MRI of the spinal cord: How to make the correct diagnosis of

non-traumatic medullar pathology

Poster No.:

C-2582

Congress:

ECR 2010

Type:

Educational Exhibit

Topic:

Neuro

Authors:

M. Vidal , B. Asenjo , A. Del Toro , M. Bernab , E. Cuartero , B.

1 1

Avila ; Mlaga/ES, Malaga/ES

Keywords:

MRI of the spinal cord, spinal multiple sclerosis, myelopathy

DOI:

10.1594/ecr2010/C-2582

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Learning objectives
1. To show a spectrum of non-traumatic spinal cord abnormalities diagnosed by
MRI.
2. To appreciate additional benefits of spinal MRI plus brain and angioMRI in the
differential diagnosis of spinal cord diseases.

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Background

MRI is essential for the detection and diagnosis of lesions of the spinal cord. When a
patient presents an acute-subacute myelopathy, excluding an compressive cause is of
utmost priority, for which MRI is invaluable. Having excluded a compressive cause and
having found an intrinsic spinal cord lesion on MRI, a detailed history and an examination
followed by focused investigations are needed.

INTRODUCTION:
- Anatomy of the spinal cord. (Fig.1, Fig.2 and Fig.3)
- Clinical presentation of spinal cord disorders. (Fig.4) on page 8

Spinal Cord Syndrome

EXAMPLES

Complete myelopathy

Trauma

Brown - Squard hemicord syndrome

Compression, multiple sclerosis

Central myelopathy

Optic neuromyelitis, syrinx

Anterior cord syndrome

Anterior spinal artery occlusion

Posterior cord syndrome

B12 deficiency

Tractopathies

Multiple sclerosis, infectious myelitis

BASIC MR IMAGING TECHNIQUE:

The basic MRI protocol includes T1- and T2-weighted sequences, on sagittal and axial
planes. Sagittal T1- and T2-weighted FSE, sagittal STIR and axial T2 FSE or GE are
the most widely used. STIR sequence has a high sensitivity to detect lesions of the spinal
cord; therefore, STIR often replaces T2-weighted FSE sequences. Contrast-enhanced
sagittal and axial T1-weighted FSE are routinely used to evaluate lesion activity. In all
cases, slice thickness should not be more than 3 mm.

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Contrast 3D MR angiography is the standard method to asses vascular morphology.

However, it could be difficult to identify small vessels or vascular spine malformation due
to their small size. MR myelography using HASTE (Half Fourier Acquisition Single Shot
Turbo Spin Echo) sequences can be used to detect intra and extradural pathology as
well as anomalous vessels on vascular malformations.

NON-COMPRESSIVE AND NON-NEOPLASTIC MYELOPATHY:

A. Inflammatory disorders:
Clinicians may suspect the inflammatory origin of myelopathy due to the presence of
biological markers such as pleocytosis and elevated IgG index in cerebral spine fluid
(CSF).
There are three major groups within inflammatory disorders:
A.1. Demyelinating disorders:
They are the most common, including multiple sclerosis, neuromyelitis optica, acute
disseminated encephalomyelitis and idiopathic transverse myelitis.

General Features:
- Usually, neurological symptoms occur over days.
- Most lesions are hyperintense on T2-weighted images on MR.
- When patient recovers, spinal cord appears normal. The persistence of imaging findings
on MRI in radiological controls is often associated with poor clinical recovery.
- Whether clinical recovery is incomplete, spinal cord atrophy is usually seen as well as
hypointensity on T1-weighted images due to axonal loss and extensive gliosis.

A.2. Infections: Infectious myelitis and intramedullary abscess.

Infectious myelitis are uncommon and intramedullary cord abscess are extremely rare.
Different agents can invade the spinal cord and cause infectious myelitis (viruses, fungi,
mycobacterium tuberculosis, cysticercus, toxoplasma ). Mostly are of hematogenous
origin and the primary sources are usually the respiratory tract and bacterial endocarditis
(althought also skeletal, genitourinary, gastrointestinal, and cutaneous infections).
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A.3. Other inflammatory pathology: Connective tissue diseases, granulomatous

disorders and vitamin deficiency may present with acute or subacute myelitis.

