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Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) is a noninvasive method that allows for fast and reproducible measurements of adipose tissue content in neonates with low intra- and intercoefficients of variability.

From: Fetal and Neonatal Physiology (Third Edition), 2004

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Positron Emission Tomography

Neoplasm

Multiple Sclerosis

Lesion

Biopsy

Computer Assisted Tomography

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Magnetic Resonance Imaging

J.O.S.H. Cleary, A.R. Guimarães, in Pathobiology of Human Disease, 2014

Introduction

Magnetic resonance imaging (MRI) is a noninvasive modality, which produces multiplanar and true 3D datasets of subjects in vivo. It achieves high spatial resolution, typically of the order of millimeters in the clinical setting. Crucially, it differs from other techniques such as computed tomography (CT) by producing excellent soft tissue contrast without harmful ionizing radiation. MRI has transformed the role of radiology in medicine since its initial applications in structural imaging in the early 1980s and now encompasses wider areas of functional and molecular imaging. In the first part of this article, we give an overview of the principles of MRI and some common uses in the diagnosis of pathologies such as stroke and cancer. We go on to discuss the role of MR contrast agents, including their application to the exciting new areas of molecular and cellular imaging. Next, we address the role of MR spectroscopy, a technique often complementary to MRI for the identification of disease processes through the assessment of metabolites. Finally, we then look at an emerging application of MRI – high-resolution MR histology – as an adjunct to pathology studies.

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Volume 2

Rachel W. Chan, ... Angus Z. Lau, in Encyclopedia of Biomedical Engineering, 2019

Introduction

Magnetic resonance imaging (MRI) is a noninvasive imaging technique that enables the observation of anatomic structures, physiological functions, and molecular composition of tissues. MRI is based on nuclear magnetic resonance (NMR), whose name comes from the interaction of certain atomic nuclei in the presence of an external magnetic field when exposed to radiofrequency (RF) electromagnetic waves of a specific resonance frequency. This article is intended to give an overview of selected topics in MRI beginning with a brief history.

NMR was first documented in 1939 in a molecular beam by Isidor Rabi, who received the Nobel Prize in Physics in 1944. In 1946, techniques were developed independently by Felix Bloch and Edward Purcell that extended NMR to liquids and solids. Bloch and Purcell shared the Nobel Prize in Physics in 1952 for other important contributions to methods in magnetic resonance. It was not until 1973 that Paul Lauterbur devised a technique to create the first 2-D image from NMR signals. This is now known as MRI. Strategies to improve imaging speed were introduced by Peter Mansfield in 1978. For their contributions, Lauterbur and Mansfield were awarded the Nobel Prize in Physiology or Medicine in 2003. Raymond Damadian also made significant contributions to the development of MRI for human imaging by demonstrating that tumors and normal tissue could be distinguished. Since then, MRI has become a vital imaging modality for clinical use.

The basis of MRI is that certain atomic nuclei, typically those of hydrogen, in the tissue, become magnetized when placed in an external magnetic field. This produces, in the tissue, a net magnetization, M, that is initially aligned with the direction of the main magnetic field, B0. A typical MRI experiment starts with the transmission of an RF pulse, B1, to perturb this magnetization. This is termed RF excitation and requires hardware called transmit coils. The excitation process involves 'tipping' the magnetization away from the longitudinal axis (i.e., parallel to B0, where signal cannot be detected) to the transverse plane (i.e., orthogonal to B0), where it can then be detected by hardware known as receiver coils. After the RF pulse is turned off, the magnetization undergoes processes called relaxation and precession as it returns to its thermal equilibrium configuration. It is possible to detect the magnetization because the transverse component of processing magnetization induces an electromotive force in the receiver coil. This is detected as the NMR signal. In MRI, the received signal can be spatially encoded by the application of magnetic field gradients that are superimposed on the uniform, main magnetic field. Excitation and detection modules are repeated until all data are collected. The data are recorded and processed to form an image.

MRI is able to produce cross-sectional images of the body with excellent soft tissue contrast. MRI operates in the RF range, so it does not have any harmful ionizing radiation. The versatility of MRI is illustrated in Fig. 1, which shows several of many possible types of images that can be produced, where each type of image has a different image contrast or 'weighting.' Each contrast mechanism offers some unique information for the noninvasive detection, diagnosis, and characterization of disease.

Fig. 1. Different types of image contrast produced by MRI. (A) T2, (B) T1, and (C) proton-density-weighted images are shown of the same slice of the brain. (D) Also shown is an image acquired with the fluid-attenuated inversion-recovery (FLAIR) sequence, which nulls the signal from cerebrospinal fluid. Arrows indicate the presence of a silent brain infarct (SBI).

Reproduced from Zhu YC, Dufouil C, Tzourio C, and Chabriat H. (2011). Silent Brain Infarcts. Stroke 42(4):1140–1145.

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Magnetic Resonance Imaging

John A. Detre MD, in Neurobiology of Disease, 2007

I. History of Magnetic Resonance Imaging

Clinical MRI is the result of an extraordinary number of scientific and engineering advances [1]. The first successful nuclear magnetic resonance (NMR) spectroscopy experiments were independently demonstrated in the 1945 by Felix Bloch and Edward Purcell, who shared the Nobel Prize in Physics in 1952 for the finding. For the next few decades, NMR experiments were mainly used for chemical and physical analysis of small samples that could be fit into small-bore NMR spectrometers. High-resolution NMR continued to evolve into a powerful modality for detailed chemical analysis of molecules, but NMR imaging of spatially resolved signals developed in a different direction. Spatial encoding in NMR is accomplished through the use of magnetic field gradients, which can introduce spatial variations in the main magnetic field. The concept of generating images with NMR arose from Paul Lauterbur's 1972 idea of applying field gradients in all three dimensions, using back-projection methods borrowed from CT scanning to generate images. This inspired development of Fourier transform reconstruction by Richard Ernst in 1974, which is the predominant approach used today. Around that time, wide-bore NMR systems capable of imaging living animals and human limbs were available, and larger magnets capable of accommodating a human body were being considered. Peter Mansfield reported the first in vivo image of human anatomy in 1977, a cross-sectional image through a finger. The potential diagnostic value of changes in NMR relaxation was suggested by Raymond Damadian and others and further motivated the development of MRI for clinical use. Nuclear magnetic resonance imaging was renamed magnetic resonance imaging to avoid the undesirable connotations of the word nuclear among the lay public. In 2003, Lauterbur and Mansfield shared the Nobel Prize in Medicine for MRI.

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Magnetic Resonance Imaging

Eric T. Chou, John A. Carrino, in Pain Management, 2007

▪ DESCRIPTION OF MODALITY

Magnetic resonance imaging (MRI) is based on the principles of nuclear magnetic resonance (NMR), a spectroscopic technique used to obtain microscopic chemical and physical information about molecules. MRI is based on the absorption and emission of energy in the radiofrequency (RF) range of the electromagnetic spectrum. It produces images based on spatial variations in the phase and frequency of the RF energy being absorbed and emitted by the imaged object. A number of biologically relevant elements, such as hydrogen, oxygen-16, oxygen-17, fluorine-19, sodium-23, and phosphorus-31 are potential candidates for producing MR images. The human body is primarily fat and water, both of which have many hydrogen atoms, making the human body approximately 63% hydrogen atoms. Hydrogen nuclei have an NMR signal, so for these reasons clinical MRI primarily images the NMR signal from the hydrogen nuclei given its abundance in the human body. Protons behave like small bar magnets, with north and south poles within the magnetic field. The magnetic moment of a single proton is extremely small and not detectable. Without an external magnetic field, a group of protons assumes a random orientation of magnetic moments. Under the influence of an applied external magnetic field, the protons assume a nonrandom alignment, resulting in a measurable magnetic moment in the direction of the external magnetic field. By applying RF pulses, images can then be created based on the differences in signal from hydrogen atoms in different types of tissue. A variety of systems are used in medical imaging ranging from open MRI units with magnetic field strength of 0.3 Tesla (T) to extremity MRI systems with field strengths up to 1.0 T and whole-body scanners with field strengths up to 3.0 T (in clinical use). Because of its superior soft tissue contrast resolution, MRI is best suited for evaluation of internal derangement of joints, central nervous system abnormalities, as well as other pathologic processes in the patient with pain.

The advantages of MRI over other imaging modalities include absence of ionizing radiation, superior soft tissue contrast resolution, high-resolution imaging, and multiplanar imaging capabilities. The time to acquire an MRI image has been a major weakness and continues to be so with the advent of faster CT scanners (with multislice CT). However, newer imaging techniques (e.g., parallel imaging), faster pulse sequences, and higher field strength systems are addressing this issue.

A number of pulse sequences have been invented to highlight differences in signal of various soft tissues. The most common and most basic of pulse sequences include T1-weighted and T2-weighted sequences. T1-weighted sequences have traditionally been considered good for evaluation of anatomic structures. Tissues that show a high signal (bright) and T1-weighted images include fat, blood (methemoglobin), proteinaceous fluid, some forms of calcium, melanin, and gadolinium (a contrast agent). T2-weighted sequences have generally been considered fluid-conspicuity pulse sequences, useful for identifying pathologic processes. Tissues that show a high signal on T2-weighted images include fluid-containing structures (i.e., cysts, joint fluid, cerebrospinal fluid) and pathologic states causing increased extracellular fluid (i.e., sources of infection or inflammation).

Advanced imaging techniques used in medical imaging include magnetic resonance angiography (MRA), diffusion weighted imaging, chemical shift imaging (fat suppression), functional imaging of the brain, and MR spectroscopy (MRS). Many of these techniques are especially useful in brain imaging. MRA (either time-of-flight or phase contrast) and diffusion weighted imaging are useful for the detection and characterization of ischemic insults in the brain. MRS uses the differences in chemical composition in tissues to differentiate necrosis or normal brain matter from tumor.

