Keywords
magnetic resonance neurography - MRN - peripheral nerve MRI - neuropathy - structured
interpretation
Magnetic resonance neurography (MRN), or MR neurography, is a dedicated magnetic resonance
imaging (MRI) technique that uses state-of-the-art pulse sequences and imaging protocols
to visualize the peripheral nerves. First introduced by Filler et al,[1] MRN techniques have considerably evolved over the last decade with the introduction
of three-dimensional (3D) imaging pulse sequences and improvement in diffusion MR
techniques.[2]
[3]
Peripheral nerves are traditionally evaluated using a combination of clinical findings
and electrodiagnostic studies such as electromyography (EMG) and nerve conduction
studies (NCS). Although these techniques can confirm the presence of neuropathy and
approximate the site of nerve pathology, they are operator and subject dependent,
minimally invasive, and uncomfortable. They also do not define the structural cause
of neuropathy or precisely localize the site of the neuropathy.[4]
[5] In addition, electrodiagnostic tests can be normal up to 14 to 21 days after mild
nerve injury.[6]
[7]
[8]
Ultrasound (US) is also used for the diagnosis of common nerve entrapment syndromes
and neuropathies as well as for guiding treatment intervention.[9]
[10]
[11] US is operator dependent and unable to show the subtle changes in neural composition
seen by MRN, especially in mild neuropathy. US is also limited in the assessment of
deeper anatomical locations and postoperative cases due to poor contrast resolution
when echogenic perineural fat is obliterated. It also does not readily show changes
in muscle composition induced by acute or subacute denervation.[12]
The small caliber of peripheral nerves as well as the presence of adjacent vascular
structures of similar intensity limits the assessment of peripheral nerves if routine
MR imaging is used. State-of-the-art advances in MR technology including dedicated
multichannel radiofrequency surface coils have made it feasible to obtain high-resolution,
high-contrast MRN imaging to delineate the small peripheral nerves, their abnormalities,
and related features.
MRN was shown to be a useful adjunct to clinical electrodiagnostic (EMG/NCS) assessment.[13]
[14] In addition, it can allow direct visualization of a neuropathy, more precise anatomical
localization of the nerve abnormality and its cause ([Fig. 1]), grading of the nerve injury, and depiction of muscle denervation. Consequently,
MRN is now considered probably the best way to image peripheral neuropathy and is
becoming more widely used in nonspecialized centers.[15]
Fig. 1 A 60-year-old man with a motor vehicle accident some years previously presented with
symptoms of right C6 neuropathy. (a) Axial T2 3D turbo spin-echo image shows moderate to severe right neural foraminal
stenosis at the C6–C7 level. (b) Small field-of-view coronal 3D 18-mm slab maximum intensity projection (MIP) short
tau inversion recovery (STIR) image depicts asymmetric thickening of right C6 preganglionic
and postganglionic segments (arrow). (c) An unexpected mass (thin arrow) was found at the right lung apex on large field-of-view
coronal MIP STIR imaging. There is traction of the right lower brachial plexus nerve
roots by desmoplastic reaction of the apical lung mass. The nerves in the axillary
pouch are bright and thickened (thick arrow). (d) Right sagittal STIR image demonstrates a thickened and bright C6 nerve root, normal
appearance of the C7 and C8 nerve roots, and bright T1 nerve root due to desmoplastic
reaction by the right lung apical mass. The final diagnosis was Pancoast tumor invading
the inferior brachial plexus.
Nevertheless, introducing MRN imaging into an MR clinical practice can be challenging.
Education of patients and referring clinicians is essential in terms of expectations.
Acute nerve injuries as seen commonly in trauma centers will have a different imaging
approach than chronic neuropathies as seen more commonly in rehabilitation centers
and pain control clinics.[15]
MRN should be approached as a team task for both radiologists and clinicians because
there is learning curve on both sides. Radiologists need to know clinicians' expectations
of imaging, terminology, clinical pathologies, and operative approaches. Clinicians
should be aware of the clinical indications for MRN, as well as the limitations and
pitfalls of the technique. Multidisciplinary conferences or case discussions are beneficial
in this regard and can potentially prevent unnecessary imaging and miscommunication.
This review focuses on the 10 practical tips considered most useful for radiologists
wishing to get started with MRN, focusing on the technical challenges, image acquisition,
the common interpretation pearls, and writing a clinically relevant report.
Tip 1: Acquire a Good Knowledge of Neuromuscular Anatomy
Tip 1: Acquire a Good Knowledge of Neuromuscular Anatomy
The nervous system encompasses the central nervous system (CNS), made up of the brain,
spinal cord, and retina, and the peripheral nervous system (PNS). The PNS comprises
all other neural structures including nerves, ganglia, receptors, and motor nerve
endings. All PNS structures are crucial in transmitting to and from the CNS. Nerves
are the main focus of PNS imaging due to their length, function, and predisposition
to pathologic entities.[12]
A peripheral nerve has a unique structure that enables it to conduct nerve stimuli.
The main component is the nerve axon, an elongated extension of the nerve body specialized
for electrical impulse conduction. The presence of supporting Schwann cells that cover
the axons differentiate nerves into myelinated or unmyelinated fibers. The myelinated
nature of a nerve fiber determines the nerve conduction velocity. Myelinated and unmyelinated
nerve fibers lie in a connective tissue called the endoneurium, comprising a collagen
matrix, fibroblasts, and fine blood capillaries. Multiple nerve fibers and their surrounding
endoneurium create nerve fascicles encased by a concentric supporting cell layer,
called the perineurium. Multiple nerve fascicles (ranging from 1 to 3 in small peripheral
sensory nerves to 250 in large more centrally located nerves such as the sciatic nerve)
are grouped by a dense connective tissue, the epineurium. The epineurium has outer
and inner layers. The outer epineurium is made up of a denser connective tissue; the
inner epineurium contains adipose tissue and blood vessels called vasa nervorum.[16]
[17] Intraneural fat and vessels become more prominent with aging.[8] In addition, asymptomatic muscle atrophy and fatty infiltration are seen with aging,
not to be confused with chronic denervation.[18] Nerves can be bifid and can demonstrate an intramuscular course as a normal variant.[19]
From a functional standpoint, peripheral nerves are divided into sensory, motor, and
mixed nerves. There is usually a predictable internal topographic distribution of
nerve fascicles within mixed peripheral nerves. For instance, the ulnar nerve at the
elbow contains sensory, motor, and cutaneous fascicles, distributed from its lateral
to medial side.[20] Knowledge of peripheral nerve locations, the common sites of nerve entrapment, common
normal variants, and aberrant nerve courses will help the radiologist avoid misinterpretation.
