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Thoracic outlet syndrome (TOS) is a disorder characterized by compression of the lower trunk of the brachial plexus, most often in association with anomalous congenital fibromuscular bands in the scalenic region. Early diagnosis is important, because the neurologic deficit associated with TOS may be irreversible. Using high-resolution ultrasound, we investigated 20 consecutive patients with clinical signs suggestive of TOS (all females, average age: 40.4 ± 14.9 y) and 25 control patients. In 19 patients, we identified a hyper-echoic fibromuscular structure at the medial edge of the middle scalene muscle, which indented the lower trunk of the brachial plexus (“wedge-sickle sign”). It was associated with the significant enlargement (p < 0.0001) and hypo-echogenicity of the lower trunk. This novel and distinctive ultrasonographic sign allows pre-surgical identification of anomalous fibromuscular bands causing TOS. It is especially useful in patients without neurologic deficit, in whom the diagnosis may not be as straightforward.
The term thoracic outlet syndrome (TOS) was coined for a group of disorders characterized by compression of the brachial plexus or the subclavian vessels at any point in the thoracic outlet region (
). According to the classification presently in use, it comprises five distinct clinical syndromes: arterial vascular TOS, venous vascular TOS, traumatic neurovascular TOS, true neurologic (neurogenic) TOS and non-specific TOS (
). In neurogenic TOS, the brachial plexus is typically compressed in the scalenic triangle at the level of the lower trunk or the distal portion of its constituents, the C8 and Th1 anterior primary rami (roots). This gives rise to a characteristic clinical syndrome with selective wasting of the thenar and the first dorsal interosseous muscle (
) and sensory disturbance on the medial aspect of the forearm, with or without pain in the affected arm. The electrophysiologic hallmark of neurogenic TOS is the demonstration of post-ganglionic sensorimotor C8–Th1 axon loss, with Th1 being more affected and earlier (
), is a controversial category with a lack of consensus on its etiology, pathomechanism and treatment. It is characterized by subjective symptoms such as pain and paresthesia in the arm and the feeling of fatigue of the arm, especially when lifted overhead, with no clinical deficit.
Congenital anomalies or anatomic variations of the thoracic outlet region, particularly the supernumerary cervical rib attached to the seventh cervical vertebra, have been historically implicated in TOS (
). Roos, with extensive surgical experience in TOS, was the first to focus attention on anomalous fibromuscular bands with or without a cervical rib in the thoracic outlet region as the real culprit in neurogenic TOS (
). These “Roos ligaments” were originally identified based on surgical and cadaveric studies, but today, modern imaging techniques such as magnetic resonance imaging (MRI) and high-resolution ultrasound (HRUS) are available for their possible pre-surgical detection and the facilitation of diagnosis. Some MRI data are already available (
). We present here a consecutive case series of patients with neurogenic and non-specific TOS assessed by HRUS.
Methods
Approval for the retrospective analysis of patient data was obtained from both institutional ethics committees. Twenty consecutive patients, assessed at two tertiary referral centres for neuromuscular disorders between 2014 and 2016, were included in the analysis (Table 1). Criteria for inclusion of patients in the study were clinical symptoms and signs suggestive of TOS and the exclusion of other disorders, such as carpal tunnel syndrome, ulnar nerve lesion and C8–Th1 radiculopathy. All patients gave informed consent for the examinations, and retrospective analysis was performed using anonymized patient data. Healthy controls were examined prospectively with informed consent.
Table 1Patient characteristics and findings
Case no.
