REVIEWARTICLE MRI findings in thoracic outlet syndrome Ayse Aralasmak & Can Cevikol & Kamil Karaali & Utku Senol & Rasul Sharifov & Rukiye Kilicarslan & Alpay Alkan Received: 8 March 2012 /Revised: 14 June 2012 /Accepted: 21 June 2012 /Published online: 11 July 2012 # ISS 2012 Abstract We discuss MRI findings in patients with thoracic outlet syndrome (TOS). A total of 100 neurovascular bun- dles were evaluated in the interscalene triangle (IS), costo- clavicular (CC), and retropectoralis minor (RPM) spaces. To exclude neurogenic abnormality, MRIs of the cervical spine and brachial plexus (BPL) were obtained in neutral. To exclude compression on neurovascular bundles, sagittal T1W images were obtained vertical to the longitudinal axis of BPL from spinal cord to the medial part of the humerus, in abduction and neutral. To exclude vascular TOS, MR angiography (MRA) and venography (MRV) of the subcla- vian artery (SA) and vein (SV) in abduction were obtained. If there is compression on the vessels, MRA and MRVof the subclavian vessels were repeated in neutral. Seventy-one neu- rovascular bundles were found to be abnormal: 16 arterial– venous–neurogenic, 20 neurogenic, 1 arterial, 15 venous, 8 arterial–venous, 3 arterial–neurogenic, and 8 venous– neurogenic TOS. Overall, neurogenic TOS was noted in 69%, venous TOS in 66%, and arterial TOS in 39%. The neurovascular bundle was most commonly compressed in the CC, mostly secondary to position, and very rarely com- pressed in the RPM. The cause of TOS was congenital bone variations in 36%, congenital fibromuscular anomalies in 11%, and position in 53%. In 5%, there was unilateral brachial plexitis in addition to compression of the neurovascular bun- dle. Severe cervical spondylosis was noted in 14%, contribut- ing to TOS symptoms. For evaluation of patients with TOS, visualization of the brachial plexus and cervical spine and dynamic evaluation of neurovascular bundles in the cervico- thoracobrachial region are mandatory. Keywords Arterial . Venous . Neurogenic thoracic outlet syndrome . Neurovascular syndrome . Brachial plexus . Scalenus anticus syndrome . Costoclavicular syndrome . Congenital bone variations . Congenital fibromuscular anomalies . Positional Introduction Thoracic outlet syndrome (TOS) arises from dynamic compression of the subclavian artery (SA) or subclavian vein (SV) or brachial plexus (BPL) in the cervicothora- cobrachial region, in combination or separately. Patients sustain symptoms depending on the compressed compo- nents of the neurovascular bundle. Compression could be due to cervical or anomalous first rib, long C7 transverse process (longer than the T1 transverse process), exosto- sis, hypertrophic callus of the first rib or clavicula, con- genital fibromuscular anomalies, muscle anomalies, posture (position), repetitive movements, post-traumatic fibrosis of the scalene muscles, short scalene muscles, and vessels passing through the substance of muscles [1–6]. Anatomy of the neurovascular bundle in the cervicothoracobrachial region The neurovascular bundle can be compressed in the three compartments of the cervicothoracobrachial region: the interscalene triangle (IS), costoclavicular (CC), and retropectoralis minor (RPM) spaces (Fig. 1). The IS is bounded by the first rib inferiorly, the anterior scalene muscle anteriorly, and the middle scalene muscle poste- riorly. The SA forms the floor of this space. Neuro- vascular compression in the IS may result from muscle injuries, muscle hypertrophy with repetitive overhead A. Aralasmak (*) :R. Sharifov : R. Kilicarslan :A. Alkan Department of Radiology, Bezmialem Vakif University, Fatih/Istanbul, Turkey e-mail: aysearalasmak@hotmail.com C. Cevikol :K. Karaali :U. Senol Department of Radiology, Akdeniz University, Antalya, Turkey Skeletal Radiol (2012) 41:1365–1374 DOI 10.1007/s00256-012-1485-3 activities, congenital fibromuscular anomalies, and cer- vical and anomalous first ribs. The CC is formed by the clavicle superiorly, subclavius muscle anteriorly, and first rib posteriorly. The CC is compromised during shoulder abduction as the clavicle moves posteriorly. The long cervical rib extending into the CC, subclavius muscle hypertrophy, the accessory muscles, and hyper- trophic callus of the first rib and clavicula narrow the CC. The RPM (subcoracoid space) is situated lateral to the first