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eEdE-239
Diffuse Involvement of the Cauda Equina
Nerve Roots in Adults: a Practical
Approach to Differential Diagnosis
Alamer A1,2, Cortes M1, Tampieri D1
1Radiology
Department, Montreal Neurological Institute, McGill University,
Montreal, Quebec, Canada
2Radiology Department, Qassim College of Medicine, Qassim University, Saudi
Arabia
Disclosure
The authors have nothing to disclose.
Objectives
Review the MR anatomy of the cauda equina nerve roots.
Discuss the most appropriate MR technique for evaluation of
the cauda equina.
Illustrate image-based diagnostic approach and clinical
assessment for different pathologies with diffuse involvement
of the cauda equina nerve roots.
Cases.
Introduction
Diffuse abnormality of the cauda equina nerve roots is non-specific
finding on MR and can be observed in a wide variety of conditions.
The most common etiologies include infectious/inflammatory
diseases versus neoplastic processes.
The MR finding itself in isolation lacks specificity, and correlation
with the clinical information, laboratory results such as CSF
analysis are usually necessary to reach to the correct diagnosis.
Biopsy is necessary in some cases to confirm the diagnosis.
Generally, the disease process of the cauda equina nerve roots can
involve solitary or multiple nerve roots.
Solitary nerve root involvement is much more specific for single
diagnosis and its beyond our scope of this exhibit.
Introduction
Diffuse or multiple nerve roots involvement is least specific for
single diagnosis and can manifest in MR imaging either as diffuse
thickening of the cauda equina nerve roots and/or diffuse
enhancement.
The pattern of post contrast enhancement can be smooth or
nodular which can help to narrow the differential diagnosis taking
in consideration smooth enhancement is the most common and the
least specific.
The presence of tumoral masses is another valuable finding which
suggests neoplastic processes.
The purpose of this educational electronic exhibit is to describe
the relevant radiological anatomy of the cauda equina nerve roots
using Magnetic Resonance Imaging (MRI) and to review various
pathologies with diffuse involvement of the cauda equina nerve
roots.
Cauda Nerve Roots Anatomy
The spinal nerve roots emerge from the ventrolateral (motor)
and dorsolateral (sensory) surfaces of the spinal cord. Then,
they traverse the subarachnoid space for variable distance
before exiting the spinal canal.
Compared to the cervical and thoracic nerve roots, the
lumbar and sacral nerve roots have a much longer course in
the subarachnoid space extending from the conus medullaris
to their respective neural foramina3.
The lumbar and sacral nerve roots within the subarachnoid
space are called the cauda equina.
Below the conus the nerve roots are predominately situated
in the posterior part of the dural sac and they become more
diffusely spread within the subarachnoid space (Figure 1).
Cauda Nerve Roots Anatomy
In the sagittal images, they together appear as a uniform structure.
However, the individual nerve roots become visible as they descend
anteriorly and laterally toward their exits under the pedicles. At this
point they invariably appear thin (less than 2 mm in diameter),
smooth, and linear16.
Spinal dura surrounds the exiting spinal nerve roots, forming root
sleeves, which terminate proximal to the dorsal root ganglia. In the
sagittal images at the pedicular level, the nerve-root sleeve unit is
clearly shown in the upper part of the neural foramen contrasted by
the surrounding fat. Just distal to the dorsal root ganglia, the
ventral and dorsal nerve roots join to form the spinal nerves.
The dorsal root ganglia in the lumbosacral region are located more
medially than in the cervicothoracic region3. 61 % of the dorsal
root ganglia lie inside the foramina, 21% lie outside the foramina,
and 18% lie within the spinal canal6.
(a)
(b)
Figure 1 (a): Sagittal T2-wieghted image show the conus (*) and the cauda equina
nerve roots. (b): Axial T2-wieghted images show the cauda equina nerve roots
posteriorly oriented in the dural sac. Note normal thin uniform thickness of the roots.
MR Technique
While the imaging findings are sometime complimentary,
MRI is the imaging modality of choice when evaluating
patient with extremity weakness, paresthesias, or GI/GU
dysfunction.
