Vertebral Column & Spinal Cord Flashcards
Vertebral Malformations
Malformations of the vertebrae are common, and although some are clinically significant, many are seen as incidental findings on imaging studies. Malformations can be categorized as simple or complex, and a recent review of spinal anomalies proposed specific classification of anomalous vertebrae based on a similar scheme used in people.
- Those anomalies that occur during the early embryonic period include centrum median cleft (butterfly vertebrae), true hemivertebrae, mediolateral wedged vertebrae, and transitional vertebrae.
- Anomalies that develop during the later fetal period include block vertebrae, articular process hypoplasia, and centrum hypoplasia or aplasia (dorsoventral wedged vertebrae).
- Vertebral anomalies can be further classified as arising from defects in formation (e.g. wedged, hemi‐, and butterfly vertebrae) versus incomplete or absent segmentation (e.g. block vertebrae).
German Shepherd Dogs are overrepresented for developing transitional vertebrae at the lumbosacral junction. Certain screw‐tailed breeds, such as Bulldogs, French Bulldogs, Pugs, and Boston Terriers, are highly predisposed to complex vertebral anomalies, particularly in the midthoracic region.
Vertebral anomalies can result in a combination of scoliosis, kyphosis, lordosis, or rotational spinal abnormalities; can cause spinal canal stenosis; and may predispose to spinal injury from what might otherwise be clinically insignificant trauma. In animals with vertebral canal stenosis, spinal cord diameter is often focally decreased as a result of chronic compression atrophy, even in patients without overt neurologic deficits.
An uncommon vertebral anomaly, caudal articular facet hypoplasia or aplasia in the thoracolumbar vertebral column, has been reported with spinal cord compression due to contralateral facet and ligamentum flavum hypertrophy.
The CT appearance of vertebral anomalies will vary depending on the specific malformation, but common findings include alteration in vertebral shape, reduced attenuation when mineralization is incomplete, and vertebral column curvature abnormalities. Vertebral canal stenosis suggests spinal cord impingement or compression, which can be documented using CT myelography. Lumbosacral transitional vertebrae can predispose to cauda equina syndrome, and asymmetrical transitional vertebra at this level can result in pelvic rotation leading to coxofemoral malarticulation.
MR features are similar to those seen with CT, and spinal cord pathology is often more clearly detected.
Atlantoaxial instability
Atlantoaxial instability
Atlantoaxial instability can be caused by malformation of either or both of the first two cervical vertebrae, with dorsal subluxation of the axis in relation to the atlas causing spinal cord compression. Malformations can include:
- Fusion of adjacent vertebrae
- Grossly abnormal vertebral shape
- Hypoplastic, aplastic, or misshaped dens
- The latter feature is associated with abnormalities of ligaments of the dens, which in turn exacerbate instability.
Caution should be used when imaging patients with suspected craniocervical junction malformations since abnormalities are often unstable.
CT imaging features of atlantoaxial malformations include the abnormalities described above as well as separation of the cranial part of the spinous process of the atlas from the dorsal arch of the atlas with mild cervical flexion. Abnormalities of the dens can some times be more clearly seen on sagittal or dorsal plane reformatted images. Dorsal subluxation of the axis in relation to the atlas also results in decreased vertebral canal diameter.
MR features of atlantoaxial malformations include those described for CT imaging. Spinal cord compression can also be seen as a narrowing of the hyperintense subarachnoid column on T2 images and narrowed spinal cord diameter due to dorsal–ventral cord compression. The MR appearance of the ligamentous structures of the normal canine occipitoatlantoaxial region has been described in a cadaveric study, but they can be challenging to accurately identify in small patients.
Chiari-like Malformation
Although imaging features of Chiari‐like malformation are detailed in Chapter 2.3, a striking imaging feature of the disorder worth mentioning here is the often pronounced saccular syringohydromyelia that can result from altered cerebrospinal fluid dynamics and is best seen on T2 images as a hyperintense dilatation of the central canal.