B. Vascular pathology:
General Considerations:
Spinal cord vascular lesions are uncommon. Among the vascular lesions of the spinal
cord and its meninges, anterior spinal artery occlusion and vascular malformation
(arteriovenous fistulas and arteriovenous malformations), are the most prevalent.
The diagnosis by MRI is predominantly based on changes of the cord tissue appearance
but not on direct visualization of abnormal vessels.
CSF is usually normal, although spinal arteriovenous malformations can lead to elevated
CSF protein concentration without pleocytosis.

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Images for this section:

Fig. 1: Spinal Cord Anatomy

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Fig. 2: Spinal Cord Anatomy

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Fig. 3: Spinal Cord Anatomy

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Fig. 4: Spinal Cord Syndromes

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Imaging findings OR Procedure details

A. INFLAMMATORY DISORDERS:

A.1 Demyelinating diseases:

Multiple Sclerosis (Fig.1 and Fig.2)

Introduction:
Multiple sclerosis (MS) is a chronic and relapsing disorder that affects the central
nervous system. Its characterized by multiple demyelinating lesions over time and
space.
It is more frequent in women aged 20 - 40 years old.
30% of patients with MS have spinal cord lesions and 90% of them is associated with
brain lesion (this is very important for the diagnosis).
Clinical Presentation:
The characteristic syndrome for spinal MS is partial myelopathy as Brown-Squard
syndrome or, more commonly, incomplete versions thereof. Repeated episodes of
neurological dysfunction with posterior recovery are frequent.
Spinal Cord MRI:
Cervical involvement is much more common than thoracic one.
Lesions are usually small: they affect a spinal cord section less than 2 vertebral bodies
and less than half the cross - sectional area of the cord.
The most common plaques location is the medullar periphery (the anatomic location
of the white matter in the cord), and frequently the dorsolateral columns.
It seems contrast enhancement correlates with the presence of an active inflammatory
process. A majority of patients with new clinical manifestations of myelopathy have
enhancing lesions in the cord. Most enhancing lesions are homogeneous, nodular and
relatively small (although patchy and ring enhancement may present in some plaques).
Diagnostic Criteria For MS:
Brain MRI helps establish the diagnosis of spinal cord MS because typical brain
lesion locations (periventricular, subcortical, brainstem and cerebellar white matter)

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associated with spinal cord lesions suggest the diagnosis. In the absence of intracranial
white matter lesions may be necessary spinal cord biopsy.

Optic Neuromyelitis (de Devic) (Fig.3)

Introduction:
Optic neuromyelitis -NMO- is a relapsing demyelinating condition of the central
nervous system affecting predominantly optic nerves and spinal cord, of unknown
etiology.
90% of patients are women and its relatively more common in asian and african
individuals.
Clinical Presentation:
This disease is characterized by optic neuritis and acute myelitis, being able to
produce blindness and great neurological disability. The clinical medullar syndrome
usually is central myelopathy.

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The prognosis for these patients is very poor.

Spinal Cord MRI:
NMO affects both the cervical and thoracic spinal cord.
Lesions are typically large: they affect a spinal cord section more than 3 vertebral
bodies.
The central medula is the most common site involved.
Often its observed an extensive widening of the spinal cord in acute phase. Signal
intensity of these lesions is more heterogeneus than typical demyelinating lesions and
after gadolinium adminitration they show a poorly defined and patchy enhancement.
Diagnostic Criteria For NMO:
- Optic neuritis.
- Acute myelitis.
- And at least two of three supportive criteria:
Contiguous spinal cord MRI lesion extends over 3 vertebral segments.
Brain MRI does not satisfy diagnostic criteria for multiple sclerosis.
NMO-IgG is seropositive (NMO-IgG is a recently identified serum antibody that is
highly specific and sensitive for NMO).
Brain MRI can be abnormal in 50% of patient and typically lesions are periventricular
(occasionally hypothalamic or brainstem lesions).