rib, posterior to the pectoralis muscles below the coracoid process. The RPM volume decreases dur- ing shoulder hyperabduction and is compromised by pectoralis minor muscle hypertrophy or the accessory muscles [1–5]. Neurogenic TOS Pain, paresthesia, and weakness in the hand, arm, and shoulder, neck pain, and occipital headaches may occur. Raynaud’s phenomenon is frequently seen owing to an overactive sympathetic nervous system since fibers of the sympathetic nervous system run on the circumference of the nerve roots of the lower trunk of the brachial plexus (C8 and T1). Neurogenic TOS is more common in women and in the IS. It usually results from cervical hyperextension trauma or overuse injury in patients with congenital abnormalities such as cervical or anomalous first ribs, congenital fibromuscular bands, or scalene muscle variants. However, 80% of neurogenic TOS cases have a previous history of trauma; in cadaver studies, IS was more frequently found to be narrowed in neurogenic TOS cases compared with in an asymptomatic population [1–5]. Arterial TOS Compression of the SA may result in stenosis, aneurysm, mural thrombus or distal emboli and cause digital ischemia, claudication, pallor, coldness, paresthesia, and pain in the hand but rarely in the shoulder or neck. It is usually caused by a cervical or anomalous first rib, scalene muscle, fibro- muscular bands, or pectoralis minor tendon, and rarely secondary to passage of the SA through the substance of the scalene muscle [1–6]. Venous TOS Thrombotic or nonthrombotic occlusion of the SV may result in swelling of the arm, cyanosis, pain, and paresthesia in the fingers and hands. Venous TOS can be seen in three different situations: intermittent/positional venous obstruc- tion, secondary SV thrombosis (in the setting of catheters or pacemaker leads), and primary effort thrombosis (Paget– Schrotter disease) preceded by excessive activity with the arms. Paget–Schrotter disease affects mostly young healthy men [1–5]. Herein, we discuss the MRI findings and the imaging details based on the patients presenting with TOS. MR imaging protocols We retrospectively reviewed and evaluated MRI findings of 50 adult subjects referred for suspected TOS. Patients were recruited consecutively upon admission to the MRI unit within 2 years. Informed consent was obtained from all subjects. Applied MRI TOS protocol was the same for all Fig. 1 a–c In a normal subject in neutral position, sagittal T1W views from medial to lateral demonstrate three potential spaces of the cervi- cothoracobrachial region, in which the neurovascular bundle can be compressed. a At the interscalene triangular space (IS) between the anterior scalene muscle (AS) and the middle scalene muscle (MS), roots and trunks of the brachial plexus (BPL) are present. The subclavian artery (SA) forms the floor of the IS, the subclavian vein (SV) is not a component of the IS and is situated at the anteroinferior aspect of the SA. b In the costoclavicular space (CC) between the first rib and the clavicula (CL), divisions of the BPL are seen in the superior and posterior aspects of the SA. c In the retropectoralis minor space (RPM), cords and terminal branches of the BPL are situated in the posterior and superior aspect of the axillary artery (AA). The SA and SV take the name of the AA and axillary vein (AV) at the lateral border of the first rib. PMA pectoralis major muscle, PMI pectoralis minor muscle 1366 Skeletal Radiol (2012) 41:1365–1374 patients. During evaluation, radiologists were blinded to the clinical symptoms and the electrophysiological and provoc- ative test results of the patients, as they were reported as being vague and nonspecific in the diagnosis of TOS [2, 7, 8]. To exclude neurogenic abnormality, sagittal and axial T2W for radiculopathy and spinal cord lesions, and pre- and fat-saturated postcontrast axial T1W and pre- and post- contrast coronal T1W and coronal fat-saturated T2W for the brachial plexus were obtained with arms alongside the body (neutral). Axial views were obtained from C4 to T2 perpen- dicular to the long axis of the vertebrae in the coronal plane. Coronal views were obtained parallel to the long axis of the C4–C7 vertebrae. To exclude compression on the neuro- vascular bundle, in abduction and neutral positions, sagittal T1W images were obtained vertical to the longitudinal