Axial T2, Sagittal T1 and T2 weighted images are standard
sequences for imaging the lumbar spine.
Other pulse sequences such as fluid attenuated inversion
recovery is also useful for assessment of the spinal nerve
roots5.
MR Technique
Sagittal and axial post gadolinium T1-wieghted images are
additionally used for the evaluation of spinal nerve roots.
Coronal sequence can be helpful for disease extent distal to
the neural foramen such as in Neurofibromatosis.
Concomitant use of fat suppression technique and contrast
enhancement increases the conspicuity of enhancing nerve
roots and allow better delineation of the disease extension
beyond the spine4.
The enhancement is also more conspicuous with a dose of
0.3 mmol/kg than with a dose of 0.1 mmol/kg12.
Approach
The differential consideration for diffuse abnormality of the
nerve roots can be distinguished partly on the basis of the
dominant imaging findings and correlate that with the
pertinent clinical information1.
The dominant radiological findings can be:
① Abnormal enlargement of the nerve roots (Morphology).
② Unusual pattern of enhancement.
③ Presence of tumoral masses.
Morphology of the Nerve Roots
Abnormal morphology or hypertrophy of the cauda equina
nerve roots is nonspecific finding and may be seen in
hereditary neuropathy such as Charcot Marie Tooth disease
(CMT) or in acquired demyelination like Chronic
Inflammatory Demyelinating Polyneuropathy (CIDP) or due
to infiltration of the nerve roots by malignancy.
Generally, hypertrophic neuropathy can also be caused by
acromegaly, diabetes mellitus, amyloidosis, lymphoma,
leprosy,
localized
hypertrophic
mononeuropathy,
neurofibromatosis, Refsum’s disease, and sarcoidosis53,54.
Nerve root hypertrophy can rarely involve the cauda equina
and produce symptoms of back pain and lumbar stenosis54.
Morphology of the Nerve Roots
Thickening of the nerve root can be define as more than 50%
increase in diameter compared to the contralateral nerve root
at the same level44. However, the assessment of diffuse nerve
roots can be much more difficult due to lack of comparison.
Developmental anomaly such as conjoined nerve roots can
be mistaken for morphological abnormality. The nerve root
anomaly itself dose not cause symptoms, but can lead to
complication if overlooked prior to spinal surgery (Figure 2).
(a)
(b)
Figure 2 (a): Tow consecutive axial T2-wieghted images of lumbar spine at L5-S1
level shows normal variant conjoined S1 and S2 nerve roots on the right side (arrow).
(b): More lower axial cut at the foramina level shows separation of the conjoined
nerve roots towards their corresponding foramina (arrows).
Spinal Nerve Roots Enhancement
The nerve is cable-like bundle of axons containing nerve fibers.
The epineurium, perineurium and endoneurium are three layers of
loose connective tissue surrounding the nerve, axons, and nerve
fibers respectively7.
The endoneurial and perineural capillaries constitute the true
blood-nerve barrier8. This barrier is less effective with extensive
permeability in the intradural roots and even more in the spinal
ganglia9.
Normally, the cauda equina nerve root doesn’t enhance (Figure 3a).
However, minimal normal enhancement can be observed probably
due to efficiency of the blood-nerve barrier9. This subtle
enhancement can be detected only if pre and post contrast images
are compared side by side and resolved in delayed images. So, any
non-specific insult can disrupt the blood-nerve barrier and cause
gadolinium enhancement of the nerve root.
Spinal Nerve Roots Enhancement
The dorsal root ganglia are void of a blood-nerve barrier and their
for will normally enhance after the injection of contrast material.
This can be easily mistaken for pathology especially the position of
dorsal root ganglia can be asymmetrical (Figure 3 b).
Abnormal enhancement of the nerve roots is non-specific finding
on MR which suggests breakdown of the blood-nerve barrier and
can be seen in wide variety of conditions including neoplastic,
infectious, and inflammatory/autoimmune causes. The abnormal
accumulation of toxic metabolites may be implicated in hereditary
disorders. In cases of leptomeningeal carcinomatosis, the
enhancement likely represents tumoral angiogenesis11.