Radiologists should stay abreast with new knowledge from scientific journal articles
and online teaching aids, especially early on after implementation of a clinical MRN
practice. Use of anatomy atlases in similar planes to MRN imaging increases the reader's
ability to find abnormalities as well as normal variants, such as atypical nerve courses.
Tip 2: Understand the Pathophysiology and Classification of Neuropathies
Tip 2: Understand the Pathophysiology and Classification of Neuropathies
Nerve lesions may be divided into traumatic, inflammatory, infectious, hereditary,
radiation-induced, neoplastic, and neoplastic-like entities.[21] Following nerve injury, the axon and the supporting Schwann cells begin to disintegrate
within a few hours. This process, called Wallerian degeneration, starts immediately
distal to the site of injury and extends distally. Wallerian degeneration is due to
the interruption of axoplasmic flow that delivers substances essential to nerve survival.
There are different classifications for peripheral nerve injuries. One of the most
frequently used grading systems, which shows moderate to good correlation with MRN
findings,[22] is the Seddon and Sunderland classification, introduced by Seddon[23] in 1943 and modified by Sunderland[24] in 1951 ([Table 1]).
Table 1
Classification of peripheral neuropathy with clinical, electrodiagnostic, MRN findings,
and prognosis
|
Sunderland
|
Seddon
|
Myelin
|
Axon
|
Endo
|
Peri
|
Epi
|
Electrodiagnostic tests
|
Tinel's sign
|
Recovery
|
MRN findings
|
|
EMG
|
CMAP
|
SNAP
|
|
I
|
Neuropraxia
|
−
|
+
|
+
|
+
|
+
|
Nl, IP
|
Nl or CB
|
Nl
|
−
|
Complete (2 mo)
|
Nerve T2 SI
Muscle Nl
|
|
II
|
Axonotmesis
|
−
|
−
|
+
|
+
|
+
|
SA, IP
|
Amp
|
Amp
|
+
|
Complete (4 mo)
|
Nerve diffusely enlarged + T2 SI
Muscle denervation changes
|
|
III
|
−
|
−
|
−
|
−
|
+
|
+
|
SA, IP
|
Amp
|
Amp
|
+
|
Variable (12 mo)
|
Nerve T2 SI
Fascicular enlargement/effacement
Muscle denervation changes
|
|
IV
|
−
|
−
|
−
|
−
|
−
|
+
|
SA, IP
|
Amp
|
Amp
|
+ not beyond
|
Needs surgery
|
Nerve focal enlargement + heterogeneous T2 SI
Fascicle disruption
Muscle denervation changes
|
|
V
|
Neurotmesis
|
−
|
−
|
−
|
−
|
−
|
No MUP
|
Absent
|
Absent
|
+ not beyond
|
Needs surgery
|
Complete nerve discontinuity
+/− Hemorrhage/fibrosis in nerve gap
Muscle denervation changes
|
|
VI[a]
|
−
|
Mixed pattern depends on degree of damage
|
Depends on the degree of damage
|
Abbreviations: Amp, amplitude; CB, conduction block; CMAP, compound motor action potential;
EMG, electromyography; Endo, endoneurium; Epi, epineurium; IP, interference pattern;
MUP, motor unit potential; Peri, perineurium; SA, spontaneous activity; SNAP, sensory
nerve action potential; T2 SI, T2 signal intensity.
a Mackinnon and Dellon pattern of injury.
-
Sunderland class I (neuropraxia according to Seddon) usually follows a moderate compression
injury leading to segmental demyelination and focal conduction block although otherwise no axonal injury. Recovery is full
and seen within a few days to 2 months of injury. There is no Tinel's sign; EMG is
normal but interference potential can be decreased. On MRI, there are no signs of
Wallerian degeneration including muscle denervation, although the affected nerve demonstrates
mild increased T2 signal intensity (SI) on MRN.
-
Sunderland class II (axonotmesis according to Seddon) usually follows a crush or severe
compression injury causing segmental demyelination and axonal injury, although the endoneurium, perineurium, and epineurium are preserved. Recovery is
complete but slower than with Sunderland class I, taking 2 to 4 months. There is complete
loss of nerve function distally leading to Wallerian degeneration, a positive Tinel's
sign, an abnormal EMG, and muscle denervation. On MRI, there is diffuse nerve enlargement
(< 50% increase in nerve thickness) with increased nerve T2 SI and appreciable muscle
denervation changes.
-
Sunderland class III usually follows a severe crush or transection injury creating
segmental demyelination, axonal injury, and disruption of the endoneurium with preservation
of the perineurium and epineurium. Recovery is variable and could be complete but takes time, with a typical pace of
1 mm/day for nerve regeneration. Nerve function, EMG, and Tinel's sign are the same
as for Sunderland class II. On MRN, diffuse fascicular enlargement/effacement within
the nerve due to edema is seen, as well as muscle denervation changes. There is > 50%
increase in nerve thickness as well as more fascicular edema/atrophy compared with
Sunderland class II.
-
Sunderland class IV usually follows a transection injury resulting in segmental demyelination, axonal injury, and disruption of the endoneurium and perineurium
although with preservation of the epineurium. Therefore, no visible nerve discontinuity is seen. Recovery is unlikely without surgical
intervention such as direct suturing or nerve grafting following neuroma resection.
Nerve function and EMG are the same as Sunderland class II/III. Tinel's sign is present
but not beyond the level of the injury. MRN shows focal nerve enlargement with heterogeneous
T2 SI and fascicular disruption as well as muscle denervation changes. Hemorrhage
and fibrous tissue entangle the regenerating neural islands inhibiting distal axonal
growth and leading to formation of a neuroma-in-continuity (NIC).
-
Sunderland class V (neurotmesis according to Seddon) usually follows a transection injury with complete disruption of all the nerve tissues including the
axons, endoneurium, perineurium, and epineurium. There is complete nerve discontinuity with a gap that may be filled by hemorrhage
or fibrous tissue. There will be no recovery without surgical intervention. EMG fails
to show a motor unit potential. Tinel's sign is positive but not beyond the level
of injury as in Sunderland class IV. MRN depicts complete nerve discontinuity with
a fluid gap or possible fibrosis/hemorrhage filling the gap and muscle denervation.
An end-bulb neuroma might be present.
Later on, Mackinnon and Dellon[25] described another class of nerve injury pattern (outside-in model) as an addition
to the Seddon and Sunderland classification (inside-out model). This type of injury,
often considered class VI, is a mixed injury involving variable tissue injury across
the transverse section of the nerve. Clinical, electrodiagnostic, and MRN findings
as well as recovery rate are variable depending on the tissues most damaged. This
injury usually results from direct nerve injury due to penetrating trauma or fracture/dislocation.
