Table 1.
Signalment, clinical and initial imaging data of patients with negative outcome.
Table 2.
Signalment, clinical and initial imaging data of patients with positive outcome.
Table 3.
Time points of MRI investigations following SCI.
Fig 1.
Transverse T2W and T1W MR images of intramedullary lesions/cavitations at the level of the SCI epicentre in the 3 dogs that were subsequently submitted for post-mortem histopathological examination.
Note the intramedullary hyperintense signal (arrow) in T2W (A, B) and hypointense signal in T1W MR images (A’, B’) in comparison to normal spinal cord parenchyma in the spinal cords of the French bulldog (A, A': patient ID 7) and dachshund (B, B': patient ID 11) 3 months following SCI. These signal changes are compatible with fluid-filled intramedullary cavitations, as they are isointense to the CSF signal. More subtle changes were observed in a Jack Russel terrier (C, C': patient ID 16) spinal cord 6 months following SCI (C). In some areas, the intramedullary signal is hyperintense in comparison to the normal spinal cord signal in T2W MR images, but it is hypointense in comparison to the CSF signal (arrowhead). Corresponding areas look isointense to spinal cord in T1W MR images (C’).
Fig 2.
Measurement of the length, maximal cross-sectional area (mCSA) of intramedullary lesions/cavitations and spinal cord diameter at the lesion epicentre.
The length of intramedullary lesions/cavitations was estimated by measuring the length of the intramedullary lesions/cavitations in T2W MR images and calculating the ratio to the length of the L2 vertebra (A). Maximal CSA of spinal cord lesions/cavitations was measured by measuring the area of the spinal cord lesion/cavitation in the T2W MR images (B) and dividing it by the area of the spinal cord at the same level (B‘), which led to a percentage of the damaged spinal cord. Spinal cord diameter was measured in T2W MRI at the lesion epicentre (C ‘) and at the level of the normal spinal cord cranially (C) and caudally (C ‘‘). The difference of diameters led to the estimated reduction of spinal cord diameter.
Table 4.
Chronic intramedullary lesion, cavitation, mCSA and SCA distribution among patients with positive and negative outcome and initial neurological grades IV and V.
Table 5.
Initial SCI location, length and location of chronic intramedullary lesions/cavitations, mCSA of intramedullary lesions/cavitations and severity of spinal cord atrophy in patients with negative outcome.
Table 6.
Initial SCI location, length and location of chronic intramedullary lesions/cavitation, mCSA of intramedullary lesions/cavitations and severity of spinal cord atrophy in patients with positive outcome.
Fig 3.
Overview of haematoxylin and eosin-stained sections of the spinal cord epicentre of the 3 dogs with severe, chronic spinal cord injury.
Patient ID 7: severe myelomalacia, especially prominent in the grey matter (open asterisk) (A). Patient ID 11: severe pan-myelomalacia with complete loss of organotypic architecture and distinction between grey and white matter (B). Patient ID 16: severe myelomalacia with accentuation in the grey matter (asterisk) (C). Patient ID 7: myelomalacia with gliosis in the grey matter (open asterisk), while the white matter (asterisk) is less prominently affected (D). Patient ID 16: grey matter with severe gliosis and infiltration of phagocytic gitter cells (arrows) (E). Patient ID 16: severe malacia with gitter cell infiltration within the grey matter (open asterisk) (F). The white matter exhibits multiple dilated myelin sheaths and several axonal spheroids (arrowheads).
Table 7.
Histopathological findings in the 3 patients (patient ID 7, 11 and 16).
Fig 4.
Association between length of chronic intramedullary lesions/cavitations and neurological grade following SCI (≤48 hours).
Statistically significant difference between grade IV and V in regard to extension of intramedullary lesions (P = 0.002) and intramedullary cavitations (P = 0.008).
Fig 5.
Association between length of chronic intramedullary lesions/cavitations and neurological outcome (P<0.0001).
Dogs with negative neurological outcomes did not regain ambulation within 7 months after presentation in the hospital. Dogs with positive neurological outcomes regained ambulation within 7 months after presentation in the hospital.