The pattern of enhancement, chronicity, and other imaging
findings coupled with a thorough history can help pare down this
differential diagnosis1.
(a)
(b)
Figure 3 (a): Sagittal post gadolinium image shows normal lack of enhancement of
the cauda equina nerve roots (arrow). Note avid enhancement of the basivertebral
vein (*). (b): Axial and coronal post gadolinium images of the lumber spine show
avid enhancement of the dorsal root ganglia (arrows).
Presence of Tumoral Masses
The presence of tumoral masses in the cauda equina region is likely
related to neoplastic process.
The presence of solitary tumor of the peripheral nerve is suggested
by an enhancing mass that grows along the nerve, often extending
out of the neural foramina. A solitary nerve sheath tumor may
represent either a solitary neurofibroma or schwannoma or a
malignant peripheral nerve sheath tumor.
If its associated with diffuse enlargement of the peripheral nerve
roots, entities such as neurofibromatosis (NF) type 1 or 2 should be
considered1. Metastasis and lymphoma are also suggested in cases
of diffuse involvement of the cauda equina with tumoral masses.
Differential Diagnosis
Diagnosis
Congenital
Hereditary motor-sensory neuropathies (i.e. CMT and DejerineSottas disease), metachromatic leukodystrophy & krabbe disease2,
and Cockayne syndrome.
Infectious
Can be bacterial, viral or due to atypical pathogen. Such as
tuberculosis, herpes radiculitis, AIDS related polyradiculopathy as
result of CMV, Lyme disease, and Neuroborreliosis.
Inflammatory
Vascular
Spinal Disk
Disease
Arachnoiditis
Toxic
Neoplastic
Sarcoidosis, Guillain-barré syndrome, and CIDP.
Spinal cord infraction15 or dural arteriovenous fistula.
Spinal Disk Disease or rarely the redundant nerve root syndrome
of the cauda equina.
Based on different etiologies.
Intrathecal methotrexate, radiation-induced lumbosacral
radiculopathy13 or post spinal-epidural anesthesia.
Neurofibromatosis, meningeal carcinomatosis and lymphoma.
The Above D.Ds are based on literature review and not necessary presented in adult age group
D.D Based on the Morphology
and Pattern of Enhancement
Smooth
Nodular
GBS (anterior
roots).
Infection: TB.
CIDP.
Sarcoid.
Spinal meningitis.
Arachnoidits
and radiation.
Vascular: infract
(ventral roots) or
SDAVF.
NF.
Spinal Disk
disease and
arachnoidits.
Meningeal
carcinomatosis.
Lymphoma.
Lymphoma.
The Above classification are based on the most common MR pattern
D.D Based on the Presence of
Tumoral Masses
Neurofibromatosis.
Meningeal
carcinomatosis.
Lymphoma.
Multiple tumoral masses are noted (arrows)
along the cauda equina nerve roots in a patient
known to have NF 1.
Clinical Correlation
Disease
Pertinent Clinical
CSF
MR
Note
Infectious:
viral,
bacterial
& atypical
e.g.: TB
Features of meningitis
in general such as fever
with back pain.
TB: presents with
radicular pain which
usually chronic
+ protein
- glucose
Smooth
enhancement, can
be nodular in case
of TB due to
tuberculoma
Spondylodiscits
Abscess
Brain MR: basal
meningitis
HIV
Rapidly progressive leg
weakness. Back pain
and numbness are also
common.
+ protein
Smooth or
- glucose nodular thickening
and enhancement
GBS
Antecedent infection.
Progressive ascending
and symmetrical
flaccid paralysis , < 2
months
+protein
CIDP
Chronic counterpart of
GBS, > 2 months
+ protein Smooth thickening
IgG, IgA and enhancement
Smooth thickening
and enhancement
(ventral roots)
CMV retinitis
Brain MR: facial
nerve
enhancement
Muscles
denervation
Clinical Correlation
Disease
Pertinent Clinical
CSF
MR
Note
Sarcoid
History of
pulmonary
sarcoidosis.