Cervical spondylomyelopathy
Cervical spondylomyelopathy
Canine cervical spondylomyelopathy (CSM) is challeng ing to concisely summarize because the etiology is unclear, the underlying pathology is variable, and the clinical presentation varies with breed and age of the patient. Genetic, congenital, body conformational, and nutritional etiologies have all been postulated, and the disorder may stem from a combination of these factors. CSM usually occurs in large‐ to giant‐breed dogs between 2 and 8 years of age, and Doberman Pinschers are overrepresented. Although the disorder appears to occur more often in males, there is no confirmed sex predilection.
Clinical signs include cervical pain and spinal cord compressive myelopathy that is neuroanatomically localized to the cervical region. Cord compression is due to some combination of three distinct mechanisms:
- Compression can occur from intervertebral disk protrusion, which tends to occur most frequently between C5 and C7. This manifestation of the disorder occurs in older large‐breed dogs and is common in Doberman Pinschers.
- Osseous stenotic compression is due to inherent vertebral canal stenosis and from proliferative new bone formation occurring on the lamina, pedicles, and articular facet margins of affected vertebrae. This manifestation occurs in younger large‐ and giant‐breed dogs and often involves many of the cervical vertebrae.
- Intermittent or dynamic compression can also occur with change in cervical spine position, usually in extension.
CT imaging features can include:
- Angulation of the endplate subchondral bone margin, associated with vertebral bodies having a rhomboidal rather than rectangular shape as viewed on sagittal images.
- Dogs with a component of intervertebral disk disease will have imaging signs referable to intervertebral disk protrusion.
- In dogs with osseous stenotic manifes tations, bone‐attenuating proliferative changes are seen involving the lamina, pedicles, and articular facets, result ing in decreased vertebral canal diameter, which is most pronounced in the lateromedial direction.
- This results in a change of canal cross‐sectional shape from round to rectangular or triangular and causes predominantly lateral or dorsolateral spinal cord compression and atrophy, which can be documented using CT myelography.
- In those dogs with a dynamic component to spinal cord compression, traction studies can be used to document reduction.
Anatomical features of CSM on MR images are similar to those in CT.
- Dense new bone will appear T1 and T2 hypointense.
- Spinal cord compression is usually clearly defined by attenuation of the subarachnoid column and cord flattening, seen best on T2 images.
- The affected region of the spinal cord may be reduced in diameter from atrophy, and change in signal intensity sometimes occurs as a result of central canal dilation, edema, or gliosis
Osteochondrosis
Osteochondrosis
Osteochondrosis involving the lumbosacral junction has been reported in dogs, and articular facet subchondral bone fragmentation is occasionally seen either in isolation or as a sequela to other disorders, such as cervical spondylomyelopathy. For lumbosacral osteochondrosis, male dogs and Boxer, Rottweiler, and German Shepherd Dog breeds are overrepresented. Clinical signs are those of cauda equina neuropathy, and mean age at presentation is 6.3 years. Approximately 90% of lesions involve the craniodorsal margin of the body of the sacrum, while the remainder involve the caudodorsal margin of the body of the last lumbar vertebra.
On CT images, lumbosacral osteochondrosis lesions appear as one or more separate, bone‐attenuating bodies associated with an underlying defect within the subchondral bone of the parent vertebra. Osteochondrosis lesions may be isolated or associated with other develop mental or degenerative processes of the lumbosacral junction.
In a report of MR features of lumbosacral osteochon drosis in seven dogs, affected endplates were predominantly T1 spin‐echo hypointense, T1 gradient‐echo hyperintense, variably T2 hyperintense, and contrast enhanced. Concurrent intervertebral disk disease was present in five of seven dogs.
Intradural arachnoid diverticula
Intradural arachnoid diverticula
Intradural arachnoid diverticula, sometimes termed arachnoid or subarachnoid cysts, are focal, subdural, and usually dorsally located dilatations containing cerebrospinal fluid and most often confluent with the subarachnoid space. The etiology of intradural arachnoid diverticula is not known, but when seen in young animals they are thought to be developmental. A broader discussion of the various forms of arachnoid diverticula, both developmental and acquired, is included in Chapter 3.5.
- In young dogs, presumed developmental arachnoid diverticula commonly occur in the C2–C4 region in large breeds and in the thoracolumbar region in all breeds.
