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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2745_Библиотеки_им_академика_М_И_Перельмана
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CIS, clinically isolated syndrome; MS, multiple sclerosis.
When properly applied, the 2001 McDonald criteria showed
high specificity (83%) and sensitivity (83%) for clinically
definite MS at 3 years in patients presenting with a clinically
isolated syndrome (CIS) suggestive of demyelinating disease.
13
In 2002, a retrospective analysis reported that, with MRI and
the McDonald Criteria, 50% of patients with a first clinical
attack would receive a diagnosis of definite MS within a year
compared with only 20% when using the Poser criteria. 16 In
the light of subsequent studies, the 2001 McDonald criteria
were revised in 2005, 2010, and most recently in 2017,
11
further clarifying the role of MRI in the diagnosis of MS.
The first revision to the McDonald criteria was published in
2005. 18 One key difference from the prior iteration was that
DIT could be established on the basis of a gadoliniumenhancing or a new T2 lesion in an MRI scan performed
30 days (rather than 90 d) or more after the baseline scan. In
addition, for the first time, spinal cord lesions were
incorporated in the total lesion count. These criteria
maintained the high specificity of the original 2001 McDonald
criteria 13 and achieved a sensitivity of 77% according to some
studies.
13,21,22
In 2010, new evidence and consensus using the
Swanton/MAGNIMS (Magnetic Resonance Imaging in
Multiple Sclerosis) criteria led to further revision of the
McDonald criteria.
17,23,24
In the 2010 revision, the definition
for DIS was simplified to include one or more T2 lesions in at
least two of four key locations: juxtacortical, periventricular,
infratentorial, and spinal cord. 14 Gadolinium-enhancing
lesions were no longer required for the determination of DIS.
The criteria for DIT were modified to include any new T2 or
gadolinium-enhancing lesions on follow-up scan at any time
after the baseline scan or the simultaneous presence of
asymptomatic enhancing and nonenhancing lesions on the
same scan regardless of timing. 14 The sensitivity and
specificity of the 2010 McDonald criteria reported by different
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studies range from 70% to 80% and 48% to 63%, respectively.
11,22,25
The McDonald criteria were redefined in 2017 (Table 4.3). As
with previous revisions, these newly revised criteria are
expected to speed the diagnostic process with increased
sensitivity while preserving specificity and to reduce the
possibility of misdiagnosis, although this will need to be
evaluated prospectively. The core requirement of the diagnosis
of MS remains the objective demonstration of dissemination
of CNS lesions in both space and time, based on either clinical
findings alone or a combination of clinical and MRI findings.
12
DIS is demonstrated with MRI alone by one or more T2
lesions in at least two of the four MS-typical regions of the
CNS: periventricular, juxtacortical (and now also cortical),
infratentorial, and spinal cord, or by the development of a
further clinical attack implicating a different CNS site. 26 Both
symptomatic and asymptomatic lesions contribute to lesion
count. DIT is demonstrated by the simultaneous presence of
both symptomatic or asymptomatic gadolinium-enhancing and
nonenhancing lesions at any point in time or a new T2 and/or
gadolinium-enhancing lesion(s) on follow-up MRI irrespective
of its timing with reference to a baseline MRI. Positive
findings of oligoclonal bands in the spinal fluid can now
substitute for demonstration of DIT in some settings. 12 Table
4.4 shows the definitions of DIS and DIT according to the
newly revised 2017 McDonald criteria. The sensitivity and
specificity of the complete set of the 2017 McDonald criteria
have not been fully evaluated yet.