Chronic neuropathy
+ protein
Nodular
Brain MR: basal
meningitis.
Enhancement of
the cranial nerve
epically the facial
Infract
Acute back pain,
paralysis, areflexia
*
Smooth
enhancement
(ventral roots)
Intramedullary
lesion with bone
marrow infract
SDAVF
Slowly progressive
paraplegia and
sensory symptoms
*
Smooth thickening
and enhancement
Prominent
perimedullary
vessels
Arachnoiditis
Progressive
weakness, sphinteric
dysfunction and
saddle anesthesia
*
Thickened
clumped nerve
roots
Depends on the
etiologies
Clinical Correlation
Disease
Pertinent Clinical
CSF
MR
Note
Meningeal
carcinomatosis
History of primary
malignancy.
Cauda equina
syndrome
+ Protein
- Glucose
Malignant
cells
Nodular
Other sites of
metastasis like
vertebral body and
brain
Lymphoma
History of
lymphoma at other
site. Rapidly
progressive
symptoms
Positive
CSF
cytology
Smooth or
nodular
Chest, abdomen and
pelvic imaging
NF
Stigmata of NF
*
Nodular
Features of chronicity
with large lesions such
as boney scaloping
Infection – Spinal Meningitis
The most common causative organism in spinal meningitis is
tuberculosis (TB). Actually, spinal involvement is rare in nontuberculous bacterial meningitis and most of the cases have been
reported in children59.
CNS involvement occurs in about 1% of patients with TB, and carries
the highest mortality60. More than 50% of cases are associated with
brain meningitis or spondylodiscitis61.
Enhancement of the nerve roots is the hallmark of spinal meningitis
which can be smooth or nodular and its not typical for specific
organism3 (figure 4,& 5).
In TB, the reported MR findings are thickening, clumping and
enhancement of the nerve roots61. The enhancement pattern is usually
smooth. However, intra-dural nodules have been also described which
usually attribuited to the presence of tubercloma.
Figure 4: 55 years old male presented with fever and previous nerve and facet blocks done outside the
hospital 1 week ago. The MR images the of the lumber spine shows diffuse smooth swelling and faint
enhancement of the cauda equina nerve roots related to spinal meningitis. Note paraspinal abscesses
(arrows). The causative organism was staphylococcus aureus.
Figure 5: 24 years old male known case of sickle cell disease (SCD) with bilateral leg paraesthesia
associated with urinary retention and loss of reflexes. The MR images of the lumber spine shows
diffuse smooth edematous swelling and intense enhancement of the cauda equina nerve roots (arrows)
related to pneumococcal spinal meningitis. Note vertebral body bone marrow infracts in case of SCD.
Infection – HIV
Tow third of HIV-positive patients presenting with myelopathy
have an infectious etiology. TB was found as the most common
organism in recent study done in an endemic area63.
However, CMV was the commonest organism causing intradural
extramedullary spine abnormalities in HIV-positive patients
presenting with polyradiculopathy in another study64. All cases
show nerve root enhancement with thickening and clumping in
30% of cases. The pattern of the enhancement was linear, diffuse
or nodular (figure 6).
Most of patient had also CMV retinitis64.
The MR findings of infectious origin polyradiculopathy in HIV
patients is indistinguishable from neoplastic causes such as
lymphoma.
Figure 6: 38 years old HIV positive male with polyradiculopathy. Sagittal and axial
T2-wieghted images of the lumbar spine show nodular thickening of the cauda
equina nerve roots (arrows).
Inflammatory - GBS
Guillain-Barré syndrome is an acute, symmetrically
progressive, inflammatory demyelinating polyneuropathy.
Clinical presentation is usually characterized by progressive
ascending and symmetric paralysis of the extremities and
marked hyporeflexia or areflexia57.
Cerebrospinal fluid analysis typically reveals elevated protein
concentrations without pleocytosis58.
The imaging is often performed to rule out other pathologies
due to the diagnosis usually made through clinical findings
and CSF analysis.
