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lack of specificity compared with MRI imaging and CSF
testing.
16
Conclusion
Confirming a diagnosis of MS can be a difficult process
because of the significant variability in disease presentation
and the extensive workup needed to rule out other common
neurologic conditions. Because of this, it is commonly
overlooked by many general practitioners. However, MS
continues to be the most common neurologic disorder
affecting young adults, numbering nearly 1 million people in
the United States, with prevalence continuing to rise. Often
times, workup and diagnosis are performed by a neurologist
after significant functional decline has already occurred. It is
essential for nonneurologists to keep MS as a differential
diagnosis when evaluating patients with intermittent
neurologic symptoms, in an effort to facilitate earlier diagnosis
and potentially earlier treatment. Understanding the different
disease phenotypes, most common signs and symptoms, and
effective preliminary workup is a crucial step for not only
providing high-quality patient care but also identifying MS
and minimizing functional decline.
References
National MS Society. MS Prevalence. https://www.nationalmssociety.org/About-
the-Society/MS-Prevalence.
Lublin FD, Reingold SC, Cohen JA, et al. Defining the clinical course of multiple
sclerosis. Neurology. 2014;83:1-9. doi:10.1212/WNL.0000000000000560.
Picone MA, Vincent H, Blitz-Shabbir K, West CY, Akinsanya J. Lower extremity
signs and symptoms of multiple sclerosis. In: Positano RG , Borer J ,
DiGiovanni C , Trepal M , eds. Systemic Disease Manifestation in the Foot,
Ankle, and Lower Extremity. Wolters Kluwer; 2017. vol. 3:284-300.
Thompson AJ, Banwell BL, Barkhof F, et al. Diagnosis of multiple sclerosis: 2017
revisions of the McDonald criteria. Lancet Neurol. 2018;17(2):162-173.
Parmenter BA, Weinstock-Guttman B, Garg N, Munschauer F, Benedict RHB.
Screening for cognitive impairment in multiple sclerosis using the symbol digit
modalities test. Mult Scler J. 2007;13(1):52-57.
doi:10.1177/1352458506070750.
Smith A. Symbol Digits Modalities Test: Manual. Los Angeles: Western
Psychological Services; 1973. https://www.communicate-
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ed.org.uk/assets/downloads/SDMT_Formula_Chart_Communicate-ed_2.pdf.
Accessed on October 30, 2018.
Thömke F, Lensch E, Ringel K, Hopf HC. Isolated cranial nerve palsies in multiple
sclerosis. J Neurol Neurosurg Psychiatry. 1997;63:682-685.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2169805/pdf/v063p00682.pdf.
Frohman EM, Fujimoto JG, Frohman TC, Calabresi PA, Cutter G, Balcer LJ.
Optical coherence tomography: a window into the mechanisms of MS. Nat Clin
Pract Neurol. 2008;4(12):664-675. doi:10.1038/ncpneuro0950.
Balcer LJ, Miller DH, Reingold SC, Cohen JA. Vision and vision-related outcome
measures in multiple sclerosis. Brain. 2015;138(1):11-27.
doi:10.1093/brain/awu335.
Khare S, Seth D. Lhermitte’s sign: the current status. Ann Indian Acad Neurol.
2015;18(2):154-156. doi:10.4103/0972-2327.150622.
Gijbels D, Eijnde BO, Feys P. Comparison of the 2- and 6-minute walk test in
multiple sclerosis. Mult Scler. 2011;17(10):1269-1272.
doi:10.1177/1352458511408475.
Filippi M, Rocca MA, Ciccarelli O, et al. MRI criteria for the diagnosis of multiple
sclerosis: MAGNIMS consensus guidelines. Lancet Neurol. 2016;15(3):292-
303. doi:10.1016/S1474-4422(15)00393-2.
Traboulsee A, Simon JH, Stone L, et al. Revised recommendations of the
consortium of MS centers task force for a standardized MRI protocol and
clinical guidelines for the diagnosis and follow-up of multiple sclerosis. AJNR
Am J Neuroradiol. 2016;37:394-401. doi:10.3174/ajnr.A4539.
