Fig. 10.1
Suprascapular neuropathy at the scapular notch in a 27-year-old patient. Sagittal (a) and axial (b) fat-suppressed T2-weighted MRI show edema of the supraspinatus and infraspinatus muscles. (c) Axial contrast-enhanced fat-suppressed T1-weighted MRI shows a homogeneous enhancement of the infraspinatus muscle. (d) Sagittal T1-weighted MRI shows muscle atrophy and signal increase of the supraspinatus and infraspinatus muscles
Peripheral nerve damage may also be due to many other causes. An acute trauma is also a frequent situation in athletes (direct contusion, blunt trauma, acute stretch injury…) (Figs. 10.2 and 10.3). Most of them are associated with complete recovery.
Fig. 10.2
A 26-year-old soccer player with a hematoma of the common peroneal nerve after a knee trauma. Axial (a) T1- and (b) fat-suppressed T2-weighted MRI show an enlargement of the common peroneal nerve with a loss of the fascicular structure, above the level of fibular head. (c) Axial fat-suppressed T2-weighted MRI shows patchy high signal in tibialis anterior, extensor digitorum, extensor hallucis longus muscles
Fig. 10.3
Axillary nerve trauma after an anterior glenohumeral dislocation. (a) Axial T1-weighted MRI shows a Hill-Sachs lesion and fatty degeneration of the deltoid muscle. (b) Sagittal fat-suppressed T2-weighted MRI shows mild muscle atrophy and a high signal of the teres minor (TM) and deltoid (D) muscles
The nerves close to joints may be compressed by synovial and ganglion cysts, both of them being connected to a joint (Figs. 10.4 and 10.5). According to Spinner, a connection to an articular branch of the nerve, cyst fluid propagation along the path of least resistance, and the variation of intra cystic fluid pressure explain the pathophysiology and the different aspect of intra-neural ganglion cysts [12]. Finally, as for all patients, neurogenic tumors, soft tissue or bone tumors and any inflammatory tissue compressing the nerves may affect athletes (Figs. 10.6, 10.7, and 10.8).
Fig. 10.4
A 28-year-old woman with a spinoglenoidal cyst and a posterosuperior impingement of the shoulder. (a) Axial, (b) coronal and (c) sagittal fat-suppressed T2-weighted MRI show a large cyst of the spinoglenoidal notch responsible for compression of the suprascapular nerve. Note the muscle atrophy and edema of the infraspinatus muscle. MRI also shows some heterogeneity of the posterosuperior labrum with a suspicion of a tear. (d) Axial and (e) coronal reformatted CT arthrography images clearly demonstrates the posterosuperior labral tear connecting with the cyst (arrow). Due to its highly viscous content, the cyst is not completely filled by the contrast medium. (f) Short axis ultrasound image shows the cyst. (g) Picture shows the gelatinous aspect of the cyst content
Fig. 10.5
Spinoglenoidal cyst associated with a SLAP lesion. Its long and tortuous path is in agreement with Spinner’s theory [12]. (a) Coronal fat-suppressed T1-weighted MR arthrography image with fat suppression shows multiseptated associated with the SLAP lesion. (b) Volume rendering CT arthrography image confirms the MRI findings. (From Blum et al. [25])
Fig. 10.6
A 34-year-old patient with schwannoma of the radial nerve. Longitudinal ultrasound of the radial nerve shows a schwannoma (curved arrow) affecting the radial nerve (straight arrow) encompassing its division into superficial and deep branches (arrowheads)
Fig. 10.7
Multiple small neurogenic tumors of the medial antebrachial cutaneous and radial nerves. (a) Ultrasound shows two small neurogenic tumors (arrows) affecting the medial antebrachial cutaneous nerve. (b) Axial, (c) coronal and (d) coronal multiplanar volume reformation fat-suppressed T2-weighted 3 T MRI show two small nerve tumors (arrows) affecting the medial antebrachial cutaneous nerve (arrowhead) and tiny neurogenic tumors of the radial nerve (curved arrow). Note the vascular inflow signal reduction and the absence of ghost artifacts caused by vascular pulsatility facilitating the depiction of the tumors
Fig. 10.8
Quadrilateral space syndrome of the left shoulder due to calcific tendonitis of the triceps tendon at the resorptive stage, 2 months after trauma. (a) Photograph of the patient showing atrophy of the deltoid and teres minor muscles. Initial (b) anteroposterior and (c) Y-view radiographs show calcific tendonitis of the supraspinatus tendon and the triceps tendon (arrow). Follow-up (d) anteroposterior and (e) Y-view radiographs 2 months later show a partial resorption of calcium hydroxyapatite deposits of the triceps. (f) Sagittal reformatted CT image shows the calcification affecting the triceps tendon. (g, h) Sagittal fat-suppressed T2-weighted MRI show muscle edema of the teres minor (TM) and deltoid (D) muscles as well as some inflammatory tissue (arrow) affecting the triceps tendon and the upper part of the quadrilateral space. Note the good depiction of the axillary nerve (arrowhead)
Iatrogenic nerve injuries in one series accounted for 17.4 % of all traumatic nerve injuries [13]. Nerve injuries can result from direct surgical trauma, mechanical stress on a nerve due to faulty positioning during anesthesia, injection of neurotoxic substances into a nerve, compression by a hematoma secondary to drawing blood or through anticoagulation, tourniquets, dressings, casts or orthotic devices (Fig. 10.9). Sites especially likely to be affected include the carpal tunnel and wrist, as well as the knee and the shoulder [14–16]. Neurologic complications associated with regional anesthesia are uncommon. Although intraneural injection during regional anesthesia has a higher incidence than previously appreciated it is not necessarily associated with nerve injury [17].
