History

A 1-year-old neutered male Weimaraner was referred for evaluation of an acute onset of paraplegia. For 2 days prior to the onset of neurologic signs, the dog was lethargic and had episodic signs of pain. At the time of admission, no abnormalities were found on physical examination. Neurologic examination revealed normal mentation and cranial nerve function. The patient was paraplegic, with intact spinal reflexes and deep pain perception in both pelvic limbs and the tail. Signs of pain were evident over the cranial thoracic region of the vertebral column. The neuroanatomic localization was at the T3-L3 spinal cord segments. Findings on a CBC and serum biochemical analysis were unremarkable. With the dog under general anesthesia, MRI of the thoracolumbar portion of the vertebral column was performed with a 1.5-T magnet (Figure 1).

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Sagittal (A–C) and transverse (D–G) MRI images of the thoracic portion of the vertebral column of a 1-year-old neutered male Weimaraner with an acute onset of paraplegia. Spin echo T2-weighted (T2W) images (A and D), spin echo T1-weighted (T1W) images before (B and E) and after contrast enhancement (C and F), and a T2* gradient echo sequence (G) are shown.

Citation: Journal of the American Veterinary Medical Association 242, 10; 10.2460/javma.242.10.1345

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Determine whether additional imaging studies are required, or make your diagnosis from Figure 1—then turn the page →

Diagnostic Imaging Findings and Interpretation

No abnormalities of the vertebral column and intervertebral disks are evident. Centered at the junction between T1 and T2, within the vertebral canal, there is a single, well-defined lesion that appears hyperintense to the spinal cord on spin echo T2-weighted (T2W) images (Figure 2). This lesion is situated ventral to the spinal cord. It occupies approximately one-third of the vertebral canal diameter on transverse images, extends from the middle of T1 to the cranial aspect of T2, and results in moderate spinal cord compression. The lesion is isointense to the spinal cord on spin echo T1-weighted (T1W) images, with a thin rim of contrast enhancement separating it from the spinal cord following administration of gadopentetate dimeglumine. The lesion itself does not enhance. The lesion appears to be situated within the subarachnoid space because, on T2W images, the epidural fat signal is preserved, there is attenuation of the hyperintense subarachnoid CSF signal with some widening of the subarachnoid space, and the hypointense dura mater is visible between the lesion and the epidural fat. There is signal void on T2* gradient echo sequences, which, in combination with the other sequences, is most consistent with hemorrhage. The MRI diagnosis was an intradural, extramedullary lesion causing spinal cord compression at the level of T1–2, compatible with an acute hematoma. Hemorrhage may also occur secondary to other conditions, with possible differential diagnoses including granulomas or poorly enhancing neoplasia with concurrent hemorrhage, although these would be uncommon in a young patient.

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The same MRI images as in Figure 1. Signal intensity in all sequences is compared with that of the spinal cord. A single, well-defined extramedullary lesion resulting in substantial spinal cord compression is evident within the vertebral canal at the level of T1–2. The lesion is hyperintense on T2W images (arrows; A and D) and isointense on T1W images (arrowheads; B and E). There is a signal void on the T2* gradient echo sequence (arrow; G). After administration of gadopentetate dimeglumine, a thin line of contrast enhancement is evident between the lesion and the spinal cord parenchyma (arrowheads; C and F), but the lesion itself does not have any enhancement.

Citation: Journal of the American Veterinary Medical Association 242, 10; 10.2460/javma.242.10.1345

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Treatment and Outcome

The patient underwent a left-sided hemilaminectomy at T1–2. A durotomy was performed, and a large intradural hematoma was removed. Histologic examination confirmed this to be hemorrhage. The dog made an uneventful recovery and was clinically normal 1 month later, and no underlying cause was identified on further investigation.

Comments

Magnetic resonance imaging is a sensitive imaging modality for detecting hemorrhage in the CNS and estimating the chronicity. Five stages of intracranial hematomas have been defined in human patients, each associated with specific MRI findings: hyperacute (duration, < 24 hours; intracellular oxyhemoglobin; hypo- to isointense on T1W images and hyperintense on T2W MRI images), acute (duration, 1 to 3 days; intracellular deoxyhemoglobin; iso- to hyperintense on T1W MRI images and hypointense on T2W MRI images), early subacute (duration, 4 to 7 days; intracellular methemoglobin; hyperintense on T1W MRI images and hypointense on T2W MRI images), late subacute (duration, 7 to 14 days; extracellular methemoglobin; hyperintense on T1W and T2W MRI images), and chronic (duration, > 2 weeks; ferritin and hemosiderin; hypointense on T1W and T2W MRI images).^1,2 Subdural and epidural spinal hematomas also have similar changes, but the highly vascularized dura mater results in a higher local oxygen tension, which may delay the progression.² Spinal hemorrhage is an unusual finding in veterinary patients.¹ Spontaneous epidural and subdural spinal hematomas have been reported in human patients with similar imaging characteristics in the hyperacute stage to those in the dog of the present report (hypo- or isointense on T1W images, hyperintense on T2W images, and no contrast enhancement).^2,3 Magnetic resonance imaging is useful in the detection of CNS hemorrhage and in determining the time course.