- Many neurological disorders simultaneously or consecutively affect the brain and spinal cord, however most neurologist find their comfort zone in attending the diagnosis via the brain access. - This concept resulted in lagging of spinal cord imaging researches compared to brain ones and consecutive underestimation of the opportunity of an important tool sometimes essential to reach a definite diagnosis.

3. ◘ Since the introduction of MRI, a breakthrough had
happened in neurological diagnosis.
◘ Many neurological disorders simultaneously or
consecutively affect the brain and spinal cord,
however most neurologist find their comfort zone in
attending the diagnosis via the brain access.
◘ This concept resulted in lagging of spinal cord imaging
researches compared to brain ones and consecutive
underestimation of the opportunity of an important
tool sometimes essential to reach a definite diagnosis.

4. To break the ice upon getting the diagnosis through the spinal axis and
increase the utilization of this important investigation

5. (1) In sagittal section:
- The region of the lesion (cervical, dorsal, conus)
- The extent of the lesion (SSTM, LETM).
- Cord swelling at the lesion.
(2) In axial sections:
- The location of the lesion (central, lateral, dorsal).
- The width of the lesion.
- Location of the spinal cord within the canal.
(3) Gadolinium enhancement:
- Pattern of enhancement (patchy, ring, flame).
- Persistent enhancement (> 3-months).
- Associated meningeal or vertebral enhancement.
(4) The vertebrae:
- Associated spondylitis.
- Spinal cord compression (disc bulge, spondylosis).

7. (A) Demyelinating:
- MS, NMOSD, ADEM and idiopathic
ATM.
(B) Autoimmune/Inflammatory:
- Systemic lupus erythematosus.
- Sjogren syndrome.
- Antiphospholipid syndrome.
- Neuro-sarcoidosis.
- Behcet disease.
- Mixed connective tissue disease.
(C) Paraneoplastic:
- Antiamphiphysin (breast carcinoma).
- Anti-CRMP-5 (small cell lung cancer).
(D) Infectious:
- Bacterial: Syphilis, TB, spinal cord
abscess, Lyme disease.
- Viral: Herpes simplex virus type-2,
varicella-zoster virus, cytomegalovirus,
Epstein-Barr virus, coxsackie virus,
enterovirus, hepatitis A and C.
- Parasitic: Neurocysticercosis,
Schistosoma, Gnathostoma
angiostrongylosis.
- Fungal: Actinomyces, Coccidioides
immitis, Aspergillus, Blastomyces
dermatitidis.

8. ◘ MS spinal cord MRI criteria:
(1) Short segment (≤ 2 vertebral bodies).
(2) Eccentric (predominantly dorso-lateral).
(3) < 50% of the cross spinal cord section.
(4) Ring enhancement (32% of cases).
◘ Value of MRI in MS:
(1) Support the diagnosis (DIT, DIS).
(2) Detects subclinical activities.
(3) Predicts treatment response as well as
functional outcome.

9. ◘ LETM ≥ 3 contiguous vertebral bodies.
◘ In axial sections:
(1) > 50% of the spinal cord cross section.
(2) Central cord predominance with > 70% of the
lesion resides around the central canal in the
central grey matter.
◘ Gadolinium enhancement may be patchy or the
more characteristic elliptical lens shaped ring-
enhancement which distinguishes NMOSD
from other causes of LETM but not MS.
◘ Enhancement disappears in < 3-months or
shortly after steroid therapy.

10. ◘ Usually affects the conus and thoracolumbar
spinal segment.
◘ T2 hyperintense lesion in axial sections, highly
restricted to the grey matter (H sign).
◘ Bilateral anterior ON involvement.
◘ Younger age of onset and a more favorable
outcome than AQP–4 positive cases.
◘ Characterized by simultaneous or rapid
sequential ONs and TM.

