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The sacral plexus and sciatic nerve are formed within the pelvis from contributions of the ventral nerve roots of L4 through S4. The sciatic nerve originates from the sacral plexus within the pelvis and then exits the pelvis through the greater sciatic foramen. Technical advances in the surface coils and pulse sequences used for MRI now make it possible to display the normal anatomy and pathology of the sacral plexus and sciatic nerve in great detail. Introduction of the surgical operating microscope and improved surgical technique have opened the possibility of surgical, medical, or combined therapy for pathologic processes involving this plexus. Successful therapy will then depend on accurate display of the anatomy and pathology of this region.
The sacral plexus is formed by the ventral rami of nerve roots L4 to S4. A variable portion of the L4 ramus joins with L5 to form the lumbosacral trunk. The lumbosacral trunk consistently courses medial to the psoas muscle and enters the pelvis just anterior to the sacral ala and medial to the sacroiliac joint. The ventral rami of S1 to S4 enter the pelvis through the anterior sacral foramina S1 to S4. As the lumbosacral trunk enters the pelvis, it joins the ventral ramus of S1 to form a large upper band. The rami of S2, S3, and S4 join together to form a small inferior band. These bands pursue an inferior, posterior, and lateral course within the pelvis, pass between the internal iliac vessels anteriorly and the piriformis muscle posteriorly, and converge at the greater sciatic foramen to form the sciatic nerve ( Fig. 27-1 ).
The piriformis muscle is the key landmark for identifying the anatomy of the sacral plexus and sciatic nerve. The piriformis originates from the anterolateral aspect of the sacrum at S3 to S5 and passes through the greater sciatic foramen to insert on the greater trochanter of the femur. The nerve roots that comprise the sacral plexus come together on the ventral surface of the piriformis. The piriformis muscle divides the sacral plexus into three anatomic sections. The preplexal portion of the sacral plexus includes the lumbosacral trunk and the portion of S1 situated cranial to the superior border of the piriformis muscle. The plexal segment of the sacral plexus is the portion that lies anterior to the piriformis muscle. The sciatic nerve originates at the inferior margin of the pyriformis. The postplexal segment of the sacral plexus includes the proximal sciatic nerve caudal to the inferior margin of the piriformis muscle in the greater sciatic foramen.
The sciatic nerve is the largest nerve in the body and measures 10 to 20 mm in its largest cross-sectional dimension. It contains contributions from the L4 through S3 nerve roots. The sciatic nerve arises at the anteroinferior surface of the piriformis muscle and exits the pelvis through the anterior third of the greater sciatic foramen, posterior to the ischial spine.
Other important branches of the sacral plexus include the superior gluteal nerve (L4-S1), the inferior gluteal nerve (L5-S2), the pudendal nerve (S2-S4), the nerve to the quadratus femoris and inferior gemellus muscles (L4-S1), the nerve to the internal obturator and superior gemellus muscles (L5-S2), the posterior femoral cutaneous nerve (S1-S3), and the parasympathetic splanchnic nerves of the pelvis (S2-S4). Many important vascular landmarks are present in this region. The common iliac vessels and bifurcations are situated anteromedial to the lumbosacral trunk at the level of the sacral promontory. The superior gluteal vessels pass between the lumbosacral trunk and the S1 (or S1 and S2) nerve(s), exiting the pelvis by turning laterally just inferior to the sacroiliac joint. The inferior gluteal vessels pass between S1 and S2 (or S2 and S3) to lie adjacent to the medial aspect of the sciatic nerve and accompany the sciatic nerve through the greater sciatic foramen. The internal pudendal vessels are located between the pudendal nerve and ischial spine. After coursing through the greater sciatic foramen, the nerve and vessels turn through the lesser sciatic foramen to enter the pudendal canal.
The basic unit of the peripheral nerve is the axon. This axon may be myelinated or unmyelinated and may carry efferent (motor) or afferent (sensory) electrical impulses. Bundles of axons form the individual peripheral nerves in the extremities, as well as the nerves composing the sacral plexus. Large peripheral nerves like the sciatic nerve consist of compartments bounded by three connective tissue sheaths, which support and protect the complex ( Fig. 27-2 ). The innermost compartment is the endoneurium. It consists of loose vascular connective tissue and extracellular fluid. The endoneurial sheath invests the Schwann cell/axon complex. Its inner border is the basement membrane of the Schwann cell. Its outer border is the second connective tissue sheath, the perineurium. The axons, Schwann cells, and endoneurium are bundled together into fascicles, each of which is encompassed by a dense perineurial sheath. The endoneurial fluid within each fascicle is isolated from the general extracellular space by tightly adherent epithelial-like cells, which form the perineurium. The endoneurial space within each fascicle is isolated from the circulating blood by the tight junctions between endothelial cells of the endoneurial capillaries. The perineurium normally acts as a protective barrier against infectious or toxic agents. However, once this barrier is penetrated, there is the potential for spread of disease along the fascicle. The epineurium is the outermost connective tissue sheath. It envelops the nerve and has extensions that encompass each of the perineurial-lined fascicles. This arrangement provides mechanical support for the axons when they are subjected to stretching forces. The epineurium consists of dense, irregular connective tissue, with thick collagen and elastin fibers. Variable amounts of interfascicular adipose tissue are present within the larger nerves. At the central or proximal end of the spinal nerves, the epineurium is continuous with the dura mater. At the distal or peripheral end of the peripheral nerves, the epineurium is progressively reduced in thickness, eventually becoming incorporated into the perineurium.