In musculoskeletal imaging, MR arthrography is a technique available to augment the depiction of internal derangements of joints.1 Arthrography can be either indirect (intravenous gadolinium is administered and allowed to diffuse into the joint) or direct (a dilute gadolinium solution is percutaneously injected into the joint) to provide distention of a joint, assisting in the evaluation of ligaments, cartilage, synovial proliferation, or intraarticular bodies. MR arthrography has been most extensively used in the shoulder to outline labral-ligamentous abnormalities as well as to distinguish partial-thickness from full-thickness tears in the rotator cuff. It is also helpful in demonstrating labral tears in the hip, partial- and full-thickness tears of the collateral ligament of the elbow, and bands in the elbow. This technique is also useful in patients after meniscectomy in the knee to detect recurrent or residual meniscal tears, evaluate perforations of the ligaments and triangular fibrocartilage in the wrist, and assess the stability of osteochondral lesions in the articular surface of joints. T1-weighted images are often employed with MR arthrography to bring out the T1 shortening effects of gadolinium. Fat saturation is also added to help differentiate fat from gadolinium. A T2-weighted sequence in at least one plane is also necessary to detect cysts and edema in other soft tissues and bone marrow.

Patients in whom MRI is contraindicated include those who have the following: cardiac pacemaker, implanted cardiac defibrillator, aneurysm clips, carotid artery vascular clamp, neurostimulator, insulin or infusion pump, implanted drug infusion device, bond growth/fusion stimulator, and a cochlear or ear implant. In addition, patients who have a history of metalworking should have a pre-MRI screening radiograph of the orbits to evaluate for radiopaque foreign bodies near the ocular globe.

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Magnetic Resonance Imaging

Cihan Duran, ... Frank J. Rybicki, in Vascular Medicine: A Companion to Braunwald's Heart Disease (Second Edition), 2013

Basic Principles

Magnetic resonance imaging (MRI) relies upon the inherent magnetic properties of human tissue and the ability to use these properties to produce tissue contrast. Magnetic resonance imaging detects the magnetic moment created by single protons in omnipresent hydrogen atoms. Because any moving electric charge produces a magnetic field, spinning protons produce small magnetic fields and can be thought of as little magnets or "spins." When a patient is placed in the bore of a large magnet (i.e., MRI scanner), hydrogen protons align with the externally applied static magnetic field (B0) to create a net magnetization vector. On a quantum level, most protons will distribute randomly, either with or against the scanner's B0. However, a slight excess of spins aligns with the field, causing net tissue magnetization. The time required for this alignment is denoted by the longitudinal relaxation time, T1. T1 variations between tissues is used to provide contrast.

Spinning protons wobble or "precess" about the axis of B0. The frequency of the wobble is proportional to the strength of B0. If a radiofrequency (RF) pulse is applied at the resonance frequency of the wobble, protons can absorb energy and jump to a higher energy state. This RF pulse deflects the protons, creating a new net magnetization vector distinct from the major axis of the applied magnetic field. The net magnetization vector tips from the longitudinal to the transverse plane (transverse magnetization). The protons are "flipped" by the RF pulse, and the net magnetization vector is defined by a "flip angle." The stronger the RF pulse applied, the greater the angle of deflection for the magnetization. Common flip angles for spin echo are 90° and 180°. For gradient echo (GRE) MRI, flip angles typically range between 10° and 70°. After the RF pulse tips the spinning protons out of alignment with the main magnetic field, new protons begin to align with the main magnetic field at a rate determined by the T1 relaxation time.

Energy is given off as the spins move from high to low energy states. The absorbed RF energy is retransmitted at the resonance frequency and can be detected with RF antennas or "coils" placed around the patient. These signals are compiled, and after mathematical processes become the MR images. Proton excitation with an externally applied RF field is repeated at short intervals to obtain signals. This MR parameter is referred to as repetition time (TR). For conventional MRI, TR is typically 0.5 to 2 seconds, whereas for MRA, TR ranges from 30 to less than 5 milliseconds. When the spins are tipped to the transverse plane, they all precess in phase. The speed of wobbling depends on the strength of the magnetic field each proton experiences. Some protons spin faster while others spin slower, and they quickly get out of phase relative to one another. Throughout the dephasing process, the MR signal decays. This loss of phase is termed T2 relaxation time or transverse relaxation. T2, like T1, is unique among tissues and is used for image contrast. In addition to the intrinsic T2 of tissue, inhomogeneity of B0 results in rapid loss of transverse magnetization. The relaxation time that reflects the sum of these random defects with tissue T2 is called T2*. To obtain an MRI signal, these spins must be brought back in phase and produce a signal or echo. The time at which it happens is referred to as echo time (TE). In spin echo imaging technique, the echo is obtained by using a refocusing 180° RF pulse, after which the spins begin to dephase. Another 180° RF pulse can be applied to generate a second echo and so on. Signal loss at longer echo times reflects tissue T2. In GRE imaging, the echo is obtained by gradient reversal rather than RF pulse. Because this includes effects from tissue homogeneity, TE-dependent signal loss reflects T2*. Recently, GRE sequences (balanced GRE steady-state free precession [SSFP]) have been developed that are insensitive to magnet field inhomogeneities and reflective of actual tissue T2.

Longitudinal and transverse magnetizations occur simultaneously but are two different processes that reflect properties of various tissues in the body. Since T1 measures signal recovery, tissues with short T1 are bright, whereas tissues with long T1 are dark. Fat has a very short T1. In contrast, T2 is a measure of signal loss. Therefore, tissues with short T2 are dark, and those with long T2 are bright. Simple fluids, such as cerebrospinal fluid and urine, have long T2. To differentiate between the tissues based on these relaxation times, MR images can be designed to be T1-weighted, T2-weighted, or proton-density weighted. Exogenous contrast such as gadolinium-based agents are routinely used to alter tissue conspicuity. Spatial encoding of signals obtained from tissues is required for imaging. Additional external time-varying magnetic fields are applied to spatially encode the MR signal. Spatially dependent gradients are used to locate the MR signal in space. In two-dimensional (2D) MRI, these are slice-selection, frequency-encoding, and phase-encoding gradients. In three-dimensional (3D) MRI, the slice-selection gradient is replaced by a second phase-encoding gradient.

Magnetic resonance echoes are digitized and stored in "k-space" composed of either two axes (for 2D imaging) or three axes (for 3D imaging). K-space represents frequency data and is related to image space by Fourier transformation. An important feature of k-space is that tissue contrast is determined by the center of k-space (central phase encoding lines), whereas the periphery of the k-space encodes the image detail. The order in which k-space lines are collected can be varied, strongly influencing tissue contrast. For example, in CE-MRA, the central contrast-defining portion of k-space may be acquired early in the scan (centric acquisition) during peak intraarterial contrast concentration to maximize arterial contrast. In addition to simple line-by-line k-space acquisition schemes, more complex schemes have been described. In spiral imaging, data acquisition begins at the center of k-space and spirals to the periphery. Slice-selective gradients applied along the z-axis will form axial images. Those along the y-axis will yield coronal images, and the x-axis gradients will provide sagittal images. An oblique slice can be selected by a combination of two or more gradients.

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Magnetic Resonance Imaging

In Imaging of Pain, 2011

Concept

•

Magnetic resonance imaging (MRI) uses the movement of protons within a magnetic field to generate an image.

•

Within the constant magnetic field of an MRI scanner, tissues that contain free hydrogen nuclei (protons) generate varying signals when pulses of radiofrequency (RF) energy are applied to them.

•

These signals, which depend on the type of tissue and the speed at which the tissue "relaxes" or gives up its movement, are then mathematically converted into an image.

•

The contrast of the image thus depends on the signal intensity (SI) of different tissues. Certain tissues that are rich in free protons, such as water and fat, are very responsive to the RF pulses. Other tissues with fewer free protons, such as cortical bone and air, are less responsive and generate much less signal.

•

Different tissue contrasts can be determined, depending on the strength and timing of the RF pulse; this parameter is known as an MR sequence. The most basic forms of MR sequences include:

•

T1-weighted (T1W) imaging, on which fluid appears dark and fat appears bright.

•

T2-weighted (T2W) imaging, on which both fluid and fat appear bright.

•

Proton density (PD) imaging, on which fluid appears intermediate-SI and fat appears bright.

•

Manipulating the MR sequences allows the demonstration of different tissue characteristics. For instance, the signal from fat can be cancelled out (made dark) using a technique known as fat suppression. Fat suppression with T2 weighting is very useful in musculoskeletal imaging to increase contrast between bright pathologic tissue and fat. Common fat suppression techniques include:

•

Short TI inversion recovery (STIR) imaging.

•

Fat suppression with T2 weighting (FST2W imaging).

•

Intravenous contrast agents such as gadolinium can be administered to enhance the visualization of vessels and inflammatory tissue. T1W with fat suppression (FST1W) images are often used to improve contrast between enhanced tissue and adjacent fat structures.

•

Intra-articular contrast agents may also be administered, producing an MR arthrogram effect to enhance the evaluation of intra-articular structures such as articular cartilage, fibrocartilage, and ligaments. This method is often employed in shoulder, wrist, elbow, and hip imaging.

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Certain metals, such as stainless steel and cobalt-chrome, distort the magnetic field and thus produce image artifact. Other metals, such as titanium, produce much less image distortion. Such distortion may degrade the image quality and is an important consideration in referring patients with metal devices such as orthopaedic hardware for evaluation by MRI.

•

Implantable electronic devices, such as cardiac pacemakers and neural stimulators, are affected by the magnetic field and are also incompatible with MRI evaluation.

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Magnetic Resonance Imaging

Hiroshi. Yoshioka MD, PhD, ... Katsumi. Kose PhD, in Imaging of Arthritis and Metabolic Bone Disease, 2009

•

Clinical magnetic resonance imaging (MRI) measures the spatial distribution of protons in the body.

•

Gradient coils are used to provide spatial information. The changing gradients are associated with noise produced during imaging.

•

Relaxation times T1, T2, and T2* are important tissue characteristics for imaging.