- Male dogs and Pug, French Bulldog, and Rottweiler breeds are overrepre sented.
- Imaging features of intradural arachnoid diverticula are described in Chapter 3.5
Spinal neural tube defects (spinal dysraphism)
Spinal neural tube defects (spinal dysraphism)
Neural tube defects result from abnormal closure or failure of closure of the developing neural tube.
- Closure errors in the rostral part of the tube lead to cranial defects
- While those that occur caudally lead to vertebral column and spinal cord anomalies
Folate deficiency is one well‐established cause of the disorder in people, and a hereditary link has been identified in neural tube defects described in Weimaraner dogs.
Terminology and classification of the various spinal neural tube defects are both inconsistent and confusing, and we choose to use a simplified scheme for this discussion.
- Errors of ectoderm, mesoderm, and neuro ectoderm development and differentiation, primarily associated with incomplete dorsal migration and closure, result in a grouping of related disorders under the overarching term spina bifida, which often involves the caudal lumbar and sacral region.
- Spina bifida can be further subclassified as spina bifida occulta or spina bifida cystica.
- Spina bifida occulta is limited to incomplete dorsal closure of affected vertebra and is periodically seen on imaging studies as an incidental finding.
- Spina bifida cystica includes dorsal meningeal defects leading to meningocele alone or the most clinically significant form that includes defective meningeal and cord development resulting in myelomeningocele.
- Spina bifida can further be characterized as closed or open to the external environment.
- Sacrocaudal dysgenesis of the Manx cat is a complex spinal neural tube defect that includes developmental abnormalities of the sacral and caudal vertebrae and associated spinal cord segments, which can include meningomyelocele and can be closed or open.
- Other manifestations of abnormal neural tube development, such as spinal duplication, are rare.
Spina Bifida
Spina bifida occulta
- The specific CT or MR imaging feature of spina bifida occulta is incomplete closure of the dorsal arch and spinous process of one or more vertebrae.
- The meninges and spinal cord should appear unaffected.
Spina bifida cystica
- MR imaging features of meningocele include T1 hypointense, STIR and T2 hyperintense dorsal dilation of the subarachnoid space in the region of the lumbosacral junction. The terminal spinal cord and associated spinal nerves remain within the vertebral canal. Meningocele is also present in patients with myelomeningocele, but the terminal spinal cord or the associated spinal nerves are displaced dorsally into the meningocele. If the lesion is open, sagittal or transverse STIR or T2 images can be used to document a communicating tract as a linear hyperintensity
Spinal Dermoid Sinus
Dermoid sinus is an uncommon disorder that also results from neural tube closure errors. Failure of normal cell separation and differentiation into developing spine and skin leads to a dorsal sinus that histologically contains skin elements, such as hair follicles and sebaceous glands. The sinus can have a closed end at its most internal extent or connect to the meninges or spinal cord via a closed or patent tract. A grading scheme has been proposed, ranging from I to IV depending on the internal extent and character of the sinus, with increasing grade reflecting a more invasive lesion. Of the few reported cases, most are at the level of the cervical or cranial thoracic vertebral column. Dermoid sinuses have been reported in dogs and cats, and Rhodesian Ridgebacks are predisposed.
CT imaging features may be unremarkable other than a possible skin surface defect. Conventional radiographic sinusography has been used to determine the internal margin of the sinus and assess its association to the underlying vertebral column, meninges, and spinal cord, and CT would likely be of similar value. Reported MR imaging features include superficial mass with mixed T1 intensity, mild T2 hyperintensity, and STIR hyperintensity. In some instances, a sinus tract was not seen, and the depth of the lesion was underestimated. In one other patient, a T2 hyperintense tract was clearly identified coursing from the superficial mass to the dura matter.
Atlantoaxial Instability (Canine)
5mo MC Yorkshire Terrier with acute onset cervical pain of 1‐week duration. Image a is the same as image b without annotations.
- Dorsal subluxation of the axis (b: large arrows) is present in relation to the atlas (b: arrowheads), causing marked narrowing of the vertebral canal in the dorsal–ventral axis (b: asterisk).