The diagnosis of plexal involvement has traditionally relied on information obtained from the clinical history, physical and neurologic examinations, and electrophysiologic studies. Clinical evidence of nerve involvement is generally based on dermatomal assessment (areas of anesthesia or hyperesthesia), changes in reflexes, patterns of muscle weakness, and points of tenderness.
Electrophysiologic and nerve conduction studies are widely used and have high sensitivity for detecting a conduction abnormality and hence are an important part of assessing nerve abnormality. These studies aid in confirming the presence of disease and may also help to localize it. However, these studies have significant shortcomings. Nerve conduction measurements reflect the status of the best surviving nerve fibers, so test results may be normal even if a few fibers remain unaffected by the disease process. Focal compression of the nerve may produce localized slowing of conduction; however, presence of normal conduction time does not exclude the compression. Conditions that affect extended portions of the nerve such as segmental demyelination may also cause slowed velocities and are poorly evaluated. Lastly, conduction studies lack specificity and cannot display the anatomic detail needed for precise localization and treatment planning.
Before the advent of ultrasonography, CT, and MRI, radiologic examination of sacral plexus lesions was largely limited to demonstration of the secondary skeletal changes caused by a plexal lesion. Expansion of neural foramina, periosteal reaction, and scoliosis of the lower spine were a few of the indirect signs of plexal involvement.
Ultrasonography has been applied to visualize and evaluate the sacral plexuses and the sciatic nerve. On ultrasonography, the normal nerve appears as a tubular echogenic structure with parallel linear internal echoes on longitudinal sonograms and as a round echogenic structure with punctate echoes on transverse scans ( Fig. 27-3 ). The internal echogenic structure presumably represents fascicles within the nerve. Ultrasonography may demonstrate early changes in neural architecture with peripheral compressive neuropathies similar to those seen with compression of the median nerve in the carpal tunnel. However, the major limitation to using ultrasound in the evaluation of the sacral plexus is its inability to demonstrate the intrapelvic segment of the sacral plexus and the sciatic nerve. Ultrasonography also has inherent limitations with operator dependency, lack of the multiplanar capability, and inferior contrast resolution.
CT has had limited success in demonstrating the detailed anatomy of the sacral plexus. The sciatic nerve itself can readily be identified on axial CT images of the lower pelvis, but the individual extradural peripheral nerves (L4 to S4) that form the sacral plexus and the sciatic nerve cannot be distinguished reliably from adjacent normal intrapelvic soft tissues such as the piriformis muscle, blood vessels, and lymph nodes ( Fig. 27-4 ). In the future, multidetector CT scanners that can image large areas rapidly and that achieve isotropic voxels suitable for multiplanar display may permit the use of CT for imaging the sacral plexus.
MRI of the peripheral nerves (MR neurography) is now the modality of choice for evaluating peripheral nerves and the sacral plexus. MR neurography enables the physician to examine major peripheral nerves for the presence, extent, and localization of structural abnormalities. The ultimate goal of MR neurography is to generate tissuespecific images of nerves analogous to angiograms. To date, this is still a work in progress.
T2-based MR neurography can be applied reliably using existing top-of-the-line clinical MR scanners of 1.5 to 3.0 T with only minor modifications to technique and to radiofrequency coils used for these studies. The predominant technique for MR neurography uses T2-weighted (T2W) techniques. Nerves contain multiple different “types” of tissue water. Evidence suggests that the low-protein endoneurial fluid is what is seen most prominently on T2W MR neurograms. Although endoneurial fluid is responsible for only a fraction of the protons in a nerve that can be imaged, it has distinct properties that increase its detectability and display by T2W MRI. The low protein endoneurial fluid lies within the privileged space of the endoneurium. It is confined by the perineurial blood/nerve barrier and bathes the axons. It exhibits bulk flow directed from proximal to distal along the nerve, and that bulk flow can be disrupted by nerve compression and edema. Technically, by applying a chemical shift-selective pulse, it is possible to suppress the signal from the fat around the nerve and from much of the fat from within the nerve. By selecting an echo time longer than 90 ms, it is possible to achieve a T2 weighting that results in relative suppression of muscle signal. By employing flow suppression techniques, it is possible to eliminate the high signal of flowing blood. Use of all three measures—fat suppression, T2W, and flow suppression—together creates the conditions that allow the generation of peripheral nerve images.