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Acute Disseminated Encephalomyelitis (Fig.4 and Fig.5)

Introduction:
Acute disseminated encephalomyelitis -ADEM- is an uncommon immune-mediated
inflammatory demyelinating disease of the central nervous system (brain and
occasionally, spinal cord). Usually it is a monophasic illness, which may occur after
viral infection, after vaccination, in association with rheumatic fever, or without any
recognized antecedent disease.
ADEM is more common in children.
Clinical Presentation:
It is a multifocal and unspecific disease with altered level of consciousness, ataxia,
focal motor deficits, headache, aphasia, seizures, impaired sphincter control, optic
neuritis or involvement of other cranial nerves.
ADEM may evolve over the course of up to 3 months.
Spinal Cord MRI:
Lesions are the variable length.
Typically, lesions enhance after administration of gadolinium because there is a
bloodbrain barrier alteration.
Diagnostic Criteria for ADEM:

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The diagnosis is based on patient history (viral infection or vaccination previous),

clinic and brain and spinal cord MRI.
ADEM only can be diagnosed in patients with concomitant encephalopathy (brain MRI:
Large and often confluent white matter lesions; also, lesions of the same or similar
duration).
ADEM may evolve over the course of up to 3 months.

Idiopatic Acute Transverse Myelitis (Fig.6)

Introduction:
Inflammatory acute transverse myelitis (IATM), in the absence of a specific cause, is
the most common cause of acute myelitis. Clinical course of this disease is variable
and it is not clear why is usually monophasic.
Pathologically, there is a demyelination and necrosis affecting both gray and white
matter.
The bimodal peaks in onset ages are 10 to 19 years old and 30 to 39 years old.
Clinical Presentation:

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The clinical criteria for IATM include a rapid onset of bilateral motor, sensory
and autonomic dysfunction in absence of spinal cord compression or other known
neurologic disease.
Some cases of IATM are linked to a previous viral infection or vaccination.
It is important to note that IATM havent brain lesions.
Spinal Cord MRI:
Without predilection for a spinal cord segment.
Lesions are usually large: they affect a spinal cord section more than 3-4 vertebral
bodies and more than half the cross - sectional area of the cord.
Lesions may be associated to spinal edema and may enhance after contrast
administration.
Diagnostic Criteria For IATM:
IATM is often a diagnosis of exclusion. Its important to note that IATM havent brain
lesions.

A.2 Infectious Myelitis and Intramedullary Abscess:

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Infectious Myelitis and Intramedullary Abscess (Fig.7)

Introduction:
They are uncommon disorders and may be caused by diferent agents as viruses,
fungi or bacteria.
Clinical Presentation:
Patients have usually fever and meningismus; infectious myelitis should be suspected
when medullar syndrome is associated with rash, concurrent systemic infection,
recurrent genital infection or lymphadenopathy.
Also, its essential to know whether the patient is immunocompromised (for
opportunistic infections) or resides in endemic area for determinated infection.
Spinal Cord MRI:
Spinal cord infection initially appears as variable increased signal intensity on T2weighted images and as poorly defined enhancement on postcontrast T1-weighted
images.
An anatomic site of preferential involvement is the distal thoracic cord and conus
medullaris.
Diagnostic Criteria For Infectious Myelitis:
Septica myelitis diagnosis must be considered in those patients with an appropriate
clinical context and intramedullar high signal intensity on T2-weighted images and
abnormal enhancement on postcontrast T1-weighted images.

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A.3 Other Inflammatory Disorders:

Connective tissue diseases, granulomatous disorders and vitamin deficiency (for
instance, vitamin B12 deficiency) may present with acute or subacute myelopathy. There
are established diagnostic criteria for these disorders and, in general, these should
be satisfied before myelitis is atributed to these disorders.

