVDH was present, and in that study,9 a few dogs that had a long region of abnormal signal intensity died because of suspected PM.

The mechanisms underlying PM have not been established. One suggestion is that spinal cord trauma (IVDH) disrupts the spinal cord vasculature (primary injury), followed by ischemic spinal cord injury (secondary injury).2 This process is usually well established within 8 hours after the primary injury and may ultimately result in PM.2 Conversely, edema due to spinal cord injury is reportedly maximal at 8 hours after primary injury12 and begins to resolve by 4 days after injury.13 When a spinal cord is injured, the lesion reportedly begins to appear in the gray matter and extends from the center to the periphery, and extension of the lesion is related to the degree of injury and the interval to manifestation of clinical signs after injury.14 However, no significant correlations were identified between length of abnormal signal intensity and interval from onset of clinical signs to performance of MRI in our study.

Considering the clinical course to the point of death in the study dogs, an area of hyperintensity of the spinal cord on T2WI scans extending > 6 times the length of L2 was presumably not simple edema but instead irreversible progressive necrosis of the parenchyma with or without intradural hemorrhage progressing to the cranial and caudal portions of the spinal cord. In addition, T2WI signal intensity may change. In 1 study dog (dog 10), transverse T2WI revealed hypointensity within the center of the spinal cord and the area was surrounded by a hyperintense lesion. This signal pattern was similar to the hemorrhage pattern observed via MRI in humans with acute spinal cord injury.15 In the acute phase after injury, deoxyhemoglobin is most commonly generated at the site of hemorrhage and appears on high field-strength scans as a discrete area of hypointensity via T2WI.1 The reason these hemorrhagic changes were detected via MRI only in dog 10 might be that the 1.5-T MRI unit used for that dog was capable of producing high-resolution images. Although disk extrusion was seen at T12-13, abnormal hypointensity and hyperintensity of the spinal cord between T1 and T7 might have represented progressive hemorrhagic changes.

In the present study, signs of PM in CSF samples included neutrophilic pleocytosis, high total nucleated cell count, and high protein concentration. Although pleocytosis within CSF is reportedly related to PM,16,17 pleocytosis and high protein concentration are also reportedly related to acute IVDH.16,18–21 Pleocytosis caused by IVDH might be related to immune system reactions to extruded disk material, not only spinal cord injury.18 Another important CSF finding in our study was xanthochromia, which was detected in all CSF samples examined, suggesting the existence of previous hemorrhage. Xanthochromia, the yellow discoloration of CSF caused by hemoglobin catabolism, is classically believed to arise within several hours after subarachnoid hemorrhage.22 Although the interval between onset of clinical signs and collection of CSF samples differed widely among study dogs (2 to 6 days after onset), this may not have influenced the xanthochromic status of those samples because some believe xanthochromia can remain for approximately 2 weeks after hemorrhage.22 Whereas subarachnoid hemorrhage also occurs with focal injuries due to IVDH, this suggests that xanthochromia including pleocytosis and high protein concentration is an important variable for distinguishing PM from other diseases but is not sufficient on its own.

Although vertebral column hyperesthesia in dogs with PM has been reported,11 only 3 dogs in our study had signs of this phenomenon. Vertebral column hyperesthesia is a common sequel to clinical disk herniation in dogs. However, because our study was retrospective in nature, hyperesthesia may have been present in other study dogs but simply not recorded.

Most reports of PM include descriptions of analgesia immediately after onset of clinical signs.1,6,7,10 Analgesia develops caudal to focal spinal cord lesions that disrupt the cranially projecting spinal cord tracts. When myelomalacia expands cranial and caudal to the focal lesion, it destroys not only these tracts but also the sensory neurons that enter the spinal cord as well as the dorsal gray column cell bodies involved in the nociceptive pathway. Either site of neuronal loss has a poor prognosis for patients. Acute loss of nociception has been suggested to be associated with severe spinal cord damage,10 so the prognosis in such situations is poor. Eleven of the 12 dogs in our study lost nociception within 48 hours after peracute thoracolumbar IVDH occurred; thus, our results support previous findings.