Fig. 10.9
A 26-year-old woman with an iatrogenic sciatic nerve injury due to a nerve block and resultant permanent residual deficits. (a) Axial fat-suppressed T2-weighted MRI shows an enlargement of the sciatic nerve (arrow) surrounded by soft tissue edema. (b) Axial fat-suppressed T2-weighted MRI of the calf shows patchy muscle edema mostly affecting the gastrocnemius muscles
Disabled athletes face many challenges during training and competition [18]. Stump pain is a common problem following limb amputation. The etiology is often multifactorial and the treatment challenging [19, 20]. Nerve section is responsible for scar tissue formation, so-called traumatic neuroma that occurs at the end of an injured nerve, usually 1–12 months after amputation (Fig. 10.10). During amputation, careful management of the peripheral nerves is critical to minimize painful neuroma formation. Most traumatic neuromas are asymptomatic but a painful neuroma makes it virtually impossible to mount a well-fitting prosthesis socket. MRI is the key examination to localize the neuroma, show its relationship with adjacent bone and eventual heterotopic bone formation, make the differential diagnosis with stump bursitis and evaluate the soft-tissue coverage [21–23].
Fig. 10.10
Neuroma of the posterior tibial nerve after leg amputation. Axial (a) unenhanced and (b) contrast-enhanced fat-suppressed and T1-weighted MRI show the neuroma (arrow). (c) Sagittal fat-suppressed T2-weighted MRI shows the neuroma covered by muscles. Note also bursitis under the lower extremity of the tibia
Parsonage-Turner syndrome, also called brachial neuritis and idiopathic neuralgic amyotrophy, is the main differential diagnosis of entrapment syndromes as it may simulate suprascapular nerve entrapment, quadrilateral space syndrome or long thoracic nerve neuropathy (Figs. 10.11 and 10.12) [24–26]. This syndrome is characterized by a sudden onset of severe shoulder pain lasting about 2–4 weeks. It affects young men without a history of trauma; pain is followed by paralysis and atrophy of muscles of the scapular girdle and sometimes of more distal arm muscles. The anarchic distribution of muscle denervation depending on which of the brachial plexus nerves are affected is the hallmark of this syndrome. Parsonage-Turner syndrome can affect almost any nerve in the brachial plexus, although damage in the upper and middle trunk distribution with involvement of the long thoracic and/or suprascapular nerve occurs most frequently (70–97 %) [26–28]. Other nerve trunks can be affected (phrenic nerve, cranial nerves). The presence of sensory signs is common. Bilateral but asymmetrical symptoms occur in 2–34 % of cases [27]. Persistent neuropathic pain may follow the acute setting. The clinical diagnosis is confirmed by EMG or MRI, which plays a major role in the differential diagnosis.