axis of the brachial plexus from the spinal cord to the medial part of the humerus. To exclude vascular TOS, contrast- enhanced MRA and MRV of the SA and SV in abduction were obtained. If there were compression on the vessels, MRA and MRV of SA and SV were repeated in neutral if necessary. Slice thickness was 3 mm and the total imaging time was around 40 min. In the evaluation of vascular TOS, if there is compression of the vessels depicted on both sagittal T1W and MRA/ MRV in abduction with resolution in neutral, it was reported to be vascular TOS. The region of compression was assessed on sagittal T1W images. In the evaluation of neu- rogenic TOS, if there were loss of normal fat signal around the fibrils of the BPL on sagittal T1W images in abduction with resolution in neutral in the CC and RPM, we called neurogenic TOS. If there were congenital bone variations such as cervical or anomalous first rib or long transverse C7 process and muscle anomalies in the IS, we called neuro- genic TOS. If bone variations extend into the CC, we called neurogenic TOS in both the IS and CC. For muscle anoma- lies in the CC and RPM, depending on the compressed component of the neurovascular bundle in abduction, we called arterial, venous or neurogenic TOS. Results A total of 100 neurovascular bundles in the cervicothoraco- brachial region were evaluated. Twenty-nine of the 100 neurovascular bundles were normal (16 cases). Seventy- one neurovascular bundles were abnormal (pathological) (34 cases). Among the normal appearing neurovascular bundles (29), 8 were associated with cervical spondylosis severe enough to explain the patients’ symptoms (27%). Among the pathologically appearing neurovascular bundles (71), only 10 were associated with cervical spondylosis severe enough to explain the patients’ symptoms (14%). In 26 neurovascular bundles (26 out of 71036%; 14 patients; 12 patients were bilateral, 2 patients were unilater- al), there were congenital bone variations causing TOS such as long C7 transverse process, short or long cervical rib, cervical rib–first thoracic rib articulation (Fig. 2). In 8 neurovascular bundles (8 out of 71011%; 6 patients were unilateral, 1 patient was bilateral), there were congen- ital muscle anomalies causing TOS (Figs. 3–5). In 4 neurovascular bundles (4 out of 71 0 5%; 4 patients), there is unilateral brachial plexitis in addition to compres- sion of the neurovascular bundles of the same sides (the first case is plexitis with venous TOS in the CC, the second is plexitis with arterial–venous–neurogenic TOS in the CC, the third is plexitis with both venous TOS in the CC and neurogenic TOS in the IS due to the scalenus minimus muscle, and the fourth is plexitis with neurogenic TOS due to a short cervical rib) In 16 out of 71, arterial–venous–neurogenic TOS was noted in CC. In 6 out of 16, compression was due to position and the long cervical rib extending into the CC (Fig. 2) and 10 out of 16 was only positional. In 10 out of 16, additional neurogenic TOS was noted in the IS owing to congenital bone variations. Short or long cer- vical rib and the long C7 transverse process pass through the IS very close to the BPL, causing neuro- genic TOS in the IS. Furthermore, if it is long enough, the cervical rib extends into the CC and compresses the neurovascular bundle in this region. In 20 out of 71, only neurogenic TOS was noted. Compression in 4 out of 20 was in the CC and RPM due to accessory or hypertrophied muscle. Eight out of 20 were in the IS owing to congenital bone variations. One out of 20 was in the IS and CC because of congenital bone variation extending into the CC. One out of 20 was in the IS owing to both congenital bone variation and the scalenus minimus muscle. Five out of 20 were in the CC and positional. One out of 20 was in the RPM and positional. In 1 out of 71, only arterial TOS was noted at the lateral border of the IS (Fig. 6). The anterior scalene muscle could be short or fibrotic owing to previous whiplash injury and compressing the SA during contraction, or the SA itself may be piercing the anterior scalene muscle, resulting in narrowing during contraction [6]. In 15 out of 71, only venous TOS was noted in the CC with one observed in the RPM additionally (Fig. 7). In 8 out of 71, arterial–venous TOS was noted: 2 out of 8 in both the CC and RPM, and 6 out of 8 only in the