The document discusses various types of acute myelopathies affecting the spinal cord, categorizing them into compressive and non-compressive myelopathies, with detailed descriptions of conditions such as multiple sclerosis, neuromyelitis optica, acute disseminated encephalomyelitis, and others. It outlines diagnostic approaches, imaging findings, and clinical features associated with these myelopathies, emphasizing the significance of understanding symptoms and MRI characteristics for accurate diagnosis. The document also highlights key differences between conditions and the impact of inflammatory and vascular factors on spinal cord health.

1. IMAGING OF SPINAL CORD
ACUTE MYELOPATHIES
DR.NAVNI GARG
DNB RESIDENT
MEDANTA-THE MEDICITY

2. • Myelopathy refers to pathology of the spinal
cord ,can occur due to a lesion arising within
the spinal cord or due to compression of the
spinal cord originating outside of it.
• When due to trauma, it is known as spinal
cord injury.
• When inflammatory, it is known as myelitis.
• Disease that is vascular in nature is known as
vascular myelopathy.

3. COMPRESSIVE MYELOPATHIES
 Cervical spondylosis
 Epidural, intradural neoplasm
 Epidural abscess
 Epidural hemorrhage/hematoma
 Herniated disc
 Posttraumatic compression by fractured or
displaced vertebra or hemorrhage

4. NON-COMPRESSIVE MYELOPATHIES
 Vascular
 Arteriovenous malformation
 Antiphospholipid syndrome and other hypercoagulable states
 Inflammatory
 Multiple sclerosis
 Neuromyelitis optica (Devic’s Disease)
 Transverse myelitis (idiopathic)
 Sarcoidosis
 Vasculitis
 Infectious/Postinfectious
 Viral: VZV, HSV-1 & -2, CMV, HIV, HTLV-I, enteroviruses, flaivaviruses
 Bacterial and mycobacterial: Borrelia, Listeria, syphilis, Mycoplasma
pneumoniae
 Parasitic: schistosomiasis, toxoplasmosis
 Metabolic
 Vitamin B12 deficiency (subacute combined degeneration)
 Copper deficiency

5. If we exclude myelopathy due to cord
compression as seen in trauma, degeneration and
metastatic disease, which is usually not a
diagnostic dilemma, then the most common
diseases of the spinal cord are demyelinating
diseases.
MS is by far the most common demyelinating
disease.

7. APPROACH TO MYELOPATHY
1. SHORT SEGMENT INVOLVEMENT OR LONG
SEGMENT INVOLVEMENT ??
2. HOW MUCH CORD IS INVOLVED ??
3. LOCATION OF INVOLVEMENT ??
4. IS THE CORD SWOLLEN ??
5. ENHANCEMENT ??

8. QUES 1. SEGMENT ??
• Short segment involvement
– common in:
• MS
– uncommon in:
• Transverse myelitis - partial
form
• Long segment involvement
– common in:
• Transverse myelitis - complete
form
• Neuromyelitis Optica
– uncommon in:
• MS

9. QUES 2. HOW MUCH CORD IS
INVOLVED ??
• PARTIAL : MULTIPLE
SCLEROSIS
• COMPLETE :
TRANSVERSE MYELITIS
AND NMO

10. QUES 3. LOCATION ??

11. QUES 4. CORD EXPANSION ??
• Tumors , transverse myelitis : swollen cord
• MS, ADEM : usually not swollen

12. DIFFERENTIAL DIAGNOSIS
(excluding trauma and degenerative diseases )

13. NON COMPRESSIVE
MYELOPATHIES

14. MULTIPLE SCLEROSIS
• MS is an immune-mediated inflammatory
demyelinating disease of the brain and the spinal cord.
• Multiple lesions disseminated over time and space.
• One third of MS patients will have spinal symptoms
• One third of patients have isolated spinal MS without
any findings in the brain.
However pathologic studies have shown that 95% of
MS patients have spinal cord lesions, whether they
have spinal symptoms or not.

15. MULTIPLE SCLEROSIS

16. CLINICAL FEATURES
• Clinical course of MS is extremely variable
• Most common signs/symptoms
o Variable; initially impaired/double vision of acute
optic neuritis
o Weakness, numbness, tingling, gait disturbances
o Loss of sphincter control, blindness, paralysis,
dementia
o Cranial nerve palsy; usually multiple, (CNs 5, 6
most common)
o Spinal cord symptoms in 80%

17. CLINICAL COURSE

19. BRAIN LESIONS
• Brain lesions are
typically in
periventricular,
subcortical and
cerebellar white matter
and also in brainstem
and corpus callosum.