A newer technique, described by Filler and colleagues, utilizes diffusion-weighted imaging to visualize the nerves. To date, diffusion-weighted neurography has shown limited resolution and no clear advantage over T2W neurography.
Imaging of the regional musculature innervated by the sacral plexus contributes little to the diagnosis of sacral plexus neuropathy because most of the muscles innervated by the plexus lie in the lower extremity outside the imaging field of view (FOV). Within the pelvic FOV the gluteal muscles and the piriformis are the most important muscles innervated by the sacral plexus. When detected, increased T2 signal intensity within denervated muscle can help to confirm the presence of, and to localize the specific segments of, nerve injury or disease ( Fig. 27-5 ).
The major change seen with acute or subacute denervation is increased T2 signal in the affected muscle(s) on either T2W or short tau inversion recovery (STIR) images. These changes begin between 4 and 14 days after onset of nerve abnormality or after nerve injury. They may persist for weeks or months if the nerve does not recover. T1W images can also be helpful for diagnosis, by identifying atrophy and fatty infiltration of the musculature, which occur in later stages of denervation ( Fig. 27-6 ). The specific imaging features of denervation atrophy evolve with time, so the pattern of change observed may also help to identify the chronicity of the lesion.
Improvement or normalization of signal intensity within a denervated muscle correlates with re-innervation of the musculature. In our experience, improvement of muscle signal toward normal in the absence of fatty infiltration correlates with recovery of nerve function.
Good visualization of small nerve structures within the sacral plexus requires very highly detailed images. The combination of thin slices, the smallest imaging FOV required, and a matrix size adequate to yield small, submillimeter pixel sizes are all necessary to obtain good images of the nerves. Clinically, diagnostic nerve imaging, therefore, requires an MR scanner of 1.5 T or higher, good magnetic field homogeneity over a relatively large volume, steep gradients to provide high-resolution imaging, and multi-element phased-array surface coils. Sacral plexus imaging typically requires an FOV in the range of 20 to 25 cm and a matrix of 512 × 512.
The imaging protocol for sacral plexus evaluation should include a set of T1-weighted (T1W) images to provide good anatomic definition of (1) nerves outlined by perineural fat, (2) regional muscles, (3) bony landmarks, and (4) regional blood vessels. A fat-saturated T2W imaging sequence is also obtained as a conventional T2W turbo spin-echo image with selective fat saturation, a STIR series, or both. T2W images with fat saturation have the advantage of providing higher signal-to-noise ratio (SNR) compared with STIR images. However, T2W spin-echo imaging sometimes shows a lower sensitivity for detection of abnormal signal change within the nerve and the T2W images can also demonstrate inhomogeneous and inadequate fat saturation due to magnetic susceptibility changes. In such situations STIR imaging is preferred.
In cases in which contrast enhancement is utilized, additional postcontrast fat-saturated T1W series are also obtained to detect subtle enhancement within and around the nerves. In difficult cases a set of precontrast, fatsaturated T1W images may be obtained just before contrast injection to enable direct comparison with the postcontrast images. Having both sets of images improves the sensitivity for detection for contrast enhancement and permits an increased level of confidence for the interpreting physician.
The most reliable imaging plane for assessing nerve pathology is the plane that is orthogonal to the longitudinal axis of the nerve under study. Orthogonal images provide cross-sectional full-thickness images of the nerve, which are free of partial volume artifacts. In-plane imaging oriented parallel or nearly parallel to the long axis of the nerve can help to display the course of the nerve and possible changes in nerve caliber. Because it courses obliquely, the sacral plexus is best imaged with a combination of true coronal and axial plane images through the pelvis. In suspected cases of piriformis syndrome, additional oblique coronal plane images oriented perpendicular to the long axis of the piriformis muscle can be used to accurately assess the sciatic nerve and its relation to the piriformis ( Fig. 27-7 ).
Interpretation of the sacral plexus requires direct comparison of the T1W and fat-saturated T2W or STIR images. The T1W images are needed to see the anatomic detail of the regional nerves, muscles, and bones, because fatsaturated T2W images tend to obscure anatomic landmarks and render all structures a relatively uniform intensity of gray. By comparing T1W and fat-saturated T2W images obtained in the same plane with the same centering and the same FOV, one can visually co-register any two images to identify the nerves and other key structures on the fat-saturated T2W images. In sequential images obtained perpendicular to the long axis of the nerve the course and continuity of the nerve can be readily followed. In some cases multiplanar reformatting is done in oblique planes to obtain an image that provides better visualization of nerve continuity.