Based on clinical and electrodiagnostic tests, it is:
-
Difficult to detect mild nerve damage (neuropraxia).
-
Electrical responses can be normal despite complete nerve transection up to a week
after insult.[26]
-
Electrodiagnostic tests do not clearly differentiate between higher grades of nerve
injury (class II–IV).
Understanding the degree of neural tissue injury is crucial to estimating recovery
potential and need for surgery. For instance, class II nerve injury is usually treated
medically, whereas class IV or V nerve injury needs surgical intervention. Early diagnosis
is important because a delay leads to muscle atrophy, slow rehabilitation, and poor
functional recovery.[27] Currently, serial electrodiagnostic studies with or without surgical explorations
are used to determine the severity of nerve injury. MRN helps minimize the time between
injury, assessment, and treatment.
Familiarity with common disease entities helps derive the correct MRN diagnosis. These
include predominant motor dysfunction neuropathies, such as multifocal motor neuropathy,
amyotrophic lateral sclerosis, polio, and perineurioma; predominant sensory dysfunction
neuropathies such as Sjögren's syndrome and sensory-type chronic demyelinating polyneuropathy;
mixed motor/sensory dysfunction neuropathies such as radiculopathy and chronic demyelinating
polyneuropathy; toxic/dying back neuropathies, such as Charcot-Marie-Tooth (CMT) disease
and diabetes mellitus (DM); and autonomic dysfunction with peripheral neuropathy such
as DM and amyloidosis.
Tip 3: Use MRN for the Proper Clinical Indication
Tip 3: Use MRN for the Proper Clinical Indication
Peripheral nerve pathologies can be broadly classified as systemic and local diseases.[28] A myriad of systemic diseases affects the peripheral nerves. These can be categorized
as vasculitides; radiation-induced neuropathy/plexopathy; metabolic diseases such
as DM, hyperlipidemia, and amyloidosis; neurocutaneous syndromes such as neurofibromatosis
and schwannomatosis; infectious including viruses or mycobacterium leprae; hereditary
diseases such as CMT; acute or chronic demyelinating conditions such as chronic inflammatory
demyelinating polyneuropathy; and idiopathic diseases such as multifocal motor neuropathy.[21]
[29] Systemic conditions produce a multifocal/multicompartmental neuropathy and are usually
diagnosed clinically. Biochemical markers and electrodiagnostic tests are currently
the most useful diagnostic tests. MRN in systemic polyneuropathy is used in cases
when there is mass lesion or a worsening focal neuropathy raising concern of a primary
or superimposed nerve entrapment. Sometimes, these systemic neuropathic conditions
may be incidentally discovered if the patient is imaged for pain or internal joint
derangement, and in this sense, it is also helpful to be aware of the imaging appearances
and common patterns of diffuse neuropathy.
Local conditions affecting peripheral nerves include neuropathies due to trauma; compressive
neuropathies, such as tunnel syndromes in various anatomical locations; traction neuropathies
due to repetitive activities, bad footwear, ankle instability, and functional compartment
syndromes; neoplastic conditions such as perineural tumors or peripheral nerve sheath
tumors; and focal infections.[8]
[29]
As discussed earlier, nerve injuries were traditionally classified according to the
Seddon and Sunderland systems ([Table 1]). Compressive neuropathies are usually due to increased pressure within an anatomical
tunnel. Increased pressure leads to venous congestion, hyperemia, blockade of axoplasmic
flow, and finally proximal epineurial edema and distal Wallerian degeneration. That
is why larger peripheral neural fascicles are first affected. Space-occupying lesions
are a less frequent cause of compressive neuropathy. The mass can be intraneural involving
the fascicles or perineural creating nerve entrapment, encasement, or displacement.
The primary mechanism of traction neuropathy is shear force followed by ischemia.
For systematic conditions, MRN is used as a complementary or problem-solving technique,
whereas for local conditions, it serves as the primary investigative modality. In
both conditions, MRN is performed without intravenous contrast unless there is a suspicion
of tumor or infection.
Tip 4: Use Appropriate Hardware and Software
Tip 4: Use Appropriate Hardware and Software
MRN reporting relies on seeing and assessing specific subtle morphological features
of the peripheral nerves, such as SI alteration, fascicular size and morphology, and
perineural fat plane obliteration or fibrosis. Therefore, imaging peripheral nerves
benefits from the use of higher field magnets, dedicated high-resolution coils, updated
pulse sequences with optimal image parameters, and occasionally the use of specific
pulse sequences with lengthier acquisition times.[29]
Obtaining images with high signal-to-noise ratio (SNR) and the best possible resolution
is desired, although it is technically challenging and often a major limiting factor
in MRN. Hence the use of 3-T scanners is recommended. High-field scanners provide
higher SNR and allow thin section (2–3.3 mm) acquisition and higher matrix size leading
to improved in-plane resolution. In addition, 3-T scanners allow use of parallel imaging
that helps reduce acquisition time and, as a result, minimize motion and breathing
artifacts. Compressed sense and partial Fourier techniques are also available on some
newer scanners that helps reduce acquisition times.[30]
MRN studies have been performed on 1.5-T systems including the use of diffusion tensor
imaging (DTI).[30]
[31] However, a longer acquisition time is required to obtain good SNR, and image resolution
may be degraded by motion due to longer scan time and possibly smaller matrix size.
In addition, 3D imaging is often limited on 1.5 T with suboptimal fat suppression.
The 3-T imaging allows longer T1 and shorter T2 relaxation times, and therefore 3-T
protocols cannot be automatically transferred to 1.5-T systems without modifying the
imaging parameters including reducing bandwidth. We highly recommend using 3-T systems,
whenever possible, for peripheral nerve imaging.[32]
[33] The 1.5-T might be preferred over 3T when there is metal in the immediate field
of view (FOV).
To further increase SNR, dedicated high-resolution multichannel phased-array surface
coils should be used even over a large FOV. Examples of best use cases include a 60-channel
surface body coil for the lumbosacral plexus and pelvic nerves, 18- to 60-channel
coil for the brachial plexus, 16-channel wrist coil for the median and ulnar nerves
at the wrist, 16-channel ankle coil for the tarsal tunnel, and a 15-channel knee coil
for the peroneal nerve.
Multichannel flexible coils are also useful for the extremities. For example, a 36-channel
peripheral coil can be used to image the leg, and a 4- to 8-channel flexible coil
can be used for the forearm.[29]
[34] It is important to image the joint and nonjoint extremity separately with different
FOVs and not to have > 30% blank air space around the extremity area being imaged.