Age (y)
Duration (y)
Side (L/R)
Neurologic deficit
Pain
EDX (C8–Th1 axon loss)
CSA of lower trunk (mm2)
Radiography (cervical rib/elongated C7)
Surgery
1
64
16
R
Th1 > C8
−
Th1 > C8
29
C7
−
2
27
1
L
Th1 > C8
−
Th1 > C8
47
—
−
3
38
1
L
Th1 > C8
+
Th1 > C8
40
Rib
+
4
36
<1
R
Th1 > C8
+
Th1 > C8
40
—
−
5
37
3
R
Th1 > C8
−
Th1 > C8
20
Rib
−
6
28
5
L
Th1 > C8
−
Th1 > C8
50
Rib
−
7
27
3
R
—
+
Th1 (sens)
45
—
−
8
46
10
R
—
+
—
20
Rib
−
9
40
2
R
—
+
C8-Th1 (sens)
25
C7
−
10
19
2
R
—
+
—
22
—
−
11
74
5
R
Th1 > C8
−
Th1 > C8
29
—
+
12
43
2
R
Th1 > C8
+
Th1 > C8
34
—
+
13
54
5
R
Th1 > C8
+
Th1 > C8
30
Rib
+
14
49
15
R
Th1 > C8
+
Th1 > C8
36
C7
+
15
53
3
R
Th1-C8
+
C8-Th1
34
—
−
16
43
2
R
Th1 > C8
+
Th1 > C8
22
—
−
17
57
13
R
C8-Th1
−
C8-Th1
30
C7
+
18
21
2
R
C8-Th1
−
C8-Th1
37
C7
+
19
24
2
R
C8-Th1
+
C8-Th1
32
Rib
+
20
28
14
R
—
+
—
30
Rib
−
CSA = cross-sectional area; sens = only sensory; EDX = electrophysiologic examination.
All patients underwent clinical, electrophysiologic and ultrasound assessments and radiographic examination of the cervical spine to look for a cervical rib or elongated transverse process of the seventh cervical vertebra. Additional examinations (e.g., MRI of the cervical spine) were also carried out if deemed necessary for differential diagnosis. Neurogenic TOS was diagnosed if unequivocal clinical and electrophysiologic signs of post-ganglionic sensorimotor C8–Th1 axon loss were observed, unexplained by any other cause. Non-specific TOS was diagnosed when subjective complaints suggesting TOS were present without neurologic deficit (clinical signs of C8–Th1 lesion), with or without electrophysiologic alterations typical of TOS.
Subjective complaints suggesting TOS included pain and paresthesia in the arm, especially when lifted overhead, the feeling of fatigability of the arm and the Tinel sign at the supraclavicular fossa. The paresthesia typically involves the medial side of the forearm and hand, but some patients may not be able to localize it and complain of paresthesia of the whole arm. Provocative maneuvers, such as the Roos test (elevated arm stress test), were not used as a diagnostic element, as they were deemed unreliable (
For demonstration of postganglionic sensorimotor C8–Th1 axon loss, all patients underwent motor and sensory nerve conduction studies and F waves of the median and ulnar nerves, and nerve conduction study of the medial antebrachii cutaneous nerve, all with side comparison. Additional examinations, such as needle electromyography of C8–Th1 innervated small hand and forearm muscles were carried out on individual basis. A Viking EMG device manufactured by CareFusion (San Diego, CA, USA) was used for electrophysiologic examination.
Ultrasonography
The scanning was performed by three of the authors, Z.A., J.B. and T.S., all of whom are neurologists and clinical neurophysiologists and have 4, 10 and 8 y of experience, respectively, in nerve sonography. A Philips HD15 XE Pure Wave device with a 12- to 5-MHz 50-mm linear array transducer and a Philips Epiq 5 device with a 18- to 5-MHz linear array transducer, manufactured by Philips (Amsterdam, Netherlands), as well as a Siemens Acuson Antaris 5.0 device with a 13-MHz linear array transducer, manufactured by Siemens (Munich. Germany), were used. Settings were optimized for nerve imaging, including the use of compound imaging mode. In all patients, the whole supraclavicular portion of the brachial plexus was scanned, according to standard methods and landmarks (
). Axial scanning was started at the supraclavicular fossa, where the lower trunk of the brachial plexus was identified adjacent to the subclavian artery. Scanning was continued cranially up to the C5 root level. Color Doppler was used to identify blood vessels in the region. Special attention was paid to the lower trunk of the brachial plexus, and any structures in its vicinity. The cross-sectional area (CSA) of the lower trunk was measured by outlining its outer border, using the continuous trace function of the ultrasound device, at the site of abnormality. More proximally (cranially), the lower trunk breaks up into its constituents, the C8 and Th1 nerve roots, which were not measured because of their deep position and unreliable identification. The shape of the lower trunk was examined and whether it deviated from the normal round shape was noted. Its echogenicity-fascicular structure was also visually assessed compared with the other elements of the brachial plexus (i.e., upper and middle trunks) in the same patient. No quantification of echogenicity was performed. Sonographic Tinel sign was tested by pressing with the transducer on the region of abnormality. The unaffected side was also examined to check for the presence of any abnormality and sonographic Tinel sign, but CSA measurements were not made.