11. ◘ TM Consortium Working Group diagnostic criteria:
- Acute bilateral symptoms and signs with a clear sensory level.
- Progression from onset to nadir in 4 h to 21 days.
- Evidence of inflammation demonstrated by CSF pleocytosis,
elevated IgG index or MRI gadolinium enhancing lesion(s).
- Exclusion of other intra- or extra-axial pathologies (diagnosis of
exclusion).
- T2 / FLAIR hyperintense edematous spinal cord lesion (1–2
vertebral bodies length, but rarely LETM).
- Typically involving > 50% of the cord in cross-section.
- Variable enhancement in 38% of cases (not ring enhancement)
which rapidly disappear after steroid therapy.
(a, b) LETM.
(c, d) short segment
myelitis.

12. ֎ Spinal cord involvement is reported in up to 83% of
cases of ADEM.
◘ MRI is important to confirm the diagnosis of ADEM
despite the picture is not totally specific.
֎ Spinal cord MRI may show confluent, intramedullary
lesion(s), swollen cord in acute phase and variable
contrast enhancement.
◘ Brain T2 / FLAIR MRI reveals multifocal, hyperintense
poorly margined, white matter lesions (> 1 – 2 cm),
with/without grey matter involvement (especially
putamen and thalamus) and no evidence of DIT.

13. - Preceding infection or vaccination (> 70% of cases).
- Typically monophasic (> 90% of cases), but in few cases
may be multiphasic or recurrent.
- Multifocal, polyfocal initial presentation.
- More common in pediatric population (< 10 years).
- Encephalopathy with either altered consciousness or
behavioral change.
- Bilateral simultaneous optic neuritis (in NMOSD always
sequential).
- CSF pleocytosis without oligoclonal bands.

14. ◘ Causes LETM with possible associated vertebral pathological collapse.
◘ Contrasted films show linear dorsal subpial and central canal enhancements (Trident Sign).
◘ Enhancement > 3 months is in favor of sarcoidosis rather than NMOSD.

15. ◘ Myelitis is a rare neuropsychiatric manifestations of
SLE.
◘ SLE results in acute short segment TM (LETM is
exceptional).
◘ In axial sections, SLE myelitis causes hyperintense
lesion involving both the grey and white matter to
a variable degree and the cord is swollen over it.
SLE myelitis; LETM (left) and
short segment (right)

17. ◘ VDDSC is an increasingly used term in past decade,
due to better diagnosis in MRI films and as it
constitutes a potentially treatable disease.
◘ The thoracic spine cord has normal anterior position
owing to the normal dorsal kyphosis.
◘ Spinal cord attachments are predominantly lateral,
when laxed, the cord get stretched against the
dome of the mid-dorsal spine with consecutive
anterior displacement.

18. Notice the eccentric cord and the dilated heterogenous retro-spinal subarachnoid
space

19. ◘ The paired denticulate ligaments are lateral
extensions of the pia between the nerve roots
which anchor the spinal cord to the dura mater
and provide stability during flexion/extension
of the vertebral column.
◘ The subarachnoid space has fibrous trabeculae
attaching the pia matter to the arachnoid
membranes.
◘ The pia also extend as the filum terminal to fix
the lower spinal cord border with the coccyx.

20. ◘ A midline bi-layered arachnoid membrane
dissecting the retro-spinal subarachnoid space.
◘ In the cervical region, the septum is interrupted
and is formed of irregular bands.
◘ In the dorsal region, it is well developed and forms
a true membrane till the conus which could be
identified as a retro-spinal filling defect in CT
myelogram.
◘ The septum may have irregular developmental or
post-traumatic perforations.
Perforations in the septum
posticum

21. ◘ Consists of fibrous connective tissue bands of variable size that anchor the ventral aspect
of the dural sac with the anterior longitudinal ligament of the spinal canal.
Septum Posticum
Hofmann’s ligaments

22. (1) Lax denticulate ligament.
(2) Septum posticum fenestration followed by
focal arachnoiditis and thickening.
(3) Congenital dural defects.
(4) Tear and/or anterior traction of the Hoffman
ligament due to trauma or inflammation.
(5) Turbulent CSF flow and shearing stress result
in dural inflammation and tear.