The MRI usually show diffuse thickening and enhancement
of the cauda equina nerve roots. Byun et al57 suggested that
enhancement solely of the anterior roots was strongly
suggestive of GBS (figure 7).
Figure 7: 68 years old male with progressive bilateral weakness. Sagittal T2 and Sagittal/axial T1 post
gadolinium images of the lumbar spine show smooth diffuse minimal hypertrophy and faint
enhancement of the cauda equina nerve roots. Note specific involvement of the ventral roots (arrows)
in case of GBS.
Inflammatory - CIDP
CIDP is a acquired neuropathy that has various clinical
manifestations, but its main symptoms are symmetrical sensory
deficit and motor weakness51. This disease may arise at any age,
but it usually affects adults with a progressive course over just a few
months.
The cause of CIDP is largely unknown, although an autoimmune
attack on myelin proteins is the suspected pathogenesis55.
CIDP and CMT can have similar clinical, radiological and
pathological presentations. However, CMT usually presents in the
first decade of life. Electrophysiology testing and CSF study with
elevated CSF proteins in CIDP can differentiate between these tow
entities52.
CIDP is the chronic counterpart of GBS, sharing similar diagnostic
evaluation and clinical findings55. GBS is more common than
CIDP with shorter clinical course and antecedent infections which
usually absent in CIDP53,55.
Inflammatory - CIDP
MRI with gadolinium is the radiological modality of choice which
can shows diffuse cauda equina nerve roots hypertrophy and
enhancement (figure 8). However, the prevalence of spinal nerve
root enlargement in the setting of CIDP, is unclear, because few
patients have undergone lumbosacral MRI56.
There are many variants of CIDP which possess important
differences in clinical presentation, laboratory features and
prognosis but not radiologically. One of those variants is distal
acquired demyelinating symmetrical neuropathy (DADS) which is
restricted to a distal, symmetrical distribution with predominantly
sensory symptoms (figure 9). In 50–70% of patients with the
clinical picture of DADS phenotype, the cause is a distinctly
separate condition in which an IgM paraprotein having antimyelinassociated glycoprotein (anti-MAG) antibody activity is responsible
for the pathogenesis62.
Figure 8: 46 years old male with 4 months history of progressive bilateral myelopathic symptoms.
Sagittal T2 and Sagittal/axial T1 post gadolinium images of the lumbar spine show diffuse smooth
hypertrophy and enhancement of the cauda equina nerve roots in keeping with CIDP.
Figure 9: 69 years old male with severe sensory neuropathy. Sagittal and axial T2-wieghted
images of the lumbar spine show hypertrophy of the cauda equina nerve roots (arrows) in
patient with DADS. Note preferential involvement of the anterior roots.
Inflammatory - Sarcoidosis
5% of all patients with sarcoidosis may develop neurosarcoidosis,
affecting predominantly the basilar meninges or the cranial nerves
(especially the facial nerve)47.
Spinal cord sarcoidosis is even more rare, less than 10% have
involvement of the cauda equina48.
The radiological diagnosis is challenging with non-specific findings
especially without history of previous systemic sarcoidosis.
Enhancing nodules and leptomeningeal involvement are observed
on MR (figure 10) which can be easily mistaken with
carcinomatosis. However, MR can be also negative early in the
course of the disease49.
Inflammatory - Sarcoidosis
Diffuse smooth enhancement of the cauda equina nerve
roots has also ben reported50.
Imaging of the chest and CSF analysis can be helpful to
reach the correct diagnosis with subsequent MR regression
after steroid therapy.
Figure 10: Sagittal T2 and T1 post gadolinium images of the lumbar spine show
multiple enhancing nodules along the cauda in 51 years old male with
Neurosarcoidosis.
Vascular – Spinal Cord Infract
There are tow secondary findings which can confirm the
diagnosis of spinal cord infract: concomitant vertebral body
infract and enhancement of the cauda equina nerve roots17.
The reports of cauda equina nerve roots enhancement in
case of spinal cord infract is rare with only 4 cases reported
in the English literature17.
The ventral cauda nerve roots usually affected.