If imaging the whole body, coils should be wrapped close to the body and can be strapped
to each other to avoid blank air space between different torso coils. The torso coils
can be combined with the spine array coils to obtain uniform imaging of the lumbosacral
plexus. For occipital nerve imaging or peripheral trigeminal nerve imaging in the
face, we use a 32-channel head coil.
Available independent software that allows thick slab maximum intensity and oblique/curved
planar reformat projections should be used for evaluation of the longitudinal nerve
axes similar to angiography. In-line reconstruction using thin client tools is preferred
for image interpretation, and images can be sent directly to the picture archiving
and communication system (PACS) for consultation and future review.
Tip 5: Follow the Correct Imaging Protocol
Tip 5: Follow the Correct Imaging Protocol
Different institutions/radiologists have different approaches to how to protocol MRN
studies. Some radiologists tailor patient-specific protocols based on the clinical
question, body part to be imaged, and required FOV. We recommend implementing standard
protocols for different body parts and, if necessary, for some specific disease entities,
(e.g., for carpal tunnel, use a wrist MRN protocol; for forearm and hand pain, use
a forearm and wrist MRN protocol; for chest wall pain, use an intercostal neuralgia
protocol that includes imaging of the thoracic spine and 3D imaging of the chest wall).
This standardized approach has benefits for the interpreting radiologists, referring
clinicians, MR technicians, and patients. Having preset protocols shortens the learning
curve for radiologists and clinicians by having the same set of images for specific
body parts. This helps everyone get used to the normal anatomy and become familiar
with nerve appearances in certain planes. Standard imaging protocols are particularly
important for less experienced MR technicians. From the patient's standpoint, standardized
protocols allow them to have an estimate of acquisition time. An intranet-based in-house
electronic ordering system in our institution enables clinicians to request specific
study types from a predefined dropdown list (e.g., brachial plexus, lumbosacral plexus,
sciatic nerve, wrist nerves, etc.).
The FOV should be adjusted to the area of interest and be as small as possible for
small extremity nerves and as large as necessary to cover all nerves in the brachial
or lumbosacral plexus. A small FOV may create wraparound artifact in the extremities,
and therefore applying a certain percentage of phase oversampling is recommended.[35] Peripheral nerves are elongated structures with some extending > 1 m in length such
as the sciatic, tibial, or peroneal nerves. It is important to have sufficient coverage
of the body area so as not to miss important pathologies.
In addition, it is often unclear clinically where a nerve injury is located, especially
in cases of diffuse neuropathy or nonspecific signs/symptoms, and therefore imaging
of the entire nerve course is often necessary. In fact, missing pathology due to limited
nerve coverage is a common imaging pitfall that should be avoided. In these circumstances,
it is recommended to increase axial slice thickness (up to 5–6 mm) while keeping high
axial in-plane resolution.[29] After screening a large area, small FOV imaging of an area of interest can then
be performed to obtain multiplanar high-resolution MRN imaging.
Generally speaking, MRN relies on high-resolution two-dimensional (2D) and isotropic
3D spin-echo (turbo spin-echo or fast spin-echo) sequences with T1- and T2-weighted
contrast. The 2D T2-weighted sequences are the workhorse of MRN due to their wide
availability, familiarity, and easy reproducibility.[36]
[37] Spectral adiabatic inversion recovery (SPAIR) or Dixon-based fat suppression provides
excellent fat suppression for these T2-weighted images. For the brachial plexus, sagittal
plane short tau inversion recovery (STIR) images are useful because SPAIR fat suppression
commonly fails along the curvatures for the neck and thoracic inlet.
Although high-resolution 2D images obtained in the perpendicular plane are usually
sufficient for detecting and characterizing nerve lesions, corresponding axial T1-weighted
images outline the nerve anatomy and perineural fat planes; and respective axial diffusion
images (especially high b-value, 600–1000 s/mm2) render the nerve abnormality conspicuous ([Fig. 2]). Isotropic 3D images demonstrate the nerve abnormality in its longitudinal axis
in multiple arbitrary planes. Thick slab maximum intensity projection (MIP) reconstructions
from these 3D images better emphasize the nerve pathologies (signal alterations, NIC,
and end-bulb neuroma). These MIP reconstructions are particularly helpful for surgical
mapping as well as facilitating discussion during multidisciplinary conferences.[29]
Fig. 2 A 41-year-old woman with history of a complicated vaginal delivery presented with
pain and a swollen feeling in the perineum. (a) Axial T1-weighted image shows fibrotic bands and scar tissue along the right posterolateral
pelvic wall in close proximity to the course of sciatic and pudendal nerves (arrow).
(b) Axial T2 SPAIR image demonstrates an asymmetrically bright right sciatic nerve (thick
arrow), right pudendal nerve (long thin arrow), and its inferior hemorrhoidal branch
(small thin arrow). (c) Axial diffusion tensor imaging (b factor: 600 s/mm2) confirms signal abnormality in the previously mentioned nerves correlating with
the patient's symptoms and consistent with iatrogenic fibrotic entrapment neuropathy
of the sciatic nerve (thick arrow) and pudendal nerve (thin arrow).