Some dogs in the present study had Horner syndrome, indicating that ascending progressive lesions had reached the cranial thoracic region of the spinal cord. All dogs developed Horner syndrome the day after onset of the syndrome. Veterinarians should thus inform owners of dogs with suspected PM of the possibility of pending pet death whenever Horner syndrome is evident.

The predominant breed among the study dogs was Miniature Dachshund (9/12 dogs). Breed characteristics of PM have not yet been reported; however, the reason Miniature Dachshunds may have been overrepresented in our study may be that this breed is popular in Japan. Nonetheless, in a study9 in which associations between MRI findings and outcomes for dogs with IVDH were evaluated, the majority (approx 80%) of dogs were Miniature Dachshunds.

Overall, our findings suggested that T2WI detection of a long area of abnormal hyperintensity with focal compression in the spinal cord as well as detection of xanthochromia in CSF samples may have diagnostic value. Such characteristics may allow a presumptive diagnosis of PM to be made before LMN deficits appear in the pelvic limbs, before extinction of the cutaneous trunci reflex occurs, and before the extent of analgesia in the caudal aspect of affected dogs begins to migrate cranially.

ABBREVIATIONS

IVDH

Intervertebral disk herniation

LMN

Lower motor neuron

MRI

Magnetic resonance imaging

PM

Progressive myelomalacia

T1WI

T1-weighted magnetic resonance imaging

T2WI

T2-weighted magnetic resonance imaging

TE

Echo time

TR

Repetition time
a.

APERTO Inspire, Hitachi Ltd, Tokyo, Japan.

b.

0.5-T FLEXART, Toshiba, Tokyo, Japan.

c.

1.5-T FLEXART, Toshiba, Tokyo, Japan.

d.

Uropaper III, Eiken Chemical Co Ltd, Tokyo, Japan.

References

  • 1.↑

    Platt SR, McConnell JF, Bestbier M. Magnetic resonance imaging characteristics of ascending hemorrhagic myelomalacia in a dog. Vet Radiol Ultrasound 2006; 47:78–82.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 2.↑

    Amsellem PM, Toombs JP & Laverty PH, et al. Loss of deep pain sensation following thoracolumbar intervertebral disk herniation in dogs: pathophysiology. Compend Contin Educ Pract Vet 2003; 25:256–264.

    • Search Google Scholar
    • Export Citation
  • 3.

    Lu D, Lamb CR, Targett MP. Results of myelography in seven dogs with myelomalacia. Vet Radiol Ultrasound 2002; 43:326–330.

  • 4.

    Summers BA, Cummings JF, de Lahunta A. Injuries to the central nervous system. In: Veterinary neuropathology. St Louis: Mosby, 1995;189–207.

    • Search Google Scholar
    • Export Citation
  • 5.

    Griffiths IR. The extensive myelopathy of intervertebral disc protrusions in dogs (“the ascending syndrome”). J Small Anim Pract 1972; 13:425–438.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 6.

    Olby N, Levine J & Harris T, et al. Long-term functional outcome of dogs with severe injuries of thoracolumbar spinal cord: 87 cases (1996–2001). J Am Vet Med Assoc 2003; 222:762–769.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7.

    Scott HW, McKee WM. Laminectomy for 34 dogs with thoracolumbar intervertebral disc disease and loss of deep pain perception. J Small Anim Pract 1999; 40:417–422.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8.

    Griffin JF, Levine JM, Kerwin SC. Canine thoracolumbar intervertebral disk disease: pathophesiology, neurologic examination, and emergency medical therapy. Compend Contin Educ Pract Vet 2009; 31:E1-E13.

