High-resolution MR imaging of the peripheral nervous system (MR neurography) has gained acceptance as a clinical tool in the diagnosis of peripheral neuropathy and plexopathy. Clinical indications include the following: 1) suspected mass involving a peripheral nerve, 2) entrapment syndrome, 3) traumatic nerve injury, 4) post-treatment evaluation, and 5) symptoms unexplained by clinical examination (1). Morphologic and MR signal intensity characteristics of individual nerves or nerve plexuses are assessed visually in determining whether a nerve is normal or likely to have pathologic changes. Secondary imaging characteristics such as muscle denervation changes are used to aid in identification of the affected nerve(s). Focal or diffuse enlargement, a markedly nonuniform fascicular pattern, and loss of surrounding fat planes, as well as postcontrast enhancement of a nerve, are features that have been associated with neuropathy in the clinical settings noted above. The feature that has been most often used as a marker of disease is hyperintensity on short tau inversion recovery (STIR) or fat-saturated (fatsat) T2-weighted fast-spin-echo (FSE) images. This feature, as pointed out by Chappell et al in their article in this issue of the AJNR, must now be evaluated more cautiously because normal peripheral nerves can exhibit increased signal intensity, mimicking disease, depending on the orientation of the nerve relative to the main magnetic field Bo of the MR system—“the magic angle” effect. In retrospect, this orientational dependence of signal intensity may be one of the factors—along with partial volume effects, signal intensity variation associated with the use of surface coils, inhomogeneous fat suppression with fatsat acquisitions, and differences between investigators in the choice of pulse sequence parameters—that have complicated the qualitative and quantitative differentiation of diseased nerves (especially the components of the brachial plexus) with mild or moderate hyperintensity from normal nerves, which are usually described as isointense to mildly hyperintense to adjacent muscle on STIR or fatsat T2-weighted FSE images.
Chappell et al have provided evidence of a magic angle effect for peripheral nerves by showing that there is a 46–175% increase in signal intensity in the median nerve as its orientation relative to the main Bo magnetic field changes from 0° (parallel to Bo) to 55° (the magic angle), accompanied by an increase in mean T2 relaxation times from 47.2 to 65.8 ms. Images depicting the signal intensity changes in the ulnar and sciatic nerves and brachial plexus as a function of orientation relative to Bo suggest that the effect is likely to be generalized for peripheral nerves and nerve plexuses. By presenting data acquired at 0.5 and 1.5 T, the authors demonstrate that the effect is not an “artifact” limited to one system or field strength. Finally, the authors show that a two-compartment model with chemical exchange, in which one compartment has protons with angle-dependent T2 and the other compartment has protons with angle-independent T2, provides a good fit to the data for the median nerve and the flexor tendon. The similar fit for peripheral nerve and tendon data strengthens the argument for a magic angle effect and implicates collagen as the structural component responsible for the effect.
The magic angle effect in tendons has been well characterized and results from the abundance of collagen, which has a highly ordered structure with bound water molecules (2–4). The protons in the bound water typically produce very short T2 values because of dipole-dipole interactions between nearby spins that result in dephasing of the MR signal intensity. Hence, tendons usually appear dark on MR images. The dipole-dipole interactions however, are minimized when the collagen fiber makes an angle of 55° (or 125°) with the direction of Bo. This contribution to relaxation is then diminished and results in increased T2 and higher signal intensity within tendons. As illustrated by Chappell et al in Figure 1 of their article, and as described by many earlier investigators (3), the mean T2 for tendons is generally short enough, and the dependence on orientation narrow enough, that tendons often remain visibly dark on STIR or T2-weighted images even as the magic angle is approached. The mean T2 for the median nerve reported by Chappell et al, though, is longer than the value for tendons, and as the magic angle is approached, the isointense or mildly hyperintense nerve becomes visibly brighter as a result of the increase in signal intensity. Figure 1 demonstrates clearly that the magic angle effect for nerves may be more evident to the eye of the radiologist than the effect for tendons.
Why do peripheral nerves exhibit T2 anisotropy, resulting in the magic angle effect? Probably because peripheral nerves, like tendons, have collagen as a major structural component. Tendons consist of thick bundles of parallel, densely packed, Type I collagen fibers, and these hydrated fibers account for the T2 anisotropy. The largest peripheral nerves have three distinct layers of connective tissue: 1) endoneurium, which invests the axon–Schwann cell complex, is a loose connective tissue consisting of small, variably oriented, collagen fibrils, along with cellular elements and extracellular fluid; 2) perineurium, which ensheaths the endoneurium/axon–Schwann cell complexes forming fascicles, is more dense and consists of flat fibroblast-like cells interleaved with layers of longitudinally oriented collagen fibers and a few elastic fibers; and 3) epineurium, which envelops the nerve and sends extensions to surround the separate fascicles, is a dense, irregular connective tissue dominated by longitudinally oriented collagen fibers. As noted by Chappell et al, 49% of the total protein in whole nerve is collagen, primarily type I, and most of the collagen is located in epineurium, which occupies 22–88% of the nerve cross-sectional area.
Thus, the T2 anisotropy of peripheral nerves results from densely packed hydrated collagen, which is primarily located in epineurium. Although this conclusion seems reasonable, scrutiny of Figure 1 raises questions about the strict analogy with tendon. First, the marked increase in signal intensity in the median nerve at the magic angle (55°) in Figure 1 appears to be located within the perineurium-lined fascicles and not within the surrounding epineurium. This apparent discrepancy between the expected and the apparent location of the magic angle effect may be clarified by a correlative MR-anatomic study of the median nerve from cadaver wrist specimens, analogous to the work of Ikeda et al (5). Second, intrafascicular tissue, which appears to be responsible for the magic angle effect, has mild hyperintensity at 0° rather than the marked hypointensity of collagen in tendon. The etiology of this difference may be clarified by studies of the multicomponent T2 relaxation time behavior of peripheral nerves in vivo and in vitro (6) with histologic correlation.
In summary, Chappell et al have made a significant contribution to the literature on MR imaging of peripheral nerves. Neuroradiologists performing MR neurography studies should be just as aware of the magic angle effect for peripheral nerves as musculoskeletal radiologists are of the effect for tendons and ligaments. The potential for confusion in image interpretation should be considered when positioning the patient for the MR study, when employing unusual orientations or provocative tests involving flexion or extension of joints, and when evaluating the brachial and lumbosacral plexuses. Although the anatomic basis for orientational dependence of the signal intensity of peripheral nerves in vivo will require additional studies, Chappell et al have established the importance of recognizing the clinical diagnostic implications of the magic angle effect. Furthermore, they have suggested that the effect, rather than being viewed as a pitfall in interpretation, may be exploited as a tool to assess the integrity of nerves. A decrease in the magic angle effect, secondary to an abnormal accumulation of free water or disruption of highly ordered structures like collagen, may be sought as a sign of an injured or diseased nerve.
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