CC. Because of the long C7 transverse process, additional neu- rogenic TOS in IS was noted in 2 out of 8 arterial–venous TOS in the CC. In 3 out of 71, arterial–neurogenic TOS was noted: 1 out of 3 was arterial–neurogenic TOS in the CC; 1 out Skeletal Radiol (2012) 41:1365–1374 1367 of 3 was arterial–neurogenic TOS in the RPM; and 1 out of 3 was neurogenic TOS in the IS due to congen- ital bone variation and arterial TOS at the lateral border of the IS. In 8 out of 71, venous–neurogenic TOS was noted: 2 out of 8 were venous–neurogenic TOS in the CC; 2 out of 8 were venous TOS in the CC and neurogenic TOS in the IS due to accessory muscle (scalenus minimus muscle); 1 out of 8 was venous TOS in the CC and neurogenic TOS in the RPM due to accessory muscle; and 3 out of 8 were venous TOS in the CC and neurogenic TOS in the IS due to long C7 transverse process. Overall, we noticed neurogenic TOS in 49 out of 71 (69%), venous TOS in 47 out of 71 (66 %) and arterial TOS in 28 out of 71 (39%). In 36% of the neurovascular bundles (26 out of 71), there were congenital bone varia- tions causing TOS. In 11% (8 out of 71) of the neurovas- cular bundles, there were congenital muscle anomalies causing TOS. In 53% of the neurovascular bundles (37 out of 71), the only cause of TOS was positional (postural) (Fig. 8). Discussion In the diagnosis of TOS, electrophysiological and provoca- tive tests are mostly vague and nonspecific, and imaging is required to identify a cause and location to provide infor- mation for surgical repair [2, 7, 8]. Many diagnostic radiological procedures are used to con- firm neurovascular compression. Radiography is used to detect osseous pathologies. Contrast-enhanced CT is used to detect both the osseous structures and the vascular struc- tures with the disadvantage of ionizing radiation and poten- tially nephrotoxic and allergic iodinated contrast material. The catheter angiography is another invasive technique in the diagnosis of vascular TOS, with possible local and systematic complications (hematoma, emboli, occlusion) and it is not possible to repeat it frequently. Ultrasound is able to detect arterial and venous pathologies, but obesity and surrounding osseous structures may prevent an accurate diagnosis. Neither of these modalities is easy to repeat or successful in the demonstration of accessory muscles or fibrous bands. Fig. 2 Magnetic resonance angiography in abduction reveals a severe compression of SAs and SVs with b resolution of compressions in neutral. Filling of left SV is not seen in this image. c Coronal T1W image shows bilateral cervical ribs (arrows). d–j Sagittal views from the right side in abduction from medial to lateral reveal a cervical rib (thick arrows) extending through the IS into the CC with compression of the SA and SV and nonvisualization of normal fat signal around the fibrils of the BPL in the CC (g, h), suggesting neurogenic, arterial, and venous TOS in the CC due to cervical rib and position. At the lateral aspect of the CC (h, i), there is no visualization of the cervical rib, but compression of the SA and SV and loss of fat signal around the BPL fibrils continues, suggesting positional compression as well. Cervical rib also impinges the BPL in the IS (d, e). Restoration of the caliber of the SA and SV begins in the lateral aspect of the CC (i, j) and normal caliber of the SA in the IS (d, e, f). Thin arrows on h, i and j show the first rib 1368 Skeletal Radiol (2012) 41:1365–1374 Magnetic resonance imaging is a noninvasive and non- ionizing technique with excellent soft-tissue contrast. MRI with contrast-enhanced MRA/MRV enables dynamic evalu- ation of the neurovascular bundle in the cervicothoracobra- chial region, and is more efficient in the diagnosis of vascular TOS and in the depiction of accessory muscle (scalenus minimus, subclavius posticus, duplicated omo- hyoid inferior belly, pectoralis minimus muscle), muscle hypertrophy (omohyoid inferior belly, pectoralis minor, sca- lene, subclavius), and fibrous bands [4, 5, 8]. There are also Fig. 3 a–c, f Accessory muscle (thick white arrows) causes neurogenic TOS on the right. Accessory muscle extends from the sternal end of the first rib to the upper border of the scapula and normal subclavius muscle is not visualized. d, e On the left, normal subclavius muscle extending under the clavicula (thin white