•

Low-field magnets have lower signal to noise ratio (SNR); longer scan times, making patient motion a potential problem; decreased resolution; decreased sensitivity to old blood and calcified lesions; lower gadolinium enhancement; and difficulty in spectral fat suppression.

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Gadolinium contrast medium is often used combined with fat-suppressed T1-weighted imaging to increase contrast between enhanced tissue and surrounding tissue.

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Artifacts are numerous in MRI and can lead to erroneous diagnosis if not understood or eliminated. The magic angle phenomenon produces increased signal in portions of tendons oriented at approximately 55 degrees to the main magnetic field. These areas will appear bright on short TE sequences (e.g., T1) and can lead to an erroneous diagnosis of degeneration or tear.

•

Patient safety is paramount and can be maximized by thorough prescreening and other safety measures.

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Handbook of in Vivo Neural Plasticity Techniques

Julie Hamaide, ... Annemie Van der Linden, in Handbook of Behavioral Neuroscience, 2018

2.1 In Vivo Visualization of the Song Control Nuclei

About the same time as Van der Linden et al. implemented MRI in songbirds, different research laboratories used manganese-enhanced MRI (MEMRI, Box 25.1) to investigate brain activation to, e.g., somatosensory stimulation (Lin and Koretsky, 1997) or to perform in vivo tract tracing experiments (Pautler et al., 1998). Given the modular arrangement of the songbird brain, injection of MnCl2 in one component of the song control system was hypothesized to enable a successful visualization of the entire song control circuitry.

To test this hypothesis, MnCl2 was injected locally in HVC in adult European starlings (Van der Linden et al., 2002). HVC is situated on the caudodorsal surface of the telencephalon, making it an ideal target for stereotactic injections, and sends afferent projections to Area X and RA. Eight hours after injection, both RA and Area X appeared clearly on the T1-weighted images, and their shape clearly matched previous descriptions (Fig. 25.2). Furthermore, volumetric analysis of Area X and RA confirmed the previously described disparity of these nuclei between both sexes (Bernard et al., 1993).

Figure 25.2. Dynamic manganese-enhanced magnetic resonance imaging measurements in starlings. (A) Schematic overview of the songbird song control system. The red arrow indicates the injection site of manganese [into high vocal center (HVC)]. The red boxes indicate the projection areas where manganese is transported and measured, i.e., Area X and nucleus robustus arcopallialis (RA). (B) Sigmoid curves describing the kinetics of manganese transport to Area X and RA in adult male and female starlings. (C) Overview of manganese-enhanced images obtained at different times after injection. A clear difference in the size of Area X (top rows) and RA (bottom rows) between male and female starlings can be observed.

Modified from Van der Linden et al. (2002), with permission from Elsevier.

The previously described study focused on Area X and RA. However, as Mn2+ can be transported transsynaptically, it should be possible to enhance entire circuitries. This was illustrated by Tindemans et al. in canaries (Tindemans et al., 2006). After injecting MnCl2 in HVC and the contralateral MAN, they could discriminate the different (alternating) layers of the chiasma opticum, several laminae, distinct cell layers of the cerebellum, and the deep cerebellar nuclei, etc. This study literally highlighted and confirmed histological tract tracing studies that remote areas, often not directly associated with song control, clearly connect to the song control system. In contrast to previous studies, they used an inversion recovery sequence that required lower doses of Mn2+ but retained a sufficient contrast-to-noise ratio to trace different song control nuclei. Moreover, while exploring the full potential of spin echo inversion recovery sequences in the songbird brain, they were able to achieve anatomical contrast of several song control nuclei even without administration of MnCl2. This highly favorable finding was a first step toward truly noninvasive—without application of exogenous contrast agent—in vivo imaging of the songbird neuroanatomy. More recently, another research group used T2-weighted anatomical scans to evaluate brain regeneration following neurotoxic lesion in adult male zebra finches (Lukacova et al., 2017).

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Magnetic Resonance Imaging

Piotr Sobieszczyk, ... E. Kent Yucel, in Vascular Medicine, 2006

Aortic Dissection

Among the four imaging modalities used in the diagnosis of aortic dissection (see Chapter 34), MRA has the highest sensitivity and specificity in diagnosing types A and B aortic dissections. Similarly, it is 100% sensitive for detection of intramural hematoma.11 MRA offers information beyond the mere diagnosis of dissection. Multiplanar reconstructions identify the location and extent of the intimal tear and its relationship to the branch vessels. Cine images of the proximal aorta can identify aortic regurgitation complicating type A dissection. Cross-sectional delayed phase images allow identification of aortic wall pathology such as intramural hematoma or ulceration. On T1-weighted spin-echo sequences, the intramural hematoma can be seen as a concentric thickening of the wall with increased intramural signal intensity. Inflammatory changes can be seen as arterial wall enhancement. Magnetic resonance imaging is superior to conventional CT in differentiating acute intramural hematoma from atherosclerotic plaque and chronic intraluminal thrombus.12 It is also well suited for evaluation of penetrating atherosclerotic ulcers, defined as ulcerated atherosclerotic lesions penetrating the elastic lamina and forming a hematoma within the media of the aortic wall. This condition is distinct from the classic aortic dissection and aortic rupture. Although life-threatening complications such as aortic rupture are rare, patients with penetrating atherosclerotic ulcers must be closely followed, particularly during the first month after diagnosis. Signs of expanding intramural hematoma or impending rupture, as well as inability to control pain and blood pressure changes, should prompt surgical treatment.12

Comprehensive aortic magnetic resonance examinations of the thoracic aorta currently include multiple nonenhanced and contrast-enhanced sequences, that hinder prompt evaluation of unstable, acutely ill patients. Recent reports suggest the noncontrast MRA techniques can determine the presence or absence of aortic dissection with 100% accuracy in less than 4 minutes.13 The constraints of time and local expertise, however, make CT a more appropriate technique in initial evaluation of an unstable patient. MRA, however, plays an important role in the long-term follow-up of patients with surgically or medically managed disease of the thoracic aorta.14

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Implantable Pacemakers

Paul J. Wang, David L. Hayes, in Cardiac Electrophysiology: From Cell to Bedside (Sixth Edition), 2014

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) has been shown to pose serious risks, including life-threatening arrhythmias and death. A pacemaker system has been designed for safe use in MRIs. Wilkoff et al.29 examined 464 patients randomized to undergo MRI scan between 9 and 12 weeks after implantation or not to undergo an MRI scan. During 1.5-T brain and lumbar MRI scans, there were no clinically significant ventricular arrhythmias, pacemaker inhibition, or changes in threshold.30 MRI imaging can pose serious risks if preexisting leads are in place, even if a pacemaker system designed for MRI is in place.

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Terms and conditions

Tibial Nerve

The tibial nerve is a branch of the sciatic nerve that passes through the popliteal fossa superficial to the popliteal artery.

From: Surgical Pitfalls, 2009

Related terms:

Electromyography

Sural Nerve

Median Nerve

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Digitalis

Nerve Conduction Study

Axon

Hoffmann Reflex

Somatosensory Evoked Potential

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Tibial Nerve

Petra Kaufmann, in Encyclopedia of the Neurological Sciences, 2003

Anatomy

The tibial nerve is derived from the tibial portion of the sciatic nerve and ultimately the lower lumbosacral plexus. It contains predominantly fibers from the L5–S3 roots.

The tibial nerve travels through the popliteal fossa and passes between the two heads of the gastrocnemius muscle. The continuation of the tibial nerve below the upper level of the fibrous arch of the soleus muscle is sometimes referred to as the posterior tibial nerve. In this entry, the term tibial nerve is used for the nerve throughout its course.

The tibial nerve gives of an anastomotic branch to form the sural nerve (together with an anastomotic branch derived from the peroneal nerve), supplying sensation to the lateral ankle and heel area. In addition to the two heads of the gastrocnemius muscle, the tibial nerve innervates the plantaris, soleus, popliteus, posterior tibialis, flexor digitorum longus, and flexor hallucis longus muscles (Fig. 1).

Figure 1. Schematic representation of the tibial nerve and its branches.

As the tibial nerve descends to the ankle, it passes beneath the flexor retinaculum through the tarsal tunnel at the medial malleolus. Within the tarsal tunnel it divides into three or four branches: the medial and lateral plantar nerves and the calcaneal branch (or medial and lateral calcaneal branches). The site of division is variable, particularly for the calcaneal nerve, and can occasionally occur proximally or distally to the tarsal tunnel.

The medial and lateral plantar nerves carry motor and sensory fibers. The motor fibers innervate the small intrinsic muscles of the foot. The medial plantar nerve travels to the sole of the foot under the bony attachment of the abductor hallucis to innervate that muscle and the flexor digitorum brevis and flexor hallucis brevis. The lateral plantar nerve passes between the flexor digitorum brevis and quadratus plantae muscles to innervate the abductor and flexor digiti minimi, the adductor hallucis, and the interossei. The sensory fibers of the medial plantar nerve supply sensation to the area of the great toe and the second and third toes. The lateral plantar nerve supplies sensation to the plantar aspects of the fifth or little toe. The sensory supply to areas under the fourth toe is variable and is often derived from the medial, but occasionally from the lateral, plantar nerves. The medial and lateral calcaneal branches are purely sensory and supply the heel area of the sole (Fig. 2).

Figure 2. Schematic representation of the sensory innervation of the sole of the left foot.

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Tibial Nerve

Y. So, in Encyclopedia of the Neurological Sciences (Second Edition), 2014

Anatomy

The tibial nerve receives nerve fibers from the L5, S1, and S2 spinal roots. After it separates from the common fibular (peroneal) nerve, it travels through the popliteal fossa and passes deep between the two heads of the gastrocnemius muscle. In the posterior compartment of the leg, it gives off branches to the calf muscles (gastrocnemius, soleus, tibialis posterior, flexor digitorum longus, and flexor hallucis longus). As the nerve descends toward the ankle, it travels along the medial aspect of the Achilles tendon and its course becomes superficial. It passes under the flexor retinaculum into the tarsal tunnel, at a location just inferior and posterior to the medial malleolus. Here, the nerve divides into several branches: one or two calcaneal nerve branches that provide sensory innervation to the heel, and the medial and lateral plantar nerves that continue into the sole.