Table 4.3
2017 McDonald Criteria for Diagnosis of Multiple Sclerosis (MS)
Clinical Presentation Additional Data Needed for a Diagnosis of
MS
≥2 Attacks and objective clinical
evidence of ≥2 lesions
≥2 Attacks and objective clinical
evidence of 1 lesion with historical
evidence of prior attack involving a
lesion in a different location
None. Dissemination in space (DIS) and
dissemination in time (DIT) criteria have
been met
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Clinical Presentation Additional Data Needed for a Diagnosis of
MS
≥2 Attacks and objective clinical
evidence of 1 lesion
One of these criteria:
DIS: additional clinical attack
implicating different CNS site
DIS: ≥1 symptomatic or
asymptomatic MS-typical T2
lesions in ≥2 areas of the CNS:
periventricular,
cortical/juxtacortical, infratentorial,
or spinal cord
1 Attack and objective clinical
evidence of ≥2 lesions
One of these criteria:
DIT: additional clinical attack
DIT: simultaneous presence of both
enhancing and nonenhancing
symptomatic or asymptomatic MRtypical MRI lesions
DIT: new T2 or enhancing MRI
lesion compared with baseline
lesion scan (without regard to
timing of baseline scan)
CSF-specific oligoclonal bands (not
present in serum)
1 Attack and objective clinical
evidence of 1 lesion
One of these criteria:
DIS: additional clinical attack
implicating different CNS site
DIS: ≥1 symptomatic or
asymptomatic MS-typical T2
lesions in ≥2 areas of the CNS:
periventricular,
cortical/juxtacortical, infratentorial,
or spinal cord
AND one of these criteria:
DIT: additional clinical attack
DIT: simultaneous presence of both
enhancing and nonenhancing
symptomatic or asymptomatic MRtypical MRI lesions
DIT: new T2 or enhancing MRI
lesion compared with baseline
lesion scan (without regard to
timing of baseline scan)
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CNS, central nervous system; CSF, cerebrospinal fluid.
Table 4.4
2017 McDonald Criteria for Demonstration of Dissemination in Space
and Time by MRI
Dissemination in space
≥1 T2-hyperintense lesion(s) in two or more areas of the CNS:
periventricular, cortical or juxtacortical, infratentorial, and spinal cord
Dissemination in time
Simultaneous presence of gadolinium-enhancing and nonenhancing
lesions at any time or by a new T2-hyperintense or gadolinium-enhancing
lesion on follow-up MRI, irrespective of the timing of the baseline MRI
CNS, central nervous system; MRI, magnetic resonance
imaging.
It should be noted that even with the wide utility of MRI, a
diagnosis of MS should follow the exclusion of other possible
etiologies that can mimic MS in clinical presentation and/or
MRI findings. 13 MRI, like other clinical features or laboratory
tests, is one piece of evidence that must be placed in the
appropriate context to arrive at a correct diagnosis.
MRI in Multiple Sclerosis
Based on the chronologic changes to lesion morphology, MS
lesion formation and activity can be divided into two phases:
an acute phase characterized by contrast enhancement of
lesions and a subacute phase characterized by changes in
lesion signal intensity and size on unenhanced T1- and T2weighted images.
2,27
In the acute phase, lesions are typically isointense to the
normal white matter on T1-weighted imaging and therefore
cannot be seen on an unenhanced T1 scan.
1,2
However, the
formation of new MS lesions is nearly always associated with
a focal area of contrast enhancement on T1-weighted scans,
which correlates with BBB disruption in the setting of acute
perivascular inflammation.
8,13
Gadolinium enhancement may
last up to 2 months in acute lesions, although the average
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duration of enhancement is 3 weeks. 2 According to the pattern
of contrast uptake, lesions can be classified as nodular or
ringlike. 1 New contrast-enhanced lesions are usually
associated with a hyperintense lesion in the same location on
T2-weighted images but can also be detected before T2
abnormalities develop. 27 Clinical relapses often occur when a
new lesion involves an eloquent area of the brain or cord.
However, many new lesions occur in noneloquent or clinically
silent brain regions. Because contrast-enhanced T1-weighted
scans can detect disease activity 5 to 10 times more frequently
than the clinical evaluation of relapses, it is generally believed
that a significant number of these lesions can be clinically
silent at any given time.
1,8,14,15,28
The subacute phase of MS lesion morphology and activity can
be subdivided into early and late periods. 3 In the early
subacute period, observed within the initial 10 weeks, the T2hyperintense lesion is a combination of an influx of
inflammatory cells resulting in demyelination, axonal
transection, and edema. During this time, there is also
cessation of lesion contrast enhancement on postgadolinium
T1-weighted imaging. 1 In the late subacute period, 3 to
5 months after initial inflammation, the T2-hyperintense lesion
often decreases in size, because of not only decreased
vasogenic edema but also a combination of degenerative and
regenerative processes (gliosis and remyelination),
respectively. Over the initial 6-month period, less than 40% of
lesions become persistently hypointense on T1-weighted
imaging, presumably secondary to permanent demyelination
and severe axonal loss, and are referred to as “T1 black holes.”