arrows) and c, e, f the inferior belly of the omohyoid muscle (black arrows) are seen. Apart from the accessory muscle, we do not see the inferior belly of the omohyoid muscle on the right. The accessory muscle is named the subclavius posticus, variational subclavius muscle or hypertrophied inferior belly of the omohyoid muscle, depending on innervation. In the abduction and neutral positions, the accessory muscle runs very close to the right BPL in the CC and RPM, suggestive of neurogenic TOS (a, b) Fig. 4 There is no vascular TOS on MRA and MRV views in abduc- tion (not shown here). a–d There is accessory muscle on the right (white arrows), extending from the sternal end of the first rib to the upper border of the scapula, very close to the BPL in abduction, causing neurogenic TOS on the right in the CC and RPM. c–f Normal inferior bellies of the omohyoid muscles are seen (black arrows) on both sides. The accessory muscle on the right can be named the subclavius posticus muscle or variational subclavius muscle or dupli- cated inferior belly of the omohyoid muscle, depending on its innervation Skeletal Radiol (2012) 41:1365–1374 1369 some disadvantages of MRI as well. First is the long imag- ing time. Forty minutes scanning time is intolerable for some patients, especially those with symptoms. Second, gadolinium, one of the contrast agents, is toxic to patients with kidney and liver diseases. MRA and MRV cannot be performed in patients with a low glomerular filtration rate. Third, it can sometimes be hard to detect bony abnormalities on MRI; in this situation CT or radiography might be needed for confirmation. Most of the time, patients have cervical radiography to assess congenital bony variations and hypertrophic callus. If not, bone abnormalities are best depicted on coronal T1W and coronal fat-saturated T2W images. Sagittal T1W images in abduction demonstrate well their extension as well as their relation to the neurovascular bundle [4, 5]. According to the literature, cervical ribs are present in less than 1% of the normal population and in 5–9% of patients with TOS [2, 4]. We found congenital bone variations such as long C7 transverse process, short or long cervical rib (incomplete cervical rib), cervical rib–first thoracic rib articulation (com- plete cervical rib) in 36% of the TOS cases. Short cervical rib and long C7 transverse process can cause neurogenic TOS in IS. If the cervical rib is long enough, it extends into the CC, and may also compress the SA, SV, and BPL fibrils. Fig. 5 a Axial T2W and b sagittal T1W views in abduction show accessory muscle (arrows) between the anterior and middle scalene muscles on the right. This muscle extends within the inferior aspect of the IS, very close to the BPL fibrils. This is the reason for neurogenic TOS on the right. This muscle is called the scalenus minimus muscle, and runs between the anterior and middle scalene muscles from the transverse processes of the lower cervical vertebrae to the apical pleura and inner border of the first rib behind the subclavian groove Fig. 6 Magnetic resonance angiography views of a patient a com- plaining of right arm weakness reveal compression of the right SA in abduction with b resolution in neutral. Sagittal T1W views in abduction show c the normal caliber of the SA in the IS, but d prominent narrowing of the SA at the lateral border of the IS, just posterior to the anterior scalene muscle. The anterior scalene muscle could be short or fibrotic because of previous whiplash injury and compressing the subclavian artery during contraction, or the subclavian artery itself may be piercing the anterior scalenemuscle, resulting in narrowing during contraction. e, f There is restoration of the caliber of the SA in the CC 1370 Skeletal Radiol (2012) 41:1365–1374 Bone abnormalities may lead to severe vascular compli- cations, in time. Repetitive trauma at the site of com- pression can damage the artery and lead to atherosclerotic changes, aneurysm, and thrombosis or embolism. With ongoing inflammation, thickening, and fibrosis of the arterial wall, initially dynamically induced symptoms may later become permanent owing to fixed stenosis [4]. Congenital fibromuscular anomalies and muscle abnor- malities and their relation to the neurovascular bundle can be demonstrated better on sagittal T1W images [4, 5]. Axial and coronal