    • Search Google Scholar
    • Export Citation
  • 9.↑

    Ito D, Matsunaga S & Jeffery ND, et al. Prognostic value of magnetic resonance imaging in dogs with paraplegia caused by thoracolumbar intervertebral disk extrusion: 77 cases (2000–2003). J Am Vet Med Assoc 2005; 227:1454–1460.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10.↑

    Duval J, Dewey C & Roberts R, et al. Spinal cord swelling as a myelographic indicator of prognosis: a retrospective study in dogs with intervertebral disc disease and loss of deep pain perception. Vet Surg 1996; 25:6–12.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11.↑

    Wheeler SJ, Sharp NJH. Thoracolumbar disc disease. In: Wheeler SJ, Sharp NJH, eds. Small animal spinal disorders diagnosis and surgery. 2nd ed. Edinburgh: Elsevier Mosby, 2005 122–159.

    • Search Google Scholar
    • Export Citation
  • 12.↑

    Janssens LAA. Mechanical and pathophysiological aspects of acute spinal cord trauma. J Small Anim Pract 1991; 32:572–578.

  • 13.↑

    Narayana P, Abbe R & Liu SJ, et al. Does loss of gray- and white-matter contrast in injured spinal cord signify secondary injury? In vivo longitudinal MRI studies. Magn Reson Med 1999; 41:315–320.

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

    Schouman-Claeys E, Frija G & Cuenod CA, et al. MR imaging of acute spinal cord injury: results of experimental study in dogs. AJNR Am J Neuroradiol 1990; 11:959–965.

    • Search Google Scholar
    • Export Citation
  • 15.↑

    Weirich SD, Cotler HB & Narayana PA, et al. Histopathologic correlation of magnetic resonance imaging signal patterns in a spinal cord injury model. Spine 1990; 15:630–638.

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

    Chrisman CL. Cerebrospinal fluid analysis. Vet Clin North Am Small Anim Pract 1992; 22:781–810.

  • 17.

    Vandevelde M, Spano JS. Cerebrospinal fluid cytology in canine neurologic disease. Am J Vet Res 1977; 38:1827–1832.

  • 18.↑

    Windsor RC, Vernau KM & Sturges BK, et al. Lumbar cerebrospinal fluid in dogs with type I intervertebral disc herniation. J Vet Intern Med 2008; 22:954–960.

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

    Sorjonen DC. Total protein, albumin quota, and electrophoretic patterns in cerebrospinal fluid of dogs with central nervous system disorders. Am J Vet Res 1987; 48:301–305.

    • Search Google Scholar
    • Export Citation
  • 20.

    Bohn AA, Wills TB & West CL, et al. Cerebrospinal fluid analysis and magnetic resonance imaging in the diagnosis of neurologic disease in dogs: a retrospective study. Vet Clin Pathol 2006; 35:315–320.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 21.

    Thomson CE, Kornegay JN, Stevens JB. Canine intervertebral disc disease: changes in the cerebrospinal fluid. J Small Anim Pract 1989; 30:685–688.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 22.↑

    Shah KH, Edlow JA. Distinguishing traumatic lumbar puncture from true subarachnoid hemorrhage. J Emerg Med 2002; 23:67–74.

Contributor Notes

Address correspondence to Dr. Kitagawa (kitagawa@brs.nihon-u.ac.jp).
Cover Journal of the American Veterinary Medical Association
Journal of the American Veterinary Medical Association
Publication Date:
15 Nov 2010
  • Figure 1—
    View in gallery
    Figure 1—

    Photograph of the thoracolumbar portion of the spinal cord in the cadaver of a 6-year-old Miniature Dachshund with suspected PM. Red to dark coloration is evident in the caudal region. The junction of healthy and diseased spinal cord segments is indicated (arrow).

  • Figure 2—
    View in gallery
    Figure 2—

    Sagittal T1WI (A) andT2WI (B) and transverseT2WI (C and D) views of portions of the spinal cord in the same dog as in Figure 1. In panels A and B, compression of the spinal cord is evident betweenT12 andT13 (short arrow). The spinal cord appears isointense relative to the healthy spinal cord on the T1WI view, and abnormal hyperintensity of the spinal cord extends from T9 to L3 on the T2WI view. The length of signal hyperintensity was calculated as the length of the area of hyperintensity (long double-headed arrow) divided by length of the L2 vertebral body (short double-headed arrow) and equalled 10.1. In panel C, abnormal hyperintensity of the spinal cord is detectable on the transverse section, which reveals slight compression of the spinal cord and extruded intervertebral disk material (arrow). Panel D shows the continuation of L1-2 to the caudal aspect of the spinal cord.