A control group was also examined to obtain normal values for the CSA of the lower trunk and to check for the occurrence of any abnormality and sonographic Tinel sign in the supraclavicular region. None of the subjects had subjective or objective symptoms and signs suggestive of TOS. Control subjects did not undergo electrophysiologic assessment. In all subjects, measurement was performed on the right side.
Statistics
Descriptive statistics (mean, standard deviation and range) were applied to describe the age of patients and controls, age of onset of TOS symptoms in patients and CSA values of the lower trunk in the affected arms of patients and controls. A two-tailed unpaired t-test was used to test the difference between the age and CSA values of the control and patient groups. A two-tailed Fisher exact test was used to test for association between the clinical symptoms and signs suggestive of TOS (including both neurogenic and non-specific TOS) and the presence of the wedge-sickle sign, and between the sonographic Tinel sign and the presence of the wedge-sickle sign. With respect to the clinical symptoms suggestive of TOS, the sensitivity and positive predictive value of the presence of the wedge-sickle sign and the sonographic Tinel sign were also calculated. For tests evaluating the wedge-sickle and sonographic Tinel signs, the control group and the unaffected arms of the patient group were pooled. Statistical significance was set at p < 0.05. GraphPad software (GraphPad Software, San Diego, CA, USA) was used for statistical calculations.
Results
The patient group included 20 females with a mean age of 40.4 ± 14.9 y (range: 19–74 y). The control group included 25 females with a mean age of 38.9 ± 9.8 y (range: 17–51 y). There was no significant difference in age between the two groups (p = 0.6917). Thus, the composition of the patient and the control groups with respect to age and sex was homogeneous. Table 1 summarizes the demographic, clinical, electrophysiologic and radiographic data, including individual CSA measurements of the lower trunk, for all patients. The mean age at the onset of symptoms in the patient group was 34.9 ± 13.5 y (range: 14-69 y). All patients were right-handed, and all patients had unilateral symptoms. In 17 patients, symptoms were on the right side. Fifteen patients were diagnosed with neurogenic TOS, with clinical and electrophysiologic signs of post-ganglionic sensorimotor C8–Th1 axon loss. C8 involvement was usually less severe than Th1 involvement. Figure 1 depicts the typical electrophysiologic findings in a patient with neurogenic TOS. Five patients without clinical neurologic deficit were diagnosed with non-specific TOS. In 2 of these patients, subclinical C8–Th1 axon loss was detected by electrophysiologic assessment.
Fig. 1Typical electrophysiologic findings in neurogenic thoracic outlet syndrome (TOS). Motor and sensory nerve conduction studies were performed in a patient with neurogenic TOS on the left side (patient 6). Note the low-amplitude motor and sensory responses in C8–Th1 distribution and the innervation area of the lower trunk of the brachial plexus on the left side, compared with the unaffected right side. Note also that the amplitude reduction in Th1-supplied areas (thenar muscle–median nerve motor response, MABC sensory response) is greater than that in C8-supplied areas (ulnar nerve motor and sensory responses). Amplitude reduction indicates axon loss. All side comparisons are depicted with the same gain and sweep settings. NCS = nerve conduction studies; MABC = medial antebrachii cutaneous nerve; NR = no response.