T1W and T2W images are also helpful. Anom- alous fibrous bands may arise from a cervical rib, the first thoracic rib, an elongated C7 transverse process, or the anterior and middle scalene muscles and insert onto the first thoracic rib or the cupola of the lung. They may be Fig. 7 a Magnetic resonance venography (MRV) in abduction reveals narrowing of the right SV (short arrow) at the entrance of the CC and nonvisualization of the left SV (long arrow) distal to the entrance of the CC and b normal filling of both SVs (short and long arrows) in neutral. c Sagittal T1W views of the right hand side in abduction are shown from medial to lateral. The Sagittal views of the left hand side are not shown here. There is compression of the right SV (short arrows) at the entrance of the CC in abduction and d resolution in neutral. Long arrows show the SA on c and d. Findings are suggestive of venous TOS on the right. It is difficult to differentiate the physiological compression from the pathological (symptomatic) compression, although compression is seen on both MRV and sagittal T1W views. Correlation with clinical history and electrophysiological and provocative tests is recommended. Stars show the internal jugular vein (c, d) Fig. 8 a Sagittal T1W views of the right hand side in abduction from medial to lateral reveal loss of the fat signal around the fibrils of the BPL in the RPM. The BPL is situated in the posterior and superior aspect of the SA in the CC and RPM. Note that the normal appearance of the BPL in the CC. b In neutral positional compression is resolved with normal fat signal noticeable around the fibrils of the BPL in the RPM. This is suggestive of positional neurogenic TOS in the RPM. Thin arrows show the first rib, and thick arrows show the second rib (a, b). The CC takes the name of the RPM lateral to the first rib Skeletal Radiol (2012) 41:1365–1374 1371 fibromuscular in nature. Hypertrophy of the anterior scalene muscle, common origin of the anterior and middle scalene muscles with division in two distally, passage of the brachial plexus through the substance of the anterior scalene muscle, a broad middle scalene muscle inserting more anteriorly on the first rib, interdigitation between the anterior and middle scalene muscles, and accessory muscles compromise the BPL in the IS. The scalenus minimus is an accessory muscle situated within the IS, between the anterior and middle scalenus muscles, extending from the anterior tubercle of the transverse process of the C6 and C7 vertebrae to the apical pleura and inner border of the first rib behind the subclavian groove [4, 6, 9]. It extends along the BPL, close to the inferior trunk (C8–T1), and, with trauma or repetitive movements, it may cause neural irritation and SA compres- sion or elevation from behind [4, 6]. Fat-saturated coronal T2W images better differentiate this muscle from the rela- tively T2 hyperintense BPL fibrils within the IS. Congenital fibromuscular anomalies running from the first rib to the scapula across the supraclavicular fossa may compress the BPL and subclavian vessels from above and the subclavian vessels from anterior in TOS [10, 11]. Hypertrophy of the subclavius muscle, subclavius posticus muscle with or with- out a normal subclavius muscle or duplicated or hypertro- phy of the omohyoid inferior belly muscles, pectoralis minor muscle hypertrophy and the accessory pectoralis minimus muscle can compress the BPL in the CC and RPM [10]. Accessory muscle usually accompanies the mus- cle from which it was duplicated. However, distinctions of accessory muscles are primarily made according to the source of their innervation [10, 11]. It has been hypothesized that the inferior belly of the omohyoid and subclavius muscles develop from one single matrix that divides into two portions—the cranial and caudal portions becoming the inferior belly of the omohyoid and subclavius respectively. In the case of an aberrant muscle, the common matrix divides into three portions, forming two normal muscles and the anomalous muscle; the latter known as the subcla- vius posticus [10, 11]. Congenital fibromuscular anomalies are not rare in the normal population (63% in the normal population in cadaver studies, 98% in TOS patients on surgery) [10, 12]. A higher proportion of anomalies in normal subjects implies that together with anatomical