  • Figure 3—
    View in gallery
    Figure 3—

    Two adjacent sagittal images from T2WI (A and B) and transverse T2WI (C and D) views for an 8-year-old Miniture Dachshund with suspected PM. Compression of the spinal cord is seen between T12 and T13 (A and B; short arrow). L2 ratio = Length of the area of hyperintensity (long double-headed arrow) divided by length of the L2 vertebral body (short double-headed arrow). Transverse T2WI of the spinal cord from T1 to T7 showed hypointensity in the center of the spinal cord and surrounded by a hyperintense area (C;T2-3). Transverse T2WI of the spinal cord from T7 to L5 showed hyperintensity of the spinal cord without hypointensity in the center of the spinal cord (D;T12-13). See Figure 3C for different signal intensity in the center of the spinal cord.

Figure 1—

Photograph of the thoracolumbar portion of the spinal cord in the cadaver of a 6-year-old Miniature Dachshund with suspected PM. Red to dark coloration is evident in the caudal region. The junction of healthy and diseased spinal cord segments is indicated (arrow).
Figure 2—

Sagittal T1WI (A) andT2WI (B) and transverseT2WI (C and D) views of portions of the spinal cord in the same dog as in Figure 1. In panels A and B, compression of the spinal cord is evident betweenT12 andT13 (short arrow). The spinal cord appears isointense relative to the healthy spinal cord on the T1WI view, and abnormal hyperintensity of the spinal cord extends from T9 to L3 on the T2WI view. The length of signal hyperintensity was calculated as the length of the area of hyperintensity (long double-headed arrow) divided by length of the L2 vertebral body (short double-headed arrow) and equalled 10.1. In panel C, abnormal hyperintensity of the spinal cord is detectable on the transverse section, which reveals slight compression of the spinal cord and extruded intervertebral disk material (arrow). Panel D shows the continuation of L1-2 to the caudal aspect of the spinal cord.
Figure 3—

Two adjacent sagittal images from T2WI (A and B) and transverse T2WI (C and D) views for an 8-year-old Miniture Dachshund with suspected PM. Compression of the spinal cord is seen between T12 and T13 (A and B; short arrow). L2 ratio = Length of the area of hyperintensity (long double-headed arrow) divided by length of the L2 vertebral body (short double-headed arrow). Transverse T2WI of the spinal cord from T1 to T7 showed hypointensity in the center of the spinal cord and surrounded by a hyperintense area (C;T2-3). Transverse T2WI of the spinal cord from T7 to L5 showed hyperintensity of the spinal cord without hypointensity in the center of the spinal cord (D;T12-13). See Figure 3C for different signal intensity in the center of the spinal cord.
  • 1.

    Platt SR, McConnell JF, Bestbier M. Magnetic resonance imaging characteristics of ascending hemorrhagic myelomalacia in a dog. Vet Radiol Ultrasound 2006; 47:78–82.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 2.

    Amsellem PM, Toombs JP & Laverty PH, et al. Loss of deep pain sensation following thoracolumbar intervertebral disk herniation in dogs: pathophysiology. Compend Contin Educ Pract Vet 2003; 25:256–264.

    • Search Google Scholar
    • Export Citation
  • 3.

    Lu D, Lamb CR, Targett MP. Results of myelography in seven dogs with myelomalacia. Vet Radiol Ultrasound 2002; 43:326–330.

  • 4.

    Summers BA, Cummings JF, de Lahunta A. Injuries to the central nervous system. In: Veterinary neuropathology. St Louis: Mosby, 1995;189–207.

    • Search Google Scholar
    • Export Citation
  • 5.