20. DAWSONS FINGERS

21. DOUBLE INVERSION RECOVERY SEQUENCE
a new sequence that suppress both CSF and white matter signal and better
delineation of the plaques.

22. SPINAL CORD LESIONS
• Aligned along the length of the cord
• Usually less than 2 vertebral segments in length
• Involves less than half of the axial cord area
• Usually wedge shaped and reach outer surface of
the cord
• Usually posteriorly or laterally in cord
• May involve the gray matter
• MC affects cervical spinal cord
• Gadolinium enhancement of acute lesions :
patchy, homogeneous or ring shaped

23. Well defined focal lesions in the cord, typically triangular in shape, located
posteriorly ; no enhancement on post contrast studies .

24. Diffuse spinal cord involvement : more
commonly seen in primary progressive and
secondary progressive MS
D/D : TM,NMO

25. ENHANCEMENT
Active lesions can enhance, but enhancement is not as common as in the
brain.
The enhancement patterns are non-specific : ring enhancement, intense and
less-intense enhancement.
The less intense or vague enhancement is the most common pattern.

26. CORD ATROPHY
• Spinal cord atrophy is
specific for primary
progressive MS (PPMS).
• The atrophy correlates
very well with the clinical
disability.
• It is more prominent in
the upper part of the
spinal cord.
• Duration of the disease is
the most important
determinant of cord
atrophy.

27. MULTIPLE SCLEROSIS : IMAGING : MRI
• Focal lesions.
• No diffuse abnormality on sagittal images.Type I
• Focal lesions plus diffuse abnormality of
cord on sagittal images.
Type II
• Diffuse abnormality of spinal cord.
• No focal lesions.
Type III
TYPES OF MR FINDINGS ON PD AND
T2W IMAGES.

28. MULTIPLE SCLEROSIS : IMAGING : MRI
:
TYPE I : FOCAL LESIONS ONLY

29. MULTIPLE SCLEROSIS : IMAGING : MRI :
TYPE II : FOCAL AND DIFFUSE LESIONS
BOTH

30. MULTIPLE SCLEROSIS : IMAGING : MRI :
TYPE III : DIFFUSE LESIONS ONLY

31. MULTIPLE SCLEROSIS : IMAGING : MRI
CLINICO-PATHOLOGIC
CORRELATION :
TYPE I :
Focal only.
• C: RRMS
• P : Focal ares
of
demyelination.
TYPE II :
Focal & Diffuse.
• C : SPMS
• P : Focal areas
progressing to
gliosis.
TYPE III :
Diffuse only.
• C : PPMS and
PRMS
• P : Axonal loss
or gliosis.

32. NEUROMYELITIS OPTICA
• Neuromyelitis Optica (NMO) is an autoimmune
demyelinating disease induced by a specific auto-antibody,
the NMO-IgG.
• NMO preferentially affects the optic nerve and spinal cord.
• Brain lesions do occur and often are distinct from those
seen in MS.
• Demyelination of the spinal cord looks like transverse
myelitis, i.e. often extensive over 4 -7 vertebral segments
and the full transverse diameter.
• NMO IgG is a specific biomarker for NMO.
• Female:male = 9:1
• Also called Devic disease

33. REVISED NMO DIAGNOSTIC CRITERIA
REQUIRED :
• Optic neuritis
• Acute myelitis
PLUS TWO OR MORE SUPPORTIVE CRITERIA
• Disease onset MR imaging non diagnostic for MS
• Contiguous spinal cord lesions on MR > 3
vertebral segments
• NMO –IgG seropositivity

34. OPTIC NEURITIS
• Unilateral or bilateral
• Optic nerve
hyperintensity on T2
and/or enhancement
on MRI
• Bilateral involvement
and extension of the
signal back into the
chiasm is particularly
suggestive of NMO.

35. BRAIN LESIONS IN NMO
• They are often distinct
from those seen in MS.
In Asia 60-80% of
patients with NMO have
brain abnormalities.
• The location of the
brain lesions in NMO is
usually around the
ventricles.

