1. eEdE#: eEdE-222 (Shared Display) CAUDA EQUINA: EMBROYOLOGY,
Control #: 2527
eEdE#: eEdE-222 (Shared Display)
CAUDA EQUINA: EMBROYOLOGY,
ANATOMY & PATHOLOGY:
A SYSTEMATIC APPROACH
PARVEZ MASOOD, MD
JAWAD TSAY, MD
VIRGINIA HILL, MD
CLEVELAND CLINIC
FOUNDATION

2. No disclosures
Parvez Masood, MD, Jawad Tsay, MD, and Virginia Hill, MD, have nothing to disclose.

3. ANATOMY
Cauda equina = “horse’s tail” of lumbar, sacral, coccygeal nerve roots below conus
More lumbar nerve roots are lateral
More sacral/coccygeal nerve roots are medial
Lumbosacral nerve roots exit under same numbered pedicle: eg, L5 exits under L5 pedicle

4. ANATOMY Nerve roots exiting conus:
Ventral: efferent somatic, some sympathetic
Dorsal: afferent somatic, visceral
Filum terminale connects conus and dura of coccyx
Intrathecal roots don’t enhance, dorsal root ganglion
does enhance

5. EMBROYOLOGY Differential elongation of the
spinal cord and the vertebral
column resulting in superior
migration of the terminal spinal
cord and elongation of the
nerve roots.
This secondarily causes a
“horse-tail” appearance of
those nerves results in the
formation of the cauda equina

6. CONGENITAL
ABNORMALITIES

7. 45 Y/O MALE WITH BOWEL & BLADDER COMPLAINTS
QUESTION
45 Y/O MALE WITH BOWEL & BLADDER COMPLAINTS

8. MOST COMMON MATERNAL FACTOR ASSOCIATED WITH THIS ENTITY IS?
ANSWER OPTIONS
MOST COMMON MATERNAL FACTOR ASSOCIATED WITH THIS ENTITY IS?
FOLATE DEFICIENCY
ALCOHOL ABUSE
MATERNAL DIABETES
TORCH INFECTION

9. MATERNAL DIABETES: ANSWER
15-20% OF CHILDREN WITH CAUDAL REGRESSION SYNDROME ARE BORN
TO DAIBATIC MOTHERS.
ALSO
B. 1% OF INFANTS OF DIABETIC MOTHERS ARE AFFECTED

10. CAUDAL REGRESSION SYNDROME
High lying club shaped cord terminus
(amputation of the terminal spinal cord)
Sacral dysgenesis
Sacral dysgenesis

11. CAUDAL REGRESSION SYNDROME
INTRODUCTION: A rare congenital anomaly assocaited with absent lower
vertebral bodies, malformed genitalia, anal atresia and potential lower
extremity anomaly (worst case scenario – sirenomyelia).
CLINICAL PRESENTATION: Neurogenic urinary bladder dysfunction.
Structural anomaly of lower extremity & sacrum
Sacral dysgensis with high lying club
shaped cord (Group I)
CLASSIFICATION:
Sacral dysgensis with low lying cord with
associated tethered anomalies and
lipo-myelo-meningo anomalies (Group II)

12. IMAGING HALLMARKS:
Lumbosacral dysgenesis (both with group I & II)
Amputated high lying spinal cord (Group I)
Tethered low lying cord with variable associated anomalies of the
meninges – fat – skin.
IMAGING GOLD STANDARD/DIAGNOSIS: MRI imaging
TREATMENT PROGNOSIS:
With group II: Untethering with repair of associated anomalies
Surgery to improve lower extremity & bowel bladder function

13. NEWBORN WITH DORSAL MENINGOCELE
QUESTION
NEWBORN WITH DORSAL MENINGOCELE

14. WHAT IS THE MOST COMMON MALFORMATION ASSOCIATED WITH THIS
ANSWER OPTIONS
WHAT IS THE MOST COMMON MALFORMATION ASSOCIATED WITH THIS
ENTITY?
CHIARI
DANDY WALKER
CARDIAC SEPTAL DEFECTS
SEPTO-OPTIC DYSPLASIA

15. ANSWER
CHAIRI II:
15-20% OF CHIARI MALFORMATION PATIENTS ARE ASSOCIATED WITH
DIASTOMETAMYELIA.

16. DIASTOMETAMYELIA Low lying spinal cord (tethered)
No imaging identifiable spur
Split spinal cord
(each side has its own unilateral nerve roots)

17. DIASTOMETAMYELIA
INTRODUCTION: Split cord malformation with 2 hemi-cords. Each has a single
dorsal horn and ventral horn as well as central canal.
CLINICAL PRESENTATION: Neurologic dysfunction. Later on progressive
vertebral body (kypho-scoliotic) changes and orthopedic issues.
Bony or fibrous or fat band separating the two
hemi-cords (Type I). Extends from posterior
Elements to merge with the vertebral body
CLASSIFICATION:
No mesenchymal band seperation. Just
spinal cord splitting (Type II)