The medial and lateral plantar nerves carry both motor and sensory fibers. The motor fibers innervate the small intrinsic muscles of the foot. The medial plantar nerve innervates the abductor hallucis, flexor digitorum brevis, and flexor hallucis brevis muscles. The lateral plantar nerve innervates the abductor and flexor digiti minimi, the adductor hallucis, and the interossei muscles (Figure 1). The sensory portions of the medial and lateral plantar nerves provide innervation of the soles. Both plantar nerves terminate at the toes by dividing into interdigital sensory branches. The medial plantar nerve supplies sensation to the first, second, and third toes. The lateral plantar nerve supplies sensation to the fifth toe. The sensory supply to the fourth toe is variable and is often derived from the medial, but occasionally from the lateral, plantar nerves (Figure 2). The sural nerve provides the remainder of the sensory innervation of the distal leg. It is composed of sensory fibers arising from the tibial nerve at the popliteal fossa, supplemented by fibers from the common peroneal nerve. The nerve descends down the middle of the calf and provides sensory innervation to the posterior aspect of the distal leg and lateral aspect of the foot.

Figure 1. Schematic representation of the tibial nerve and its branches.

Figure 2. Schematic representation of the sensory innervation of the sole of the left foot.

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Entrapment Syndromes

Mary G. Hochman MD, in Imaging of Arthritis and Metabolic Bone Disease, 2009

Tibial Nerve Compression in the Popliteal Fossa

The tibial nerve (L4-S3) is not part of the conventional popliteal artery entrapment syndrome. Occasionally, however, the tibial nerve may be compressed in the popliteal fossa. Nerve compression by popliteal cysts and by hemorrhage associated with popliteal muscle rupture has been reported111,112 (Figure 14-20, A, B). Mastaglia described six surgically proven cases of tibial nerve entrapment by the tendinous arch of the origin of the soleus muscle.113 The tibial nerve is well depicted on axial T1-weighted and T2-weighted MRI scans. Although dedicated images of the symptomatic leg provide high spatial resolution to better visualize the nerve, imaging both legs can highlight asymmetry of surrounding soft tissues.

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Monitoring somatosensory evoked potentials

David B. MacDonald, in Neurophysiology in Neurosurgery (Second Edition), 2020

3.5.2 Tibial and trigeminal nerves

Tibial nerve stimulation evokes a radial positive (P37) response from the mesial leg area S1 crest [70]. Maximum amplitude is the main localizing criterion because there is no consistent phase reversal. Tibial nerve SEP mapping is less often done partly because of greater difficulty in placing a recording array on leg cortex, but may be indicated with craniotomy near the midline to approach a mesial lesion.

Trigeminal nerve stimulation at the chin, lip, anterior tongue, or palate evokes mainly a positive radial response from the face area S1 crest near the sylvian fissure [71]. Maximal amplitude is the main localizing criterion for this infrequently employed method. Phase reversal is less consistent but may occur with lip stimulation [72].

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Nerves

Lyn Weiss MD, FAAPMR, FAANEM, ... Jay M. Weiss MD, FAAPMR, FAANEM, in Easy Injections, 2007

Local Anatomy

The tibial nerve travels under the flexor retinaculum, which lies between the medial malleolus and the Achilles tendon. The tibial artery and vein, as well as the tibialis posterior and the flexor digitorum tendons, also travel in this space. The tibial nerve runs posterior to the tibial artery. The tibial nerve divides into its two main branches in the region of the tarsal tunnel. These branches are the medial plantar nerve and the lateral plantar nerve. The medial calcaneal nerve generally branches off the tibial nerve at or above the tarsal tunnel and supplies sensation to the medial and plantar surfaces of the heel. The medial plantar nerve supplies sensation to the medial 2–3 toes on the surface of the foot. The first branch of the lateral plantar nerve supplies the abductor digiti quinti muscle. It is also called the inferior calcaneal nerve or Baxter's nerve. Entrapment of this branch is thought by some to be a cause of intractable heel pain. The lateral plantar nerve supplies sensation to the lateral 2–3 toes on the plantar surface of the foot.

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Neurological Rehabilitation

Kevin R. Scott, ... Milind J. Kothari, in Handbook of Clinical Neurology, 2013

Introduction

The tibial nerve arises from the sciatic nerve just proximal to the knee. It descends to the level of the medial malleolus from where it travels under the flexor retinaculum at the medial side of the ankle. The distal tibial nerve then divides into four terminal branches. The medial and lateral calcaneal sensory nerves are purely sensory and supply sensation to the heel of the foot. The medial and lateral plantar nerves contain both motor and sensory fibers, which supply the medial and lateral sole, respectively (Ellis et al., 2005; Preston and Shapiro, 2005).

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Paresis of One Limb

Michael D. Lorenz BS, DVM, DACVIM, ... Marc Kent DVM, BA, DACVIM, in Handbook of Veterinary Neurology (Fifth Edition), 2011

Tibial Nerve

The tibial nerve supplies the muscles that extend the hock and flex the digits. It provides cutaneous sensory innervation to the plantar surface of the foot and the caudal surface of the limb. In most animals, tibial nerve lesions occur in association with peroneal nerve injuries, and a mixture of neurologic signs occurs. In a pure tibial nerve injury, the hock joint is dropped when the animal walks or supports weight (Figure 5-6). The gastrocnemius muscle is atrophied. Loss of sensation occurs from the plantar aspect of the foot. The flexor reflex is severely depressed when the plantar surface of the foot is stimulated. Pinching the dorsal surface of the foot elicits a definite conscious response when stimulated, and the flexor reflex is present even though the toes are not flexed. Isolated tibial nerve injury may follow injections into the thigh muscles. Large so-called trophic ulcers may develop in the digital pads of small animals because of decreased circulation over bony prominences.21,22 Affected animals apparently do not move their limbs to the degree necessary to relieve soft tissue compression.23 In those animals unsuccessfully treated conservatively, surgical correction necessitates grafting of skin from normally innervated cutaneous regions.24

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Pain, Invasive Procedures for

Edgar L. Ross, Edward Michna, in Encyclopedia of the Neurological Sciences, 2003

Tibial Nerve Block

Anatomy

The tibial nerve is one of two major branches of the sciatic nerve. It provides sensation to the posterior portion of the calf, heel, and medial plantar surface of the foot. The tibial nerve begins in the popliteal fossa and descends between the two heads of the gastrocnemius muscle deep to the soleus and then medially between the Achilles tendon and the medial malleolus into the foot.

Indications

Tibial nerve blockade is useful for evaluation and treatment of foot and ankle pain. Injection of the tibial nerve at the ankle can be useful in the diagnosis and treatment of tarsal tunnel syndrome.

Procedure

The nerve is accessible to blockade in the posterior popliteal fossa and ankle. With the ankle approach, the leg is externally rotated and the posterior tibial artery is palpated between the medial malleolus and the Achilles tendon. A 25-gauge needle is introduced slowly toward the posterior groove of the medial malleolus. A paresthesia is often obtained at a depth of approximately 0.5 in. The needle is then slightly redirected and the desired solution injected.

Complications

The main complications of this block are postblock pain, hematoma, and ecchymosis. Because this block can elicit paresthesia, nerve damage is possible if the needle is not slightly withdrawn before injection.

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Structure and Function of the Ankle and Foot

Paul Jackson Mansfield DPT, BS, MS, Donald A. Neumann PhD, PT, FAPTA, in Essentials of Kinesiology for the Physical Therapist Assistant (Third Edition), 2019

Tibial nerve (see Fig. 11.24A)Innervates all of the muscles in the posterior compartment of the leg (see Fig. 11.24B). These muscles perform plantar flexion or combined plantar flexion and inversion as their primary actions. Note that the deep plantar flexor muscles (bottom three) are not visible in this figureGastrocnemius

Soleus

Plantaris

Tibialis posterior

Flexor digitorum longus

Flexor hallucis longusDeep fibular nerve (see Fig. 11.25A)Innervates all muscles in the anterior compartment of the leg (see Fig. 11.25B). These muscles perform dorsiflexion as one of their primary actions.Tibialis anterior

Extensor digitorum longus

Extensor hallucis longus

Fibularis tertiusSuperficial fibular nerve (see Fig. 11.25A)Innervates the two muscles in the lateral compartment of the leg; both perform plantar flexion and eversion (see Fig. 11.25B).Fibularis longus

Fibularis brevis

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Knee Pain of Neural Origin

A. Lee Dellon, in Noyes' Knee Disorders: Surgery, Rehabilitation, Clinical Outcomes (Second Edition), 2017

Proximal Tibial Nerve

Although the tibial nerve (like the common peroneal nerve) arises at the sciatic notch as the medial component of the sciatic nerve and is often clearly a distinct nerve in the thigh, the only well-described site for tibial nerve compression was at the medial ankle in the tarsal tunnel.31 It is now evident that the tibial nerve can be compressed in a site more proximal than the tarsal tunnel, and this site (just distal to the knee) is best described as the proximal tibial nerve, to distinguish it from the tarsal tunnel region. Tibial nerve compression in the popliteal fossa has been described related to the presence of compartment syndrome or space-occupying masses, such as a popliteal artery or a Baker cyst.26,34 Although anatomy texts clearly depict a fibrous arch or soleal sling from which the soleus muscle arises, only recently has there been an anatomic study describing the relationship of this sling to the proximal tibial nerve (unpublished data). This sling lies at a mean distance of 9.3 cm (range, 7-13 cm) from the middle of the popliteal fossa and causes a visible narrowing of the tibial nerve over a length of 1.5 cm in 55% of the cadavers, with a severe constriction being found in 2% of the specimens. With injury to the knee, especially one associated with postoperative bleeding into the popliteal fossa, tibial nerve compression at this proximal site must be considered as a source of symptoms of numbness in the plantar aspect of the foot, with proximal referral to the knee region.