Stangle M, Fredrikson SM, Meinl E, Petzold A, Stuve O, Tumani H. The utility of
cerebrospinal fluid analysis in patients with multiple sclerosis. Nat Rev Neurol.
2013;9:267-276.
Walsh P, Kane N, Butler S. The clinical role of evoked potentials. J Neurol
Neurosurg Psychiatry. 2005;76:16-22. doi:10.1136/jnnp.2005.068130.
National Multiple Sclerosis Center. Evoked Potentials.
https://www.nationalmssociety.org/Symptoms-Diagnosis/DiagnosingTools/Evoked-Potentials. Accessed on November 4, 2018.
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C H A P T E R 4
Magnetic Resonance Imaging
in Multiple Sclerosis
Carlos A. Pérez John A. Lincoln
Introduction
Since its clinical introduction in the 1980s, magnetic
resonance imaging (MRI) has become an essential tool in
supporting the diagnosis, longitudinal monitoring, and
evaluation of therapeutic response in multiple sclerosis (MS).
1
Although the diagnosis of MS is mostly based on clinical
findings, MRI has become an integral part of the overall
diagnostic process because of its ability to sensitively and
noninvasively demonstrate the spatial and temporal
dissemination of demyelinating plaques in the brain and spinal
cord.
2,3
In some cases, MRI can be useful for ruling out
alternative neurological diseases. 4 In this chapter, we discuss
the underlying principles and clinical utility of MRI with the
aim of helping clinicians understand how to better apply this
valuable tool in the assessment of MS and related conditions.
How MRI Works
MRI provides exquisite detail of the brain and the spinal cord
in the axial, sagittal, and coronal planes. 5 Unlike computed
tomography (CT) scans, it does not require the use of ionizing
radiation. Instead, MRI uses a powerful magnetic field that
aligns protons (hydrogen atoms) within water molecules that
are normally randomly oriented in the same or opposite
direction as the external field. 6 The alignment is briefly
disrupted by the introduction of an external radiofrequency
(RF) pulse, and the excited hydrogen atoms emit resonance
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signals as they return to their previously aligned (equilibrium)
state that are then measured by a receiving coil. 3 The
frequency information contained in the signal from each
location in the imaged plane is then converted to
corresponding intensity levels that are displayed as shades of
gray in a matrix arrangement of pixels. 1 By varying the
sequence of the RF pulses applied and collected, different
types of images are created. 7 The contrast between different
tissues is determined by the rate at which excited atoms return
to their equilibrium state. The amount of time between
successive RF pulses is referred to as repetition time, and the
time between the delivery of the RF pulse and the receipt of
the echo signal is referred to as the time to echo.
7
T1-Weighted Sequencing
The longitudinal relaxation time, or T1, is the time constant
that determines the rate at which the excited protons realign
with the external magnetic field. 3 The more quickly the
protons realign, the greater (and brighter) the signal. The rate
at which this occurs is determined by the T1 properties of a
tissue. Fat quickly realigns its longitudinal magnetization with
the magnetic field, short T1, and it therefore appears bright
(i.e., hyperintense) on a T1-weighted image. 8 Conversely,
water has a much slower longitudinal magnetization
realignment after an RF pulse, long T1, and therefore it
appears dark (i.e., hypointense) on a T1-weighted image.
8
Therefore, tissues with high fat content (such as white matter)
will be bright, and compartments filled with water (such as
cerebrospinal fluid [CSF]) will be dark on T1-weighted scans.
In this way, T1-weighted images are good for demonstrating
anatomy (Figure 4.1).
8
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FIGURE 4.1 Appearance of tissue on T1, T2, and FLAIR
(fluid attenuated inversion recovery) sequences. (A) T1
precontrast sequence showing the caudate nucleus (long
arrow) and putamen (arrow head), (B) T2 sequence showing
multiple sclerosis (MS) lesions (short arrow), (C) FLAIR
sequence showing the same MS lesions (short arrow).