pre- disposition, repetitive movements and trauma are also addi- tional elements in the development of TOS [10, 12]. Brachial plexitis can be seen in TOS either as a primary condition or secondary to irritation of the BPL. There are no data in the literature on the frequency of brachial plexitis in TOS cases. Brachial plexitis was very rare (5%) in our patient group (Fig. 9). We do not know if it was primary or secondary. However, 3 of the 4 cases with brachial plexitis were associated with neurogenic TOS suggesting that it is secondary to TOS (entrapment neuritis). One out of 4 was associated with only venous TOS, suggesting that it is primary (idiopathic, viral, allergic, toxic, etc.) rather than entrapment neuritis. T2 fat-saturated coronal T2WI are most valuable in demonstrating brachial plexitis [5]. Contrast enhancement of the BPL may not always be present in brachial plexitis [5]. In the literature, neurogenic TOS is the most common, comprising 90–95% of TOS cases; more common in the IS because of cervical whiplash injury or congenital bone variations [1]. In our patient population, neurogenic TOS was observed in 69% of the neurovascular bundle (total 49 neurovascular bundles: 17 in the IS due to either muscle anomalies and/or congenital bone variations, 14 in the CC due to position, 11 in both the IS and the CC due to congenital bone variations and/or position, 4 in both the CC and the RPM due to muscle anomalies, and 3 in the RPM due to either position or muscle anomalies). We noticed neurogenic TOS almost similar in frequency in the IS and CC, but very rarely in the RPM. As a causative factor, in the IS congenital bone variations are more common than muscle anomalies; in the CC positional compression was more common than congen- ital bone variations or muscle anomalies; in the RPM muscle anomalies were more common than position. Only Demondion et al. found similar results to us in that in neurogenic TOS, compression is as frequent in the CC as in the IS. The RPM is very rare potential site of compression [4, 13]. According to the literature, arterial TOS comprises 1 to 2% of TOS cases and is most commonly associated with cervical or anomalous first rib; more common in the IS [1–3]. In our patient population, arterial TOS was observed in 39% of the neurovascular bundles (total 28 neurovascular bundles: 23 in the CC, 2 in the IS, 1 in the RPM, and 2 in both the CC and the RPM). In arterial TOS cases in the IS, compression was at the lateral border of the IS in both, one was related to an anterior scalenus muscle anomaly and the other was related to a congenital bone variation. Six cases were in the CC due to congenital bone variations and posi- tion. The cause of the rest was the position. In contrast to the literature [1–3], in our patient population, most common compression for arterial TOS was in the CC and due to position. On the other hand, Demondion et al. found fairly similar results to ours in that the SA was most frequently compressed in the CC, second most frequently compressed in the IS, and very rarely com- pressed in the RPM [4, 13]. Venous compression is frequently observed in asymp- tomatic individuals in all the compartments of the thoracic outlet after arm elevation [4, 13, 14]. It is hard to differen- tiate benign physiological compression from symptomatic pathological compression. Venous TOS, comprising 2–5% 1372 Skeletal Radiol (2012) 41:1365–1374 of TOS cases according to the literature, usually occurs at the junction of the clavicle and the first rib in the CC, is the result of strenuous hyperabduction of the affected limb, and is most commonly seen in young athletes as a result of a repetitive action with the affected limb, such as pitch- ing a baseball or weight lifting [1, 4, 13]. In our case group, we called venous TOS if we saw narrowing in both sagittal T1 and MRV views in abduction and we observed venous TOS in 66% of the neurovascular bundles, the majority in the CC and very rarely in the RPM, most commonly due to position (a total of 47 neurovascular bundles: 38 in the CC due to position, 3 in both the CC and the RPM due to position, and 6 in the CC due to both position and congenital bone variations extending into the CC). Because of the higher frequency of venous TOS, we thought it would be benign physiological compression and we recommended clinical correlation to