In general, the echo time (TE) for 2D T2-weighted imaging is kept at ∼ 60 to 65 ms
and matrix > 256 to obtain enough SNR to depict the nerve fascicles while minimizing
the magic angle artifact. For 3D imaging, the TE time is kept at ∼ 78 ms with an isotropic
voxel of 1.4 to 1.5 mm for imaging of the plexuses.[38] For extremities and facial nerve imaging, 3D reversed fast imaging in steady-state
precession (PSIF) is used for selective nerve demonstration with a TE of 2.5 ms and
an isotropic voxel size of 0.9 mm. Steady-state imaging using 0.65-mm isotropic voxels
is helpful to depict intrathecal rootlets, and 3D STIR provides excellent imaging
of the extrathecal segments ([Fig. 3]). Suggested protocols for brachial plexus, lumbosacral plexus, and extremity MR
neurography are outlined in [Tables 2], [3], and [4]. If metal is present in the immediate FOV, 1.5-T imaging and various metal reduction
strategies are used (e.g., low TE, high bandwidth, high echo train length, frequency
encoding gradient along the metal axis, and high matrix and low echo spacing) and
techniques such as the commercially available MARS, WARP, or OMAR techniques.[39]
Table 2
Brachial plexus 3-T MRN protocol
|
Sequence
|
Plane
|
Matrix
|
Gap, %
|
Voxel size, mm
|
TR
|
TE
|
Comment
|
|
3D STIR SPACE
|
Coronal
|
400 × 400
|
0
|
Isotropic 1.4–1.5
|
1,500–2,000
|
75–80
|
Cover both sides. Make 7- to 10-mm coronal MIP slabs. TI of 230 ms
|
|
3D T2 SPACE
|
Sagittal
|
320 × 290
|
0
|
Isotropic 0.9
|
1,500–2,000
|
110–120
|
Cover neural foramina on both sides
|
|
FIESTA/bFFE/TrueFISP
|
Coronal
|
330 × 330
|
0
|
Isotropic 0.6–0.65
|
6
|
4
|
Generate axial and sagittal reconstructions
|
|
2D T1 TSE
|
Axial
|
> 256
|
10
|
4 mm
|
700
|
6–9
|
Cover both sides
|
|
STIR right
|
Sagittal
|
> 256
|
10
|
3.5–4.0
|
1,500–2,000
|
25–35
|
Cover from left para-midline to right shoulder
|
|
STIR left
|
Sagittal
|
> 256
|
10
|
3.5–4.0
|
1,500–2,000
|
25–35
|
Cover from right para-midline to left shoulder
|
|
DTI
|
Axial
|
128–192
|
0
|
4.0
|
10,000
|
60–70
|
b-values of 50 and 800, 12 directions. SPAIR fat saturation
|
|
3D T1 mDixon (optional)
|
Coronal
|
340 × 340
|
0
|
Isotropic 1.0–1.5
|
8–12
|
4
|
Cover both sides. Pre- and postcontrast if needed
|
Abbreviations: bFFE, balanced fast field echo; D, dimensional; DTI, diffusion tensor
imaging; FIESTA, fast imaging employing steady-state acquisition; MIP, maximum intensity
projection; SPACE, sampling perfection with application optimized contrasts using
different flip angle evolution; STIR, short tau inversion recovery; TE, time of echo;
TI, time of inversion; TR, time of repetition; TrueFISP, fast imaging with steady-state
precession; TSE, turbo spin echo.
• On coronal 3D STIR SPACE, coverage is from base of skull to T3–T4 level. Side-to-side
coverage is shoulder point to shoulder point and includes both sides.
• On sagittal T2 SPACE and coronal FIESTA, focus only on C spine including both neural
foramina.
• Sagittal STIRs are critical to the examination, so repeat if there is pulsation
artifact or motion present.
• For large subjects, increase voxel size to 1.5 to 2 mm.
Table 3
Lumbosacral plexus 3-T MRN protocol
|
Sequence
|
Plane
|
Matrix
|
Gap, %
|
Voxel size, mm
|
TR
|
TE
|
Comment
|
|
3D SHINKEI/STIR
|
Coronal
|
460 × 460
|
0
|
Isotropic 1.5
|
1,500
|
78–80
|
Cover both sides. Make 8-mm-thick MIP slabs
|
|
2D T2 TSE
|
Sagittal
|
370 × 300
|
10
|
3.5–4.0
|
3,500
|
45
|
Focus on lumbar spine
|
|
2D T2 TSE
|
Axial
|
300 × 300
|
10
|
3.5–4.0
|
3,500
|
45
|
Focus on lumbar spine
|
|
2D T1 TSE
|
Axial
|
700 × 600
|
10
|
4.0
|
700
|
6–9
|
Cover both sides from L1 to lesser trochanter
|
|
T2 SPAIR
|
Axial
|
400 × 400
|
10
|
4.0
|
4,000
|
60–65
|
Cover both sides from L1 to lesser trochanter
|
|
3D T1 Dixon (optional)
|
Axial
|
260 × 260
|
0
|
Isotropic 1.0
|
12
|
5
|
Cover both sides from L1 to lesser trochanter. Pre- and postcontrast if needed
|
|
DTI
|
Axial
|
128 × 192
|
0
|
4–5
|
10,000
|
60–70
|
b-values of 0 and 600, 15 directions. Cover from L3–L4 to lesser trochanter. SPAIR-
fat saturation
|
|
STIR (optional)
|
Axial
|
320 × 320
|
10
|
4.0
|
2,000
|
30–35
|
If fat saturation fails on SPAIR
|
|
FIESTA/bFFE/TrueFISP (optional)
|
Sagittal
|
340 × 340
|
0
|
Isotropic 0.6–0.65
|
12
|
4
|
Coronal and axial reconstructions
|
Abbreviations: 3D SHINKEI, 3D nerve sheath signal increased with inked rest-tissue
RARE imaging; bFFE, balanced fast field echo; D, dimensional; DTI, diffusion tensor
imaging; FIESTA, fast imaging employing steady-state acquisition; MIP, maximum intensity
projection; STIR, short tau inversion recovery; TE, time of echo; TR, time of repetition;
TrueFISP, fast imaging with steady-state precession; TSE, turbo spin echo.
• On coronal SHINKEI, cover both sides from skin to skin in anterior posterior and
lateral dimensions and L1 to lesser trochanters craniocaudally.
• Sagittal bFFE/FIESTA/TrueFISP only if patient has had surgery or has a tumor or
any known lesion.
• Ask the patient to empty urinary bladder before the examination and to breathe normally.
• Large subjects: increase voxel size to 1.5 to 2 mm.
Table 4
Upper and lower extremity 3-T MRN protocol
|
Sequence
|
Plane
|
Matrix
|
Gap, %
|
Voxel size, mm
|
TR
|
TE
|
Comment
|
|
2D T2 SPAIR/T2 Dixon
|
Axial
|
256 × 256
|
10
|
3–4
|
4,000
|
60–65
|
Cover skin to skin to include area of concern
|
|
2D T1 TSE
|
Axial
|
256 × 256
|
10
|
3–4
|
700
|
7–9
|
Cover skin to skin to include area of concern
|
|
3D SPAIR TSE
|
Coronal
|
320 × 320
|
0
|
Isotropic 1.0–1.1
|
1,500
|
78
|
Cover 10–15 cm including the area of interest
|
|
3D DW PSIF
|
Coronal
|
|
0
|
Isotropic 0.9
|
12
|
2.5
|
Cover 10–15 cm including the area of concern; b-value 50–60
|
|
DTI
|
Axial
|
128 × 192
|
0
|
4
|
10,000
|
60–70
|
b-values of 0 and 600, 12 directions. Perform around the palpable or pain site. Keep
FOV under 15 cm. SPAIR fat saturation
|
|
STIR (optional)
|
Axial
|
256 × 256
|
10
|
|
3000
|
25–35
|
If fat saturation fails on SPAIR
|
|
3D T1 VIBE (optional)
|
Axial
|
320 × 320
|
0
|
Isotropic 1.5
|
12
|
5
|
Pre- and postcontrast if needed
|
Abbreviations: D, dimensional; DTI, diffusion tensor imaging; MIP, maximum intensity
projection; PSIF, time-reversed FISP (fast imaging with steady-state precession);
STIR, short tau inversion recovery; TE, time of echo; TR, time of repetition; TSE,
turbo spin echo; VIBE, volumetric interpolated breath-hold examination.