18. IMAGING HALLMARKS:
Two hemi-cords.
May appreciate a bony or fibrous separation (Type I)
Each hemi-cord has its own central canal and dorsal and ventral horns
IMAGING GOLD STANDARD/DIAGNOSIS: MRI imaging
TREATMENT PROGNOSIS:
Untethering of cord with resection of spur
Orthopedic procedures for spine alignment issues (kypho-scoliosis)

19. 6 Y/O MALE WITH ABDOMINAL PAIN
QUESTION
6 Y/O MALE WITH ABDOMINAL PAIN

20. ALL OF THE FOLLOWING ARE CHARACTERSTIC FOR NF-1 EXCEPT?
ANSWER OPTIONS
ALL OF THE FOLLOWING ARE CHARACTERSTIC FOR NF-1 EXCEPT?
PSEUDOARTHROSIS
LATERAL MENINGOCELE
PLEXIFORM NEUROFIBROMA
SACRAL DYSPLASIA
SPHENOID WING DYSPLASIA

21. SACRAL DYSPLASIA: ANSWER
ALL OF THE AFOREMENTIONED ARE CHARACHTERSTICS OF NF-1 EXCEPT
SACRAL DYSPLASIA.
B. HALLMARK OF NF-1 IS PLEXIFORM NEUROFIBROMA.
C. HALLMARK OFNF-2 IS VESTIBULAR SCHWANNOMA (BILATERAL).

22. Multiple separate enhancing nodules (along the entire cauda equina)
NEUROFIBROMATOSIS
Multiple separate enhancing nodules
(along the entire cauda equina)

23. NEUROFIBROMATOSIS
INTRODUCTION: NF-1 is a chromosomal disorder (#17) mesodermal dysplasia
disorder. Whereas NF-2 is an chromosomal anomaly (#22) predisposing to
multiple schwannomas and meningiomas or ependymomas (MISME tumors)
with both of them although being completely unrelated present with nerve
tumors on imaging as the most common presentation.
CLINICAL PRESENTATION: NF-2 presents typically (greater than 50% patients)
with hearing loss. Patients with cord lesions (almost 50% present with cord
compression symptoms). NF-1 presents typically with cutaneous or skeletal
deformities.

24. NF-1 (associated with chromosome 17)
typically mesodermal pathologies. Hallmark is
a plexiform neurofibroma.
NF-1 (associated with chromosome 17)
typically mesodermal pathologies. Hallmark is
a plexiform neurofibroma.
CLASSIFICATION:
CLASSIFICATION:
CLASSIFICATION:
CLASSIFICATION:
CLASSIFICATION:
NF-2 (associated with chromosome 22) typically
with MISME lesions (detailed above). Hallmark
is bilateral vestibular schwannomas.
NF-2 (associated with chromosome 22) typically
with MISME lesions (detailed above). Hallmark
is bilateral vestibular schwannomas.
NF-2 (associated with chromosome 22) typically
with MISME lesions (detailed above). Hallmark
is bilateral vestibular schwannomas.
IMAGING HALLMARKS:
NF-1:
Plexiform neurofibroma
Intracranial and optic nerve glioma
Sphenoid wing and other osseous dysplasias
Cervical kyphosis
NF-2:
MISME lesions (detailed above)

25. IMAGING GOLD STANDARD/DIAGNOSIS: MRI imaging of brain and spine
TREATMENT PROGNOSIS:
Resection of symptomatic tumors
Orthopedic procedures for spine alignment issues (kypho-scoliosis)

26. 1 Y/O MALE WITH INCONTINENCE
QUESTION
1 Y/O MALE WITH INCONTINENCE

27. NORMAL LOCATION OF CONUS?
ANSWER OPTIONS
NORMAL LOCATION OF CONUS? L1
L1-2 L2
L2-3 L3

28. ANSWER
AT OR ABOVE L2-3 LEVEL:

29. Fat along the terminal cord
TETHERED CORD
Low lying spinal cord
Fat along the terminal cord
(lipomeningocele)

30. TETHERED CORD
INTRODUCTION: Low lying terminal spinal cord below inferior L2 which may
or may not be associated with a soft tissue – fatty mass or may or may not
be adherent to the posterior spinal canal.
CLINICAL PRESENTATION: Neurologic dysfunction. Low back and leg pain.
May be associated with gait disturbance.
IMAGING GOLD STANDARD/DIAGNOSIS: MRI imaging

31. Conus ends below inferior L2.
IMAGING HALLMARKS:
Conus ends below inferior L2.
Thickened filum (greater than 2 mm at L5-S1 on MRI).
May or may not be associated with spectrum of spinal dysraphisms
TREATMENT PROGNOSIS:
Untethering of cord
May be followed with CSF flow study to look for re-tethering
(Caveat: return of normal CSF flow is seen in less 1/3 of patients even if symptoms resolve)
3. Re-tethering is based mainly on clinical grounds

32. 5 MONTH FEMALE WITH DORSAL SINUS
QUESTION
5 MONTH FEMALE WITH DORSAL SINUS

33. WHICH NEUTRITIONAL DEFICIENCY IS ASSOCIATED WITH THIS ENTITY?
ANSWER OPTIONS
WHICH NEUTRITIONAL DEFICIENCY IS ASSOCIATED WITH THIS ENTITY?
Thiamine
Riboflavin
Folic acid
Leucine
Cholecalciferol