In cases for which timing is available, this finding was noted
in the sub-acute phase18.
The mechanism may includes: Wallerian degeneration19 or
direct ischemia to the cauda equina20.
Vascular- SDAVF
Vascular malformation such as spinal dural arteriovenous
fistula (SDAVD) can cause edematous swelling of the cauda
equina nerve roots due to venous congestion (Figure 11).
SDAVF is a rare vascular malformation that can induce
progressive upper motor neuron signs21.
Increased blood flow to the vein through a fistula causes
venous congestion, which reduces blood supply to the spinal
cord and nerve roots, induces neurological dysfunctions and
subsequently manifests a variety of clinical symptoms22.
Figure 11: Sagittal and axial T2-wieghted images of the lumbar spine show conus
edema (arrowhead) and peri-medullary flow voids (arrow) related to SDAVF. Note
diffuse edematous swelling of the cauda equina nerve roots.
Arachnoiditis
Spinal arachnoiditis is a difficult clinical diagnosis because it has
distinct clinical complex38.
The causes of arachnoiditis would include infection, intrathecal
steroid, anesthesia agents, trauma, surgery and hemorraghe40. It’s a
cause of persistent symptoms in 6-16% of postoperative patients39.
Jeffrey S. Ross et al38 reviewed the pattern of lumbar arachnoiditis
into: central thickening of the nerve roots without dural thickening
(mild), clumped nerve roots attached to thickened dura given the
appearance of empty sac (moderate), and increased soft tissue
signal within the thecal sac obliterating the majority of the
subarachnoid space (severe). (figure 12,13,&14)
Enhancement of the nerve roots also can be seen probably
secondary to development of vascular network within the
proliferating fibrous stroma41. Its inconstant finding and should not
be relied upon for the diagnosis.
Figure 12: Sagittal and axial T2-wieghted of the lumbar spine show central thickening
of the nerve roots within the thecal sac (arrows) suggestive of mild arachnoiditis. The
dura is not thickened.
Figure 13: 74 years old male with history of previous lumbar surgery for disk disease.
Sagittal and axial T2-wieghted of the lumbar spine show clumped nerve roots
attached to the dura represents empty sac sign (arrow) suggestive of moderate
arachnoiditis. The dura is thickened.
Figure 14: 54 years old male known case of traumatic thoracic cord injury with intra
thecal Baclofen pump to control spasticity. Sagittal and axial T2-wieghted of the lumbar
spine show obliteration of the subarachnoid space by soft tissue signal intensity (arrow)
with lack of definition of individual nerve roots suggestive of severe arachnoiditis. The
dura is thickened.
Spinal Disk Disease
Occasionally, the compressed nerve root can enlarged and shows
increased T2 signal due to inflammation or edema43 (figure 16).
Enhancement of the compressed nerve roots are also noted in 30%
of cases from the site of involvement to their origin which
attributed to breakdown of the blood-nerve barrier9.
There is known discrepancy between clinical symptoms, pathology
and radiological findings in disc disease. However, nerve
enhancement is often observed in acute phase9. Its transient
phenomena and decreased enhancement doesn't necessary means
symptoms resolution.
In post operative spine, nerve root changes such as thickening,
displacement and more important enhancement well matched to
the site of radiculopathy45.
However, the timing of post operative imaging is important due to
enhancement up to 6 months after the surgery can be considered as
normal. Nerve root enhancement after 6 months is pathological46.
Figure 15: Sagittal and axial T2-wieghted images of the lumbar spine show L5-S1
disk herniation causing severe spinal canal stenosis and diffuse swelling the cauda
nerve roots.
Figure 16: Sagittal and axial T2-wieghted images of the lumbar spine show L5-S1
right paracentral disk protrusion (*) with faint enhancement of the compressed S1
nerve root (arrow) as compared to the contralateral nerve root in the same level.
Neoplastic - Metastasis
The spine is the third most common site for metastatic disease,
following the lung and the liver23. Metastases to the spine can
involve the bone, epidural space, leptomeninges, and spinal cord.