1
The accumulation of T1 black holes has been shown to
correlate with disease progression and disability.
5,23
Although
not uncommon in the brain, T1 black holes are rarely seen in
the spinal cord, although, in part, this is because imaging of
the spinal cord is more challenging because of the small crosssectional size, motion artifacts, and low lesion contrast.
2
Although MS lesions can occur anywhere in the CNS, above
the tentorium cerebri, they have a predilection for
periventricular white matter and tend to have an ovoid
configuration with the major axes perpendicular to the
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ventricular surface (Dawson fingers) 1 (Figure 4.4). During
their initial stage, the lesions are typically thin and appear to
be linear, which is likely associated with the inflammatory
changes around the long axis of the medullary vein that create
the dilated perivenular space.
1,29
In addition to the
periventricular regions, the corpus callosum, brainstem, Ufibers, optic nerves, and subcortical region are areas where MS
lesions are frequently located. 30 In addition, lesions occur in
the gray matter. Gray matter lesions are more easily detected
on FLAIR imaging and other advanced sequencing techniques,
including double inversion recovery (DIR) 31 and phase-
sensitive inversion recovery (PSIR) (Figure 4.5).
32-34
FIGURE 4.4 Dawson finger. Sagittal FLAIR (fluid attenuated
inversion recovery) sequence showing “Dawson finger”
appearance of multiple sclerosis (MS) lesions.
FLAIR and T2-weighted sequencing are the mainstays in the
diagnostic workup of patients with MS (Figure 4.6). 35 The T2
and FLAIR lesion loads reflect the accumulation of gross
tissue changes. 35 Although newly formed or enlarging T2
lesions might indicate new areas of MS-related tissue damage,
T2 hyperintensities are nonspecific with respect to the actual
pathological changes within the lesions and can represent
areas of inflammation, edema, abnormal myelination, gliosis,
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or axonal loss.
4,15,36,37
Table 4.5 shows the MRI characteristics
of brain lesions typical of MS.
FIGURE 4.5 (A) Axial FLAIR (fluid attenuated inversion
recovery) sequence showing “typical” multiple sclerosis (MS)
lesions compared with (B) axial FLAIR sequence showing
large amorphous tumefactive MS lesion. Demyelinating lesion
often show early involvement of cortico-cortical fibers (U-
fibers) as seen in this lesion (long arrows shown in both
panels a and b).
Table 4.5
MRI Characteristics of Brain Lesions Typical of MS
Lesion size: usually >5 mm
Asymmetric
Nonconfluent
Location: cortical/juxtacortical, periventricular (Dawson fingers),
infratentorial, spinal cord, corpus callosum
Gadolinium-enhancing lesions (incomplete rim enhancement)
Central vein sign
New lesions on repeat imaging are common
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MRI, magnetic resonance imaging; MS, multiple sclerosis.
The majority of conventional MRI scanners use different
magnet strengths, typically 1.5 or 3.0 T. In general, an increase
in magnet strength is expected to lead to an increase in the
number of identifiable MS lesions. 38 Of note, open-
configuration MRI scanners, which may be used when patients
have difficulty tolerating a closed MRI machine, are usually
less than 1.5 T, and the quality of images they provide is often
suboptimal for detecting MS activity. 39 Additionally, there
may be variability in scanning protocols and voxel size
(resolution). Newer protocols use a “3D” image representing
an isotropic voxel with dimensions of 1 × 1 × 1 mm cubed. By
contrast, conventional “2D” images utilize a nonisotropic
voxel with variable dimensions, commonly 2 × 2 × 5 mm.
Because facilities may have different MRI scanners with
different magnet strengths and imaging protocols, patients
should be encouraged to use the same MRI facility for followup imaging. When possible, the same scanner should be used
for a more accurate comparison of new and old MRI scans.