In one patient (patient 20), a large bony cervical rib articulating with the first rib was found on the affected, right side. The anterior, articulating end of the cervical rib bulging into the supraclavicular fossa compressed the subclavian artery from the lateral direction and elevated and compressed the lower trunk of the brachial plexus from underneath (Fig. 2). The lower trunk was enlarged and hypo-echoic. This patient also experienced Raynaud's phenomenon in the right arm. On the contralateral side, a smaller, non-articulating cervical rib was present, without any signs of brachial plexus abnormality or compression.
Fig. 2Cervical rib compressing the brachial plexus. Axial image of the supraclavicular brachial plexus of patient 20, revealing the bony anterior end of a large cervical rib articulating with the first rib and bulging into the supraclavicular fossa (arrow). Note how it elevates and compresses the lower trunk, the medial part of the brachial plexus (dotted line), and compresses the subclavian artery (dashed line) from the lateral direction. The lower trunk is hypo-echoic. Med = medial; Lat = lateral; AS = anterior scalene muscle; Art = subclavian artery.
In the remaining 19 patients, in the supraclavicular fossa, slightly cranial to the attachment of the scalene muscles on the first rib, the lower trunk of the brachial plexus was indented (compressed from the lateral direction) by a wedge-shaped, hyper-echoic fibromuscular structure at the medial edge of the middle scalene muscle, resulting in a sickle-shaped lower trunk (Fig. 3, Fig. 4). Furthermore, at the site of indentation, the lower trunk was markedly hypo-echoic, associated with complete loss of fascicular structure, as visually compared with the other trunks of the brachial plexus in the same patient, and also enlarged, as statistically compared with the control group. The mean CSA of the lower trunk, measured at the site of compression, including the whole sickle-shaped structure (i.e., the flattened indented site and the enlarged superficial and deep parts) was 32.6 ± 8.7 mm2 (range: 20–50 mm2) in the patient group and 16.7 ± 3.9 mm2 (range: 9–23 mm2) in the control group. The difference between the two groups was statistically significant (p < 0.0001). In 4 patients, a similar but less conspicuous wedge-sickle sign was seen also on the unaffected side, and in 1 patient, the anomalous attachment of the anterior scalene muscle was seen between the subclavian artery and the brachial plexus on the unaffected side. However, in none of the controls was a wedge-sickle sign or other anomaly detected. The association between clinical symptoms and signs suggestive of TOS (including both neurogenic and non-specific TOS) and the presence of the wedge-sickle sign was statistically highly significant (p < 0.0001). With respect to the clinical signs and symptoms suggestive of TOS (including both neurogenic and non-specific TOS), the presence of the wedge-sickle sign had a sensitivity of 95% (95% confidence interval [CI]: 75.13%–99.87%) and a positive predictive value of 82.6% (95% CI: 61.22%–95.05%) in our cohort. In addition to the wedge-sickle sign, in patient 10 the anomalous insertion of the anterior scalene muscle between the subclavian artery and the brachial plexus was also seen (Fig. 4b).
Fig. 3Spectrum of the wedge-sickle sign. Axial images reveal the lower trunk (dotted line) in the supraclavicular fossa: (a) normal control, (b) patient 4, (c) patient 5, (d) patient 1, (e) patient 6, (f) patient 12. Note the hyper-echoic pointed fibromuscular structure at the caudal medial aspect of the middle scalene muscle indenting the lower trunk adjacent to the subclavian artery. The asterisk indicates the hyper-echoic tip of the fibromuscular structure. Med = medial; Lat = lateral; AS = anterior scalene muscle; MS = middle scalene muscle; Art = subclavian artery.
Fig. 4Wedge-sickle sign in two patients without neurologic deficit: (a) patient 9, (b) patient 10. The dotted line outlines the lower trunk. Note also the anomalous insertion of the anterior scalene muscle in (b). The asterisk indicates the hyper-echoic tip of the fibromuscular structure. Med = medial; Lat = lateral; AS = anterior scalene muscle; MS = middle scalene muscle; Art = subclavian artery.