• Upper extremity: Perform in superman position with extremity at the center of the
field of view. Cover from skin to skin (not > 20% air space around the extremity).
Use appropriate coil: wrist coil, flex coil for hand and forearm, etc.
• Lower extremity: Perform only one side at a time. Cover from skin to skin (not > 20%
air space around the extremity). Use appropriate coil: knee coil, flex coil for thigh,
leg, foot, boot coil for ankle, etc. For dedicated ankle MRN, replace coronal fat-saturated
PD with sagittal fat-saturated PD.
• Large subjects: Increase voxel size to 1.5 to 2 mm.
Fig. 3 (a) Multiplanar reconstruction (MPR) coronal oblique FIESTA image clearly depicts the
intrathecal preganglionic nerve roots and is extremely helpful when evaluating suspected
nerve root avulsion or other intrathecal pathologies. (b) MPR coronal oblique FIESTA image in a 21-year-old patient referred with left upper
extremity weakness reveals extensive posttraumatic left-sided preganglionic nerve
root avulsions from C4 through T2 with large pseudomeningoceles compatible with Sunderland
class V nerve injury. (c) Coronal 3D 18-mm slab maximum intensity projection short tau inversion recovery
image better demonstrates postganglionic extrathecal nerve roots and plexus. Note
is made of bright postganglionic right C5 nerve root (arrow) consistent with a stretch
injury (Sunderland class II/III).
Tip 6: Know How to Use Diffusion Imaging
Tip 6: Know How to Use Diffusion Imaging
MRN protocols include more advanced imaging techniques such as diffusion-weighted
imaging (DWI) including DTI and tractography. Using diffusion imaging along with MRN
and tractography might be needed to get the most out of MRN studies. However, application
of these techniques for small peripheral nerves can be technically challenging and
difficult to implement.[36]
[40]
The surrounding fat and vessels are essentially suppressed in DWI, and this effective
background suppression enhances the nerve conspicuity, helping to diagnose subtle
nerve pathologies.[41]
[42] DWI provides quantitative parameter for nerve evaluation, such as apparent diffusion
coefficient (ADC), and DTI in addition provides fractional anisotropy (FA) and tractography.
When nerve pathology is present, ADC values increase, and FA values decrease.[32]
[40]
[41]
[42] Evaluation of peripheral nerve microarchitecture and fascicles has been made feasible
by DTI. Although some applications such as the ADC value measurement is easy to perform
in routine clinical settings for tumors, application of DTI including tractography
of the small peripheral nerves is still challenging and time consuming. It has the
potential to allow differentiation of axonal versus demyelinating pathologies similar
to electrophysiology but is currently mainly reserved for tumors and research purposes.[29]
[43]
[44]
[45]
[46]
Tip 7: How to Interpret MRN Studies
Tip 7: How to Interpret MRN Studies
The normal peripheral nerve has a continuous course, uniform contour, and a diameter
similar to the accompanying arteries or contralateral nerve.[47] Normal peripheral nerves should have a smooth course without sharp angulation or
deviation, or focal caliber change at nonbranching sites. This is diagnostically important
for nerve entrapments where there is deviation in the normal neural course as well
as compressive features upon the nerve. Irregular contour, abrupt change in caliber,
or diffuse persistent increased caliber without distal tapering are abnormal and indicative
of neuropathy. Discontinuity of the nerve with end-bulb-neuroma is indicative of a
high-grade neural injury (Sunderland class IV and V).
The fascicular morphology has important diagnostic significance and should be identifiable
on the axial images. Nerve thickness and image quality are key factors for this identification.
Generally speaking, evaluation of the fascicular morphology is feasible in nerves > 3 mm
thick.[48] Fascicles should be examined regarding their uniformity, signal, size, and continuity.
Enlarged, atrophied, nonuniform, or disrupted fascicles are pathologic. Comparison
with the contralateral nerve (if imaged) or adjacent similar size nerves can be helpful
for more precise interpretation.
SI is one of the most important features to be evaluated on MRN after suppressing
adjacent perineural fat and vascular flow signal to obtain optimal SNR. The perineurium
and outer epineurium demonstrate a thin low SI lining. As a rule, the SI of a peripheral
nerve should be close to the adjacent skeletal muscle on all pulse sequences.[34] High SI is seen on T2-weighted images at areas of neuropathy. This change in SI
is usually evident within the first 24 hours following an insult.[49]
[50] Nerve SI changes are maximum adjacent to the area of entrapment or injury that helps
localize the site of insult. For instance, ulnar nerve hyperintensity is most pronounced
at the cubital tunnel in cubital tunnel syndrome, and sciatic nerve signal alteration
is most pronounced at the sciatic notch in piriformis syndrome. A longer extent of
signal alteration is seen on the neuropathic side as compared with the contralateral
normal nerve (e.g., in piriformis syndrome, a longer extent and more hyperintense
signal is seen in the sciatic nerve as compared with minimal signal at the sciatic
notch on the contralateral side). Diffuse signal or caliber changes in one or more
regional nerves is indicative of a systemic neuropathy. That said, not all neural
T2 hyperintensity is necessarily abnormal. Neural T2 hyperintensity can be found in
asymptomatic subjects at the cubital and carpal tunnels in particular. In these situations,
the degree and length of hyperintensity, the nerve caliber, and, whenever possible,
comparison with the contralateral side should also be considered.
Nerves are generally wrapped in a fine fatty background referred to as the perineural
fat. Obliteration of perineural fat planes by fibrosis is an indirect sign of entrapment
or adhesive neuropathy secondary to a regional insult (e.g., in a failed back surgery
syndrome, perineural scarring of the preganglionic segment with nerve entrapment and
resultant downstream neuropathy or the femoral with or without sciatic nerves) ([Fig. 4]). Other indirect signs of prior dural injury may be present such as dural diverticula,
peridural iatrogenic fat patch, or pseudomeningocele apart from the regional scar
tissue. In extremity nerve entrapment cases, perineural space-occupying lesions or
nerve entrapment along the anatomical tunnels due to tight fascia, tenosynovitis,
ganglion, accessory muscles, or other secondary cause can result in displacement of
perineural fat planes and predispose to secondary changes in nerve course, caliber,
and abnormal fascicular morphology and SI.