34. ANSWER
FOLIC ACID:

35. Sina bifida with outpouching of the meninges
MYELOMENINGOCELE
Sina bifida with outpouching of the meninges
Fetal ultrasound

36. MYELOMENINGOCELE
INTRODUCTION: Dorsal spinal defect without skin covering exposing
meninges with or without neural tissue and or CSF.
CLINICAL PRESENTATION: New born with exposed midline neural tissue.
Level of abnormality reflects neurological deficits.
ASSOCIATIONS: Chiari malformation.
(type II with lumbar and type II with cranio-cervical)

37. IMAGING HALLMARKS:
Open spinal dysraphism
Low lying spinal cord
Open neural arch
Intracranial Chiari findings
IMAGING GOLD STANDARD/DIAGNOSIS: MRI imaging
TREATMENT PROGNOSIS:
Prevention (Folate supplementation for conceiving & pregnant women)
In-utero surgery if possible
3. Repair of the meningomyelocele in early neonate period

38. 50 Y/O MALE WITH LOW BACK PAIN – INCIDENTAL FINDING
QUESTION
50 Y/O MALE WITH LOW BACK PAIN – INCIDENTAL FINDING

39. ALL THE FOLLOWNG RESTRIC DIFFUSION EXCEPT?
ANSWER OPTIONS
ALL THE FOLLOWNG RESTRIC DIFFUSION EXCEPT?
EPIDERMOID
ARACHNOID CYST
ABSCESS
INTRACRANIAL PNET

40. ARACHNOID CYST: Follows CSF
ANSWER
ARACHNOID CYST: Follows CSF
intensity (density) on all imaging parameters

41. ARACHNOID CYST CSF intensity collection without
restricted diffusion with
associated mass effect and
bone remodeling

42. ARACHNOID CYST
INTRODUCTION: Extramedullary intraspinal CSF collection.
CLINICAL PRESENTATION: Most patients are incidentally detected.
Presentation may be in relation to mass effect and compression of cauda
equina, especially if present in sacral region.
Intradural.
CLASSIFICATION:
Extradural (herniating thru the dura)

43. IMAGING HALLMARKS:
CSF intensity circumscribed collection
Mass effect (bone scalloping & compression of cauda equina – thecal sac)
(bone remodeling is more common with extradural form)
3. Cap sign: Seen with extradural type – epidural fat at superior & inferior
aspect
IMAGING GOLD STANDARD/DIAGNOSIS: MRI imaging
TREATMENT - PROGNOSIS:
Only if symptomatic (nerve or cord compression)
Decompression – fenestration of the arachnoid cyst

44. TRAUMA - IATROGENIC
ABNORMALITIES

45. MOST COMMON PRESENTATION OF CHRONIC SPINE SUBARACHNOID HEMORRHAGE IS?
QUESTION
MOST COMMON PRESENTATION OF CHRONIC SPINE SUBARACHNOID
HEMORRHAGE IS?
MOST COMMON PRESENTATION OF CHRONIC SPINE SUBARACHNOID
HEMORRHAGE IS?
Headache
Hearing loss
Vomiting
Back pain
Headache
Hearing loss
Vomiting
Back pain

46. HEARING LOSS: Due to cortical superficial siderosis
ANSWER
HEARING LOSS: Due to cortical superficial siderosis
(most common extra spinal presentation of myxopapillary ependymoma).

47. MOST COMMON CAUSE OF EPIDURAL HEMATOMA IN SPINE IS?
QUESTION
MOST COMMON CAUSE OF EPIDURAL HEMATOMA IN SPINE IS?
Coagulopathies
Trauma
Spontaneous
Iatrogenic

48. SPONTANEOUS EPIDURAL HEMTOMA:
ANSWER
SPONTANEOUS EPIDURAL HEMTOMA:

49. DESIRED LOCATION OF COLLECTION IN CSF LEAK BLOOD PATCH IS:
QUESTION
DESIRED LOCATION OF COLLECTION IN CSF LEAK BLOOD PATCH IS:
Subdural
Epidural
Subarachnoid

50. ANSWER
EPIDURAL - BLOOD PATCH

51. Dorsal subdural hematoma
NONACCIDENTAL TRAUMA
Ventral displacement
with impingement of
the thecal sac
Dorsal subdural hematoma

52. Spinal cord compression
EPIDURAL HEMATOMA:
Ventral displacement
with impingement of
the thecal sac
Hematocrit level
Spinal cord compression

53. SUBARACHNOID HEMATOMA:
High density (blood) within the thecal sac
(Differential – post myelogram)
CSF is Iso on T1 and Hypo on T2
Mixed signal (blood) within the thecal sac
(CSF fluid intensity not identifiable)

54. INTRASPINAL BLOOD PRODUCTS
INTRODUCTION: Classically as in intracranial component depending on
the three compartments for hemorrhage will be epidural, subdural and
intrathecal location subarachnoid blood.
CLINICAL PRESENTATION: Subdural and epidural will be spontaneous and
present with lower extremity weakness of symptoms of cauda equina
syndrome (due to mass effect).
Epidural
CLASSIFICATION:
Subdural
Subarachnoid

