1) The study analyzed MRI findings of Wallerian degeneration in the spinal cords of 11 patients with traumatic spinal injuries. 2) The most common pattern observed was degeneration in both the posterior and lateral tracts of the spinal cord. 3) The signal changes observed on MRI, including hyperintensity on T1 and T2 weighted images, likely correspond to later stages (3 and 4) of Wallerian degeneration as described in the brain.

1. Wallerian Degeneration in the Spinal Cord: Study in 11
patients with traumatic spine injury
Poster No.: C-0909
Congress: ECR 2017
Type: Educational Exhibit
Authors: C. A. Robles, P. ORELLANA, A. Torres; Santiago/CL
Keywords: Neuroradiology spine, MR, Sampling, Trauma
DOI: 10.1594/ecr2017/C-0909
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2. Learning objectives
The aim of this work is to show the findings in magnetic resonance imaging (MRI) of
the spinal cord Wallerian degeneration, through the analysis of 11 cases in patients with
spinal cord injury and literature review.
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3. Background
Wallerian Degeneration (WD) are degenerative changes in the distal axons and the
myelin sheaths secondary to injury to the proximal portion of the axon or neuronal cell
body from vascular (ischemic or haemorrhagic), neoplastic, inflammatory or traumatic
origin (1).
Was described by August Waller, who severed the glossopharyngeal and hypoglossal
nerves of frogs, made histologic analysis and described coagulation and curdling of the
spine into separate particles of various sizes.
The cellular cascade of WD in the central nervous system include granular disintegration
of the cytoskeleton, which axonal proteins (microtubules and neurofilaments) degrade to
an amorphous and granular debris probably activated by calcium induced proteases (2).
The debris from breakdown of the nerve fibres and myelin sheaths in the CNS begin
after 1 week and continues for about 2 years (some authors say 8 years). There
is no macrophage invasion, the oligodendrocytes do not proliferate, instead undergo
apoptosis, the end result is a matrix dominated by astrocytes that fail to accommodate
new axonal growth (3).
MR imaging of WD in the brain has been reported in literature, and four stages have been
proposed by Kunh. These stages reveal the biochemical changes in the neuronal cell
body, that are represented on the image. These findings should be similar in the spinal
cord but there are specific structural differences that explain different imaging findings
between WD in the spinal cord vs brain.
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4. Findings and procedure details
11 patients with spinal cord injury and Wallerian degeneration diagnosis were selected.
The data was obtained from a trauma hospital in Santiago, Chile, between 2011 and
2015. All these patients were controlled with MRI with a minimum of 1 and maximum of
5 exams. MRI were obtained on a 1.5 T unit and consisted of sagittal, coronal and axial
T2 weighted images. T1 sagittal and axial images were also obtained. The interpretation
of these images were performed by 2 neuroradiologist with more than 10 years of
experience.
The signal intensity in the spine in different sequences (T1, T2 and T2 STIR) was
controlled, with emphasis in the posterior and lateral cords, above and under the spine
injury.
In order to interpret the appearances of the spine seen on MRI and to distinguish normal
from abnormal, it is important to understand the normal anatomy (figures 1 and 2).
The median age was 39 y/o, with an age range between 23 to 61 y/o. All the patients had
myelomalacia, syrinx or spine contusion, above or under which the intensity changes in
the posterior (somato-sensorial) or lateral (corticospinal) spinal tracts were affected.
The levels of the lesion are shown in Table 1.
Injury Level N %
Cervical 8 66,6
Dorsal 4 33,3
Lumbar 0 0
Table 1
Only one patient had 2 levels compromised (cervical and dorsal), with a total of 12 studies
analysed. Most of the patients had cervical injury, which correlates with the literature
findings in traumatic spine injury. All the causes of injury in the study were motor vehicle
accidents. The time since the accident was between 6 to 28 years at the moment of the
study.
If we identify WD above or under the injury we certainly know that the spinal cord
injury caused complete or partial interruption of the ascending or descending axons in
the posterior or lateral columns. The differences in size signal between cervical and
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5. dorsal compromise is a function of the number of axons damaged and the somato-topic
arrangement of the ascending fibres in the dorsal column tracts.
The analysis of the compromised tracts is showed in Table 2.