Fig. 4 A 75-year-old man presented with scoliosis and worsening pain in his left leg 4 months
after posterior decompression. (a) Coronal 3D short tau inversion recovery and (b) DWI (b600) reconstructed maximum intensity projection images with a 14-mm slab thickness
demonstrate increased signal intensity and abnormal thickening of the left L4 and
L5 nerve roots (arrows, Sunderland class III) with significant perineural fibrosis/granulation
as well as downstream sciatic (not shown) and (c) femoral neuropathy (arrow). The final diagnosis was postoperative perineural fibrosis
with left L4 and L5 constriction.
Use of contrast in routine MRN studies is controversial and differs from practice
to practice. Some endorse its use; others argue that it provides little or no incremental
value to the information obtained from noncontrast images. Normal peripheral nerves
do not show appreciable enhancement after contrast administration due to the existence
of a blood-nerve barrier. Enhancement could be physiologic as in dorsal nerve ganglia[16] or indicate disruption of the blood-nerve barrier, a sign of neuropathy distal to
the dorsal nerve root ganglion. Given the cost, increase in scan time, concerns regarding
tissue accumulation of gadolinium-based contrast media, and its limited additive diagnostic
value, the general consensus is against the routine use of contrast media in MRN studies.
Contrast use is recommended if there is concern regarding infection, tumor, or atypical
polyneuropathy.[2]
[34]
[51] Therefore, the supervising radiologist should consider each MRN case separately.
Muscle changes are of high clinical and diagnostic value in the setting of motor neuropathies
and must always be taken into consideration. Muscle denervation change helps in more
precise localization of the nerve lesion based on the anatomical distribution of the
muscle changes. The neuropathy is always proximal to the denervation change in the
muscle clinically or on MRN. Muscle changes can help determine the chronicity of the
neuropathy with muscle edema indicative of a more acute injury (within a few days)
and muscle fatty infiltration or atrophy with or without edema indicating a more chronic
process. Muscle denervation edema or fatty infiltration is differentiated from an
inflammatory myositis using key imaging signs such as diffuse involvement, lack of
hemorrhage, or fascial/subcutaneous edema findings limited to the distribution of
affected nerves and associated nerve lesions. Severe muscle atrophy is a poor prognostic
indicator for nerve injury because even if nerve regeneration occurs, the muscle is
weakened, and therefore a full functional recovery is unlikely.[29] A serial decrease in muscle edema and nerve hyperintensity is correlated with nerve
regeneration and subsequent functional improvement.[49]
[52]
Tip 8: Become Familiar with the Key Pearls and Pitfalls of Imaging Diagnosis
Tip 8: Become Familiar with the Key Pearls and Pitfalls of Imaging Diagnosis
Knowledge of and attention to the most common diagnostic pearls and pitfalls will
expedite the MRN learning process, as well as help generate accurate reports and aid
patient management.
A frequent pitfall in interpretation occurs when it comes to nerve SI. Misinterpretation
of an elevated nerve SI on fluid-sensitive sequences is common, especially for less
experienced eyes. This is even more common where nerves track along certain anatomical
tunnels, such as the ulnar nerve or median nerve along the cubital and carpal tunnels,
respectively. Mild increased SI of the ulnar nerve on T2-weighted images can be considered
normal and should be correlated clinically.[53] Conversely, some patients with clinical findings of cubital tunnel syndrome demonstrate
only mild ulnar nerve signal changes at the tunnel. The same pitfall is seen when
there is signal alteration on STIR images without a change in SI on fat-saturated
T2-weighted images. Comparison with the contralateral asymptomatic nerve is very helpful
although not always technically feasible in most cases in the upper extremities. A
contrast-to-noise ratio method, where ulnar nerve SI is compared with background noise,
may be helpful if doubt still exists.[54]
Therefore, experience and correlation with other MRN features of neuropathy such as
distal longitudinal extension of signal hyperintensity, nerve enlargement, change
in fascicular morphology, muscle denervation change, and not least correlation with
clinical findings are important to avoid overrating these subtle changes.[29]
[34]
[53]
[54] However, mild signal changes should not be overlooked because it may be the only
sign of neuropathy. Knowledge of expected increased signal of nerve at certain sites
due to magic angle artifacts is essential (e.g., the plexus nerves are bright at their
curving points; the sciatic nerve at the sciatic notch, and the femoral nerve at its
genu above the inguinal ligament, etc.).
Another important imaging feature to be aware of is the “triple B-sign” as described
by Chhabra et al, and a variant described as the “bull's-eye sign” by Sneag et al
orthogonal to the long axis of the nerve, where there is alternating bright-black-bright
SI changes along the course of a nerve at the area of concern for injury or entrapment.
This basically indicates severe focal neuropathy such as severe nerve entrapment,
nerve transection, or severe degeneration/dehiscence of a nerve graft.[29]
[48]
[55] Although isolated signal change can be associated with mild entrapment, proximal
enlargement of nerve is a sign of moderate entrapment, and proximal and distal enlargement
of the nerve is a sign of severe entrapment. In chronic entrapment cases, the SI may
fade to near normal, although enlargement of the nerve with distal flattening at the
site of entrapment will persist. In chronic neuropathies, such as DM, nerve signal
may decrease on fat-suppressed T2-weighted images due to fascicular atrophy and increased
epineurial fat.[56]
Another interpretation pitfall in nerve evaluation is the absence of perineural fat
planes. Perineural fat is generally sparse or absent especially within anatomical
tunnels and tight anatomical regions. Therefore, in its absence, it is hard to distinguish
scar tissue from normal lack of perineural fat. Radiologists must avoid overestimating
neuropathy based solely based on the absence of perineural fat, and correlation with
anatomical location and other imaging features should be used.
Careful attention should be taken when protocoling MRN studies and deciding the FOV.
Nerves are commonly enlarged with high SI proximal to the site of insult. However,
distally, the nerves might depict normal SI and size, or even a mild decrease in diameter.
Therefore, limited coverage of the FOV not including the proximal aspects of the nerve
could lead to misinterpretation. Again, comparison with the contralateral normal nerve
(if imaged) or the same size regional nerves, and paying attention to muscle denervation
changes can be helpful. As a rule, the FOV must extend above the site of visible muscle
denervation change.