55. IMAGING HALLMARKS: Blood does not follow the signal characterstics as
seen in brain (no blood brain barrier)
Epidural: Biconvex collection (+/-). Cap sign (fat lining both ends of the
collection). Peripheral (dural) enhancement is possible. Ventral component
separated by midline raphe - septum (curtain sign).
2. Subdural: Major portion is hypointense on T2.
(Dorsal epidural cannot be differentiated from subdural hematoma)
3. Subarchnoid: Mixed signal in the thecal sac. Likely to layer along the
sacral lining
IMAGING GOLD STANDARD/DIAGNOSIS: MRI imaging
TREATMENT - PROGNOSIS: Symptomatic decompression

56. PANTOPAQUE SUBARACHNOID:
Fat suppression
Chemical shift artifact

57. PANTOPAQUE SUBARACHNOID:

58. INFLAMMATORY
AUTOIMMUNE
GRANULOMATOUS:

59. 9 Y/O MALE WITH ACUTE ONSET PROGRESSIVE DIFFICULTY WALKING
QUESTION

60. WHICH OF THE FOLLOWING IS FALSE CONCERNING ABOVE PATHOLOGY
ANSWER OPTIONS
WHICH OF THE FOLLOWING IS FALSE CONCERNING ABOVE PATHOLOGY
1. UP TO 8% MORTALITY
2. 50% FACIAL NERVE INVOVLEMENT
3. CRANIAL NERVE INVOLVEMENT IS UNCOMMON
4. PRESENTS WITH ASCENDING PARALYSIS

61. CRANIAL NERVE INVOLVEMENT IS UNCOMMON: Cranial nerve is common.
ANSWER
CRANIAL NERVE INVOLVEMENT IS UNCOMMON: Cranial nerve is common.
In fact facial nerve is invovled almost upto 50%

62. Smooth uniform symmetric enhancement of cauda equina
G.B. SYNDROME
Smooth uniform symmetric
enhancement of cauda equina

63. G.B. SYNDROME
INTRODUCTION: Guillian Barre syndrome or acute demyelinating
polyneuropathy is an autoimmune inflammatory demyelination or cranial
and peripheral nerves most commonly after a predisposing viral infection
(post infection or post vaccine).
CLINICAL PRESENTATION:
Classically presents with ascending paralysis.
Starts ~ 2 weeks post insult.
Reaches peak at ~ 4 weeks.
Most patients better by 2-3 months
2 to 10 % may relapse
Up to 5 to 6% may progress to pathology that resembles CIDP

64. IMAGING HALLMARKS: (CT is non diagnostic)
Smooth + uniform +/- minimally enlarged (typically not) nerve roots
No nodularity of the nerve roots
Avid enhancement of the cauda equina (+/- cranial nerves)
Variable enhancement of the pial lining of conus
Some sources claim (???) – more prominent ventral nerve root
enhancement.

65. IMAGING GOLD STANDARD/DIAGNOSIS: MRI imaging (final diagnosis by CSF evaluation)
TREATMENT - PROGNOSIS:
Plasma exchange or IV Gamma-globulin
No proven data that steroids help
Some time supportive (breathing) therapy in severe cases
2 to 10% may replase
Up to 8% patient mortality
6% may progress to condition similar to CIDP

66. 53 Y/O MALE WITH LOWER EXTRIMITY PARESTHESIAS
QUESTION
53 Y/O MALE WITH LOWER EXTRIMITY PARESTHESIAS

67. DIFFERNTIAL FOR THE ABOVE IMAGES INCLUDES ALL OF THE FOLLOWING EXCEPT?
ANSWER OPTIONS
DIFFERNTIAL FOR THE ABOVE IMAGES INCLUDES ALL OF THE
FOLLOWING EXCEPT?
1. LYMPHOMA
2. METASTASIS
3. GUILLIAN BARRE SYNDROME
4. SARCOID
5. ATYPICAL INFECTION (TUBERCULOSIS)

68. GUILLIAN BARRE SYNDROME: G.B. syndrome typically presents as smooth,
ANSWER
GUILLIAN BARRE SYNDROME: G.B. syndrome typically presents as smooth,
non-nodular, homogenous avid enhancement of the cauda equina and
cranial nerves and not thickened nodular enhancement as in the images above

69. Cake like nodular coating
(NEURO) SARCOIDOSIS
Cake like nodular coating
and enhancement of
the cauda equina

70. (NEURO) SARCOIDOSIS
INTRODUCTION: Noncaseating granulomatous disease involving any
organ system with almost 5% involvement of the central nervous system.
CLINICAL PRESENTATION:
Lower extremity weakness
Paresthesias – radiculopathy
Bowel – bladder abnormalities
(Essentially nonspecific neurological symptomatology)
Exclusive CNS involvement in only 1.5% patients of sarcoid
15 to 25% of sarcoid patients have CNS invovlemnt (on Autopsy findings)