In 2 patients (patients 1 and 5), the fibromuscular structure with the hyper-echoic tip indented the subclavian artery as well, caudal to the level of the compression of the lower trunk (Fig. 5; Supplementary Video 1, online only, available at 10.1016/j.ultrasmedbio.2016.06.005). No vascular symptoms were present in these patients. In the patient with the bony articulating cervical rib, the subclavian artery was compressed by the cervical rib. In this patient, Raynaud symptoms were also present, indicating vascular involvement.
Fig. 5Indentation of the subclavian artery by the fibromuscular structure in patient 5 (caudal to the image in Fig. 3c), with (a) and without (b) color Doppler, respectively. The lower trunk is round at this level (dotted line). The asterisk indicates the hyper-echoic tip of the fibromuscular structure. Med = medial; Lat = lateral; AS = anterior scalene muscle; MS = middle scalene muscle; Art = subclavian artery.
In 5 patients, the cranial end of the hyper-echoic fibromuscular structure was traced to a bony structure with posterior acoustic shadowing (Supplementary Video 1). All of these patients had either a cervical rib or an elongated C7 transverse process on radiography of the cervical spine. In the remaining patients, cranially the hyper-echoic fibromuscular structure gradually melted into the middle scalene muscle.
The attachment of the middle scalene muscle on the first rib is normally found lateral-posterior to the brachial plexus, being the lateral border of the interscalenic space (Fig. 3a). In 6 patients, the attachment was more medial-anterior, intruding between the first rib and the subclavian artery–brachial plexus, and thus elevating the artery and the plexus (Fig. 6, Supplementary Video 1). This anatomic situation has a space restricting effect in the caudal aspect of the interscalenic space.
Fig. 6Axial images of anomalous attachment of the middle scalene muscle in the most caudal aspect of the supraclavicular fossa: (a) patient 1, (b) patient 5. Note the unusually medial (anterior) attachment of the middle scalene muscle (outlined by dotted line), elevating the subclavian artery and the brachial plexus from the first rib. Med = medial; Lat = lateral; AS = anterior scalene muscle; MS = middle scalene muscle; Art = subclavian artery.
A supraclavicular sonographic Tinel sign was observed in 10 patients with the wedge-sickle sign on the affected side and in the 1 patient with the articulating cervical rib. In these patients, pressing on the wedge-sickle sign/articulating rib with the transducer provoked strong radiating, electric-like pain and paresthesia in the arm or the shoulder region. This never occurred in the controls or in the unaffected arms in the patient group, including those 4 patients in whom the wedge-sickle sign was observed in the unaffected arm as well. The association between the presence of the sonographic Tinel sign and the presence of the wedge-sickle sign was statistically highly significant (p < 0.0001). With respect to the clinical symptoms of neurogenic or non-specific TOS, the presence of a supraclavicular Tinel sign had a sensitivity of 55% (95% CI: 31.53%–76.94%) and a positive predictive value of 100% (95% CI: 71.51%–100.00%) in our cohort.
Surgical findings
Eight patients underwent surgery (Table 1). The remaining patients either refused surgery or had not yet been scheduled for surgery. In patient 3, the whole middle scalene muscle was found to be hard and fibrotic, and scalenotomy was performed. In patients 11–14 and 17, at the medial edge of the middle scalene muscle, a hard, fibrotic ligament indenting the lower trunk of the brachial plexus was found. The ligament was resected (Fig. 7). Hourglass-like enlargement of the trunk was also observed. In patient 18, the ligament at the medial edge of the middle scalene muscle was found attached to the elongated transverse process of the seventh cervical vertebra. The ligament was resected. In patient 24, the ligament at the medial edge of the middle scalene muscle was attached to a cervical rib, but only the rib was removed. In all patients, pain and paresthesia in the arm decreased markedly after surgery, as reported by the patients. Long-term follow-up is pending.
Fig. 7Intraoperative confirmation of the wedge-sickle sign. (a) Axial ultrasonographic image of patient 17, revealing the wedge-sickle sign (the lower trunk is outlined by the dotted line). (b–d) Successive intra-operative steps. Note the swollen lower trunk and the indentation on the trunk, visible after resection of the ligament (d). The asterisk indicates the hyper-echoic tip of the fibromuscular structure. Med = medial; Lat = lateral; AS = anterior scalene muscle; MS = middle scalene muscle; Art = subclavian artery.