T1-weighted imaging can also be performed after the
administration of gadolinium. Gadolinium is a paramagnetic
contrast enhancement agent that facilitates the relaxation of
hydrogen atoms (i.e., shortens T1). 1 It preferentially shortens
T1 values in tissues where it accumulates, rendering them
bright on T1-weighted images. Gadolinium-enhanced images
are especially useful in looking at pathological tissues such as
tumors, and areas of inflammation or infection, because these
will demonstrate accumulation of contrast due to disruption of
the blood-brain barrier (BBB), which will make them appear
brighter than the surrounding tissue.
8
T2-Weighted Sequencing
The transverse relaxation time, or T2, is the time constant that
determines the rate at which the excited protons lose resonance
perpendicular to the main field and become out of phase with
each other after being excited by an RF pulse (i.e., dephasing).
6
Dephasing occurs because of random and time-dependent
field variations induced by spins of neighboring atoms,
because not all spins have exactly the same precession
frequency. 6 The precession frequency of an atom refers to the
rate of change in orientation of the rotational axis of protons
due to an applied external magnetic field. 7 The addition of an
external RF pulse results in augmentation of the angle of
precession of the protons, and in doing so, it converts some of
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the magnetization that exists along the axis of the dominant
magnetic field (longitudinal magnetization) into measurable
magnetization along a perpendicular axis (transverse
magnetization).
3,7
The rate at which this dephasing occurs is
determined by the T2 properties of a tissue. The slower the
dephasing, the greater (and brighter) the T2 signal. 3 On a T2-
weighted scan, compartments filled with water (such as CSF)
appear bright because of protons in phase with each other. To
illustrate, as water molecules move around in all directions,
their local magnetic fields fluctuate, averaging each other out.
Without a significant net difference in internal magnetic fields,
the protons stay in step with the applied external field for a
longer period of time. Conversely, tissues with high fat content
(such as white matter) appear dark. T2-weighted scans are
good for demonstrating pathology because most, but not all,
brain lesions tend to develop edema and are associated with an
increase in water content, which will make them appear bright.
8
In general, T1- and T2-weighted images can be differentiated
by looking at the CSF: CSF appears dark on T1-weighted
imaging and bright on T2-weighted imaging 3 (Table 4.1).
Table 4.1
T1- and T2-Weighted MRI Signal Intensities
T1 T2
Hyperintense
(bright)
Fat, cholesterol,
intravascular blood flow,
protein-rich fluid,
gadolinium, hemorrhage
Water, CSF, vasogenic edema,
intravascular slow flow or
thrombus, infarction,
inflammation, infection
Hypointense
(dark)
Water/CSF, air, bone,
hemosiderin, edema,
infection, gliosis,
intravascular flow void
Bone, air, fat, protein-rich fluid,
increased cellularity, intravascular
flow void
Data from McMahon KL, Cowin G, Galloway G. Magnetic resonance imaging:
The underlying principles. J Orthop Sport Phys Ther. 2011;41:806-819.
doi:10.2519/jospt.2011.3576. CSF, cerebrospinal fluid; MRI, magnetic resonance
imaging.
FLAIR Sequencing
A third commonly used conventional sequence is the fluid
attenuated inversion recovery (FLAIR). The FLAIR sequence
is similar to a T2-weighted image, but the high signal of
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normal CSF fluid is attenuated and made dark. 5 The CSF
signal is nullified by using a long inversion recovery sequence
with a long inversion time (TI). A long inversion time
suppresses the high CSF signal and improves the visualization
of periventricular lesions. 9 As with the T2-weighted image,
this sequence is very sensitive to pathology and makes the
differentiation between CSF and brain parenchymal
abnormalities much easier to distinguish. 9 FLAIR is
particularly useful in the detection of subtle changes at the
periphery of the hemispheres, near sulcal CSF, and in the
periventricular region close to CSF (such as those typical of
MS) (Figures 4.2A and 4.2B) where the high intensity of the
CSF signal itself may attenuate visible contrast when
compared with the high intensity of nearby lesions.