71. IMAGING HALLMARKS:
Wide spectrum imaging findings (mimicking other disease processes)
When it involves cord: Long segment patchy mass like cord/conus
enhancement
Nodular (but on rare occasions may be smooth) enhancement
Intramedullary as well as pial/surface enhancement
Cauda equina: Mass like or nodular (or on rare occasions smooth) patchy
or diffuse cauda equina enhancement
Almost certain systemic disease involvement provides for better diagnosis and easy biopsy source
When an enhancing pathology in any organ system spreads without respect
to fat or tissue planes then differential would include but not be limited to
sarcoidosis or lymphoma/leukemia or atypical granulomatous infections
(like tuberculosis and fungal infections)

72. IMAGING GOLD STANDARD/DIAGNOSIS: MRI imaging (final diagnosis by CSF evaluation)
TREATMENT - PROGNOSIS:
IV (+/- oral) corticosteroids.
Immunosuppression therapy
(Rarely) radiation therapy
Prognosis: Majority (roughly 60% patients) have a good response to steroid therapy
Approximately 30% of the patients will have a relapse

73. 63 Y/O MALE WITH POSTLAMINECTOMY SYNDROME
QUESTION
63 Y/O MALE WITH POSTLAMINECTOMY SYNDROME

74. DIFFERNTIAL FOR THE ABOVE IMAGES INCLUDES ALL OF THE FOLLOWING EXCEPT?
ANSWER OPTIONS
DIFFERNTIAL FOR THE ABOVE IMAGES INCLUDES ALL OF THE
FOLLOWING EXCEPT?
1. LYMPHOMA
2. METASTASIS
3. GUILLIAN BARRE SYNDROME
4. SARCOID
5. ATYPICAL INFECTION (TUBERCULOSIS)

75. GUILLIAN BARRE SYNDROME: G.B. syndrome typically presents as smooth,
ANSWER
GUILLIAN BARRE SYNDROME: G.B. syndrome typically presents as smooth,
non-nodular, homogenous avid enhancement of the cauda equina and
cranial nerves and not thickened nodular enhancement as in the images above

76. ARACHNOIDITIS (TYPE II) “EMPTY SAC SIGN”
Peripheral adherence of
the nerve roots
(Type II – empty thecal sac sign)

77. ARACHNOIDITIS (TYPE III)
“CONTRAST BLOCK”
Myelographic block

78. ARACHNOIDITIS
INTRODUCTION: Post iatrogenic or infectious inflammatory scarring
+/- adhesions or clumping of the nerve roots (cauda equina).
CLINICAL PRESENTATION: Low back pain +/- lower extremity pain and
paresthesias mimicking spinal stenosis or neurogenic claudication from
spinal stenosis. Sometimes imaging findings may be present without
clinical symptoms.

79. CLASSIFICATION BASED IMAGING HALLMARKS:
TYPE I: Nodular +/- kinking of nerve roots with potential central
clumping of nerve roots. Featureless thecal sac.
TYPE II: Marginalization (peripheralization) of nerve roots with
their adherence peripherally to the thecal sac potentially
resulting in an “empty thecal sac sign”
TYPE III: Marked scarring with central soft tissue mass and
complete filling (obscuring) of the thecal sac. On
myelography it will present as myelographic block.

80. IMAGING GOLD STANDARD/DIAGNOSIS: CT myelogram
TREATMENT - PROGNOSIS:
No good treatment or cure
Pain management is the approach:
Intrathecal steroid injections
Spinal cord stimulators
If possible release/lysis of adhesions
If calcific/ossific arachnoiditis: Surgical resection of the portion (mostly not effective)

81. 71 Y/O MALE WITH POSTLAMINECTOMY SYNDROME
QUESTION
71 Y/O MALE WITH POSTLAMINECTOMY SYNDROME

82. DIFFERNTIAL FOR THE ABOVE IMAGES INCLUDES ALL OF THE FOLLOWING EXCEPT?
ANSWER OPTIONS
DIFFERNTIAL FOR THE ABOVE IMAGES INCLUDES ALL OF THE
FOLLOWING EXCEPT?
1. SCHWANNOMA
2. METASTASIS (DROP)
3. NEUROFIBROMA
4. CIDP
5. MYXOPAILLARY EPENDYMOMA

83. ANSWER
CIDP: Typically associated with diffuse cauda equina involvement with multiple bilateral nerve root marked thickening with +/- patchy enhancement

84. CATHETOR TIP GRANULOMA
Enhancing nodule (granuloma)
in intradural extramedullary location

85. CATHETOR TIP GRANULOMA
Position of the catheter tip confirmed in the
location of the enhancing nodule

86. CATHETOR TIP GRANULOMA
INTRODUCTION: Reactive inflammatory nodule at the tip of a placed
intrathecal catheter (mainly associated with pain pump catheters).
Progressively increases from 0.05% incidence at 1 year to 1.2% at 6 years
of treatment.
CLINICAL PRESENTATION:
Back pain
Progressively decreasing effectiveness of pain control
(despite increase in pain medication dose)
Increasing lower extremity neurological symptoms
May or maynot have bowel bladder symptoms
(depending on location of granuloma)