36. PERIVENTRICULAR BRAIN LESIONS
• The NMO IgG auto-antibodies are directed
against Aquaporin-4 water-channels.
The highest concentration of these Aquaporin-
4 water-channels is seen around the ventricles
therefore NMO lesions are predominantly
located near the ventricles.

37. OTHER AREAS
• Hypothalamus/medial thalamus
• Dorsal pons/medulla
• Corpus callosum
– multiple callosal lesions with heterogeneous signal
leading to a marbled pattern
– splenium may be diffusely involved and expanded
Unlike MS, NMO does not appear to involve the
cortex.

38. MARBLED PATTERN IN NMO

39. ENHANCEMENT
• Patchy "cloud like" enhancement of T2 bright
lesions may be present
• Thin ependymal enhancement similar
to ependymitis
• Open ring enhancement is not a feature of
NMO .

40. Features helpful favouring NMO over
MS include
• Periventricular/aqueductal distribution
• Absent perivenular orientation of periventricular
lesions (no Dawson's fingers)
• More extensive involvement of the corpus callosum
• Larger more confluent lesions
• Lack of open ring enhancement
• Lack of cortical grey matter involvement

41. SPINAL CORD
• MC cervical cord is involved
• Hyperintense lesion that extends over three or
more consecutive segments and much of the
cross section of spinal cord
• Lesions may enhance with gadolinium for
several months
• Lesions can progress to atrophy and necrosis,
leading to syrinx like cavities

42. SPINAL CORD
Abnormal signal in the spinal cord with
swelling and some enhancement.

43. NMO

44. NMO MULTIPLE SCLEROSIS
DISTRIBUTION OF
SYMPTOMS
OPTIC NERVE AND SC ANY WHITE MATTER TRACT
BRAIN LESIONS PERIVENTICULAR
CORTEX NOT INVOLVED
PERIVENTRICULAR
JUXTACORTICAL
SC LONGITUDINAL >3
VERTEBRAL SEGMENTS
MULTIPLE SMALL LESIONS
LAB FINDINGS PLEOCYTOSIS DURING
ATTACK
RARELY WBC>25 CELLS
OLIGOCLONAL BANDS ABSENT PRESENT
NMO IgG Ab PRESENT ABSENT
INCOMPLETE RING
ENHANCEMENT
RARE COMMON

45. ACUTE DISSEMINATED
ENCEPHALOMYELITIS (ADEM)
• Acute disseminated encephalomyelitis (ADEM) is an
inflammatory demyelinating disease of the CNS after viral
infection or vaccination.
• In 75% of patients there is a clear infectious event or
vaccination (1-4 weeks)
• Typically monophasic in 90%.
• Multiphasic illness in 10%. In these cases ADEM behaves
like MS and cannot be differentiated from MS.
• Mostly seen in young children.
• In 50% of ADEM patients the anti-MOG IgG test is positive
and supports the diagnosis. This is antibody-reactivity
against Myelin Oligodendrocyte Glycoprotein (MOG).

46. CLINICAL FEATURES
• ADEM manifests with low-grade fever, headache,
meningismus, generalized seizures,drowsiness,
and encephalopathy.
• Multifocal neurologic signs and symptoms may
develop, with visual loss,hemiparesis,paraparesis,
ataxia, sphincter disturbances, sensory level,
choreoathetosis, and myoclonus.
• In fulminant cases, increased intracranial
pressure with tentorial herniation, resulting in
death within few days.

47. BRAIN LESIONS
• Patchy areas of increased
signal intensity on
conventional T2 and FLAIR in
white matter of the posterior
fossa and cerebral
hemispheres.
• Cerebellum and brainstem
involvement is more common
in children.
• Few MRI lesions may
enhance after gadolinium
administration.
• Extensive perifocal oedema
may be seen rarely.

48. ADEM VS MS
Typical for ADEM and
uncommon for MS is:
• Massive involvement of
the pons.
• Involvement of the
basal ganglia.

49. Diffuse spinal cord involvement, cord swelling
No enhancement

50. RESOLUTION OF ADEM

52. ACUTE TRANSVERSE MYELITIS
• Focal inflammatory disorder of the spinal cord
resulting in motor, sensory and autonomic
dysfunction.
• Imaging findings:
– More than 2/3 of the cross sectional area is
involved.
– Focal enlargement.
– T2WI hyperintensity
– Enhancement + / -.