- The angulation of the vertebral column at the atlantoaxial joint, the gap between the caudal margin of the dorsal arch of the atlas, and the cranial margin of the spinous process of the axis (b: two‐headed arrow) are further evidence of atlantoaxial instability.
- The dens is also absent (b: small arrow).
- The abnormal relationship of the atlas and axis is also clearly seen on 3D renderings (c,d).
- Aplasia of the dens is best seen from the dorsal view (d: arrow).
Chiari‐like Malformation with Syringohydromyelia (Canine)
1.5y F Chihuahua with recent‐onset paroxysmal episodes.
- The caudal cranial vault is small as a result of occipital hypoplasia (a: arrowhead), and moderate generalized hydrocephalus is evident (a).
- Marked saccular syringohydromyelia is present throughout the cervical and cranial thoracic spinal cord (b: arrows).
- There is also T2 hyperintensity within cord parenchyma, which is likely due to edema (b: arrowhead).
A diagnosis of Chiari‐like malformation with syringohydromyelia was made based on clinical and imaging findings.
Cervical Spondylomyelopathy (Canine)
3y MC Mastiff with hypermetria in all limbs. CT myelographic images a, b, and c are at the approximate level of the C2–3, C3–4, and C4–5 intervertebral disk spaces, respectively.
- Hyperattenuating new bone of the lamina (a–c: arrow) and articular facets (a–c: arrowheads) at all three levels results in reduction of vertebral canal cross‐sectional area and change in shape, with greatest narrowing occurring in the horizontal axis.
- Remodeled articular facet margins impinge on the spinal cord to the greatest extent at C4–5, although a thin subarachnoid contrast column is retained (c).
- Additional sites with similar abnormalities were present more caudally (not shown).
Cervical Spondylomyelopathy (Canine)
3y MC Labrador Retriever with myelopathy neuroanatomically localized to C1–5. The CT myelographic image is at the level of C4–5.
- Hyperattenuating new bone of the lamina (black arrow) and articular facets (arrowheads) results in reduction of vertebral canal cross‐sectional area and change in shape, with greatest narrowing occurring in the horizontal axis.
- The spinal cord is grossly distorted by bilateral compression from hypertrophied articular facets.
- There is also a separate osseous fragment associated with the distal margin of the right caudal aspect of the fourth cervical articular facet (white arrow), consistent with osteochondrosis.
Sacral Osteochondrosis (Canine)
4y FS Miniature Schnauzer with a diagnosis of portosystemic shunt and no neurologic abnormalities. A CT examination was performed for surgical planning.
- Multiple small but highly attenuating osseous fragments are seen within the vertebral canal at the level of the lumbosacral junction (a,b: arrow).
- There is an underlying defect of the craniodorsal margin of the first sacral body, manifest as an angular flattening of the bone (a: large arrowhead).
- The lumbosacral intervertebral disk space is widened, and a soft‐tissue mass containing the fragmented bone protrudes into the vertebral canal, indicative of intervertebral disk herniation (a: small arrowhead) and possible dorsal longitudinal ligament hypertrophy.
Intradural Arachnoid Diverticulum (Canine)
10mo FS Boxer cross with myelopathy neuroanatomically localized to C1–5.
- Conventional and CT myelographic images show an elongated teardrop‐shaped dilation of the dorsal subarachnoid space at the level of the second cervical vertebra (a–c: arrow), resulting in pronounced spinal cord compression (a–c: arrowhead).
- Contrast enhancement within this focal dilation is evidence that it communicates with the rest of the subarachnoid space.
A large cyst‐like structure was surgically removed following durotomy and was histologically confirmed to be an arachnoid diverticulum.
Myelomeningocele (Canine)
6mo M English Bulldog with urinary and fecal incontinence since birth.
- The spinous process and pedicle margins of the caudal‐most lumbar vertebra are missing, consistent with spina bifida (a,b).
- There is dorsal deviation of the dural sac (c,d: arrow), which contains neural elements (c,e,f: white arrowhead), defining this as a myelomeningocele.
- A thin stalk (e: black arrowhead) extends from the dorsum of the myelomeningocele to the skin surface, which is dimpled.