87. IMAGING HALLMARKS:
Most important: History of catheter placement (for a long duration)
(Often catheter may be difficult to see on MRI - without clinical history)
CT + Plain film: Confirm catheter with catheter tip position
CT myelogram: Nodular filling defect at catheter tip
MRI:
T2 may confirm catheter position (inluding tip)
Susceptibility artifact related to tip
Peripherally enhancing nodule (more common than solid enhancement)
Unless aware of presence of localizing catheter tip
(extensive differential)

88. IMAGING GOLD STANDARD/DIAGNOSIS: MRI + CT (or plain radiograph) imaging (to confirm catheter tip position)
TREATMENT - PROGNOSIS:
Cessation (with replacement by saline) of the lipophilic medication infusion thru the catheter.
Decrease in the concentration of drugs typically associated with granuloma formation
Withdrawal (by about 2 cm) of the catheter tip
If failure with conservative therapy (and with progressive deterioration) then surgical excision of the catheter granuloma.

89. NEOPLASM - TUMOR:

90. 6 Y/O FEMALE WITH INCONTINENCE
QUESTION
6 Y/O FEMALE WITH INCONTINENCE

91. ALL OF THE FOLLOWING ARE ASSOCIATED WITH THE DEPICTED
ANSWER OPTIONS
ALL OF THE FOLLOWING ARE ASSOCIATED WITH THE DEPICTED
ABNORMALITY EXCEPT?
1. DERMAL SINUS
2. STRUCTURAL VERTEBRAL BODY ANOMALIES
3. INTENSE ENHANCEMENT
4. RESTRICTED DIFFUSION

92. ANSWER
ENHANCEMENT: Epidermoid (shown above) as well as dermoid will have minimal to no enhancement. All of the remaining are associations for an epidermoid which is shown above.

93. ALL OF THE FOLLOWING ARE EXCLUSIVELY CONGENITAL IN ORIGIN EXCEPT?
QUESTION
ALL OF THE FOLLOWING ARE EXCLUSIVELY CONGENITAL IN ORIGIN
EXCEPT?
1. DERMOID CYST
2. EPIDERMOID CYST
3. NEUROENTERIC CYST
4. LIPOMENIGOCELE CYST

94. EPIDERMOID CYST: Greater than 50% of the epidermoid cysts are congenital in nature with up to 40% of the cysts being acquired (from iatrogenic reasons).

95. DERMOID Extrameduallary intradural fat and
mixed signal intensity mass indenting
the terminal spinal cord (up to 40%
can be intramedullary)
Fat signal in an
non-contrast T1 sequence

96. EPIDERMOID CSF intensity cystic focus along terminal
cauda equina displacing and insinuating along the spinal cords
(without diffusion sequence with restriction
may be indistinguishable from an arachnoid cyst)

97. DERMOID – EPIDERMOID - TERATOMA
INTRODUCTION: Tumors of ectodermal origin which may arise
mainly along the midline or para-midline region from inclusion rest cells
progressing to mass like nodular formation that tend to remain benign.
CLINICAL PRESENTATION:
Frequently asymptomatic with incidental detection
Gradually increasing radiculopathy/myelopathy (Due to mass effect)
Late: Cauda equina syndrome
Chemical meningitis (with dermoid secondary to rupture)
Infectious meningitis (if associated with dermal sinus)

98. CLASSIFICATION AND IMAGING HALLMARKS:
Dermoid: All parts of ectodermal tissue including
all or some of the following contents:
Hair follicles, sebaceous glands, squamous
epithelium, desquamated keratin and lipid material
(Hallmark: Fluid – fluid levels and presence of
Fat & potentially tooth)
3 TYPES
Epidermoid: Squamous epithelium with
desquamated keratin and cholesterol crystals
(Hallmark: Fluid intensity on T1 & T2 with
restricted diffusion)
Teratoma: Not included with images (may be benign or malignant) with all embryonic cell lines with very
heterogeneous signal with heterogeneous but almost certain enhancement.

99. IMAGING GOLD STANDARD/DIAGNOSIS: MRI
TREATMENT - PROGNOSIS:
Surgical complete resection
If incomplete resection: Will recur

100. 69 Y/O MALE WITH progressive lower extremity weakness
QUESTION

101. SPINAL ENTITY DEPICTED ABOVE IS MORE COMMON IN FEMALES?
ANSWER OPTIONS
SPINAL ENTITY DEPICTED ABOVE IS MORE COMMON IN FEMALES?
1. TRUE
2. FALSE

102. ANSWER
FALSE: Shown entity is an myxopapillary ependymoma which is (2:1 preponderance) more common in males.

103. MYXOPAPILLARY EPENDYMOMA
Areas of hemorrhage
Dorsal vertebral body scalloping: Due
to long standing progressive increase in size
(usually 2 -3 years before diagnosis)
Areas of hemorrhage
Intense enhancement
(+/- calcification)

104. MIMIC: CYSTIC SCHWANNOMA
Peripherally enhancing cystic lesion
(will have a variable differential).
This lesion turned out to be a cystic schwannoma
No heterogenous signal or
areas of blood products