WD Tract Compromised N %
Posterior tracts 4 36,4
Lateral tracts 2 18,2
Both tracts 5 45,4
Table 2
The most common pattern was WD in both tracts (posterior al lateral fascicles). When only
one tract was compromised, the posterior tracts were more frequently involved. (figures
3, 4 and 5)
The changes in the spinal cord through the analysis in time, were represented on the
MRI. Signs of spine WD were defined as changes in the signal intensity in posterior tracts
above the level of the injury and lateral tracts under this one, with posterior atrophic
changes.
The earliest time at which areas of increased signal intensity on T1 and T2 weighted
images can be detected by MR is 7 weeks in cadaver cords (3).
Wallerian degeneration in the brain is widely described in literature with 4 histopathologic
and imaging stages. These imaging findings could be similar in the spine, though
the signal of the white matter on MRI is lower on T1/T2 weighted images, with less
differentiation between white and grey matter. Besides the structural organization of the
axons and the composition of the different cellular elements in the spine is different to
the brain. These could explain the differences in signal and temporality of the changes
in time, in spine WD. In the brain there is a classical classification made by Kunh and
collegues. The stage 1 of Kunh (physical degradation of the axon with little biochemical
changes in myelin) during the first 4 weeks, will have a normal signal on T1/T2 and
diffusion restriction on DWI. Stage 2 (myelin protein breakdown) from 4-14 weeks will
lead to a hydrophobic environment, that explain the low signal on T2 because of the
high lipid-protein ratio (1). In our study we observed hyperintensity of the spinal tracts
compromised, most probably to changes in the lipid/water proportions, which became
more hydrophilic. The signal changes we found in our patients would be equals to stages
3 and 4 of Kuhn, with high T2 signal and tract's atrophy.
The differential diagnosis on MRI should consider:
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6. Subacute combined degeneration: Myelopathy due to B12 or Cupper deficiency
secondary to malabsorption syndromes or inadequate intake. The initial symptoms are
usually paraesthesia in the hands and feet. This may progress to sensory loss, gait
ataxia and distal weakness(4). The diagnosis is made by low serum of them. Pathologic
studies show multifocal demyelinated and vacuolates lesions in the posterior, lateral,
and sometimes anterior columns. Copper is an important cofactor in several enzymatic
processes important in the function of the CNS. Distinction from vitamin B12 deficiency
based on imaging is not possible.
The imaging findings are modest expansion of the cervical and thoracic spinal cord and
increased signal intensity on T2 weighted images, primarily in the dorsal columns, usually
contiguous in length over several vertebral bodies. (figure 6)
AIDS-Associated Myelopathy: The most common cause of spinal cord disease in AIDS
patients. It is an exclusion diagnosis based on clinical, laboratory and radiological
findings. There is intramyelin and periaxonal vacuolation, with cellular debris and lipid-
laden macrophages in the white matter of the spinal cord(5). It typically involves the lateral
and posterior tracts of the cervical and thoracic cord. The most common imaging finding
is spinal cord atrophy, typically involving the thoracic cord and increased signal intensity
on T2 weighted images in the dorsal columns and lateral columns.
Spinal Xanthomatosis: Cerebrotendinous xanthomatosis (CTX) is an autosomal
recessive disease, due to a deficiency of the sterol 27-hydroxilase, that leads to the
storage of cholestenol and cholesterol in many tissues, specially eye lens, CNS and
tendons (6). There is diffuse involvement of the long tracts in the spinal cord as well as
in the brainstem. The imaging findings are hyperintense lesions on T2 weighted images
in the dentate nucleus, substnatia nigra, globus pallidus and the spinal cord. The entire
spinal cord is compromised, with increased signal intensity localized in both lateral and
corticospinal tracts and in the gracile tracts. (figure 7)
Others: Tabes dorsalis, Friedreich's ataxia, Vitamin E deficiency, Adult-onset autosomal-
dominant leukodystrophy (ADLD) and Multiple Sclerosis.