53. Two forms of TM:
–Acute partial transverse myelitis - APTM
Lesions extending less than two Segments.
These patients are at risk of developing MS
–Acute complete transverse myelitis - ACTM
Lesions extending more than two Segments

55. ACUTE VIRAL MYELITIS
 Two Forms
 Enteroviruses (poliovirus,
coxsackie virus, and
enterovirus 71), Flaviviruses
(West Nile virus and Japanese
encephalitis virus) target the
gray matter (Anterior horn
cells) of the spinal cord,
producing acute lower motor
neuron disease.
 MRI often shows
hyperintensities in the anterior
horns of the spinal cord on T2-
weighted imaging .

56. OWL’S EYE SIGN IN SPINAL CORD- POLIOMYELITIS
Abnormal intra medullary T2 hyper intensity in the region of anterior horn cells of spinal cord, as
two white dots, one in each half of cord on axial T2w MRI images in the background of normal
gray coloured spinal cord.

57. Second form
 CMV, VZV, HSV I &II, HCV, and
EBV are associated with a
second form of viral myelitis
which has clinical and
diagnostic test features that
are similar to transverse
myelitis.

58. HIV MYELOPATHY
 HIV
 More of a chronic myelopathy, Often found mostly in late stages of AIDS and associated
with AIDS related dementia in half of the cases.
 slowly progressive spastic paraparesis is accompanied by loss of vibration and position
sense and urinary frequency, urgency, and incontinence.
MRI :
 Cord atrophy involving the thoracic spinal cord > cervical
 T2-weighted MRI often shows symmetric nonenhancing high-signal areas.
 Lesions may be confined to the posterior columns, especially the gracile tracts, or may
be diffuse.

59. Sagg T1W image : diffuse cord atrophy in mid thorasic level
T2W image of different patient : Focal Hyperintensity in cord
predominantly posteriorly.

60. BACTERIAL MYELOPATHY
 Mycoplasma (acute and post infectious), Listeria
monocytogenes
 TB
 via secondary cord compression from verterbral
osteomyelitis, aka Pott’s disease
 Also via compressive tuberculomas
 Lyme disease

61. GULLIAN BARRE SYNDROME
• Inflammatory
demyelination
(autoimmune / viral) :
Follows recent viral illness,
Campylobacter jejuni
infection
• MC- Ascending paralysis,
may ascend upto brainstem
invo. Cranial nerves, may
require respiratory support.
• Typical involvement of
Conus and Cauda
equina nerve roots –
mostly ventral.
• Nerve roots may be
slightly enlarged &
appear symmetric and
smooth (Not nodular).

62. IMAGING
• Myelography :
– May show symmetric enlargement of cauda nerve roots.
• CT :
– Difficult to diagnose with CT.
– May show enhancement of cauda nerve roots.
• MRI :
– Precontrast : T1,T2W images : essentially normal.
– T1+C :
• Avid enhancement of cauda nerve roots : enlarged but not
nodular.
• Preferential contrast accentuation of ventral roots.
• Pial enhancement along distal cord and conus.

64. TABES DORSALIS
 Form of tertiary neurosyphilis in which the nerves of the dorsal (or posterior)
columns degenerate.
 Loss of sense of position (proprioception), vibration, and discriminative touch
 Latency period of 3-20 years

65. CONNECTIVE TISSUE DISEASE
ASSOCIATED MYELITIS
 SLE
 May be the initial feature but onset is usually present with other
active lupus signs.
 Thought to be due to an arteritis, with resultant ischemic necrosis of
the spinal cord
 ANA, ds-DNA, anti-Sm, Anti-neuronal (may correlate with active CNS
lupus)
 Has been associated with antiphospholipid antibodies in some studies.
 Mixed connective tissue disease
 Sjogren's syndrome (antibodies to the Ro/SSA or La/SSB)
 Scleroderma (ANA, anti-Scl-70, anti-centromere (ACA), anti-RNA
polymerase III, and anti-beta2-glycoprotein I antibodies)

66.  Ankylosing spondylitis
 Acute myelopathy will typically occur in the setting of
fracture of ankylosed spine or atlantoaxial-axial
subluxation
 cauda equina sydrome rare but associated with long
standing disease
 Rheumatoid arthritis
 atlantoaxial subluxation, atlantoaxial impaction, and/or
subaxial subluxation
 Rarely associated with CNS vasculitis and more rarely with
myelopathy from vasculitis

67. NEUROSARCOIDOSIS
 Typically occur perivascularly, but they can be extramedullary or
intramedullary, and can involve the cauda equina.
 Occurs in 5% of Sarcoid patients
 MRI signal abnormalities are not specific
 neurosarcoid lesions can appear similar to transverse myelitis or can
resemble a tumor
 Intramedullary T1 hypo and T2 hyper lesion with cord expansion and
patchy enhancement
 CSF profile consists of variable lymphocytic pleocytosis; oligoclonal bands
are present in one-third of case .