MRI of the Spinal Cord
The detection of spinal cord lesions or other intramedullary
abnormalities is accomplished by MRI of the cervical and
thoracic cord that includes sagittal and axial images with and
without gadolinium. 40 Because of the higher density of
eloquent axons in the cord, lesions in this region are more
likely to be symptomatic. Clinically, spinal cord demyelination
can manifest as motor weakness with accompanying
ambulatory difficulties, sensory loss, neuropathic pain,
paresthesias/dysesthesias, poor coordination, spasticity, and
bladder/bowel dysfunction. 41 The length of the spinal cord
lesion or lesions, the distribution of signal abnormality seen on
axial plane imaging, and the pattern of gadolinium
enhancement are all important clues that can help narrow the
differential diagnosis.
42
In MS, spinal cord lesions are typically one vertebral segment
or less in craniocaudal length and rarely longitudinally
extensive (i.e., three or more vertebral segments). 43 They are
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characteristically located peripherally along the cord within
the dorsal or lateral columns and are mostly focal and
asymmetric. 40 Detection of longitudinally extensive lesions in
the craniocaudal plane or large central lesions involving >50%
of the cord in the axial plane on MRI in patients with myelitis
strongly suggests neuromyelitis optica spectrum disorder
(NMOSD), with diagnostic specificity surpassed only by the
presence of AQP4-IgG. 43 However, an initially longitudinally
extensive spinal cord lesion can evolve over time and appear
chronically as several small short-segment lesions.
29
Therefore, spinal cord MRI interpretation requires analysis in
the clinical context and knowledge of the timing of the scan. It
should also be noted that, although MS is rarely associated
with an acute longitudinally extensive lesions in adults, the
lesions may occur in up to 10% to 15% of patients with
childhood-onset MS. 29 As with brain lesions, the detection of
lesion enhancement after gadolinium administration implies
BBB injury and the enhancement pattern can be informative.
44
Lesion enhancement is highly variable and can show a ringlike
distribution of enhancement at the lesion periphery. 29 Table
4.6 shows the MRI characteristics of spinal cord lesions
typical of MS.
Table 4.6
MRI Characteristics of Spinal Cord Lesions Typical of MS
Little to no cord swelling
Size: at least 3 mm and less than two vertebral segments in length
Focal (i.e., clearly delineated and circumscribed on T2-weighted
sequences)
Most commonly involve the cervical region compared with the rest of the
spine
On sagittal view, lesions rarely exceed two vertebral segments in length
On cross-section, they typically occupy the lateral and posterior white
matter columns and seldom occupy more than half of the cross-sectional
area
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Enhancing spinal cord lesions are seen less frequently than in the brain
but are commonly associated with new clinical symptoms when present
MRI, magnetic resonance imaging; MS, multiple sclerosis.
Conventional MRI seems to lack sensitivity and specificity to
MS-associated pathological changes in the spine. 43 Even
though spinal cord lesions can be detected in up to 90% of
patients with MS, only weak to moderate correlations have
been observed between spinal cord abnormalities and clinical
status. 45 This phenomenon has previously been described as
the “clinicoradiological paradox.” 41 A number of factors can
contribute to the lower-than-expected correlation between
spinal cord lesion load and clinical disability. Visible lesion
contrast is decreased because the spinal cord represents a small
fraction of the total imaged spinal volume that includes bone
and CSF. In addition, the spine is a mobile structure and
artifacts related to breathing movements and intrinsic motion
caused by cardiac and respiratory cycles can complicate image
acquisition.
43
Sagittal views have been shown to
underestimate the number of lesions in the spinal cord.
Therefore, evaluation of both sagittal and axial images is
recommended to improve the accuracy of identification of
spinal cord lesions, as well as to reduce the risk of reporting
equivocal abnormalities. 41 Lastly, spinal cord lesions, however
small, can substantially contribute to disability.
27
In addition to having diagnostic value, MRI evaluation of MSassociated spinal cord lesions can provide prognostic
information. Reduced cross-sectional area of the upper
cervical cord in patients with MS is thought to indicate
disease-related atrophy. 43 Spinal cord atrophy in MS has
shown a robust correlation with physical disability. 45 In a
prospective study of patients with primary progressive MS,
increased spinal cord atrophy over the first 2 years of the
disease predicted worse outcomes at 5-year follow-up. 41 In
this setting, spinal cord atrophy has been postulated as a
potential outcome measure in clinical trials of putative
neuroprotective therapies.
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