Nerves may demonstrate anomalous course as a normal variant. Many of these alterations
are asymptomatic, often bilateral, and therefore are of no clinical importance. However,
some atypical courses are associated with entrapment/compressive neuropathies, such
as bifid brachial nerve roots or an intramuscular course of the sciatic nerve. It
is crucial to have a good knowledge of normal anatomy as well as being familiar with
the common clinically important normal variants.[47]
[57]
MRN provides valuable information complementing other more diagnostic techniques,
such as clinical examination and electrodiagnostic tests. Radiologists and clinicians
should work as a team and relay all pieces of information in a timely fashion to get
the most out of advanced diagnostic tests such as MRN. Many imaging pitfalls are related
to lack of proper clinical information, EMG/NCV results, or miscommunication. This
is especially important in inflammatory/autoimmune neuropathies (Parsonage-Turner
syndrome) or more diffuse and multifocal conditions. In these circumstances, neural
thickening and altered signal are often diffuse and may be underrated by radiologists,
especially if imaging is performed during the early, relatively asymptomatic period
when findings are more subtle.[56]
[58]
Tip 9: How and What to Report
Tip 9: How and What to Report
Important advantages of MRN over more traditional diagnostic techniques include its
ability to assess neuromuscular anatomy precisely, localize neuropathy, show the extent
and nature of neuromuscular abnormality or nerve injury, find organic lesions, and
evaluate adjacent joint or tendon derangements that could predispose or contribute
to traction neuropathy. These pieces of information put together with the clinical
history and electrodiagnostic information can help better identify the cause of any
neuropathy and target management. In addition, this information opens an array of
other therapeutic advantages, such as for surgical planning, nerve blocks, and, if
necessary, tissue sampling. Another advantage is that MRN is extremely sensitive with
a high negative predictive value. Finding normal nerves in a case of suspected neuropathy
can favor a psychological or psychosomatic etiology rather than an organic cause in
a chronic pain patient.
The radiologist should comment on the degree of neuropathy based on the MRN findings.
This is especially important prognostically and for care management. For instance,
a Sunderland class IV and V injury needs surgical intervention, whereas milder neuropathies
can be expected to improve with conservative management. The Seddon and Sunderland
classification of neuropathy is based on various layers of neural tissue involvement.
This classification can be used for MRN interpretation and reporting; however, not
all delicate neural tissue layers can be individually evaluated even on high-resolution
MRN studies. Therefore, the following grading system can alternatively be used in
addition to the Seddon and Sunderland grading, especially for less experienced readers.
This grading system is capable of conveying all the required clinically important
information, is more practical, and easier to communicate MRN findings.
-
Low-grade (stretch) injury (equivalent to Sunderland class I or neuropraxia based
on Seddon): nerve-in-continuity with increased T2 SI without focal or diffuse enlargement
-
Moderate-grade injury (equivalent to Sunderland class II/III or axonotmesis based
on Seddon): nerve-in-continuity with diffuse nerve enlargement (more than the size
of the contralateral nerve or adjacent vessel) with increased T2 SI with or without
fascicular abnormalities
-
High-grade injury (equivalent to Sunderland IV): NIC with abrupt change in nerve caliber,
effacement of or heterogeneous fascicular morphology, and increased T2 SI ([Figs. 5] and [6])
-
Severe injury: nerve transection or nerve root avulsion with or without end-bulb-neuroma
formation (equivalent to Sunderland class V or neurotmesis based on Seddon)
Fig. 5 A 68-year-old woman with pain and paresthesia along the right lateral thigh. Lumbar
plexus MR neurography was performed for suspected meralgia paresthetica. (a) Maximum intensity projection coronal oblique 3D short tau inversion recovery image
with 14-mm slice thickness depicts increased thickness and signal intensity of the
right lateral femoral cutaneous nerve (LFCN). There is a small 4-mm neuroma-in-continuity
(NIC) along the right LFCN (arrow) at the level of the inguinal ligament. (b) Intraprocedural axial computed tomography image shows LFCN block proximal to the
area affected by the NIC.
Fig. 6 A 37-year-old man with a history of carpal tunnel release presented with numbness
and tingling along the median nerve distribution. (a) Axial T2 SPAIR image shows marked thickening and bright SI on the median nerve (arrow)
at the carpal tunnel. (b) Coronal and (c) sagittal MIP 3D PSIF images depict a large neuroma-in-continuity (NIC) measuring
2.5 cm along the median nerve. (d) Diffusion tensor imaging tractography map demonstrates marked disruption of fascicles
(markedly reduced relative to the size of the nerve) at the site of NIC (large arrow)
consistent with axonal degeneration and demyelination. Fractional anisotropy (FA)
and apparent diffusion coefficient (ADC) measured 0.45 and 1.31 × 10−3 mm2/s, respectively. Notice normal ulnar nerve (small arrow, FA = 0.6, ADC = 1.10 × 10−3 mm2/s).
Radiologists must try to follow a specific search pattern and consider using a structured
template with a checklist approach while interpreting MRN studies. Having a specific
step-by-step search algorithm probably reduces the likelihood of overlooking subtler
but often critically important findings, such as anatomical variations, obliteration
of perineural fat planes, and muscle denervation changes. Use of proper and accurate
terminology is crucial in describing and communicating nerve findings. Excessive use
of “radiology language” is confusing for clinicians, and information may get overlooked
during report interpretation. Adherence of both radiologists and clinicians to a recognized
classification system is crucial in this regard to avoid preventable diagnostic pitfalls.[29]
[59] For example, myopathy in neurology literature refers to nonneurogenic muscle pathology.
Using the term muscle denervation change instead of myopathy helps multidisciplinary communication. The nerve should not just be called bright.
Interpretation must be more specific. The patient history and clinical findings need
to be reviewed, as well as a quite specific diagnosis suggested based on all available
information and included as part of the final impression in the report.
Tip 10: How to Participate in Multidisciplinary Care of Neuropathy Patients
Tip 10: How to Participate in Multidisciplinary Care of Neuropathy Patients
Radiologists are, in most cases, consultants in the multidisciplinary team. On a personal
note, we at UT Southwestern are one of the rare sites in the world with a dedicated
musculoskeletal patient care clinic where patients with musculoskeletal disorders
and neuropathy are seen by radiologists, imaged, and intervened. Whichever model exists
in your center, it is important to be part of the multidisciplinary care of the patients
with formation of disease-oriented teams in this era of patient-centered care. Regular
communication of the findings and continuous learning from your other clinical colleagues
(plastic surgeons, peripheral nerve surgeon, neurologists, fellow radiologists, etc.)
is not only helpful for proper patient care but also essential for personal and professional
growth. The treatment decisions about nerve injections, medications, and surgery are
best made with multiple teams working together facilitating cost-effective care. The
knowledge gained can be distributed in the form of case series and scientific reports
to less experienced readers in other centers.[60]
[61]
To conclude, MRN has rapidly translated into current clinical practice. We have outlined
what we consider to be the most important tips to help set up a successful MRN practice.