23. ◘ It is a mild form of VDDSC with preserved rim of subarachnoid space between the ventral
aspect of the cord and the dura.
Septum Posticum PouchArachnoid septation (web)

24. ◘ CT myelogram and MRI show VDDSC, flattening of the posterior margin in axial sections
and focal indentation of the cord in sagittal sections “scalpel sign”.

25. ◘ Presented by progressive myelopathy with MRI reveals no intervening CSF space between the
cord and the dura.
◘ Herniation is a severe form of VDDSC where the spinal cord bulges through a dural defect.

26. ◘ The spinal cord projects across a dural defect.
◘ An anterior C-shaped kink of the cord with an
irregular posterior margin on sagittal sections.
◘ On axial section, the herniated cord is visible as a
protrusion through the dural defect.
◘ The herniated cord may be thinned out and may
show signal changes due to cord atrophy.
◘ The presence of normal CSF pulsation artifacts and
free CSF flow in phase contrast pulse in MRI
differentiates it from an arachnoid cyst.

27. The spinal cord is wrapped by a sheet of Duragen at the site of dural defect

28. ◘ Spinal arachnoid cysts (SAC) result from CSF inflow
into a small diverticulum in-between the 2 layers
of the septum posticum (intradural SAS) or
through a small dural defect (extradural SAS).
◘ The most common location of SAS is the dorsal
retro-spinal subarachnoid space where the septum
posticum is well developed.
◘ The arachnoid diverticulum may be congenital or
may develop secondary to trauma, infection or
iatrogenic (lumbar puncture or postsurgical).

29. (1) Type I SAC which describes extradural
arachnoid cysts without nerve root
involvement (including sacral meningocele).
(2) Type II SAC which include extradural
arachnoid cysts with nerve root
involvement.
(3) Type III SAC incorporate intradural
arachnid cysts.

30. Arachnoid cyst in the subarachnoid space

31. ◘ Uniform fluid intense lesion in all MRI sequences, loss of normal CSF pulsation artifacts
during phase contrast imaging (spinal block) and smooth symmetric anterior spinal cord
displacements.

34. ◘ Before the era of MRI, SCI was a diagnosis of doubt with a common misdiagnosis inside the
trap of ATM while definitive diagnosis was kept only postmortem.
Aortic Atheroma Causing Cord
Ischemia

35. ◘ SCI comprises < 1% of all strokes and 5–8% of acute myelopathies.
◘ The onset is often dramatic (< 1-hour) and spinal cord MRI (DWI/ADC) show restricted
diffusion.

36. 1. Acute non-traumatic myelopathy.
2. MRI hyperintense lesion in a defined vascular
territory or watershed area on T2-WI.
3. No alternative diagnoses or cord compression.
A. Definite SCI:
- Vascular abnormality demonstrated on spinal angiogram
explanatory of the clinical presentation.
B. Probable SCI:
- Spinal angiogram negative or not available.
- Positive DWI or known stroke risk factors or mechanism
explanatory of the clinical presentation (i.e., severe
hypotension, hypercoagulable state)
C. Possible SCI:
- Spinal angiogram negative or not available.
- No identifiable risk factor or mechanism.

37. (A) Dissection or atheroma of aortic, vertebral,
subclavian arteries are the commonest causes.
(B) Procedure Related; aortic surgery, vertebral
angiography, intra-aortic balloon counter-
pulsation or renal artery embolization.
(C) Embolic; cardioembolic or decompression
sickness (diving).
(D) Vasculitis.
(E) Systemic hypotension and cardiac arrest.
(F) Hypercoagulable state and cocaine
abuse.
(G) Spinal-dural AVF. Vertebral artery dissection

38. (1) Typical ASA syndrome is bilateral loss of motor
function and pain/temperature sensation, with relative
sparing of deep sensation below the level of the lesion.
(2) Man in Barrel Syndrome due to central cervical
cord hypoperfusion (WSI between the branches of the
ASA and PSA) with consecutive painful bilateral
brachial diplegia and relative sparing of lower limbs.
(3) Progressive distal amyotrophy with wasting and
fasciculation due to chronic AHCs ischemia. May be
misdiagnosed as ALS but usually asymmetrical.

