An 11 year old spayed female Doberman pinscher was referred to the University of Tennessee Veterinary Medical Center with the complaints of progressive tetraplegia over a 3 day interval and acute onset of dyspnea. On presentation, the dog was non-ambulatory and cyanotic and showing signs of hypoventilation.
There is variable loss of high T2 and STIR signal within all intervertebral discs most notably in the caudal cervical and cranial thoracic segments. There is dorsal protrusion of low signal material from the C6-7 intervertebral disc space into the ventral spinal canal resulting in mild flattening of the adjacent ventral spinal cord with maintenance of high signal within the spinal canal dorsally separating the spinal cord from the vertebral arch. At the level of C5-C6, a larger volume similar low signal material extends dorsally from the intervertebral disc space into the ventral spinal canal extending cranially on the left side displacing the spinal cord dorsally and to the right. Additionally, there is T2 hyperintense material with a well-defined hypointense rim located primarily dorsally extending left and ventrally within the vertebral canal of C5 resulting in marked ventral and right deviation and compression of the spinal cord. This T2 high signal material is of mixed T1 hyperintensity cranially and hypointensity caudally with a well-defined division between the 2 phases. On transverse gradient echo T2* images, magnetic susceptibility artifact is present associated primarily with the caudal aspect of this material. Sagittal HASTE images show marked attenuation of the subarachnoid space centered at the caudal body of C5 with mild attenuation of the ventral subarachnoid space at the level of C6-7. Postcontrast sagittal and transverse T1-weighted images with fat saturation show focal partial enhancement of the predominantly dorsally located T2 and STIR high signal material.
Degenerative disc disease likely associated with cervical vertebral instability with intervertebral disc herniation at the level of C5-6 with concurrent chronic active spinal canal hemorrhage resulting in severe dorsal and left spinal cord compression.
Non-compressive intervertebral disc protrusion at the level of C6-7.
While spinal cord compression secondary to intervertebral disc herniation was presumed clinically significant, the more severe spinal cord impairment was attributed to the actively bleeding spinal canal hematoma. The signal characteristics of dorsal extradural lesion being hyperintense on T1, T2, and STIR sequences coupled with significant magnetic susceptibility artifact on gradient echo T2* images were diagnostic for hemorrhage. The mixed signal characteristics in the T1 images and T2 images in the time frame of the animal’s clinical signs are consistent with hyperacute and acute hemorrhage where both diamagnetic oxyhemoglobin and paramagnetic deoxyhemoglobin are intermixed. The hypointense rim of the T2 hyperintense material is consistent with rapid deoxygenation of the margin of the acute hematoma. The partial enhancement of the hematoma on post-contrast images was consistent with active bleeding.
The dog’s respiratory compromise was consistent with a mid-cervical spinal cord lesion. There are 2 potential causes of dyspnea secondary to cervical spinal cord injury. First, hypoventilation may be attributable to phrenic nerve injury interrupting normal motor activation of the muscles of respiration as the C5, C6, and C7 nerve roots are its components. Second, spinal cord compression may result in interruption of sympathetic airway innervation resulting in airway hyperresponsiveness due to excess parasympathetic tone leading to bronchoconstriction.
The dog was placed on a ventilator prior to MRI examination. Von Willebrand’s factor testing found abnormally low activity, and the dog was administered cryoprecipitate prior to surgery. A dorsal laminectomy was performed confirming the MRI diagnoses. The dog’s respiratory and neurologic clinical signs slowly progressively improved following surgery.
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