Intradural extramedullary and intramedullary seeding of systemic
cancer is unusual, accounting for 5–6% and 0.5–1% of spinal
metastases, respectively24.
Lung carcinoma (40%—85% of cases) is the most common
primary site, followed by breast carcinoma (11%), melanoma (5%),
renal cell carcinoma (4%), colorectal carcinoma (3%), and
lymphoma (3%); 5% of the primary sites are unknown25.
The route of spread usually through hematogenous or direct
extension from the leptomeninges. Intracranial lesions such as
ependymomas,
primitive
neuroectodermal
tumors,
and
glioblastomas multiforme may have drop metastases to the
lumbosacral region.
Neoplastic - Metastasis
The cauda equina syndrome is the typical clinical syndrome caused
by intrathecal metastases which is characterized by low back pain,
unilateral or usually bilateral sciatica, saddle sensory disturbances,
bladder and bowel dysfunction, and variable lower extremity motor
and sensory loss26.
MR usually shows multiple isointense and enhancing nodules
along the cauda equina nerve roots (figure 17,&18). The presence
of associated bone marrow lesions can also support the
radiological diagnosis of metastasis (figure 19).
Gomori JM et al28, reviewed the MR spine of 61 patients with
leptomeningeal metastasis and they found 57% positive MR at
multiple levels; cervical 38%, thoracic 54% and lumbar in 89% of
cases. The enhanced MR pattern was diffuse in 53%, nodular in 37
and combined in 10%. There was no correlation between the
enhancement pattern or the degree of MR involvement with the
tumor type, CSF cytology or clinical findings.
Figure 17: Sagittal T2 and T1 post gadolinium images of the lumbar spine show
multiple nodular enhancing lesions along the cauda equina nerve roots in a 86 years
old male patient known to have primary lung carcinoma and presented with left foot
drop. Hematogenous spread.
Figure 18: Sagittal T2 and Sagittal/axial post gadolinium images of the lumbar spine
show nodular thickening of the cauda equina nerve roots with T2 isosignal intensity and
intense enhancement. Note the Sagittal T1 image at the craniocervical junction shows
coating of the dorsal cervical cord by spontaneous T1 hyperintensity (arrow) related to
metastatic melanoma. CSF drop metastasis.
Figure 19: 60 years old female presented with progressive bilateral lower limb weakness in
a patient known to have metastatic sacral Ewing Sarcoma. The lumbar spine images show
diffuse nodular and smooth thickening of the cauda equina nerve roots with diffuse
enhancement. Note multiple metastatic deposits in the vertebral bone marrow. Direct
spread.
Neoplastic - Lymphoma
In the CNS, the spinal cord is the rarest site of involvement
in patients with primary CNS lymphomas (<1% of
PCNSLs)27. Moreover, among spinal cord lymphomas, cauda
equina lesions are rarest. Lymphoma can cause peripheral
neuropathy either by direct infiltration or by paraneoplastic
mechanism34.
Histologically, most cases are B-cell
lymphomas and rarely Hodgkin type35.
non-Hodgkin
Cauda equina lesions present with progressive, typically
asymmetric involvement of the lower roots, initially
manifesting with distal dysesthesias and sensory loss but less
classic root pain. Bladder and bowel function tend to be
spared until late36.
Neoplastic - Lymphoma
The radiological findings in cauda equina lymphoma may be
subtle. The MRI finding of contrast enhancement (+/ thickening)
of the cauda equina was the only abnormality in majority of the
reported cases14 (figure 20). The involvement can be diffuse or as
bulky deposits28.
There is rare type of non-Hodgkin lymphoma called
lymphomatoid granulomatosis (LG) which involve the cauda
nerve roots (figure 21).
LG is multisystem disease characterized by multifocal angiocentric
angiodestructive lymphoreticular proliferative and granulomatous
lesions32. While it may develop in the immunocompetent, LG is
more common in the immunosuppressed including human
immunodeficiency virus patients37.
LG involves the lungs most frequently, followed by the skin and
brain32. Neurological symptoms occur in up to 30% of cases with
24% of them have peripheral neuropathy32.