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Terms and conditions

Sciatic Nerve

The sciatic nerve is the most lateral structure leaving the greater sciatic foramen, with the inferior gluteal vessels and nerve, pudendal nerve and internal pudendal vessels medial to the nerve entering the thigh posterior to the adductor magnus.

From: Essential Clinically Applied Anatomy of the Peripheral Nervous System in the Limbs, 2015

Related terms:

Neuropathic Pain

Schwann Cell

Nerve Growth Factor

Central Nervous System

Dorsal Root Ganglion

Tibial Nerve

Axon

In Vivo

Myelin

Protein

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Sciatic Nerve

M.A. Ross, in Encyclopedia of the Neurological Sciences (Second Edition), 2014

Abstract

The sciatic nerve originates from the L4–S2 spinal segments and supplies motor and sensory functions below the knee and motor function to the hamstring muscles above the knee. Exceptions include sensation of the medial leg and foot supplied by the saphenous nerve. Sciatic nerve injuries may complicate hip disorders including fracture, dislocation, or surgery; traumatic injury or physical compression at any location along the nerve; medical disorders such as diabetes, vasculitis, or endometriosis; and intrinsic nerve tumors. Electromyography helps differentiate sciatic neuropathy from other conditions affecting the leg such as plexopathy, radiculopathy, or disorders of the peroneal (fibular) or tibial nerves.

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Emphasizing Histone-Related Chromatin Remodeling in the Central Nervous System of Animal Models of Chronic Pain

Hiroki Imbe, in Epigenetics of Chronic Pain, 2019

Partial Sciatic Nerve Ligation (PSL) Model (Table 1)

PSL increases HDAC1 in the ipsilateral spinal microglia of mouse (Kami et al., 2016). Treadmill running attenuates mechanical allodynia and thermal hyperalgesia resulting from PSL. This treatment dissolves the PSL-induced increase of HDAC1 and increases global acetylation of histone H3 at Lys9 (H3K9ac) in the ipsilateral spinal microglia. The authors speculate that the increase of H3K9ac in the activated microglia might induce the production of IL10 and subsequently downregulate pro-inflammatory cytokines (Kami et al., 2016). Coincident with this result, intrathecal administration of HDAC inhibitor has been reported to attenuate neuropathic pain behavior after PSL (Denk et al., 2013).

Table 1. Neuropathic pain model 1

ModelRegionHistone Modification or Enzyme ExpressionTarget GenesEffect of TreatmentRef.PSL modelThe spinal cordHDAC1 upNATreadmill running—HDAC1 down, global H3K9ac up, relief mechanical and thermal reactionsKami et al., 2016The spinal cordNANAHDAC inhibitor i.t.—relief mechanical reactionsDenk et al., 2013The spinal cordH3K27me3 down at MCP-3 promoterMCP-3MCP-3 antibody i.t.—relief mechanical and thermal reactionsImai et al., 2013The spinal cordGlobal H3K27me3 up, EZH2 upIba1, TNF alpha, IL1-beta, MCP-1EZH2 inhibitor i.t.—relief mechanical and thermal reactionsYadav and Weng, 2017SNL modelThe spinal cordGlobal H3ac down, HDAC1 upNABaicalin i.t.—HDAC1 down, global H3ac up, relief mechanical and thermal reactionsCherng et al., 2014The spinal cordNANAHDAC inhibitor i.t.—global H3K9ac up, relief mechanical and thermal reactionsDenk et al., 2013The spinal cordNAGLT-1, GLASTHDAC inhibitor p.o.—GLT-1 up, GLAST up, relief mechanical reactionHobo et al., 2011The spinal cordNAGLT-1, GLASTHDAC inhibitor p.o.—GLT-1 up, GLAST up, glutamate release down, relief mechanical reactionYoshizumi et al., 2013The spinal cordHDAC4 phosphorylation upNASGK1 inhibitor i.t.—HDAC4 phosphorylation down, relief mechanical reactionLin et al., 2015

Some studies of PSL model have demonstrated that not only acetylation but also methylation of histone plays an important role in neuropathic pain. PSL decreases local trimethylation of histone H3 at Lys27 (H3K27me3) at the monocyte chemotactic protein-3 (MCP-3) promoter in the mouse spinal cord (Imai et al., 2013). The gene transcription of MCP-3 is enhanced in the ipsilateral spinal cord. The increase of MCP-3 occurs mostly in the spinal astrocyte. MCP-3 activates the spinal microglia that express C-C chemokine receptor type 2 (CCR2), receptor for MCP-3. The activation of spinal microglia induces spinal sensitization. Intrathecal administration of MCP-3 antibody attenuates the neuropathic pain behavior and spinal microglial activation. Furthermore, the increase of MCP-3 expression after PSL is obviously reduced in IL6 knockout mice. It is worth knowing that IL6 signaling within the spinal cord is involved in the establishment of this histone modification (Imai et al., 2013). On the other hand, PSL seems to increase global H3K27me3 in the spinal cord. It has been demonstrated that PSL increases enhancer of zeste homologue 2 (EZH2), histone methyltransferase, and global H3K27me3 in the ipsilateral rat spinal cord (Yadav and Weng, 2017). The numbers of EZH2-positive neuron and microglia are increased in the ipsilateral spinal cord. Intrathecal administration of EZH2 inhibitor attenuates the neuropathic pain behavior and reduces the levels of Iba1, TNFα, IL1-β, and MCP-1 in the ipsilateral spinal cord (Yadav and Weng, 2017). Since the effect of H3K27me3 on gene expression is not consistent in these studies, further investigations need to elucidate a role of this histone modification.

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PROXIMODISTAL TRANSPORT OF ACETYLCHOLINE IN PERIPHERAL CHOLINERGIC NEURONS

A. DAHLSTRÖM, ... N.R. SAUNDERS, in Dynamics of Degeneration and Growth in Neurons, 1974

Injection of VIN and COL.

The sciatic nerves of rats were injected with 5 μl of COL (10−2, 10−1 m) or VIN (10−4–10−2) dissolved in saline. Two hours later the sciatic nerves were crushed as described above about 15 mm distal to the site of injection. After a further 6 h the sciatic nerves were removed, divided as shown in Fig. 6, and extracted for ACh. In some experiments VIN or COL was injected into the lumbar region of the spinal cord (4 × 5 μl; see Fig. 7) 6 h before crushing the sciatic nerves. Twelve hours later the 5 mm part of nerve above the crush was removed and extracted for ACh.

FIG. 6. The effect of colchicine and vinblastine on ACh-transport in rat sciatic nerve. Mean ± SEM are given, n indicates number of observations. The ordinate shows the amount of ACh in pmol per 5 or 100 mm piece of nerve after different treatments which are indicated along the abscissa. The injections to the upper right of the figure 2 h before a low crush was made. The stars indicate levels of significance in differences against control nerves, injected with saline or only crushed 6 h prior to dissection.

FIG. 7. The effect of colchicine and vinblastine injections into the lumbar part of the rat spinal cord on the accumulation of ACh in the sciatic nerve above bilateral 12 h crushes. Mean ± SEM are indicated, n = 3–5. Four injections of 5 μl each were made as indicated in the figure to the right (o) 6–7 h before crushing the nerve. Five millimeters of the nerves just above the crush were dissected out 12 h after the crush operation. The top bar shows the ACh content in 5 mm of normal, uncrushed nerve. ACh is expressed in percent of the amounts in 12 h crushed nerves of normal rats.

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Femoral Nerve Blocks

Javad Parvizi MD, FRCS, ... Associate Editor, in High Yield Orthopaedics, 2010

Anatomy:

The sciatic nerve is the largest single nerve trunk of the body, with a diameter of 16 to 20 mm. It arises from the L4, L5, S1, S2, and S3 spinal roots and exits the pelvis posteriorly through the greater sciatic foramen, running laterally along the posterior surface of the ischium anterior to the piriformis muscle. The posterior cutaneous nerve of the thigh escorts the sciatic nerve as it exits the greater sciatic foramen. The sciatic nerve has medial and lateral components, which separate into the tibial and common peroneal nerves in the superior aspect of the popliteal fossa.

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Lower Extremity Nerve Blocks

Uma Shastri, ... Admir Hadzic, in Practical Management of Pain (Fifth Edition), 2014

Anatomy

The sciatic nerve is the largest nerve of the sacral plexus, and it innervates almost the entire leg below the knee. The sciatic nerve passes from the pelvis through the sacrosciatic foramen between the ischial tuberosity and greater trochanter of the femur. It lies anterior to the gluteus maximus muscle and runs with the sciatic artery. It courses down the posterior aspect of the thigh to the popliteal fossa, where it diverges into the tibial nerve (TN) and the common peroneal nerve (CPN) (Fig. 54.12). Sensation to the posterior aspect of the thigh is provided by the posterior femoral cutaneous nerve, which also originates from the sacral plexus, follows a similar course as the sciatic nerve in the thigh, but is not formally part of the sciatic nerve (see Fig. 54.2).

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Anesthetics, local

In Meyler's Side Effects of Drugs (Sixteenth Edition), 2016

Sciatic nerve anesthesia

Sciatic nerve anesthesia can cause cardiovascular depression [581].

•

A 74-year-old man was to receive a combined sciatic nerve and psoas compartment block for a total hip arthroplasty; the classic Labat's approach was used and 30 ml of 0.75% ropivacaine was injected over 1.5 minutes, after which he suddenly became unresponsive and developed tonic–clonic movements. Propofol was administered and the seizure resolved, but he developed sinus bradycardia with progressive lengthening of the QRS interval, which converted to nodal bradycardia. A ventricular escape rhythm at 20/minute with T wave inversion was treated with ephedrine 10 mg and adrenaline 0.1 mg, resulting in supraventricular tachycardia with transient atrial fibrillation.

The authors pointed out that an equipotent dose of bupivacaine would have resulted in worse cardiovascular depression with less chance of successful resuscitation.