Maximum intensity projection (MIP) algorithms have been advocated to provide an image of the nerve distinct from adjacent structures. This is analogous to blood vessel visualization with MR angiography. In our experience, however, this technique works well in only a limited number of cases, when the nerve has abnormally high signal intensity due to intrinsic signal abnormality of the nerve. Use of this technique typically also requires editing of the source images to eliminate high signal from blood vessels and other high signal structures before obtaining the MIP, so this methodology is not often used.
Gadolinium-enhanced imaging is used selectively in sacral plexus imaging based on clinical indications. For most cases, including traumatic nerve injury or compressive neuropathy, a noncontrast examination is sufficient. Nevertheless, contrast material has proved useful— assessment of unexplained nerve enlargement, mass lesions, presence of signs or symptoms suggestive of inflammation or abscess formation, and postoperative evaluations. A standard dose of 0.1 mmol/kg of a gadolinium contrast agent is used and is administered as an intravenous bolus. T1W spin-echo images, with frequency-selective fat saturation, are acquired within 3 to 5 minutes after injection.
Understanding the normal appearance of nerves on MR neurography is the key for accurate and correct interpretation of these studies. In most cases, the only finding on MR neurography is hyperintensity of the nerve or the plexus, which can be subjective. There are no objective criteria to assess the degree or amount of hyperintensity. In interpretation, one first assesses the size, shape, and location of the nerve on T1W images. In some cases, all or part of the course of the nerve may be obscured by surrounding muscle tissue, because of a lack of intervening fat. In these cases, correlative assessment of T1W and T2W images is done to trace the course of the nerve and to monitor its appearance. The normal nerve is oval or round. The size of a sacral plexus and sciatic nerve can vary along the length of the nerve and from person to person, but they tend to be symmetric from side to side. On MR neurograms, the nerve displays a characteristic “dot-like” or honeycomb pattern, which represents the cut cross-section of rod-like collections of fascicles within the nerve ( Fig. 27-8 ). In cross section, the fascicular pattern is more easily discernible on T2W images than on corresponding T1W images. The fascicles are uniform in size and generally mildly hyperintense relative to adjacent muscle on T2W images. The signal intensity seems to vary slightly among nerves, with larger, centrally located nerves having a higher nerve/muscle signal intensity ratio than do smaller, more peripheral nerves. In-plane sections along the length of a nerve typically show uniform appearance and signal intensity within the nerve over the full extent of the FOV.
The anatomy of the sacral plexus and sciatic nerve can be effectively demonstrated with high resolution MRI in the axial and coronal planes ( Figs. 27-9 and 27-10 ). The normal lumbosacral trunk and the sacral plexus have signal intensity similar to that of muscle on T1W sequences and slightly increased signal on T2W sequences. Within the pelvis the sacral plexus and sciatic nerve are surrounded by fat, improving visualization, particularly on T1W sequences. At the level of the greater sciatic foramen, the sacral plexus is identified by its elongated, dot-dash configuration within the fat anterior to the piriformis muscle. If the S2 and S3 nerves are situated on, or interdigitate with, serrations in the piriformis muscle and are not surrounded by fat, these nerves can be difficult to distinguish from the muscle on T1W images. From its position at the apex of the plexus, the sciatic nerve courses laterally and inferiorly through the greater sciatic foramen into the gluteal region. The medially located inferior gluteal vessels can usually be identified by their brighter T2W signal intensity and contour as compared with the sacral plexus and sciatic nerve.
Loss of fat planes on T1W images is one of the abnormal findings associated with infiltrating or compressive lesions, but this appearance may be normal in younger, thinner patients, who have a low percentage of body fat.
Diffuse or focal enlargement of a nerve is definitely an abnormal finding. However, it is difficult to assess mild enlargement of the nerve, especially bilateral enlargement, without substantial clinical expertise. Marked diffuse or focal T2 hyperintensity of the nerve is also an abnormal finding, but assessment of lesser degrees of signal intensity is clearly subjective ( Fig. 27-11 ). At present, there are no reliable quantitative parameters for evaluating the signal intensity of normal versus abnormal nerves. In some compressive neuropathies, focal hyperintense areas are observed in the affected nerve at the site of compression, while normal or nearly normal T2 signal intensity is present both proximal and distal to that region. The exact pathogenesis of this focal change in signal intensity is not known, but it may represent localized edema or increased fluid accumulation within the endoneurial spaces at the site of compression. An altered fascicular pattern is another finding indicative of an abnormal nerve. In some cases, individual fascicles are not resolved even though the MR images are of sufficient quality to do so. In other cases, some fascicles are markedly enlarged and/or hyperintense relative to adjacent fascicles, resulting in a decidedly nonuniform pattern. Changes in the fascicular pattern are almost always accompanied by a marked increase in signal intensity within the abnormal nerve on T2W images.
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