68. SACD (VITAMIN B12 DEFICIENCY)
 Vitamin B12 deficiency causes typical degeneration of dorsal +/- lateral
spinal tracts.
 Damage to peripheral nerves caused by demyelination and irreversible
nerve cell death.
 Symptoms include
 paresthesias in the hands and feet
 loss of vibration and position sensation
 progressive spastic and ataxic weakness
 Loss of reflexes due to an associated peripheral neuropathy in a
patient who also has Babinski signs, is an important diagnostic clue
 Optic atrophy and irritability or other mental changes may be
prominent in advanced cases

69. Mild spinal cord enlargement, with abnormal T2 Hyperintensity
within dorsal +/- lateral columns

70. Axial MR images display the symmetric involvement of the dorsal and
lateral columns as increased T2 signal in an “inverted V” or “inverted rabbit
ears” configuration in SACD.

71. COPPER DEFICIENCY
 Very similar to subacute combined degeneration
 Progressive spasticity, severe gait abnormalities including ataxia, and
a neuropathy.
 Also associated with anemia and neutropenia in certain patients
 More common after gastric bypass, also with zinc supplementation
 Diagnosis usually confirmed with low levels of serum copper are found
and often there is also a low level of serum ceruloplasmin
 Symptoms are potentially reversible with copper supplementation and
reversal of underlying cause

73. SPINAL CORD INFARCTION
 Rare compared with CVA
 Most frequently caused by surgical procedures and pathologies
affecting the aorta
 Aortic aneurysm stenting is the most common cause of spinal cord
infarction.
 Presents with sudden spinal cord dysfunction that typically corresponds to
the territory of the anterior spinal artery
 Weakness and pinprick loss below the level of the infarction but
sparing vibration and position sense.
 No treatment available and prognosis is variable and dependent upon
severity of presenting deficit

74. ARTERY OF ADAMKIEWICZ
• Arises from left posterior intercostal artery,
which arises from aorta, supplies two third of
spinal cord via anterior spinal artery.
• It is important to identify location of artery
when surgically treating aortic aneurysm to
prevent damage which would result in
insufficient blood supply to spinal cord.

75. • In bronchial artery embolization for treatment
of massive hemoptysis , one of the most
serious complication is advertant occlusion of
artery of adamkeiwicz.

76. High signal ventrally in the cord, which is typical for
arterial infarction.
On transverse images a typical snake-eye appearance
can be seen.

77. DURAL AV FISTULA
• It consists of an abnormal connection between
the artery and the veins , which can lead to
increased venous pressure and predisposes the
cord to ischemia and less commonly to
hemorrhage.
• AVF's are mostly seen in the elderly population
and are believed to be the result of trauma.
An accurate diagnosis is important because these
lesions may represent a reversible cause of
myelopathy.

78. High signal in the lower thoracic cord and the surrounding
dilated vessels on the T2WI.
On the enhanced T1WI there is subtle enhancement.

79. COMPRESSIVE MYELOPATHIES

80. TRAUMATIC CORD COMPRESSION
• Fracture with posterior
displacement causing
cord compression and
acute myelopathy.

81. EPIDURAL ABSCESS
 Most common pathogen is Staphylococcus aureus, which
accounts for about two-thirds of cases 9
 Typically originate via contiguous spread from infections of
skin and soft tissues or as a complication of spinal surgery
and other invasive procedures, including indwelling
epidural catheters.
 Expected back and/or radicular pain usually but not always
accompanied systemic signs of infection
 MRI preferred test
 Requires emergent surgical decompression and antibiotic
therapy are indicated to treat epidural abscess

83. METASTATIC CORD COMPRESSION
• Abnormal signal in the
vertebral body as a
result of a metastasis
which extends into the
vertebral canal.

84. THANK YOU