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Sciatic Nerve Block

Radha Sukhani M.D., Honorio T. Benzon M.D., in Essentials of Pain Medicine and Regional Anesthesia (Second Edition), 2005

REGIONAL ANATOMY PERTINENT TO SCIATIC NERVE BLOCK

The sciatic nerve is the largest nerve in the body measuring 0.8 to 1.5 cm in width. It is the continuation of the sacral plexus arising from L4, L5 and S1, S2, S3 nerve roots. The roots that form the sciatic nerve exit from the pelvis through the greater sciatic foramen and travel on the anterior surface of the piriformis muscle. From its origin to its termination, the two divisions of the sciatic nerve—tibial nerve (medial position) and peroneal nerve (lateral position)—are distinctly separate. The two divisions, however, are combined into one large single nerve trunk by a connective tissue sheath. Proximally the nerve lies over the posterior surface of the ischium between the ischial tuberosity and greater trochanter of the femur. In this location the sciatic nerve is accompanied by the posterior cutaneous nerve of the thigh and the inferior gluteal artery. Distal to piriformis muscle the nerve lies sandwiched between the gemelli, quadratus femoris, and adductor magnus muscles anteriorly and gluteus maximus muscle posteriorly. In the infragluteal location the sciatic nerve lies over adductor magnus muscle and is crossed obliquely in the mediolateral direction by the long head of the biceps femoris. The sciatic nerve, therefore, lies at first lateral and subsequently deep to the long head of the biceps femoris muscle in the upper thigh. In its entire course, from its origin to its termination in the distal thigh, the sciatic nerve lies deep and covered by large muscle mass except in the infragluteal region. For a brief 3 to 4 cm distance in this location the nerve lies lateral to long head of the biceps femoris muscle covered only by subcutaneous tissue and skin with no overlying musculature.20 In the infragluteal region the nerve lies posteromedial to the femur in the close proximity of the lesser trochanter. The sciatic nerve continues distally in the thigh along the posteromedial aspect of femur under the biceps femoris muscle. At the cephalad portion of popliteal fossa or distal third of thigh, the sciatic nerve divides into its two terminal branches, the posterior tibial and common peroneal nerves. The division may occur higher in the thigh. The two divisions of the sciatic nerve are distinctly separate for the entire length of the nerve, but are combined into one large trunk by a common connective tissue sheath. The need for two separate injections to achieve surgical anesthesia of the tibial and common peroneal divisions of the sciatic nerve has been attributed to this anatomical feature.26–28

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Foot Drop

Bashar Katirji, in Encyclopedia of the Neurological Sciences, 2003

Sciatic Neuropathy

Partial sciatic nerve lesions usually affect the lateral division (peroneal nerve) more than the adjacent medial division (tibial nerve) due to greater vulnerability of the peroneal division of the sciatic nerve to physical injury. This often presents a diagnostic challenge since they imitate a distal selective peroneal nerve injury due to compression at the fibular head. Although the neurological history is useful (such as following a gluteal injection or gunshot wound), the examiner should search for signs of tibial nerve involvement. Common manifestations of sciatic nerve involvement that are inconsistent with a peroneal neuropathy at the fibular head include severe foot pain, absent or depressed ankle jerk, weak ankle inversion, and sensory loss in the sole.

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Sciatic Neuropathy

David C. Preston MD, Barbara E. Shapiro MD, PhD, in Electromyography and Neuromuscular Disorders (Third Edition), 2013

Anatomy

The sciatic nerve is derived from the L4–S3 roots, carrying fibers that eventually will become the tibial and common peroneal nerves. It leaves the pelvis through the sciatic notch (greater sciatic foramen) under the piriformis muscle accompanied by the other branches of the lumbosacral plexus (inferior and superior gluteal nerves and posterior cutaneous nerve of the thigh). In some individuals, fibers destined to become the common peroneal nerve run through the piriformis muscle before joining the sciatic nerve. Covered by the gluteus maximus, the sciatic nerve next runs medial and posterior to the hip joint between the ischial tuberosity and the greater trochanter of the femur (Figure 33–1). The knee flexors, including the medial hamstrings (semimembranosus and semitendinosus) and lateral hamstrings (long and short heads of the biceps femoris), and the lateral division of the adductor magnus are all supplied by the sciatic nerve.

Within the sciatic nerve, fibers that eventually form the common peroneal nerve often are segregated from those that distally become the tibial nerve. The peroneal division of the sciatic nerve runs lateral to the tibial division. The two divisions physically separate from each other in the mid-thigh to form their respective nerves. All sciatic innervated muscles in the thigh are derived from the tibial division of the sciatic nerve, with the important exception of the short head of the biceps femoris, which is derived from the peroneal division. In essence, the short head of the biceps femoris is the only peroneal-innervated muscle above the level of the fibular neck. This muscle assumes special importance in the EMG evaluation of peroneal palsy, sciatic neuropathy, and other more proximal lesions. As the sciatic nerve terminates in the common peroneal and tibial nerves, it supplies all motor and sensory innervation below the knee, with the exception of sensation over the medial calf and foot (saphenous sensory territory).

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Mononeuropathies of the Lower Limb

BASHAR KATIRJI, ASA J. WILBOURN, in Peripheral Neuropathy (Fourth Edition), 2005

Anatomy

The sciatic nerve is formed from convergence of the L5, S1, and S2 ventral rami, with a small contribution from the L4 ventral ramus, after the superior and inferior gluteal nerves arise.7 The nerve is composed of a lateral division (common peroneal nerve, or lateral popliteal nerve) and a medial division (tibial nerve, or medial popliteal nerve), which are enclosed in a common sheath. These two divisions are separate from each other, however, and do not exchange any fascicles.61 The sciatic nerve leaves the pelvis via the greater sciatic notch and usually passes underneath the piriformis muscle. However, in 10% to 30% of subjects the peroneal division alone, or the entire sciatic nerve, passes through or above the piriformis muscle. The sciatic nerve innervates all four hamstring muscles and, partially, the adductor magnus. All of these muscles are innervated by the tibial component of the nerve with the exception of the short head of the biceps femoris, which is innervated by the common peroneal division. Slightly proximal to the popliteal fossa, the sciatic nerve terminates by dividing into its common peroneal and tibial components7,61 (Fig. 61-3).

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Terms and conditions

Nerve Conduction Study

Nerve conduction studies (NCSs) are an essential component of the electromyogram, an electrodiagnostic procedure that is commonly used to assess the neuromuscular system.

From: Encyclopedia of the Neurological Sciences (Second Edition), 2014

Related terms:

Polyneuropathy

Electromyography

Compound Muscle Action Potential

Electrodiagnosis

Lesion

Neuropathy

Axon

Motor Nerve Conduction

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Nerve Conduction Studies

Jasper R. Daube, Devon I. Rubin, in Aminoff's Electrodiagnosis in Clinical Neurology (Sixth Edition), 2012

Nerve conduction studies assist in the evaluation of neuromuscular diseases by providing a physiologic assessment of the peripheral nerve, muscle, neuromuscular junction, dorsal root ganglion cell, and anterior horn cell. They provide the greatest help in assessing peripheral nerve disease. Motor nerve conduction studies assess motor axons by selectively recording muscle responses to nerve stimulation. Sensory nerve conduction studies assess sensory axons by stimulating or recording from peripheral nerves with predominantly sensory axons. Nerve conduction studies most often confirm a clinical diagnosis, but they are also valuable in:

Excluding other suspected disorders

Identifying unrecognized (subclinical) disorders

Localizing focal abnormalities along a nerve

Defining severity with objective measurements1

Characterizing abnormalities, such as conduction block or demyelination

Helping to distinguish axonal disorders from anterior horn cell, neuromuscular junction, muscle, and central disorders, and

Identifying anomalous innervation.

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Nerve Conduction Studies

J. Tavee, K. Levin, in Encyclopedia of the Neurological Sciences (Second Edition), 2014

Introduction

Nerve conduction studies (NCSs) are electrophysiological procedures that assess the peripheral nervous system. The technique consists of electrically stimulating a sensory or motor nerve, and then recording the evoked response. NCSs are an essential component of the electromyogram (EMG), and are typically performed alongside the needle electrode examination.

The EMG is best conceptualized as an extension of the neurological examination. Not only can it help confirm or exclude the clinical impression, but it can also be specifically constructed to serve as a screening assessment for other potential neuromuscular disorders within the differential diagnosis. The EMG is an invaluable neurological tool and helps in providing diagnostic information on disorders affecting the anterior horn cells, peripheral nerves, neuromuscular junction, and muscle fibers.

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Nerve Conduction Studies

Didier Cros, Peter Siao, in Encyclopedia of the Neurological Sciences, 2003

Conclusion

Nerve conduction studies are powerful tools for the diagnosis of peripheral nerve disorders. They are generally complemented by F response studies and needle electromyography. They are essential for the assessment of focal neuropathy and their localization and severity. In generalized neuropathy, emphasis is placed on the distinction between primary demyelinating and primary axonal neuropathies. In this regard, some findings are unequivocally diagnostic of primary demyelination, including marked prolongation of DMLs with normal or near-normal CMAP amplitudes and severe slowing of CVs and CB. Other findings are ambiguous because they may reflect either primary demyelination or axonal degeneration. These include moderate slowing of CVs, low-amplitude CMAPs (which may be caused by either motor unit loss or distal CB), and absent sensory potentials. In difficult cases, multiple nerve studies, F responses, and proximal conduction studies may be very helpful in obtaining an accurate diagnosis.