Our cohort of 20 consecutive patients with TOS indicates the clear preponderance of female sex, the early onset of symptoms in youth or middle age and the preferential involvement of the right (dominant) arm. Fifteen patients were diagnosed with neurogenic TOS, indicated by clinical signs of the damage of the lower trunk of the brachial plexus, and five fell into the category of non-specific TOS, with only subjective symptoms with or without subclinical electrophysiologic changes. In one patient with non-specific TOS, a large bony cervical rib articulating with the first rib compressed the brachial plexus (Fig. 2). In the remaining 19 patients, a distinctive ultrasonographic sign was observed, which we termed the wedge-sickle sign (Figs. 3, 4 and 8). The “wedge” corresponds to a fibromuscular structure with a pointed, hyper-echoic (fibrotic) tip along the caudal medial edge of the middle scalene muscle, indenting (compressing) the lower trunk from the lateral direction in the supraclavicular fossa, where it is lodged between the middle scalene muscle and the subclavian artery. The “sickle” is the shape assumed by the lower trunk in cross section because of the indentation.
Fig. 8Schematic representation of the wedge-sickle sign. The asterisk indicates the tip of the fibromuscular structure. LT = lower trunk; Art = subclavian artery.
The hypo-echogenicity, complete loss of fascicular structure and significant enlargement of the lower trunk, which are characteristic ultrasonographic signs of nerve compression in general, were associated features in all patients (
). The wedge-sickle sign was also seen in the unaffected arm in four patients but in none of the control subjects, possibly indicating a genetic predisposition to bilateral occurrence. With respect to the clinical symptoms of neurogenic or non-specific TOS, the wedge-sickle sign had a sensitivity of 95% and a positive predictive value of 82.6% in our cohort. The supraclavicular sonographic Tinel sign was also an important feature, with a lower sensitivity (55%), but a 100% positive predictive value. The fibromuscular structure may also indent the subclavian artery in the same fashion (Fig. 5; Supplementary Video 1), possibly leading to vascular symptoms as well. Moreover, vascular TOS may also cause neurologic symptoms secondary to blood vessel involvement, such as pain and numbness of the arm, resembling symptoms of non-specific TOS. However, in the two patients with the wedge-sickle sign and indentation of the subclavian artery, symptoms were clearly neurologic (with marked C8–Th1 axon loss), without associated vascular symptoms. On the other hand, in the one patient with non-specific TOS symptoms, where compression of both the brachial plexus and the subclavian artery was caused by a bony cervical rib, vascular symptoms (Raynaud phenomenon) were also present. It has been reported that the bony cervical rib has a higher relevance for arterial vascular TOS (
). In this patient, the difference between symptoms of brachial plexus and of arterial origin is not so clearly delineated.
The observed fibromuscular structure located between the lower trunk and the middle scalene muscle in the supraclavicular fossa may correspond to several of the 10 different types of bands causing compression of the Th1 root or the lower trunk described by
. In type 1, a tight fibrous band connects the rudimentary cervical rib to the mid-portion of the first rib, posterior to the scalene tubercle. In type 2, the band originates on an elongated C7 transverse process. In 5 of our patients with the wedge-sickle sign, the cranial end of the fibromuscular structure could be traced to a bony structure with posterior acoustic shadowing (Supplementary Video 1). As all of these patients had a cervical rib or an elongated C7 transverse process, the bony structure appearing in the interscalenic region cranial to the site of compression most likely corresponds to the anterior tip of the cervical rib or the elongated C7 transverse process. Thus, type 1 or 2 bands are probably the cause of the compression in this subset of patients. In the remaining patients with the fibromuscular abnormality, the wedge-shaped fibromuscular structure became less distinct cranially and melted into the middle scalene muscle. In these cases, the other types of Roos ligaments (types 3–10) are considered, but they cannot be reliably differentiated from each other on ultrasound. Type 3 (a fibromuscular band arising at the neck of the first rib and attaching to the inner part of the first rib, posterior to the scalene tubercle) is the most common type according to
, and type 4 (fibrous, sharp medial edge of the middle scalene muscle and medial attachment of the muscle) is also noteworthy. In the latter, the more medial (anterior) attachment of the middle scalene muscle leads to a common tendinous insertion of the anterior and middle scalene muscles, forming a V-shaped sling underneath the subclavian artery and the lower trunk (Fig. 6). This anatomic situation elevates the lower trunk from the first rib and may result in a space-occupying effect and compression of the lower trunk, especially if the middle scalene muscle has a sharp, fibrous medial edge. However, we observed this anomalous attachment in patients with type 1 or 2 bands as well, in whom it may be considered as an additional factor contributing to the compression. Furthermore, in patient 10, the anomalous insertion of the anterior scalene muscle between the subclavian artery and the brachial plexus was seen; thus, in this patient, the lower trunk became compressed between the middle and anterior scalene muscles (Fig. 4b).