differentiate symptomatic from benign physiological compression. In the differential diagnosis of TOS, cervical spondy- losis, shoulder disease, primary brachial plexitis, and neoplastic lesion of the cervicothoracobrachial region must be considered. The higher percentage of severe cervical spondylosis among the normal appearing neuro- vascular bundles (27%) than that among the pathologi- cal appearing neurovascular bundles (14%) necessitates cervical spine imaging in all patients presenting with TOS. There are some shortcomings to our study. First is the long imaging time and position in abduction, which may be intolerable for some of the patients. Second, we do not know the frequency of the findings that we used for the diagnosis of TOS in the normal population, such as loss of fat signal around the BPL fibrils in the CC and the RPM in abduction to call neurogenic TOS and compression of the SA and SV on sagittal T1W and MRA/MRV in abduction to call vascu- lar TOS. Third, we did not look for the correlation between the imaging findings and clinical symptoms and test results. Fig. 9 In a patient with left-sided intense pain radiating from the neck to the hand, a a coronal T2 fat-saturated image demonstrates thicken- ing and minimal asymmetric T2 hyperintense appearance of left BPL fibrils (short arrow) compared with that of the right hand side (long arrow). MRA and MRV in abduction demonstrate bilateral compres- sion of the SA (short arrows) and SV (long arrow). Compression of the left SV is not seen here. Sagittal T1W views in c abduction and d neutral from medial to lateral demonstrate bilateral compression of BPL fibrils, the SA (long arrows), and the SV (short arrows) in the CC with resolution of all in neutral. The fibrils of BPL run the posterior and superior aspect of the SA in all three spaces. Normal fat signals around the BPL fibrils are not seen in abduction in the CC (c). Views from the right hand side are not shown here. There is no congenital fibromuscular anomaly or cervical rib contributing to the compression. All these findings are suggestive of the bilateral positional compression of neurovascular bundles in the CC associated with a left-sided bra- chial plexitis Skeletal Radiol (2012) 41:1365–1374 1373 Therefore, we described the radiological findings and most plausible diagnosis, and recommended correlation with clin- ical history and electrophysiological and provocative tests in all TOS cases. Conclusion For evaluation of patients with TOS, visualization of the brachial plexus and cervical spine and dynamic evaluation of the neurovascular bundle in the cervicothoracobrachial region is mandatory. The neurovascular bundle is most commonly compressed in the CC, mostly secondary to position and very rarely compressed in the RPM. Congenital bone variations can cause TOS in the IS and CC depending on their extension. Congenital fibromuscular anomalies can be encountered in all three spaces. Fat-saturated coronal T2W images are needed to show brachial plexitis. Sagittal T1W, coronal T1W, and fat-saturated coronal T2W images easily show muscle and bone abnormalities and their rela- tion to the neurovascular bundle. Sagittal T1W in abduction are needed to demonstrate neurogenic compression. Vessel compression is very common in sagittal T1W in abduction. To support vascular compression, MRA and MRV views in abduction are needed. Venous compression is very common in abduction and it is hard to differentiate physiological from symptomatic compression. Correlation with clinical history and electrophysiological and provocative tests is recommended for differentiation. Acknowledgements This study was presented at ASNR 48th Annual Meeting & NER Foundation Symposium 2010, Boston, MA, USA, as a scientific exhibit. References 1. Nichols AW. Diagnosis and management of thoracic outlet syn- drome. Curr Sports Med Rep. 2009;8:240–9. 2. Sanders RJ, Hammond SL, Rao NM. Diagnosis of thoracic outlet syndrome. J Vasc Surg. 2007;46:601–4. 3. Huang JH, Zager EL. 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J Vasc Surg. 1997;26:776–83. 1374 Skeletal Radiol (2012) 41:1365–1374 MRI findings in thoracic outlet syndrome Abstract Introduction Anatomy of the neurovascular bundle in the cervicothoracobrachial region Neurogenic TOS Arterial TOS Venous TOS MR imaging protocols Results Discussion Conclusion References