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Nerve Conduction and Needle Electromyography

JUN KIMURA, in Peripheral Neuropathy (Fourth Edition), 2005

Nerve Conduction Studies

Fundamentals of Nerve Conduction Studies

Basic Principles

Motor Nerve Conduction Studies

Sensory Nerve Conduction Studies

Nerve Conduction in the Clinical Domain

Commonly Assessed Nerves

Cranial Nerves

Major Nerves in the Upper Limb

Nerves of the Shoulder Girdle

Cutaneous Nerves in the Forearm

Major Nerves in the Lower Limb

Nerves of the Pelvic Girdle

Human Reflexes and Late Responses

Blink Reflex

H and T Reflexes

Masseter Reflex

F Waves

A Wave

Clinical Applications

Common Sources of Error

Collision Technique

Anomalous Innervations

Temporal Dispersion and Phase Cancellation

Practical Assessment of Conduction Block: Criteria for Conduction Block

Long and Short Segmental Nerve Conduction Studies

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Diabetes and the Nervous System

Bruce Perkins, Vera Bril, in Handbook of Clinical Neurology, 2014

Summary

Nerve conduction studies are a highly reliable and meaningful way to detect, stage, and monitor DSP. No other test has supplanted NCS for the evaluation of DSP patients, and they are integral to the definition of this disorder. NCS are widely available and a necessary investigation when the diagnosis of DSP is uncertain or confounded by other disorders. Simpler methods, such as screening for monofilament sensitivity, can detect DSP in diabetes clinics and can identify patients at risk for foot ulceration, but confirmation of the diagnosis requires NCS. Finally, the results of the NCS have prognostic significance for end-stage complications of foot ulceration and mortality in subjects with diabetes.

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Thoracic Nerve, Long

G. Rakocevic, in Encyclopedia of the Neurological Sciences (Second Edition), 2014

Nerve Conduction Study of Long Thoracic Nerve

Nerve conduction study (NCS), along with EMG, can be a most helpful study in confirming the diagnosis of LTN dysfunction, and to distinguish other neuromuscular causes of scapular winging. NCS provides information about the type (demyelinating vs. axonal loss) and extent of the lesion. One common technique for NCS is to stimulate either nerve in the neck above the clavicle or near the upper trunk of the brachial plexus; surface recording is made from the serratus anterior muscle (fifth or sixth rib at the midaxillary line). Abnormalities are limited to the involved side and include prolonged conduction time, reduced amplitude of the muscle action potential, or absence of the potential. NCS and EMG should be performed on multiple limbs because electrical dysfunction may extend beyond the confines of the LTN and serratus anterior.

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Muscle Disorders

David Myland Kaufman MD, Mark J. Milstein MD, in Kaufman's Clinical Neurology for Psychiatrists (Seventh Edition), 2013

Nerve Conduction Studies

Nerve conduction studies (NCS) (Fig. 6-7) can determine the site of nerve damage, confirm a clinical diagnosis of polyneuropathy, and distinguish polyneuropathy from myopathy. In addition, they can help separate neuropathies that have resulted from loss of myelin, such as Guillain–Barré syndrome, in which the conduction velocities slow, from those that have resulted from axon damage, such as with chemotherapy, in which the amplitude is reduced.

Nerve damage can lower NCS amplitudes or velocities at the point of injury, which can be located by proper placement of the electrodes, e.g., across the carpal tunnel. With diffuse nerve injury, as in diabetic polyneuropathy, NCS show moderately slowed velocities. Myopathies, in contrast, do not slow NCVs, though amplitudes in motor NCS are often lowered in weak muscles.

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Case 21

Bashar Katirji M.D., F.A.C.P., in Electromyography in Clinical Practice (Second Edition), 2007

Nerve Conduction Studies

Nerve conduction studies (NCSs) in LEMS reveal normal sensory responses. However, motor NCSs disclose low or borderline-low CMAP amplitude in all motor nerves (discussed in a later section). These are usually associated with normal distal latencies, conduction velocities, and F wave latencies.

In general, low-amplitude CMAPs with normal SNAPs are infrequent findings in the EMG laboratory, especially when the findings are diffuse (i.e., every motor NCS has low CMAP, and every sensory NCS reveals normal SNAP). Figure C21-6 outlines the common site of pathology in patients manifesting low-amplitude CMAP responses in all or most motor nerves. These disorders are distinguished by a detailed needle EMG and repetitive nerve stimulation. Table C21-1 lists the common causes of such findings, as seen in the EMG laboratory.

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Clinical–Electrophysiologic Correlations

David C. Preston MD, Barbara E. Shapiro MD, PhD, in Electromyography and Neuromuscular Disorders (Third Edition), 2013

Clinical Syndromes

After recognizing the underlying pattern of NCS–EMG abnormalities as neuropathic, myopathic, central, or secondary to an NMJ disorder, the next step is to identify the distribution of abnormalities (i.e., which nerves and muscles are involved and which are spared). Together, this combination of findings enables the identification of unique clinical patterns.

Mononeuropathy: Non-localizing

NCSNeedle EMGDistributionMotorSensoryAxonal lossAxonal lossNeuropathic findingsLimited to one nerve

Non-localizing mononeuropathy is a familiar pattern in the EMG laboratory. Nerve conductions and needle EMG are normal everywhere, except in the distribution of one nerve. Depending on whether the involved nerve is a sensory, motor, or combination nerve, sensory and motor nerve conductions may be abnormal. In a non-localizing lesion, however, findings on nerve conductions are limited to signs of axonal loss (decreased amplitudes with normal or slightly slowed latencies and CVs). On EMG, neuropathic abnormalities are limited to the distribution of the involved nerve.

Abnormalities on sensory studies identify the lesion as one of peripheral nerve, at or distal to the dorsal root ganglion. Other than that, the mononeuropathy can be localized only at or proximal to the most proximal abnormal muscle identified on the needle EMG. In this pattern, there are no demyelinating findings (i.e., focal slowing or conduction block) on NCSs to localize the lesion definitively. In the EMG laboratory, this pattern is often seen in cases of ulnar neuropathy. In the case of non-localizing ulnar neuropathy, although the lesion most likely is at the elbow in most patients, ulnar conduction studies simply show evidence of axonal loss, without slowing or conduction block across the elbow to localize the lesion.

Mononeuropathy: Localizing

NCSNeedle EMGDistributionMotorSensory

Marked slowing, conduction block, or both across the lesion

Variable axonal loss

Marked slowing, conduction block, or both across the lesion

Variable axonal loss

Neuropathic findingsLimited to one nerve

In a localizing mononeuropathy, nerve conduction and needle EMG abnormalities are limited to one nerve, marking the pattern as a mononeuropathy. Localization is based on electrophysiologic evidence of demyelination at the site of the lesion, either focal slowing, conduction block, or both. Coexistent axonal loss may or may not be present. This is a common pattern, frequently seen in entrapment neuropathies where the underlying primary pathophysiology is demyelination (e.g., carpal tunnel syndrome, radial neuropathy at the spiral groove, peroneal neuropathy at the fibular neck).

Polyneuropathy: Symmetric Stocking-Glove

NCSNeedle EMGDistributionMotorSensoryAxonal loss, demyelination, or bothAxonal loss, demyelination, or bothNeuropathic

Distal affected more than proximal

Lower extremity affected more than upper extremity

Symmetric–bilateral

Length dependent

Polyneuropathies are recognized by generalized abnormalities on nerve conduction studies and neuropathic findings on needle EMG. Nerve conduction abnormalities may indicate either demyelination, axonal loss, or a combination, depending on the type of the polyneuropathy. One of the most common patterns is the stocking-glove polyneuropathy, wherein abnormalities are dependent on the length of the nerve. Longer nerves are preferentially affected. Thus, on both NCSs and EMG, abnormalities are more prominent distally, worse in the legs than in the arms, and more prominent in distal than proximal segments. The vast majority of polyneuropathies, especially those due to toxic, metabolic, or genetic factors, result in symmetric nerve conduction and EMG findings. Side-to-side comparisons often are useful in this regard. Any significant asymmetry should make one question the diagnosis of a symmetric stocking-glove polyneuropathy.

Polyneuropathy: Asymmetric Axonal

NCSNeedle EMGDistributionMotorSensoryAxonal lossAxonal lossNeuropathic findings

Asymmetric

Non-length dependent

Multiple mononeuropathies

The presence of any significant asymmetry in an axonal polyneuropathy may have important diagnostic significance. In some cases, asymmetry or a non-length dependent pattern is seen in typical, symmetric polyneuropathies with superimposed entrapment mononeuropathies or radiculopathies. More important, however, an asymmetric pattern may suggest underlying multiple mononeuropathies. Multiple mononeuropathies (often referred to as mononeuritis multiplex) produce a unique pattern in which individual peripheral nerves are affected in a stepwise manner. Most often, this pattern results from an underlying vasculitic neuropathy. If the pattern is not recognized initially, as further nerves become affected, a confluent pattern of nerve involvement will develop that is difficult to differentiate from a typical distal symmetric polyneuropathy. In such cases, the presence of any asymmetry on NCSs or needle EMG may be a clue to the true underlying mononeuritis multiplex pattern.

Chronic Demyelinating Polyneuropathy with Secondary Axonal Changes: Uniform Slowing

NCSNeedle EMGDistributionMotorSensory

Amplitude: Normal or ↓

CV: ↓↓

DL: ↑↑

LR: ↑↑

Amplitude: ↓

CV: ↓↓

DL: ↑↑

Neuropathic findings

Distal affected more than proximal

Lower extremity affected more than upper extremity

Symmetric–bilateral

↓ = reduced; ↓↓ = moderately reduced; ↑↑ = moderately increased; LR = late responses

Chronic demyelinating polyneuropathy with secondary axonal features is an important pattern to recognize. Although axonal changes are present in all chronic polyneuropathies, few are associated with primary demyelination. The differential diagnosis of a demyelinating neuropathy is further narrowed depending on whether demyelination results in uniform slowing or in conduction block at non-entrapment sites. In neuropathies where demyelination is a uniform process, all nerve segments are equally affected. Consequently, demyelination results in marked slowing of CVs (<75% of lower limit of normal), DLs and late responses (>130% of upper limit of normal), but not conduction block. This pattern of demyelination, uniform slowing without conduction block at non-entrapment sites, is the pattern seen in the inherited demyelinating polyneuropathies (e.g., Charcot–Marie–Tooth). The cardinal features of an inherited demyelinating neuropathy are symmetry comparing side to side, and uniform CV slowing without conduction block. The absence of conduction block at non-entrapment sites is the key feature that separates inherited from acquired demyelinating polyneuropathies.