39. ◘ MRI shows bilateral T2 ventral and paracentral spinal cord pencil like linear hyperintensities in
sagittal sections, owl or snake eyes appearance in axial ones, cord swelling, ill-defined patchy
enhancement and associated vertebral body infarction.
Owl or snake eyes
Contrast
enhancement
Diffusion restrictionVertebral infarction

40. (1) Posterior spinal artery occlusion
results in dorsal columns involvement.
(2) Segmental (radicular) arteries
infarctions cause complete cord syndrome
(simulating idiopathic transverse myelitis).
(3) Sulco-commissural arteries occlusion
result in hemi-cord syndrome.

41. ◘ Results in mid-thoracic spinal cord WSI due to hypo-perfusion at its anastomosis with the
ASA usually during repair of aortic aneurysm.

42. ◘ Venous infarction in a patient with epidural and paraspinal abscesses.
◘ Notice the leptomeningeal enhancement and the increased bone marrow intensities due to
associated vertebral bodies ischemia.

43. ◘ It is the most common spinal vascular malformation
with progressive or stepwise course.
◘ MRI shows serpentine dilated peri-medullary
venous plexus with puzzle shaped LETM due to
peri-AVF spinal cord ischemia.
◘ The spinal lesion is hyperintense in T2-WI with a
hypointense rim made of stagnant deoxygenated
hemoglobin in the dilated capillaries.
◘ Gadolinium enhancement persists > 3 months.

44. Dilated and tortuous
draining vein
Feeding artery from
right vertebral artery
T2-and contrasted T1 with spinal cord lesion and
serpentine, dilated peri-medullary venous plexus

46. ◘ It is the most common cause of myelopathy
accounting for 23% of cases (usually cervical).
◘ MRI shows hyperintense heterogenous T2 lesions
with flat, transversely oriented pancakelike
enhancement (width>height) at the site of
maximal compression.
◘ Axial sections show circumferential sparing grey
matter
◘ Persistent lesional enhancement > 3-months and up
to 2-years after successful surgery.

47. Enhanced gadolinium rim and flame like lesions > 3-months

50. The cross sectional distribution of lesion is of ultimate diagnostic importance

51. (1) NMOSD.
(2) Confluent ADEM lesion
(3) Anterior spinal artery occlusion.
(4) Spinal venous infarction
(5) Neuro-sarcoidosis.
(6) Paraneoplastic myelopathy.
(7) Primary CNS lymphoma.
(8) Exceptional causes of LETM:
- MS especially in pediatric
population.
- Idiopathic ATM.
- Vasulitic myelopathy.
Paraneoplastic LETM
Tract specific enhancement

52. (1) Spondylotic myelopathy.
(2) Spinal-dural AVF.
(3) Intramedullary metastasis
(4) Paraneoplastic myelopathy.
(5) Primary CNS lymphoma.
◘ Pattern and persistence of gadolinium
enhancement are important red flags to
revise your diagnosis.

53. ◘ Results from cervical spinal cord ventral
displacement during neck flexion with consecutive
chronic ASA ischemia.
◘ Characterized by progressive asymmetrical distal
amyotrophy of C7, C8 and T1 innervated muscles
with pyramidal tract and sensory sparing.
◘ T2 / MRI shows mid-cervical cord hyperintensities
with anterior displacement of the cord on flexion
and widening of the posterior epidural space.

54. ◘ The spinal cord remains one of the areas in
which ultra-high fields strength MRI have
great impacts:
(1) The small spinal cord diameter needs high spatial
resolution for lesion localization and grey/white
matter differentiation.
(2) Faster examination time.
(3) Better post-processing of structured films.
(4) Lower necessity for contrast enhancement.

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