Portfolio MRT

Staffordshire terrier Gizmo, 10 years

Bilateral toe dragging hind limbs, progressive paraparesis

T2 weighted

T2 weighted

T1 weighted without contrast

T1 weighted with i.v. contrast

With kind permission Dr. O. Lautersack, Tierärztliche Klinik für Chirurgie Ettlingen

Diagnosis

MRI description

In the T2 weighted images all included discs show a varying degree of signal loss of the nucleus pulposus. A moderate to severe degree of spondylosis is located at the TL junction and the first three lumbar vertebrae. An approx. 2cm long mass is present to the L of the spinal cord at the level of L2. At the level of the intervertebral foramen L1/2 it causes compression and displacement of the spinal cord to the right. Centrally over L2 the spinal cord is completely abnormal. The transverse images do not indicate if the spinal cord is completely infiltrated or merely severely displaced and compressed. On the T2 weighted dorsal image a “Golf-T sign”, which represents widening of the subarachnoid space, is present cranial and caudal to the lesion. In the T2 weighted images the mass is of heterogeneous hyperintensity, in the T1 weighted images it is hypointense with strong enhancement. A thin structure without contrast enhancement is evident ventral and to the R of L2; its signal intensity is that of the normal spinal cord.

On the sagittal views only part of the LS junction is included. The LS disc appears to protrude moderately into the spinal canal, replacing the ventral epidural fat so that it comes into contact with the cauda equine.

MRI diagnoses

  • Intradural, mostly extramedullary and partially intramedullary mass level with L2
  • Generalised disc degeneration
  • Spondylosis TL junction and cranial L-spine
  • Cauda equine compression secondary to disc protrusion

Discussion

The list of differential diagnoses includes peripheral nerve sheath tumor, lymphoma, malignant histiocytic sarcoma and meningioma. However, the appearance is not typical for the last three tumor types. Localisation and behavior of the mass also fit the diagnosis of neuroblastoma; however, clinical signs generally begin to show between the first and third year of life. In case the tumor is slow growing, the onset of clinical signs can be delayed until later in life.

Outcome

Photo after durotomy.
With kind permission Dr. O. Lautersack.

Gizmo’s owner elected surgery.

During surgery the tumor was intradurally located and had a greasy, friable consistency. Only a partial resection was possible.

The histological diagnosis was atypical meningioma (Grade II WHO).

Two weeks post operatively “Gizmo” had improved significantly and could walk without signs of paraparesis.

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Irish Setter Thor, 12 years

Epileptic seizures

Images courtesy of Tierklinik Hofheim. Dres Kessler, Kosfeld, Tassani-Prell, Bessmann, Rupp, Delfs, Schmohl, von Klopmann

Diagnosis

Description

The following sequences are available:

T2 weighted transverse, T2* weighted transverse, T1 weighted transverse pre and post contrast medium administration, FLAIR dorsal

A focal, approx. 0.5cm large, intraaxial lesion is present in the grey matter of the suprasylvian gyrus of the right temporal lobe. Centrally the lesion is hypointense on T1w, T2w and FLAIR images. Peripherally a thin, hypointense rim is visible. On the T2* weighted images a large signal void due to a susceptibility artefact is present.

There are no signs of a mass effect. No significant contrast medium uptake is present.

MRI diagnosis

  • Focal, intraaxial cortical lesion right suprasylvian gyrus with suceptibility artifact

Discussion

The suceptibility artefact is indicative for the presence of haemorrhage.

The most common cause for primary intraaxial bleeding is an amyloidangiopathy. Amyloidangiopathy represents perivascular accumulation of hemosiderin and generally appears as multiple very small, pin point changes. Another cause for primary intraaxial bleeding is a spontaneous rupture of vessels due to systemic hypertension, e.g in case of chronic renal disease.

Most common cause for secondary bleeding into the brain parenchyma is an infection with angiostrongylus vasorum. Further differential diagnoses for secondary bleeding include coagulopathies, such as occur with Cushing’s disease, trauma associated bleeding, tumour associated bleeding (vascular neoplasia, e.g. hemangioendothelioma, primary CNS neoplasia, metastases) or vascular malformations.

Haemorrhagic infarcts in dogs are rare, compared to humans.

Owing to the fact that in this case a single lesion with a relatively large susceptibility artefact is present, bleeding secondary to an infection with Angiostrongylus vasorum is considered the most likely diagnosis.

Furth differential diagnoses include systemic hypertension and coagulopathy. Vascular neoplasia and malformations are rare and therefore considered less likely but cannot be ruled out completely.

Due to the lack of contrast enhancement and the absence of peripheral oedema a brain metastasis is unlikely. Trauma associated bleeding can be excluded as no trauma was reported in the history and there are no changes in the overlying musculature which indicate previous trauma.

Outcome

Fecal examination proved a severe infection with Angiostrongylus vasorum.

The dog was dewormed.

Under therapy with anticonvulsant drugs seizuring was reduced and eventually ceased.

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