- The hyperintensity in image c defining the volume of the meningocele does not extend dorsally within the stalk, and clinically this was determined to be a closed meningomyelocele.
Vascular Cord Trauma
Contusion/hemorrhage
Contusion/hemorrhage
Spinal cord trauma is usually but not always accompanied by overt vertebral column trauma. Neurologic deficits range from clinically silent to complete spinal cord transection. In addition to the primary spinal cord injury that results directly from trauma, secondary injury occurs from vascular damage, local cytotoxic biochemical responses to injury, and inflammatory response, the combination of which can lead to progres sive disease. Postmortem examination of spinal cords of dogs and cats that sustained traumatic injury revealed thoracolumbar necrosis that correlated with the degree of static compression from vertebral column injury. Cervical cord injury often included central hemorrhagic necrosis that was more consistent with transient impact trauma than static cord compression.
MR features of spinal cord contusion include:
- Focal to regional increased T2 intensity with mild to no enhancement following contrast administration (Figure 3.2.18).
- T2* sequences reveal parenchymal susceptibility effects when there is a hemorrhagic component.
- Syringohydromyelia is often a late sequela to spinal cord trauma and appears as a focal to regional and central to eccentric T2 hyperintensity.
Vascular disorders of Spinal Cord
Fibrocartilagenous Embolism
Fibrocartilagenous embolism
Early reports indicated that fibrocartilaginous embolism (FCE) occurs primarily in middle‐aged to older, large‐ and giant‐breed dogs; however, a more recent review in which diagnosis was based on clinical signs and MR imaging findings suggests that small and medium‐sized dogs are also commonly affected. The disorder has also been reported in cats. The clinical presentation is often a peracute onset of symmetrical or asymmetrical motor dysfunction immediately following exercise or minor trauma, with lower motor neuron signs also present in some patients. Initial clinical signs can include transient pain and can be progressive for the first 2 hours but are often nonprogressive thereafter. The cervicothoracic (C5–T2) and lumbosacral (L3–S3) regions appear to be predisposed. Pathology in histologically confirmed patients includes spinal cord infarction and hemorrhage with cartilaginous emboli in meningeal or spinal vessels. In some patients, extensive myelomalacia may also be present, but pathology is likely to be more severe in those patients that were euthanized and confirmed as having FCE. A poorer prognosis is seen in patients with involvement of the intumescences, symmetrical neurological signs, and decreased deep pain sensation. A recent review of dogs with ischemic myelopathy found that a combination of lesion length greater than twice a vertebral length and cross‐sectional involvement of greater than 67% had a positive correlation with an unsuccessful outcome. Recovery rates for FCE are unclear since patients who do respond are not definitively diagnosed. However, a majority of patients with stable disease seem to partially or fully recover neurologic function.
CT imaging features can be limited to a noncompressive focal increase in spinal cord diameter, indicative of an intrinsic lesion.
MR features include focal T1 iso‐ to hypointensity and T2 hyperintensity within the affected spinal cord segments. Lesions preferentially affect gray matter and can be either symmetrical or asymmetrical. Spinal cord diameter can also appear locally enlarged but without compression. Intervertebral disk T2 signal intensity at the level of the spinal cord lesion is often less than that of adjacent disks
Occipitoatlantal Luxation (Canine)
1y FS Keeshond cross with acute cervical injury after being struck by an automobile earlier in the day. A CT examination was performed with the dog on a backboard in lateral recumbency. Images a–c were acquired at the level of the occipitoatlantal joint and are ordered from cranial to caudal.
- The right occipital condyle (a–d: arrow) is axially subluxated in relation to the cranial articular fovea of C1 (a–c: asterisk).
- The left occipital condyle is ventrally luxated (c,d: arrowhead).
Closed reduction of the luxation was successfully performed using fluoroscopic guidance.
Cervical Vertebral Subluxation with Articular Facet Fracture (Canine)
5y F Terrier cross bitten in the cervical region by a larger dog earlier in the day. Currently has neurologic deficits neuroanatomically localized to C6–T2.
- Survey radiographs reveal dorsal subluxation of C7 relative to C6 and narrowing of the C6–7 intervertebral disk space (a: arrowhead).