Fig. 10.11
A 22-year-old man with Parsonage-Turner syndrome due to a left suprascapular and accessory nerves palsy. (a) Photograph of the patient showing a winging scapula of the left shoulder. (b) Axial fat-suppressed T2-weighted MRI shows muscle edema of the infraspinatus and trapezius muscles (arrows). (c) Axial water-imaging with a three-point Dixon MRI shows the muscle edema of the infraspinatus and trapezius muscles (arrows). Note the good signal homogeneity of the image
Fig. 10.12
A 43-year-old man with Parsonage-Turner syndrome due to an isolated right suprascapular nerve palsy mimicking a nerve entrapment syndrome. (a) Sagittal fat-suppressed T2-weighted MRI shows a muscle edema of the supraspinatus and infraspinatus muscles. (b) Sagittal T1-weighted MRI shows atrophy and fatty degeneration of the supraspinatus and infraspinatus muscles. Note the fatty degeneration is more severe for the supraspinatus muscle
The origin of this predominantly multifocal axonal damage to the brachial plexus is still poorly understood. Immune dysfunction remains the most plausible hypothesis in the presence of infectious or vaccine triggers, and in some cases of antimyelin antibodies.
Finally, some degenerative changes of the nerves and some inflammatory neuropathies remain of unknown origin (Figs. 10.13 and 10.14).
Fig. 10.13
Idiopathic fibrosis and cystic degeneration of the common peroneal nerve. (a, b) Axial fat-suppressed T2-weighted MRI show an enlargement and a cystic degeneration of the common peroneal nerve (arrow) and edema of the tibialis anterior, extensor digitorum, extensor hallucis longus muscles
Fig. 10.14
A 37-year-old patient with inflammatory polyneuropathy of unknown origin. (a, b) Coronal water-imaging with a three-point Dixon sequence MRI show an enlargement of the right cervical roots (arrow) and a muscle edema of the muscles of the right scapular girdle (arrowheads)
10.4 Imaging Modalities of Neuropathies and Muscle Denervation
High-resolution ultrasound and magnetic resonance imaging (MRI) are the two imaging methods of choice for the study of peripheral nerves. Conventional radiography and CT scans have a more limited input. CT arthrography (with delayed acquisitions) may play a role to detect the joint anomalies associated with a ganglion cyst and show its connection with the joint.
10.4.1 Ultrasound
High-resolution ultrasound is currently the imaging modality of choice for the examination of peripheral nerves, particularly because of the unrivaled spatial resolution it provides [29–31]. In addition, ultrasound is a noninvasive and low-cost technique and has two major advantages: It allows dynamic imaging (as in the assessment of subluxation of the ulnar nerve in the elbow) and analysis of the entire length of peripheral nerves along their anatomical course. The transducer frequency is chosen based on the size of the nerve and the depth of the anatomical region to be examined.
Using musculoskeletal presets and high frequency linear probes (10–17 MHz), the majority of peripheral nerve trunks, i.e. the median, radial, ulnar, sciatic, common fibular and tibial nerves, can be examined. However, nerves that are more proximal may be more difficult to analyze. The nerve is identified and its perineuronal environment studied on axial sections in which the peripheral nerve appears as an oval structure, consisting of a network of hypoechogenic fascicles separated by hyperechogenic septa. In longitudinal sections, it appears as a tube containing hypoechogenic bands separated by hyperechogenic lines (Fig. 10.15). The characteristic fascicular structure allows peripheral nerves to be distinguished from tendons, which have a fibrillar echo structure.
Fig. 10.15
Normal appearance of the median nerve. (a) Short axis ultrasound image shows the peripheral median nerve (arrows) as an oval structure, consisting of a network of hypoechogenic fascicles separated by hyperechogenic septa. (b) Longitudinal ultrasound image shows the median nerve (arrows) as a tube containing hypoechogenic bands separated by hyperechogenic lines
Ultrasound plays three roles in the diagnosis of entrapment syndromes [1, 32]:
to look for nerve morphology abnormalities as a result of compression, which may produce two major signs:
segmental changes in diameter, usually focal thinning at the point of compression and downstream enlargement immediately after the compression; an increase in nerve diameter may also be seen proximal to the compressed area.
loss of the usual fascicular echo structure, the nerve becoming hypoechogenic and the fascicles are difficult to visualize.
to identify lesions in the perineuronal environment responsible for compression: soft tissue tumors, musculoskeletal abnormalities such as synovial cysts, tenosynovitis or supernumerary tendons and vascular abnormalities (Figs. 10.4, 10.6, and 10.7).
to guide cyst aspiration and/or corticosteroid injection.