Pre-surgical identification of the fibromuscular structure as the cause of compression of the lower trunk is especially important in the controversial “non-specific TOS” category. In our cohort, association of the wedge-sickle sign with the sonographic Tinel sign could also be observed in 4 patients with only pain and paresthesia in the arm without neurologic deficit (Fig. 4). Likewise, in a surgical series of 14 patients, it was found that anomalous fibromuscular bands compressed the lower trunk in patients with only pain, sensory symptoms and supraclavicular Tinel sign (
). Thus, it may be necessary to reconsider the validity of the category of “non-specific TOS.” Patients with only the typical subjective symptoms of TOS, associated with imaging proof of lower trunk compression, should be classified as having “neurogenic TOS,” as they represent an early stage of the disease. This has clinical relevance, because in patients with already marked C8–Th1 axon loss, surgery stops mainly progression; proximodistal axonal regrowth is unlikely because of the long distance (
) may play an important role. Ultrasound is a more easily accessible modality; however, MRI may be the appropriate choice in patients with an unfavorable body habitus.
Limitations of our study include the retrospective nature of the analysis and the lack of surgical confirmation of the fibromuscular anomaly in all patients. A further limitation may be that the examinations were carried out by different ultrasonographers using different ultrasound devices. However, inter-rater and inter-equipment reliability in nerve ultrasound has been tested previously, confirming examiner- and equipment-independent reproducibility (
Inter- and intraobserver reliability of predefined diagnostic levels in high-resolution sonography of the carpal tunnel syndrome—A validation study on healthy volunteers.
Our study provides ultrasonographic confirmation of Roos' observation that anomalous fibromuscular structures in the scalenic triangle are the major cause of neurogenic TOS. We report a novel and distinctive ultrasonographic sign, the wedge-sickle sign, which allows the easy pre-surgical identification of these bands causing TOS. This is especially useful in patients without neurologic deficit, in whom the diagnosis is not always as straightforward. On the other hand, early diagnosis is important, because the neurologic deficit associated with TOS may be irreversible.
Acknowledgments
Zsuzsanna Arányi and Anita Csillik were supported by the National Brain Research Program (NAP B) of the Hungarian government (KTIA_NAP_13-2-2014-0012). The funding source had no direct role in the design of the study, the interpretation of the data or the preparation/submission of the article.
Axial scanning of the right brachial plexus of patient 5 from caudal to cranial, starting at the supraclavicular fossa and ending at the level of the foraminal exit of root C6. First note the unusually medial attachment of the middle scalene muscle deep to the subclavian artery. Moving cranially, the middle scalene muscle moves laterally, and at its medial edge, a hyper-echoic wedge-shaped fibromuscular structure indents in succession first the subclavian artery, then the lower trunk, and ends in a bony structure with posterior acoustic shadowing. Further cranially, the contour of the transverse processes of the seventh and sixth cervical vertebrae can be seen, with their respective roots exiting the neuroforamen.
Inter- and intraobserver reliability of predefined diagnostic levels in high-resolution sonography of the carpal tunnel syndrome—A validation study on healthy volunteers.
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