- Similar findings are also seen on sagittal and 3D reformatted CT images (b,f: arrowhead). In addition, there is a highly comminuted and displaced fracture of the right cranial articular process of C7 (c–e: arrow).
- The left articular process is normal by comparison (f: arrow). On MR images, the C6–7 intervertebral disk space is reduced in width and T2 signal intensity (i: arrow), and extruded disk material is present in the right ventral vertebral canal (g,h: arrowhead).
- There is evidence of spinal cord compression (g–i) and spinal cord T2 hyperintensity at the level of C6–7 (h,i), indicative of an intrinsic component to the injury.
Disk material was removed from the canal, and the subluxation was reduced and stabilized surgically.
L3 Lamina Depression Fracture (Feline)
8y FS Domestic Shorthair bitten by a dog 2 days previously. Currently has a nonambulatory T3–L3 myelopathy.
- On CT images, a depression fracture arising from the cranial margin of the L3 lamina (a,b: arrowhead) impinges on the dorsal margin of the spinal cord.
- A ventral oblique 3D rendering with the vertebral bodies removed further illustrates the displacement of the fracture fragment into the canal (c: arrowhead).
- The fracture fragment is T2 hypointense on MR images (d,e: arrowhead) and impinges on the spinal cord, causing deformation and compression.
- There is also marked increase in spinal cord T2 signal intensity at this level due to intrinsic edema and hemorrhage.
- The T2 signal intensity of the L3–4 intervertebral disk is also reduced, suggesting possible traumatic intervertebral disk extrusion.
Spinal cord compression was relieved with a hemilaminectomy, and the L3–4 vertebral column was stabilized, resulting in gradual return of neurologic function.
Spinal Cord Contusion (Canine)
4y MC Border Collie stepped on by a bull 1 day previously, resulting in injuries to the lumbar spine and abdomen. Current neurologic deficits are referable to an L3–L5 myelopathy. Spinal radiographs were unremarkable.
- There is moderate diffuse spinal cord T2 hyperin- tensity centered at the level of L3 and L4 (a,d: arrowheads) indicative of an intrinsic lesion.
- The spinal cord mildly and diffusely enhances following contrast administration (c,f: arrowheads).
- A T2* sequence reveals pinpoint susceptibility artifacts within the spinal cord indicative of multifocal hemorrhage (g: arrow).
Hematomyelia (Canine)
12y FS Pit Bull Terrier with acute‐onset tetraparesis. The owners have administered aspirin twice weekly for chronic osteoarthrosis.
- There is T2 hyperintensity of the spinal cord parenchyma and focal central canal dilation centered on C5 (b,e: arrow).
- Cord diameter is enlarged at this level, indicative of intrinsic pathology, but there is no evidence of compression.
- The internal venous plexus also appears dilated (a,b: arrowheads).
- T2* sequences document hemorrhage within the effected spinal cord segment, as evidenced by prominent susceptibility effect (c,f: arrowhead).
Postmortem examination confirmed hematomyelia, myelomalacia, and subdural hemorrhage. An underlying cause was not determined, and chronic aspirin administration was thought to have induced a spontaneous hemorrhage. The two vertically oriented curvilinear lines superimposed on the spinal cord in image e are artifacts caused by an out‐of‐field microchip.
Fibrocartilaginous Embolism (Canine)
4y FS Yorkshire Terrier with peracute onset of tetraparesis shortly after returning from a walk with the owner.
- A myelographic examination reveals a pronounced increase in spinal cord diameter centered on C6 (a: arrowheads).
- CT myelography further documents a caudal cervical intrinsic lesion (b–d: arrowheads).
- Although there is normally an increase in diameter of the cervical intumescence, the magnitude of the diameter change is abnormal and causes annular attenuation of the subarachnoid contrast column (d: arrowhead).
- A transverse cranial thoracic image acquired caudal to the spinal cord lesion shows a more normal spinal cord diameter and prominent contrast‐enhanced subarachnoid space (e).
Postmortem examination confirmed regional myelomalacia caused by multiple fibrocartilaginous emboli. The degree of spinal cord diameter enlargement in this patient is somewhat unusual and would be less likely to occur in patients with recoverable disease.