Ultrasound may also depict the consequences of muscle denervation. On ultrasound, fatty degeneration and muscle atrophy appear as increased echogenicity of the muscle and resultant poor differentiation between the tendon and the muscle. Fatty atrophy also results in decreased muscle bulk. However, these anomalies are not specific and ultrasound is not able to depict muscle edema with any certainty.
Contrast-enhanced ultrasound could play a role in the future as animal studies have shown that it enables quantitative measurement of nerve perfusion and shows a significant signal enhancement of denervated muscle [33].
10.4.2 MRI
MRI is the most efficient technique for diagnosing neuropathies and entrapment syndromes. Improvements over the last couple of decades–high-field units, improved coil design and more robust sequences–have increased image quality with higher spatial resolution, better signal homogeneity and vascular inflow signal reduction, allowing better delineation of the nerves and an enhanced depiction of muscle edema associated with denervation.
10.4.2.1 Technical aspects
T1 sequences allow good identification of the peripheral nerves, which appear on cross-sectional images as numerous small hypointense dots (corresponding to the nerve fascicles) surrounded by high signal-intensity connective tissue (corresponding to the epineurium) that contains a certain amount of fat. With fat-suppressed T2-weighted sequences, peripheral nerves appear isointense to mildly hyperintense compared with normal muscle. Nerve fascicles, which contain endoneural fluid, may have slightly higher signal intensity than the surrounding connective tissue (Fig. 10.16). STIR, periodically rotated overlapping parallel lines with enhanced reconstruction (PROPELLER®, BLADE®) sequence and Dixon three-point sequence are very sensitive to fluid and may be used as an alternative to T2-weighted fast spin-echo sequences. MR neurography based on 3D volume acquisitions may also improve the depiction of nerves anomalies. It provides high quality isotropic images with the possibility of curvilinear multiplanar reconstructions and post-processing such as MIP or image fusion, which are particularly useful in examining complex anatomical structures like the brachial plexus [34–36].
Fig. 10.16
Axial fat-suppressed T2-weighted MRI of the median nerve (arrow) and ulnar nerve (arrowheads). Peripheral nerves appear isointense to mildly hyperintense as compared with normal muscle. Nerve fascicles, which contain endoneural fluid, may have slightly higher signal intensity than the surrounding connective tissue
It is noteworthy that even with longer echo times, the magic angle phenomenon may increase the signal intensity of the nerves when the nerve fibers are oriented at an angle of about 55° to the constant magnetic induction field B0. However, neuropathic lesions are clearly distinguishable from an artificial increase of intraneural T2 by the magic angle effect [37, 38].
Diffusion tensor imaging, a technique for imaging anisotropy based on the measurements related to the molecular motion of water, provides information on peripheral nerves, which are characterized by an anisotropic arrangement of the nerve fibers. The molecular motion of water preferentially occurs along the axis of the nerve fibers, whereas it is much less in the direction perpendicular to this axis. Tractography (or fiber tracking) allows visualization of 3D fiber tracts via a mathematical representation (Fig. 10.17). Tractography could have clinical applications in entrapment neuropathies such as carpal tunnel syndrome and in peripheral nerves injuries [39–42].
Fig. 10.17
Schwannoma of the ulnar nerve. (a) Axial fat-suppressed T2-weighted MRI shows the nerve is enlarged and hyperintense. (b) Tractography shows disorganization of the nerve fibers
MRI plays a major role in the diagnosis of entrapment syndromes by identifying nerve anomalies, lesions in the perineural environment and muscle denervation [43].
10.4.2.2 Pathological Features of the Morphology, Signal and Course of the Nerve
flattening of the nerve, particularly in areas liable to be compressed, is abnormal. This sign is particularly valuable if the flattening is segmental and associated with an increase in diameter of the upstream nerve segment;
an increase in diameter, particularly a segmental increase preceded and followed by a nerve of normal diameter, is also considered pathological;
hyperintensity on “neurography” sequences: this is reported to be the result of decrease in axonoplasmic flow due to neuronal degeneration and peri- and endoneural edema;
loss of the fascicular structure on T2-weighted sequences with fat suppression also indicates disease and is due to the same causes;
moderate contrast enhancement on T1-weighted sequences after gadolinium injection, reflects a breach of the blood-nerve barrier;
a deviation or change in direction of a nerve is evidence for compression or a pathological adhesion. It is therefore an excellent criterion to assess entrapment syndromes, particularly for recurrences or failures after surgery [1].