5,10
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FIGURE 4.2 A. Juxtacortical multiple sclerosis (MS) lesions
are more readily identified on FLAIR (fluid attenuated
inversion recovery) (a) compared with T2 (b) sequences (long
arrows). B. As with the prior figure, many periventricular MS
lesions are more readily identified on FLAIR (a) compared
with T2 (b) sequences (long arrows).
Diagnostic Role of MRI in Multiple
Sclerosis
Although there is no single diagnostic test for MS, MRI is
routinely employed to evaluate a patient clinically suspected
with MS. The diagnosis of MS is based on the principle of
dissemination in time (DIT) and dissemination in space (DIS)
of central nervous system (CNS) demyelination.
11-13
Conventional T1- and T2-weighted, as well as contrast-
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enhanced T1-weighted and FLAIR, images offer the most
sensitive way of detecting lesions and are the current standard
assessment methods to confirm the clinical diagnosis of MS.
9
The high conspicuity of MS-related abnormalities seen on
MRI provide the best view of tissue injury, lesion activity, and
disease accumulation compared with all other imaging
modalities, including CT.
1
Although the diagnosis of MS can be straightforward in
patients with a typical clinical history, when the symptoms are
nonspecific or atypical of MS, MRI is the most commonly
performed investigation that can support a clinical diagnosis.
14,15
For a considerable proportion of patients, MRI can replace
some of the clinical criteria by revealing brain and spinal cord
changes that are typical of MS 4 (Figure 4.3). The evolution of
the diagnostic criteria for MS, from solely clinically based to
the currently used McDonald criteria, reflects the increasing
importance of MRI findings in establishing a timely and
accurate diagnosis.
16
FIGURE 4.3 Characteristic multiple sclerosis (MS) lesions.
(A) Axial FLAIR (fluid attenuated inversion recovery)
sequence showing MS lesions that are perpendicular to the
callosal plane with discrete lesion borders and most
measuring more than 3 mm in diameter. (B) Sagittal T2
sequence showing discrete MS lesion at C5 (long arrow).
Diagnostic Criteria for Multiple Sclerosis
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The fundamental concept of DIT and DIS was first introduced
by Schumacher et al. in 1965 as a first attempt to standardize
diagnostic criteria for MS. 16 Initially, these criteria were based
on clinical features alone, as well as the elimination of
alternative diagnoses with similar presentations. In 1983, the
Poser criteria were proposed, which incorporated paraclinical
tests (evoked potentials, neuroimaging, and CSF analysis) to
supplement clinical evidence for the diagnosis of MS in
situations where clinical criteria were not met.
13
With the advent of MRI, the need for early diagnosis and
treatment prompted revision of the widely used Poser criteria.
17
In 2001, an international panel headed by Ian McDonald
published new guidelines for the diagnosis of MS, commonly
known as the 2001 McDonald criteria.
13,14,18
For the first time,
these guidelines proposed the use of MRI findings as
supporting evidence for lesion dissemination in time and space
with the potential to enable an earlier diagnosis. 19 The concept
of DIS was based on the Barkhof criteria 20 (Table 4.2), which
were originally developed to predict conversion to clinically
definite MS in patients presenting with an isolated first clinical
symptom. 20 They require at least 3 of 4 of: (1) one
gadolinium-enhancing lesion or nine T2-hyperintense lesions
if gadolinium-enhancing lesions are not present; (2) at least
one infratentorial lesion; (3) at least one juxtacortical lesion
(i.e., involving the subcortical U-fibers); (4) at least three
periventricular lesions. DIT was determined by a gadoliniumenhancing or a new T2 lesion detected on repeat MRI
performed 3 months (90 d) or more after the baseline scan.
19
Table 4.2
Barkhof Criteria for Prediction of CIS Conversion to Clinically Definite
MS
≥1 Gadolinium-enhancing lesion or ≥9 T2-hyperintense lesions
≥1 Infratentorial lesion
≥1 Juxtacortical lesion
≥3 Periventricular lesions
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