Fibrocartilaginous Embolism (Canine)
4y FS Irish Wolfhound with acute‐onset pelvic limb paraparesis with no known initiating cause.
- There is diffuse T2 hyperintensity in the caudal spinal cord consistent with an intrinsic lesion (a–c: arrow).
- There is mild, diffuse cord enhancement following contrast administration (e,f: arrow).
- The central T2 hyperintensity and contrast enhancement suggests predominantly gray matter involvement (b,f: arrow).
Neurologic deficits persisted for 14 days with no evidence of improvement. Postmortem examination revealed severe bilateral myelomalacia with hemorrhage from spinal segment L6 caudally. Multiple fibrocartilaginous emboli were present in both the meningeal and spinal vessels.
Fibrocartilagenous Embolism (Canine)
8y MC Labrador Retriever with acute‐onset neurologic deficits anatomically localized to C6–T2.
- There is focal T2 hyperintensity and T1 hypointensity of the spinal cord at the level of C5–6 (a,b,d,e: arrow) with no evidence of enhancement following contrast administration (c,f).
- The intensity changes are centrally distributed, and spinal cord diameter is focally increased, indicative of an intrinsic lesion.
- A T2* sequence shows no evidence of hemorrhage within the affected cord parenchyma (g).
The owners elected to euthanize the dog, and postmortem examination revealed locally extensive, primarily gray matter, myelomalacia, hemorrhage, and neuronal necrosis in the C5–C7 spinal cord segments (h). Multiple fibrocartilaginous emboli were evident in meningeal and spinal vessels. It is unclear why the T2* sequence failed to show the intraparenchymal sites of hemorrhage. One possibility is that because of the peracute nature of the disorder, MR imaging was performed early enough after the initial insult that hemoglobin degradation products were not yet present in adequate concentration to yield a susceptibility effect.
Steroid responsive meningitis–arteritis
(SRMA)
Steroid responsive meningitis–arteritis (SRMA) is a systemic immune‐mediated disorder that includes inflammatory responses of the leptomeninges and associated blood vessels, which has been reported in young Bernese Mountain Dogs, Beagles, Nova Scotia Duck Tolling Retrievers, Corgis, Boxers, and other breeds.
The disorder involves the spinal cord primarily and, to a lesser extent, the brain. Although MR features of meningeal thickening and contrast enhancement have been reported, our experience is that imaging studies in dogs with SRMA are often unremarkable.
Bacterial (suppurative) discospondylitis
In a large retrospective study involving over 500 canine patients diagnosed with discospondylitis, 2/3 were male, older dogs were more likely to be affected, and Great Danes were overrepresented.8\ Staphylococcus, Brucella, Streptococcus, and Escherichia species are most frequently isolated, although many others have been reported. Dogs with bacterial discospondylitis most often have an underlying infection of the urinary tract, skin, or other organ system, which leads to bacteremia and embolic seeding of vulnerable disks.
Conventional radiographic examination is an excellent test for diagnosis and monitoring of discospondylitis. CT and MRI are most often employed when neurologic deficits are present or the patient has other clinical signs not explained by radiographic findings or other diagnostic tests.
Imaging features vary widely and depend on the stage of the disease. CT features of early active disease can include vertebral endplate osteolysis and intervertebral joint space widening. In later phases of active disease, more pronounced endplate destruction is seen, which is associated with underlying bone sclerosis, reactive new bone formation, and collapse of the disk space. If there is significant proliferative soft‐tissue inflammatory response or intervertebral joint subluxation, spinal cord compression can occur with resultant neurologic signs. In the convalescent or reparative phase, complete collapse of the joint may occur with bridging reactive new bone. Soft tissues within the disk space, medullary bone, and surrounding soft tissues moderately to markedly contrast enhance during the active phases of disease, reflecting the presence of discitis, osteomyelitis, and cellulitis.
MR features of bacterial discospondylitis are similar and include mixed T2 intensity within the disk space and T1 hypointensity and T2 and STIR hyperintensity within affected vertebral bodies and adjacent soft tissues during the early active phase of disease. The disk, medullary bone, and adjacent soft tissues intensely contrast enhance during the active phases of disease. MR may be less sensitive than CT for monitoring bone destruction and production in the active and reparative phases, respectively.