10.4.2.3 MRI of Muscle denervation
Finally, MRI is the only imaging technique that clearly shows the consequences of muscle denervation. Initially the muscle remains normal in size and morphology, with clear global hyperintensity on T2-weighted sequences. The edema is visible early, experimentally as soon as 48 h, and persists throughout the acute and subacute phase of denervation, usually for less than 10 weeks and very rarely for more than 6 months. The intensity of the T2 signal increase is reported to be proportional to the severity of nerve damage [3, 46, 47].
However, muscle edema may be missing on MRI when inappropriate sequences with insufficient sensitivity to fluid are used, when the image quality is poor or when the denervation is either minor or chronic (Table 10.1; Fig. 10.18).
Table 10.1
Causes of lack of muscle edema on MRI in compressive neuropathy
Compression of sensory branches only |
Minor denervation |
Chronic denervation |
Poor image quality |
Inappropriate sequence |
Fig. 10.18
A 29-year-old man with suprascapular nerve entrapment at the suprascapular notch. Axial (a) fat-suppressed and (b) water-image IDEAL T2-weighted MRI show muscle edema is more visible on image b for different reasons: the signal-to-noise ratio is better and the signal homogeneity is better. However, the spatial resolution is lower on image b
Muscle edema usually affects the entire muscle with the same intensity. In some situations, edema is more prominent around the myotendinous junction. The significance of this pattern is not clear. It may reflect increased vascularity and capillary permeability around the myotendinous junction in the subacute phase. In our experience, this finding is more frequent in Parsonage-Turner syndrome than in entrapment syndromes [25, 48]. Significant muscle enhancement after gadolinium injection is seen in this phase [2].
Secondarily, loss of muscle volume (muscle atrophy) associated with hyperintense T1-signal (fatty degeneration) is seen. This chronic phase of denervation, which occurs in the months following the initial lesion, persists if re-innervation does not occur. Uncommonly, muscle denervation is associated with muscle hypertrophy (Fig. 10.19) [49]. In Parsonage-Turner syndrome, acute and chronic muscle denervation may co-exist.
Fig. 10.19
Neurogenic muscle hypertrophy associated with an S1 radiculopathy due to a disk herniation (From Zabel et al. [49]). Axial fat-suppressed T2-weighted MRI of the calf shows enlargement, edema and fatty degeneration of the medial gastrocnemius
10.5 Entrapment Neuropathies of the Shoulder
Entrapment neuropathies are relatively common, accounting for about 2 % of cases of sport-related shoulder pain. The most frequent one is the suprascapular nerve entrapment syndrome. Quadrilateral space syndrome, long thoracic nerve and accessory nerve neuropathies are less frequent. Parsonage-Turner syndrome is the main differential diagnosis [25, 46, 53, 54].
10.5.1 Suprascapular Neuropathy
Suprascapular neuropathy was first described by Thomas in the French literature in 1936 [55]. Suprascapular neuropathy is one of the most frequent manifestations of injury to the peripheral branches of the brachial plexus in athletes. It is particularly common among volleyball and tennis players, but other sports may also be implicated (notably throwing sports and weightlifting). Trauma is usually related to stretching and/or contusion of the nerve. Depending on the movement the patient made, nerve damage occurs either in the suprascapular notch or, more distally, in the spinoglenoid notch. Compression by a labral or mucoid cyst is also common. The site of compression determines the effect on the muscles [56–61].
10.5.1.1 Anatomy
The suprascapular nerve is a peripheral mixed sensorimotor nerve arising from the superior trunk of the brachial plexus (C5–C6) and in 15–22 % of cases C4. It provides motor innervation of the supraspinatus and infraspinatus muscles, and sensory branches innervate the subacromial bursa, acromioclavicular and glenohumeral joints and sometimes the lateral shoulder. Downstream from its origin in the brachial plexus, the suprascapular nerve crosses the posterior cervical triangle and then the deep face of the trapezius muscle in the direction of the suprascapular notch, which it crosses to enter the supraspinous fossa.
The suprascapular notch varies considerably in size and shape, and Rengachary has classified six types [62–64]. A U-shaped form is most common and least likely to damage the suprascapular nerve. Narrow (9 % of cases) or closed (4 %) notches are theoretically more pathogenic but this has not been proven (Fig. 10.20).
Fig. 10.20
Volume rendering technique show the great morphological diversity of the suprascapular notch in patients without neuropathy. (a) flared notch (b) indented notch (c) closed notch (From Blum et al. [25])
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