Chronic Demyelinating Polyneuropathy with Secondary Axonal Changes: Non-uniform Slowing and Conduction Block

NCSNeedle EMGDistributionMotorSensory

Amplitude: Normal or ↓

CV: ↓↓

DL: ↑↑

LR: ↑↑

Conduction block

Temporal dispersion

Amplitude: ↓

CV: ↓↓

DL: ↑↑

Neuropathic findings

Distal affected more than proximal

Lower extremity affected more than upper extremity

Asymmetric

↓ = reduced; ↓↓ = moderately reduced; ↑↑ = moderately increased; LR = late responses

On NCSs, the presence of conduction block at non-entrapment sites and asymmetry usually can differentiate acquired from inherited demyelinating neuropathies with secondary axonal loss. Acquired conditions (e.g., chronic inflammatory demyelinating polyneuropathy) often yield asymmetric NCSs, even when there is apparent clinical symmetry. In addition, conduction block and temporal dispersion at non-entrapment sites always mark the polyneuropathy as acquired; they are not seen in inherited demyelinating neuropathies. This differentiation leads to important implications for further evaluation, prognosis, and potential therapy.

Plexopathy

NCSNeedle EMGDistributionMotorSensoryAxonal lossAxonal lossNeuropathic findingsMultiple nerves of one plexus

In a plexopathy, neuropathic abnormalities are present in more than one nerve but are limited to the distribution of one plexus. To recognize this pattern, it usually is necessary to compare both NCS and needle EMG findings from side to side.

Radiculopathy

NCSNeedle EMGDistributionMotorSensoryNormal or axonal lossNormalNeuropathic findingsLimited to one myotome, including the paraspinals

Radiculopathy is one of the patterns seen most frequently in the EMG laboratory. Because the lesion is proximal to the dorsal root ganglia, sensory conduction studies are always normal in radiculopathy. Motor conductions also are normal, unless muscles used for recording are innervated by the involved nerve roots and the radiculopathy is fairly severe, in which case low CMAP amplitudes may be seen. This is the case in the median and ulnar motor studies for C8–T1 radiculopathy, and in the peroneal and tibial motor studies for L5–S1 radiculopathy. These motor studies may show changes consistent with axonal loss.

Each nerve root supplies a segment of paraspinal muscles before innervating limb muscles, usually by way of several different peripheral nerves. Accordingly, radiculopathy is recognized on needle EMG by a pattern of neuropathic abnormalities that share the same nerve root innervation (i.e., myotomal pattern). Abnormalities usually are expected in distal and proximal limb muscles innervated by the same nerve root but by different nerves. In addition, abnormalities in the paraspinal muscles are key in helping to recognize a radiculopathy. For example, in a C7 radiculopathy, both the flexor carpi radialis (a median-innervated C7 muscle) and triceps (a radial-innervated C7 muscle) may be abnormal, as well as the cervical paraspinal muscles. As with other axonal loss lesions, it is important to remember that the specific neuropathic abnormalities vary, depending on the time course of the radiculopathy.

Polyradiculopathy

NCSNeedle EMGDistributionMotorSensoryNormal or axonal lossNormalNeuropathic findingsMultiple myotomes, including the paraspinals

The polyradiculopathy pattern occurs when multiple nerve roots are involved. It may be seen in diabetes, in cervical–lumbosacral stenosis, or when multiple nerve roots are infected (e.g., by cytomegalovirus) or infiltrated (e.g., by tumor or granulomatous tissue). As in an isolated radiculopathy, sensory studies are always normal. Motor studies may show changes consistent with axonal loss if the recorded muscles are in the distribution of the abnormal nerve roots. On needle EMG, there are neuropathic changes in the paraspinal and limb muscles in the distribution of multiple myotomes. It is important to note that there is no fundamental difference between the NCS–EMG pattern seen in polyradiculopathy and that seen in motor neuron disease. However, the differentiation is easily made on clinical grounds, because patients with motor neuron disease have no sensory complaints or findings and often have additional upper motor signs.

Motor Neuron Disease

NCSNeedle EMGDistributionMotorSensoryNormal or axonal lossNormalNeuropathic findings

± Multiple myotomes

± Thoracic paraspinals

± Bulbar muscles

Because the sensory system is spared in motor neuron disease, sensory conduction studies are always normal. Motor studies can be normal but more often show evidence of axonal loss. Demyelinating features are not seen on motor NCSs. The absence of demyelinating features is critical because some demyelinating motor neuropathies can mimic lower motor neuron disease clinically but are associated with conduction block and other signs of demyelination on NCSs. On needle EMG, motor neuron disease is similar to polyradiculopathy: there are neuropathic abnormalities in the paraspinal muscles and in the distribution of multiple nerve roots. Bulbar and thoracic paraspinal muscles may also be abnormal. Abnormalities in these areas have special diagnostic significance because they are not involved in cervical–lumbar spondylosis (i.e., cervical–lumbar polyradiculopathy), a common condition that sometimes is confused with motor neuron disease.

Neuromuscular Junction: Post-synaptic Disorders

NCSNeedle EMGDistributionMotorSensory

Normal at rest

Decrement: 3 Hz RNS

Increased decrement post-exercise

NormalNormal, unstable, or "myopathic" findings

Proximal affected more than distal

Bulbar

Extraocular

In post-synaptic NMJ disorders (e.g., myasthenia gravis), routine motor and sensory nerve conduction studies are normal. Slow RNS (3 Hz) characteristically results in decrements of CMAP amplitude of more than 10%. Decrements become more marked if RNS is performed several minutes after 1 minute of exercise. Because weakness and fatigue predominantly affect extraocular, bulbar, and proximal muscles, decrements are seen more often with stimulation of more proximal nerves. On needle EMG, MUAPs often are normal in milder cases. With worsening disease, MUAPs become unstable, varying in configuration from potential to potential. If the NMJ disorder is severe enough that persistent blocking occurs, MUAPs become small, short, and polyphasic, with normal or early recruitment, similar to the findings seen in myopathy.

Neuromuscular Junction: Pre-synaptic Disorders

NCSNeedle EMGDistributionMotorSensory

Amplitude: ↓at rest

Decrement: 3 Hz RNS

Increment: 50 Hz RNS

Increment post-exercise

NormalNormal, unstable, or "myopathic" findingsProximal and distal

↓ = reduced

Pre-synaptic and post-synaptic NMJ disorders both show decremental CMAP responses on 3 Hz RNS, and they display similar findings on needle EMG studies. However, two important differences separate the two. First, CMAP amplitudes in pre-synaptic disorders usually are low at baseline compared with post-synaptic disorders, in which they are normal at rest. Second, in pre-synaptic NMJ disorders marked CMAP increments occur after brief voluntary maximal contraction or 50 Hz RNS (often >100% above baseline).

Myopathy: Proximal

NCSNeedle EMGDistributionMotorSensoryNormalNormalMyopathic MUAPs

Proximal affected more than distal

Abnormal paraspinal muscles

Proximal myopathies always result in normal sensory conductions and usually in normal motor conduction studies. Needle EMG shows myopathic findings, most prominent in the most proximal muscles, especially the paraspinal muscles.

Myopathy: Distal

NCSNeedle EMGDistributionMotorSensoryAmplitude: Normal or ↓NormalMyopathic MUAPsDistal affected more than proximal

↓ = reduced

Myopathies that preferentially affect distal muscles (e.g., myotonic dystrophy, inclusion body myositis, distal inherited myopathy) result in myopathic abnormalities that are more prominent in the distal muscles. In addition, motor conduction studies, in which distal muscles typically are used for recording, may show decreased CMAP amplitudes.

Myopathy with Denervating Features

NCSNeedle EMGDistributionMotorSensoryAmplitude: Normal or ↓Normal

Myopathic MUAPs

Fibrillation potentials/positive waves/CRDs

Variable

↓ = reduced; CRD = complex repetitive discharge

The presence of denervating potentials (fibrillation potentials, positive sharp waves, CRDs) in the setting of myopathic MUAPs on needle EMG represents an important myopathic pattern. Denervating potentials are present most commonly in myopathies associated with inflammation or necrosis and occasionally in those due to certain toxins.

Myopathy with Denervating Features: Chronic

NCSNeedle EMGDistributionMotorSensoryAmplitude: Normal or ↓Normal

Fibrillation potentials/positive waves/CRDs

Myopathic findings/neuropathic findings or both

Recruitment relatively spared

Variable

↓ = reduced; CRD = complex repetitive discharge

A chronic myopathy with denervating features is one of the most difficult patterns to recognize. Clinically, this pattern is seen most often in inclusion body myositis, which now is the most common inflammatory myopathy occurring in individuals older than 50 years. After denervation, some reinnervation normally occurs. As the condition becomes chronic, this can lead to complex needle EMG patterns of both myopathic and neuropathic MUAPs, often in the same muscle. However, the degree of neuropathic MUAP changes (large, long, and polyphasic) often appears too abnormal for the mild reduction in recruitment pattern, an important clue to a possible chronic myopathy.

Myopathy with Myotonic Discharges

NCSNeedle EMGDistributionMotorSensoryAmplitude: Normal or ↓Normal

Myotonic discharges

+/− Myopathic MUAPs

Proximal, distal or both

The presence of myotonic discharges on EMG in the setting of myopathic MUAPs has important diagnostic significance. Myotonic discharges with distal predominant myopathic MUAPs are characteristic of myotonic dystrophy. Myotonic discharges are characteristically seen in the paraspinal muscles and very proximal muscles in acid maltase deficiency myopathy. Sparse myotonic discharges in the paraspinal muscles, along with denervating potentials and myopathic MUAPs in the proximal limb muscles, may be seen in polymyositis. Widespread myotonic discharges in the presence of normal MUAPs is characteristic of myotonia congenita and several other genetic disorders.

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