105. MIMIC: HEMANGIOBLASTOMA
in the
cauda equina region
Intracranial & spinal
hemangioblastoma
(in a patient with VHL)

106. MYXOPAPILLARY EPENDYMOMA
INTRODUCTION: Gradually growing ependymal glioma at the location of
filum terminale. Typical location of myxopapillary type. This tumor is
almost 1/3 of all CNS ependymoma’s and are overwhelmingly predominant
entity of all solitary cauda equina – filum tumors.
CLINICAL PRESENTATION:
Presentation is generally 2-3 years after start
(due to slow growing nature)
Indolent nature
Progressive back pain & lower extrimity neuorlogical symptoms
Late: Bowel bladder symptoms
(in almost 25 to 30% of the patients)

107. IMAGING HALLMARKS:
Heterogenously avidly enhancing soft tissue insinuating mass
Intradural and extramedullary in location
Usually spans > 2 vertebral bodies (at presentation)
Can see (+/-) flow voids
May have terminal cord signal changes
Common to have hemorrhage
Dorsal vertebral body scalloping with larger lesions

108. IMAGING GOLD STANDARD/DIAGNOSIS: MRI + Contrast
TREATMENT - PROGNOSIS:
Surgical resection
Radiotherapy for recurrence and residual tumors

109. 30 Y/O MALE with melanoma for staging
QUESTION
30 Y/O MALE with melanoma for staging

110. DROP METASTASIS ARE SEEN CLASICALLY WITH?
ANSWER OPTIONS
DROP METASTASIS ARE SEEN CLASICALLY WITH?
ANAPLASTIC ASTROCYTOMA
MEDULLOBLASTOMA
DYSEMBROPLASTIC INFANTILE GLIOMA
MENINGIOMA

111. ANSWER
MEDULLOBLASTOMA: High grade exophytic tumors of intracranial location can be associated with drop metastasis. Typically seen with ependymoma and medulloblastoma and choroid plexus papillary carcinoma.

112. MELANOMA - METASTASIS T2 T1
T1 + C

113. BREAST CANCER - METASTASIS

114. LUNG CANCER – LEPTOMENINGEAL METASTASIS
T1 + C

115. FILUM METASTATIC DISEASE
INTRODUCTION: Intradural metastasis can spread via hematomgenous
route or contiguous route or as drop CSF dissemination from intracranial
tumors. Once it lodges to the pia-arachnoid or dural ling it drops the
prognosis of the patient (even with treatment) significantly.
Alternatively vertebral body (extradural – extramedullary [extra osseous]
cancer – metastasis may affect the cauda equina with compression due to
vertebral collapse or soft tissue component with epidural extension.
CLINICAL PRESENTATION:
Mainly detected on staging
Rare to primarily present with cauda equina metastasis

116. IMAGING HALLMARKS:
Smooth or nodular (typically) enhancement of the cauda equina
and the cord surface
May or may not be associated with underlying cord edema
Frequently associated with metastasis of the vertebral bodies,
retroperitoneum, intracranial region as well as the spinal cord
Biggest indicator: Multiplicity of lesions
EXTENSIVE DIFERENTIAL:
Hematogenous spread of infection
Granulomatous disease
Lymphoma/leukemia
Multiple nerve sheath tumors

117. IMAGING GOLD STANDARD/DIAGNOSIS:
1. LP and CSF evaluation are the gold standard.
2. Imaging gold standard will be MRI with contrast.
TREATMENT - PROGNOSIS:
Intrathecal rounds of chemotherapy
Radiation
PROGNOSIS: Extremely poor: Terminal stage of cancer with 5% patients presenting with it. Survival of less than ~3 months with aggressive treatment.

118. 50 Y/O male with progressive back pain

119. LUNG CANCER METASTASIS
Curtain sign:
Due to ventral median raphe
LUNG CANCER METASTASIS
Vertebral pathological collapse
with epidural extension
(soft tissue tumor)
Leptomeningeal carcinomatosis

120. VASCULAR:

121. 29 Y/O male with acute onset of paraplegia while surfing
QUESTION

122. TYPICAL ORIGIN OF ARTERY OF ADAMKEIWCZ IS FROM LEFT SIDE FROM AORTA?
ANSWER OPTIONS
TYPICAL ORIGIN OF ARTERY OF ADAMKEIWCZ IS FROM LEFT SIDE
FROM AORTA?
TRUE
FALSE

123. ANSWER
TRUE: Artery of Adamkeiwcz typically arises from left side of aorta between T9 to T12 levels from the left side with a classic hair-pin “U” turn of the vessel at its entry into the spinal canal

124. CORD INFARCT Butterfly (ventral & dorsal horns)
But may occasionally be only ventral cord - horn
T2 prolongation
Intramedullary spinal cord
T2 prolongation & swelling
with extension upt o the filum

125. CORD INFARCT
INTRODUCTION: Abrupt vascular occlusion or cutoff involving spinal cord
from aortic dissection or iatrogenic or vascular avulsion leading to cord
infarct or necrosis.
CLINICAL PRESENTATION:
Acute onset paraplegia or paraparesis
Symptoms peak within couple hours of onset

126. IMAGING HALLMARKS:
Long segment central cord T2 hyperintensity
Cord swelling in acute state volume decrease in chronic
(if patient survives)
Ventral & dorsal horn (butterfly appearance) or more preponderance
of ventral horn involvement
Restricted diffusion in acute state and enhancement in subacute state
Most commonly distal thoracic spinal cord extending to conus
Contiguous T2 signal abnormality
Differential: Cord edema due to inherent cord disease from tumor or
infection or inflammation or the waste basket transverse myelitis.
to be differentiated from discontinuous cord multiple sclerosis

127. IMAGING GOLD STANDARD/DIAGNOSIS:
MRI
2. Followed by angiography for vascular occlusion
TREATMENT - PROGNOSIS:
Supportive
Treatment of underlying vascular cause (like aortic dissection or aneurysm)
PROGNOSIS: Poor: Nearly quarter of the patient die within the acute hospital stay.