    Griffiths IR. The extensive myelopathy of intervertebral disc protrusions in dogs (“the ascending syndrome”). J Small Anim Pract 1972; 13:425–438.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 6.

    Olby N, Levine J & Harris T, et al. Long-term functional outcome of dogs with severe injuries of thoracolumbar spinal cord: 87 cases (1996–2001). J Am Vet Med Assoc 2003; 222:762–769.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7.

    Scott HW, McKee WM. Laminectomy for 34 dogs with thoracolumbar intervertebral disc disease and loss of deep pain perception. J Small Anim Pract 1999; 40:417–422.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8.

    Griffin JF, Levine JM, Kerwin SC. Canine thoracolumbar intervertebral disk disease: pathophesiology, neurologic examination, and emergency medical therapy. Compend Contin Educ Pract Vet 2009; 31:E1-E13.

    • Search Google Scholar
    • Export Citation
  • 9.

    Ito D, Matsunaga S & Jeffery ND, et al. Prognostic value of magnetic resonance imaging in dogs with paraplegia caused by thoracolumbar intervertebral disk extrusion: 77 cases (2000–2003). J Am Vet Med Assoc 2005; 227:1454–1460.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10.

    Duval J, Dewey C & Roberts R, et al. Spinal cord swelling as a myelographic indicator of prognosis: a retrospective study in dogs with intervertebral disc disease and loss of deep pain perception. Vet Surg 1996; 25:6–12.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11.

    Wheeler SJ, Sharp NJH. Thoracolumbar disc disease. In: Wheeler SJ, Sharp NJH, eds. Small animal spinal disorders diagnosis and surgery. 2nd ed. Edinburgh: Elsevier Mosby, 2005 122–159.

    • Search Google Scholar
    • Export Citation
  • 12.

    Janssens LAA. Mechanical and pathophysiological aspects of acute spinal cord trauma. J Small Anim Pract 1991; 32:572–578.

  • 13.

    Narayana P, Abbe R & Liu SJ, et al. Does loss of gray- and white-matter contrast in injured spinal cord signify secondary injury? In vivo longitudinal MRI studies. Magn Reson Med 1999; 41:315–320.

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

    Schouman-Claeys E, Frija G & Cuenod CA, et al. MR imaging of acute spinal cord injury: results of experimental study in dogs. AJNR Am J Neuroradiol 1990; 11:959–965.

    • Search Google Scholar
    • Export Citation
  • 15.

    Weirich SD, Cotler HB & Narayana PA, et al. Histopathologic correlation of magnetic resonance imaging signal patterns in a spinal cord injury model. Spine 1990; 15:630–638.

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

    Chrisman CL. Cerebrospinal fluid analysis. Vet Clin North Am Small Anim Pract 1992; 22:781–810.

  • 17.

    Vandevelde M, Spano JS. Cerebrospinal fluid cytology in canine neurologic disease. Am J Vet Res 1977; 38:1827–1832.

  • 18.

    Windsor RC, Vernau KM & Sturges BK, et al. Lumbar cerebrospinal fluid in dogs with type I intervertebral disc herniation. J Vet Intern Med 2008; 22:954–960.

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

    Sorjonen DC. Total protein, albumin quota, and electrophoretic patterns in cerebrospinal fluid of dogs with central nervous system disorders. Am J Vet Res 1987; 48:301–305.

    • Search Google Scholar
    • Export Citation
  • 20.

    Bohn AA, Wills TB & West CL, et al. Cerebrospinal fluid analysis and magnetic resonance imaging in the diagnosis of neurologic disease in dogs: a retrospective study. Vet Clin Pathol 2006; 35:315–320.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 21.

    Thomson CE, Kornegay JN, Stevens JB. Canine intervertebral disc disease: changes in the cerebrospinal fluid. J Small Anim Pract 1989; 30:685–688.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 22.

    Shah KH, Edlow JA. Distinguishing traumatic lumbar puncture from true subarachnoid hemorrhage. J Emerg Med 2002; 23:67–74.

Advertisement