Acute noncompressive nucleus pulposus extrusions most often occur when an otherwise healthy intervertebral disk is subjected to a brief excessive force. Such extrusions typically occur in dogs during performance of strenuous exercise or following trauma.1–4 The force placed on the intervertebral disk may result in the nucleus pulposus being rapidly projected toward the spinal cord through a rent in the annulus fibrosus. The extruded nucleus pulposus strikes the spinal cord, causing contusion, and dissipates within the epidural space without resulting in a compressive mass.1–4
Acute noncompressive nucleus pulposus extrusions in dogs and cats have been reported.1–7 Several other terms have been used to describe this condition, including traumatic disk prolapse,5 dorsolateral intervertebral disk “explosion,”1 high-velocity–low-volume disk extrusion,6 Hansen type III intervertebral disk disease,2–4 and traumatic disk extrusion.7 The term ANNPE is used here because it describes the main features of the disease and helps differentiate it from the more common type of disk extrusion that occurs following intervertebral disk degeneration (Hansen type I intervertebral disk disease) and that typically results in spinal cord contusion and compression.
In dogs with ANNPE, the neurologic signs that develop depend on the site and severity of the lesion and are characterized by an acute, often asymmetric myelopathy that is nonprogressive after the first 24 hours.1–4,a Clinical signs, course of disease, and CSF and myelographic findings of dogs with ANNPE may be similar to those reported for dogs with ischemic myelopathy.2–4 High-field MRI and experience in neuroimaging help in differentiating between these 2 diseases.2–4,7–9,a The MRI features of ANNPE include focal hyperintensity within the spinal cord overlying an intervertebral disk, with reduction in volume and signal intensity of the nucleus pulposus on T2-weighted images, narrowed intervertebral disk space, and extraneous material or signal change within the epidural space dorsal to the affected disk with absent or minimal spinal cord compression.2–4,6,7,a The region of spinal cord that corresponds to the focal hyperintensity on T2-weighted images is most commonly isointense on T1-weighted FSE images and does not have evidence of enhancement on T1-weighted FSE images obtained after administration of contrast agent. However, hypointensity on T1-weighted FSE images and mild enhancement on T1-weighted FSE images obtained after administration of contrast agent have also been described.7
A definitive diagnosis of ANNPE is only possible at postmortem examination by visual detection and histologic examination of the gelatinous nucleus pulposus extruded into the vertebral canal, the ruptured annulus fibrosus, and the contused spinal cord.1 The improved availability of MRI has resulted in an increase in the number of dogs in which a diagnosis of ANNPE is made while alive2–4; however, limited information is available on outcome, and the prognostic role of MRI has not been reported to our knowledge.
In human medicine, MRI is considered the imaging modality of choice for evaluation of spinal cords after traumatic injury.10 A distinct association between MRI signal intensity and histologic characteristics of acutely injured spinal cords has been identified in human patients with spinal cord injury11 and in animals in experimental studies.12–14 In those species, intramedullary hyperintensity on T2-weighted MR images has been associated with edema and necrosis of the spinal cord.11–14 The signal intensity of hemorrhage on T1- and T2-weighted FSE MR images varies depending on the specific form of hemoglobin present (ie, oxyhemoglobin, deoxyhemoglobin, or methemoglobin), whether the RBCs are intact or lysed, and the strength of the MRI operating field.15 Gradient echo sequences are the most sensitive means of detecting hemorrhage within the CNS because with this type of MRI sequences, hemorrhage appears hypointense at all stages.16 The degree of parenchymal spinal cord injury detected via MRI is reportedly associated with the degree of neurologic deficits and has prognostic value for predicting neurologic recovery in humans with traumatic spinal cord injury.17–23
In veterinary medicine, researchers in only 3 studies have investigated the prognostic role of MRI in the diagnosis of traumatic24 or ischemic25,b,c spinal cord injury in dogs. To the best of our knowledge, the prognostic role of MRI and clinical findings in dogs with ANNPE has not been investigated. The purpose of the study reported here was to assess associations of severity of neurologic signs, involvement of an intumescence, and MRI findings with interval to recovery and outcome in dogs with ANNPE.
Acute noncompressive nucleus pulposus extrusion
T2* gradient echo
Lesion length-to-vertebral length ratio
Methylprednisolone sodium succinate
Magnetic resonance imaging
Percentage cross-sectional area of the lesion
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1.5-Tesla Signa Echospeed MRI, General Electric Medical Systems, Milwaukee, Wis.
Gadolinium: Omniscan (gadodiamide) Nycomed, Oslo, Norway or Multihance (gadobenate dimeglumine), Bracco, Milan, Italy.
GE Advantage Windows, version ADW3.1, General Electric, Milwaukee, Wis.
E-film, Merge Emed, Milwaukee, Wis.
Stata, version 10.0, StataCorp, College Station, Tex.
SAS, version 9.1.3, SAS Institute Inc, Cary, NC.
Scores for severity of neurologic signs according to clinical neuroanatomic localization in dogs with presumptive ANNPE.
|Score||Clinical neuroanatomic localization|
|C1-C5 or C6-T2||T3-L3 or L4-S3|
|1||Clinically normal||Clinically normal|
|2||Ambulatory hemiparesis or tetra paresis||Ambulatory monoparesis or paraparesis|
|3||Nonambulatory tetraparesis with or without monoplegia or hemiplegia||Nonambulatory paraparesis with or without monoplegia|
|4||Tetraplegia with or without U1 or F1||Paraplegia with or without U1 or F1|
|5||Tetraplegia, loss of nociception, U1, and F1||Paraplegia, loss of nociception, U1, and F1|
U1 = Urinary incontinence. F1 = Fecal incontinence.