128. 53 Y/O male with progressive difficulty in walking
QUESTION

129. MOST COMMON SPINAL CORD VASCULAR MALFORMATION - FISTULA IS?
ANSWER OPTIONS
MOST COMMON SPINAL CORD VASCULAR MALFORMATION - FISTULA IS?
TYPE I
TYPE II
TYPE III
TYPE IV

130. ANSWER
TYPE I: 75 TO 85% IS THE FORMAINAL DURAL FISTULA (TYPE I) ABNORMALITY. ALSO 75 TO 85% OF THE PATIENTS WITH VASCULAR CHANNEL ABNORMALITY ARE MEN.

131. ARTERIOVENOUS FISTULA: TYPE I
Prominent flow voids
(venous drainage)
Prominent flow voids
Along neural foramen
heading centrally to
the canal venous drainage
Abnormal T2 cord
signal due to
ischemia or venous
congestion (not infarct)

132. MALFORMATIONS & FISTULAS:
ARTERIOVENOUS
MALFORMATIONS & FISTULAS:
INTRODUCTION: Direct communication of arterial channels (aspect) to
venous drainage side with or without intervening normal tissue resulting
in a early draining vein
CLINICAL PRESENTATION:
Progressive onset of paraplegia or paraparesis
Acute presentation or abrupt deterioration if hemorrhagic conversion

133. IMAGING HALLMARKS:
Long segment central (and on occaisions posterior) T2 hyperintensity
Cord swelling in acute state and volume decrease in chronic
(if patient survives)
Prominent vascular flow channels – flow voids
Vascular tuft in type II – III – IV (with nidus in II & III)
+/- cord enhancement

134. ARTERIOVENOUS ANOMALIE: IMAGING HALLMARKS
TYPE I
TYPE III
Dural arteriovenous “fistula”
with slow flow:
Ia: Single feeder
Ib: Multiple feeders
Location: Neural foramina
Juvenile: Dural arteriovenous
“malformation” with mixed
flow:
With intramedullary &
extramedullary component
(worst prognosis)
TYPE II
TYPE IV
Dural arteriovenous
“malformation”
with high flow:
Similar to intracranial
parenchymal AVM
Dural arteriovenous “fistula”
at surface of spinal cord:
IVa: Single feeder – slow flow
IVb: Multiple feeders – slow flow
IVc: Multiple feeders: fast flow

135. IMAGING GOLD STANDARD/DIAGNOSIS:
MRI followed by angiography
TREATMENT:
Embolization (when possible)
Otherwise surgical ligation or excision
Repeated treatment (mainly unsuccessful) in type II malformation
PROGNOSIS:
If patient progressed to bowel bladder symptoms: Rarely improve on treatment
Good: for type I & II & IV
Poor for: III

136. MISCELLANOUS:

137. SYNOVIAL CYST Unusual degenerative changes
Air filled focus arising from the facet joint
If arising from disc space, it would represent a disc herniation with extrusion
(but would be ventral to the thecal sac). And if arising from the central portion
of the vertebral body with air in the vertebral body, it would represent
Kummel disease (avascular necrosis of the vertebral body) and again would be
ventral to the thecal sac

138. SIMPLISTIC APPROACH TO
CAUDA EQUINA
AND
CORD PATHOLOGY:

139. CAUDA EQUINA PATHOLOGY
ENHANCING CAUDA EQUINA
NODULAR NERVE ROOTS
NORMAL THICKNESS
OF NERVE ROOTS
THICK NERVE ROOTS
GB SYNDROME
NEUROFIBROMA
SCHWANNOMA
DJERINE SOTTAS SYNDROME
CHARCOT MARIE TOOTH DISEASE
INFECTION
GRANULOMATOUS
NEOPLASTIC
CHROMOSOMAL EVALUATION
CSF EVALUATION

140. H SPINAL CORD LESIONS Anterior spinal artery infarct
Demyelinating disease
Multiple sclerosis
Lyme disease
ADEM (Post viral)
Amyotropic lateral
sclerosis (ALS)
Wallerian degeneration H
Cord infarct
AVM & AVF
Cord Ischemia
Syrinx
Hydromyelia
HOLOCORD ABNORMALITY:
Tumor
Primary
Metastasis
Infection
Trauma
Transverse myelitis
(diagnosis of exclusion)
Sub-acute combined
degeneration
(Vitamin B12 deficiency)
HIV
Syphilis
Copper metabolism
abnormality
Polio

141. THANK YOU