Subacute Combined Degeneration (Fig.8)

Introduction:
Subacute combined degeneration of the spinal cord is a result of vitamin B12 deficiency.
Its important to recognize it because it is a treatable and potentially reversible
disorder.
In Europe this deficiency is caused by an inadequate intake (in alcoholism - common
- and in strict vegetarians) or malabsorption syndromes.
Vitamin B12 deficiency has effects on brain, optic nerves, peripheral nerves, and spinal
cord.
Pathologically, its occurs a "orderly" demyelination: first, it affects to dorsal columns
and after, to lateral columns. This process is eventually symmetric and spread in
the cranial and caudal directions.
Clinical Presentation:
Myelopathy develops over the course of a few weeks to a few months.
The characteristic lesion is posterior and lateral tractopathy, bilateral and
symmetric, which causes weakness and paresthesia of lower extremities, and
progresses in a distal-to-proximal manner.
Spinal Cord MRI:
Subacute combined degeneration affects to lower cervical and upper thoracic spinal
cord, in variable lenght segment. Abnormal signal intensity is particularly prominent in
dorsal and lateral columns, bilaterally symmetrical.
Diagnostic Criteria For Subacute Combined Degeneration:
Patients have neurologic deficit and low serum B12 level (elevated metabolites
homocysteine and methylmalonic acid serum levels are seen, if B12 level is borderline).

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Hematologic abnormalities, most notably megaloblastic anemia, are not reliable

markers for B12 deficiency.
These clinical and analytical features, associated to typical spinal and brain lesions
(brain MRI in B12 deficiency shows confluent areas of abnormal signal intensity on T2weighted images in cerebral white matter), helps establish the diagnosis.
Also, it is typical the resolution of these lesions in months after initiation the B12 therapy.

B. VASCULAR PATHOLOGY:

Anterior Spinal Artery Occlusion (Fig.9)

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Introduction:
Occlusion of anterior spinal artery (or AdamKiewicz artery) is rare and must be suspect
in patient with anterior cord syndrome especially in following cases: Aortic surgery,
vasculitis, embolic source, aortic / vertebral dissection, hypotension and prothrombotic
states.
Acute vascular occlusion can lead to spinal cord infarction mimicking myelitis.
Clinical Presentation:
Spinal cord stroke has an acute onset evolving over minutes. It is the main cause of
anterior cord syndrome and clinical sign depend on the level of the cord lesion and
may vary from mild or moderate and even reversible leg weakness to quadriplegia.
Spinal Cord MRI:
Typically this pathology appears as elongated ''pencil-like'' lesion in anterior cord.
Uncomplicated spinal cord infarction is most commonly on thoracic spinal cord.
Diagnostic Criteria for anterior spinal artery occlusion:
This alteration must be suspect in patients with severe atherosclerotic disease, aortic
disection, or profouns hypotension and anterior spinal syndrome developed acutely
over minutes.

Vascular Spinal Malformation (Fig.10 and Fig.11)

Spinal cord vascular malformations are uncommon lesions and a treatable cause of
myelopathy.
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They are a direct communications between arterial and venous channels without
an intervening capillary bed.
An angioarchitecture visualization of these lesions and their correct classification are
important for therapeutic planning.
There are two vascular malformations main types:
ArterioVenous Malformation:
They are congenital lesions and are more common in younger patients. They are
subdivided into 3 types:

Intramedullary (type II or classic AVM or glomus type). They have a nidus

similar to intracranial AVMs and are more frequent in the cervical and
upper thoracic spine.
Extradural-Intradural (Type III or juvenile AVM). Fortunately, they are
uncommon and respect no tissue boundary. They are more common in the
cervical and thoracic spine, too.
Conus Medullaris (Type IV). They are lesions characterized by multiple
feeding arteries, multiple niduses, and a complex venous drainage. They
are always located in the conus medullaris and cauda equina and can
extend along the entire terminal filum.