Figure 20: 55 years old with peripheral neuropathy and lymphoma of the cauda
equina. Sagittal/axial T2 and sagittal/axial T1 Post gadolinium images of the lumbar
spine show diffuse smooth thickening and enhancement of the cauda equina nerve
roots.
(a)
(b)
Figure 21 (a): Sagittal and axial post gadolinium images of the lumbar spine show
enhancing nodules over the cauda equina nerve roots (arrows). (b): Coronal post
gadolinium images of the brain shows multiple ring enhancing lesions (arrows). The
patient is known case of HIV and diagnosed as lymphomatoid granulomatosis by biopsy.
Neoplastic - Neurofibromatosis
Neurofibromatosis (NF) type 1 and 2 are autosomal
dominant neurocutaneous disorder. NF type 1 accounts for
greater than 90% of cases of NF29. Both of them can present
with tumoral masses along the cauda equina nerve roots.
Patients with NF1 and NF2 have characteristic bilateral
peripheral nerve involvement with evidence of chronicity,
such as enlargement of the neural foramina from dural
ectasia or bony scalloping or remodeling from the nerve root
sheath tumors themselves.
Intradural, extramedullary masses are characteristic of NF2
with meningiomas and schwannomas most commonly
found. Often more than 10 schwannomas are found with
slight predominance in the lumbar region30 (figure 22).
Neoplastic - Neurofibromatosis
The spinal tumors form also a part of the clinical spectrum
of NF1, and occur in a surprisingly large number of patients,
in all segments of the spine31. However, often less clinically
significant than NF2.
Different types of spinal neurofibromas are recognized in
patients with NF1. Localized neurofibroma is seen in 90% of
patients with NF1. Plexiform neurofibroma is less common
and presents with diffuse enlargement of the nerve roots with
a bulky mass or a ropelike appearance1 (figure 23).
Schwannomatosis without features of NF is rare and has
been reported in the literature42 (figure 24).
Figure 22: 35 years old male known case of NF 2. Sagittal T2 and sagittal/coronal T1
post gadolinium images of the lumbar spine show multiple nodular lesions along the
cauda equina nerve roots.
Figure 23: 36 years old male known case of NF 1. Sagittal, coronal and axial T2 with
sagittal T1 post gadolinium images of the lumbar spine show multiple nodular lesions
along the cauda equina nerve roots. Note target sign very characteristic for
neurofibroma (arrow).
Figure 24: 34 years old male with multiple schwannomas without NF. Sagittal/axial
T2 and sagittal/axial T1 post gadolinium images of the lumbar spine show multiple
nodular lesions along the cauda equina nerve roots.
Neoplastic - Other
There are other neoplastic processes that can arise at the level
of the cauda equina such as paragangliomas and
myxopapillary ependymoma.
Those lesions are usually solitary compressing the cauda
equina nerve roots at the corresponding level and if they are
large enough (figure 25) or multiple (figure 26), can diffusely
affect the cauda equina nerve roots.
Figure 25: 71 years old male with myxopapillary ependymoma. Sagittal/axial T2 and
Sagittal/axial T1 post gadolinium show a large intradural mass with intense
enhancement extended from the conus to L3-L4 level. Note significant compression
on the cauda nerve roots (arrow).
Figure 26: 63 years old male known case of Von Hippel-Lindau disease. Sagittal T2
and sagittal/axial T1 post gadolinium images of the lumbar spine show multiple
nodular enhancing masses along the cauda equina nerve roots with prominent
adjacent vascularity representing hemingioblastomas.
Conclusion
Although MR findings is sensitive for diffuse nerve roots
pathology such as thickening or enhancement, it still lacks
specificity.
Special attention to the pattern of thickening and
enhancement either as smooth or nodular can help to narrow
the list of differential diagnoses. The presence of tumoral
masses is in keeping with neoplastic processes.
Complete imaging of the entire neuraxis and correlation with
the pertinent clinical findings, CSF analysis and EMG study
can give a clue to the diagnosis although confirmation by
biopsy sometimes is required.
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