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7. Images for this section:
Fig. 1: Schematic (a), histological (b) and GRE (c) images with the posterior tracts
(somato-sensorial) highlighted in blue (Courtesy Dr Miguel Soto)
© Universidad de Chile, Hospital Clinico Universidad de Chile - Santiago/CL
Fig. 2: Schematic (a), histological (b) and GRE (c) images with the lateral tracts (cortico-
spinal) highlighted in red. (Courtesy Dr Miguel Soto)
© Universidad de Chile, Hospital Clinico Universidad de Chile - Santiago/CL
Fig. 3: 23 y/o man with history of motor vehicle accident. (a) Sagittal T2 weighted images
with myelomalacia in the dorsal spine. (b) Posterior tracts with Wallerian Degeneration
upward to the lesion. (c) Lateral tracts Wallerian Degeneration downward to the lesion
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8. © Universidad de Chile, Hospital Clinico Universidad de Chile - Santiago/CL
Fig. 4: 47 y/o man with history of motor vehicle accident. (a) Sagittal T2 weighted images
with myelomalacia in the cervical spine. (b) Posterior tracts with Wallerian Degeneration
upward to the lesion. (c) Lateral tracts Wallerian Degeneration downward to the lesion
© Universidad de Chile, Hospital Clinico Universidad de Chile - Santiago/CL
Fig. 5: 49 y/o man with history of motor vehicle accident with lesion in the cervical and
dorsal spine. (a) Sagittal T2 weighted image. Blue arrows showing the spinal cord lesions,
the red line represents the axial image. (b) Axial T2 weighted image. Hypersignal in
the posterior and lateral tracts compatible with Wallerian Degeneration. Both tracts are
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9. compromised due to lesions in the cervical (lateral tracts) and dorsal (posterior tracts)
spine.
© Universidad de Chile, Hospital Clinico Universidad de Chile - Santiago/CL
Fig. 7: 44 y/o female with Cerebrotendinous Xanthomatosis. (a) Sagittal T2 weighted
image in the dorsal spine showing diffuse posterior tracts hyperintensity. (b) Axial T2
weighted image in the dorsal spine with posterior tracts hyperintensity. (c) Axial T1
weighted with diffuse enlargement of the Achilles tendons. (Courtesy Dr Juan Pablo Cruz)
© Department of Radiology, Hospital Clínico Universidad Católica, Pontificia Universidad
Católica de Chile, Chile 2016
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10. Fig. 6: 31 y/o man with Subacute combined degeneration. (a) Axial T2 weighted image
in the cervical spine showing anterior,posterior and lateral tracts hyperintensity. (b) Axial
T2 weighted image in the dorsal spine with anterior and lateral tracts hyperintensity. (c)
Axial T2 weighted image in the dorsal spine with posterior tracts hyperintensity
© Universidad de Chile, Hospital Clinico Universidad de Chile - Santiago/CL
Page 10 of 12

11. Conclusion
The analysis of the cases shows that our imaging findings in WS of the spine are similar
to the cases reported in literature. Due to the physiopathology, parenchyma and time of
evolution the WD is different between spine and brain lesions. Our imaging findings could
correlate with the stages 3 and 4 of Kuhn described in the brain, but further studies with
histologic analysis is needed to asses this. It's important to know the imaging findings of
WD in the spinal cord, its evolution in time, that could lead us to raise a certain imaging
diagnosis and not to be misinterpreted with other pathologies, in the correct clinical
context.
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12. References
1.-Becerra, Jose L., et al. "MR-pathologic comparisons of wallerian degeneration in spinal
cord injury." American journal of neuroradiology 16.1 (1995): 125-133.
2.-Valencia, Maria Pilar, and Mauricio Castillo. "MRI findings in posttraumatic spinal cord
Wallerian degeneration." Clinical imaging 30.6 (2006): 431-433.
3.-A. Buss, et al. Gradual loss of myelin and formation of an
astrocytic scar during Wallerian degeneration in the human spinal cord. Brain 127 (2004):
34-44.
4.-Ravina, Bernard et al. MR Findings in Subacute Combined Degeneration of the
Spinal Cord: A Case of Reversible Cervical Myelopathy. AJNR Am J Neuradiol 174
(2000):863-865.
5.-Chong, June et al. MR Findings in AIDS-Associated Myelopathy. AJNR Am J Neuradiol
20 (1999):1412-1416.
6.-Verrips, A. et al. Spinal xantomatosis: a variant of cerebrotendinous xantomatosis.
Brain 122 (1999): 1589-1595.
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