Spondylitis
In some geographic areas, inhaled plant awns can migrate through airways and lung parenchyma and exit caudally into the cranial sublumbar region, following the path of the attachment of the pars lumbalis of the diaphragm to the ventral margins of the third and fourth lumbar vertebrae. Pyogranulomatous myositis and frank abscess adjacent to the vertebrae lead to spondylitis.
Imaging features of spondylitis include:
- Periosteal new bone formation of the ventral and lateral margins of affected vertebral bodies.
- Underlying bone sclerosis may also be present depending on the duration and severity of infection, resulting in hyperattenuation on CT images and hypointensity on T1 and T2 MR images.
- Cellulitis or abscess is present with active disease, which will appear as a hypoattenuating sublumbar mass on CT images and a T1 hypointense, T2 hyperintense mass on MR images.
- Marked, heterogeneous soft‐tissue contrast enhancement occurs on images of both modalities
Spinal epidural empyema
Infections within the spinal epidural space are uncommon and can occur by direct extension of discospondylitis or other local infection or through hematogenous dissemination. Signs include fever and progressive myelopathy, which may have a compressive component.
CT findings can be equivocal but include signs of discospondylitis as described above. Subarachnoid and epidural space contrast enhancement can be incomplete or nonuniform on CT myelographic images, and there may be evidence of focal, multifocal, or diffuse spinal cord compression.
MR features include mixed or increased T2 intensity within the epidural space, as well as T2 hyperintensity within the spinal cord at the site of infection. Moderate diffuse or peripheral enhancement is seen following contrast administration with both modalities
Presumptive Spinal Granulomatous Meningoencephalomyelitis (Canine)
4y FS Chinese Crested Dog with a 3‐day history of difficulty walking, most pronounced in the thoracic limbs, and neuroanatomic localization to C1–T2.
- There is a T2 hypointense, T1 isointense focus in the dorsal spinal cord at the level of caudal C2 (a–d: arrow).
- Two smaller intrinsic foci with similar intensity are seen at the level of the C2–3 intervertebral disk space (a,c: arrowhead).
- There is diffuse T2 hyperintensity in the cranial cervical spinal cord due to surrounding edema (a).
- A discrete, uniformly enhancing mass is seen following contrast administration (e,f: arrow), and faint enhancement of the two smaller lesions is also evident (e: arrowhead).
Diagnosis was made from results of cerebrospinal fluid analysis consistent with granulomatous meningoencephalomyelitis, absence of infectious agents, and response to immunosuppressive doses of steroids.
Spinal Granulomatous Meningoencephalomyelitis (Canine)
4y FS Jack Russell Terrier with recent onset of nystagmus and circling.
- There is diffuse moderate T2 hyperintensity of the brainstem and cranial cervical spinal cord associated with parenchymal swelling (a).
- There is mild nonuniform enhancement within the brainstem following contrast administration, and three ill‐defined contrast‐enhancing intrinsic lesions are seen in the dorsal cervical spinal cord (c: arrowheads).
Postmortem examination revealed angiocentric inflammatory lesions consistent with granulomatous meningoencephalitis. Multifocal suppurative inflammation with necrosis was also noted.
Suppurative Discospondylitis (Canine)
5y FS Greyhound with back pain that developed a few weeks following treatment of an inflammatory pulmonary disorder.
- Vertebral radiographs reveal vertebral endplate osteolysis, surrounding bone sclerosis, and narrowing of the L3–4 intervertebral disk space (a,b: arrow).
- These findings are also evident on CT images, and the degree of endplate destruction is more apparent (d,e: arrow).
- There is a loss of the normally fat‐attenuating ventral epidural space (c: arrow), and there is regional enhancement adjacent to the vertebral column (f: arrowhead) and within the ventral epidural space (f: arrow) following contrast administration, indicative of local extension of the inflammatory response.
Fine‐needle aspiration cytology revealed suppurative inflammation. Microbial culture failed to yield a causative agent, although the dog had been on antibiotics prior to sampling.