ArterioVenous Fistula:
They are the most frequent. They are acquired arteriovenous shunt, more frequent
at the thoracolumbar spine level and more common in men aged 50 - 80 years old.
They are subdivided into 2 types: extradural and intradural - extradural. Both types lead
to a high-flow fistula development, epidural venous system engorgement (with venous
hypertension), spinal cord compression, and resultant progressive myelopathy.
Clinical Presentation:
Typically vascular malformations appears as stepwise progressive or recurrent
episodes of weakness related to upright posture or walking, accompanied by upper
motor neuron or lower motor neuron syndrome or both.
Pathological substrate is venous hypertension, compression, ischemia, or hemorrhage.
Spinal Cord MRI:
Vascular malformations appear as long spinal cord lesion extending into the conus
on T2 -weighted images (due to spinal edema), and multiple signal voids (tortuous
vessels) on the cord surface or in the thecal sac on MR myelography.
Diagnostic Criteria For Vascular Malformations:

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Patients with clinical suspicion associated to spinal edema and tortuous vessels
on the cord surface or in the thecal sac.
The diagnosis can be made using MRI, but angiography is necessary to define the
exact angioarchitecture.

Images for this section:

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Fig. 1: MRI of the cervical and upper thoracic spine in a 17-year-old man with
typical spinal lesions seen in multiple sclerosis. Sagittal STIR image shows small focal
hyperintensity lessions (less than 2 vertebral bodies) at C-1, C-3 and C-5 levels, with no
cord swelling. Sagittal contrast-enhanced T1-weighted image shows subtle enhancement
at C-5 (arrow).

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Fig. 2: Cervical and upper thoracic cord MRI from a 42-year-old woman with multiple
sclerosis. Sagittal STIR image shows multiple small hyperintense foci at brainstem, and
at C-2 and C-5 levels, in an otherwise normal-sized spinal cord. Axial STIR image of
lesion at C2 level shows its typical peripheral posterolateral location.

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Fig. 3: Cervical and thoracic cord MRI from 30-year-old man with optic neuromyelitis.
Sagittal STIR image shows multiple long hyperintense lesions in the cervical and thoracic
spine.

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Fig. 4: Cervical and thoracic-lumbar spine in a 2-year-old boy with acute disseminated
encephalomyelitis after viral infection. Sagittal T2-weighted image shows hyperintense
lesions of variable length located in the cervical (from C2 to C4) and thoracic-lumbar
spine with discrete cord swelling.

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Fig. 5: Sequential axial Flair images of the brain show typical large and confluent lesions
in brainstem, left cerebellar peduncle and vermis as well as in white matter (periventricular
and subcortical) and left thalamus.

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Fig. 6: 45-year-old man with monophasic myelopathy. No brain lesions or other clinical
features suggestive of specific myelitis were found. Diagnosis of acute idiopathic myelitis
was made. Sagittal STIR image shows an extensive hyperintense lesion, covering more
than 3 vertebral bodies, from thoracic spine to conus medullaris.

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Fig. 7: 78-year-old man who developed herpes zoster in the upper limbs and
simultaneously extensive thoracic myelitis. Sagittal STIR image of the thoracic spine
shows poorly defined lesions with high signal intensity and with no cord swelling. Sagittal,
contrast-enhanced T1-weighted image shows uptake of contrast at T-1 (arrow).

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Fig. 8: 73-year-old alcoholic man with subacute combined degeneration of spinal cord.
Sagittal T2-weighted image shows abnormal increased signal intensity along posterior
columns of spinal cord extending from C3 through C7.

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Fig. 9: Sagittal STIR image of a 32-year-old man who developed acute tetraplegia,
bladder and bowel dysfunction and cervical sensory level to pain. Linear lesion in the
anterior cord -presumed anterior spinal artery occlusion.

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Fig. 10: A 60-year-old man with subacute myelopathy due to combined extra-intradural
vascular malformation. Sagittal T2-weighted image shows longitudinally extensive
hyperintense lesion from T5 to conus medullaris.

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Fig. 11: Sequential coronal myelography-MR images show multiple curvilinear signal
voids representing dilated vessels localized on the posterior surface of the cord.

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Fig. 12: Diagnostic Algorithm for non-compressive mielopathy

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Conclusion
Management of a patient with non-compressive acute-subacute myelopathy is a
challenge for neurologists. Radiological findings of spine MRI, including number,
location and extension of cord lesions, are essential for the differential diagnosis
of spinal cord diseases, specially if they are evaluated together with those of
brain MRI. However, CSF analysis is still the reference to establish the definitive
diagnosis.

Personal Information
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