Histologic evidence of brachial plexus compression sites at the thoracic inlet and variations in formation of the lower trunk in cadavers.

BACKGROUND: In thoracic "outlet" syndrome (TOS), pathologic evidence is well documented for vascular but not neurologic compression. We hypothesized that histologic evidence of compression would be identified at sites where the upper trunk was impacted by the anterior scalene muscle and the lower trunk by anatomic anomalies or the first rib. The purpose of this study was to investigate this hypothesis in human cadavers. MATERIALS AND METHODS: Twenty-five cadavers' brachial plexuses were dissected and excised. Histologic and descriptive analysis was directed at juncture 1, the upper trunk and anterior scalene muscle, and juncture 2, C8 and T1 nerve roots (lower trunk) with the posterior border of the first rib. Measurements were obtained at the juncture of the T1 nerve root with the C8 nerve root in relationship to the first rib. RESULTS: Histologic analysis demonstrated epineurial and perineurial fibrosis, myelin thinning, and Renaut bodies at junctures 1 and 2. Lower trunk formation occurred on or lateral to the first rib in 66% of specimens, with asymmetry in 32% of cadavers. A muscle of Albinus was present in 18% of cadavers. A large dorsal scapular artery coursed through 36% of plexuses with a high, arched subclavian artery. CONCLUSIONS: We report histologic changes consistent with chronic compression of the upper and lower plexus in the thoracic inlet at hypothesized sites of brachial plexus compression that may correlate with clinical neck/shoulder (upper trunk) and "ulnar nervelike" (C8-T1/lower trunk) symptoms. Anatomic anomalies identified should alert the surgeon to variations of lower trunk formation at compression sites.

Imaging of non-specific complaints of the arm, neck, and/or shoulder (CANS): role of the scalene muscles and piercing variants in neurogenic thoracic outlet syndrome.

Complaints of the arm, neck and/or shoulder (CANS) are common in the general population (40%) and workers (30%) and have significant economic impact. Twenty-three conditions have been designated as specific CANS. Cases where no cause is identified are reported as non-specific CANS; these cases make up the majority of CANS. Non-specific CANS presentations overlap with clinical entities including cervicobrachial and scalene myofascial syndromes that are associated with neurogenic thoracic outlet syndrome (NTOS). The scalene muscles have been identified as the commonest site of NTOS, although this has been reported to be functional and in conjunction with cervicothoracic junction variants that compromise the brachial plexus lower trunk. Anatomical variants in relation to both the scalene muscles and brachial plexus are not widely recognised in the clinical and imaging literature; however, pass-through and pass-over (or "piercing") variants of the brachial plexus upper trunk and scalene muscles have been well described in the anatomical and anaesthetic literature. In this review, we demonstrate the presence and describe the imaging of scalene muscle pathology and variant muscle-brachial plexus anatomy affecting the upper trunk that are underdiagnosed causes of non-specific CANS presentations and NTOS.

The thoracic outlet syndromes: Part 1. Overview of the thoracic outlet syndromes and review of true neurogenic thoracic outlet syndrome.

The thoracic outlet syndromes (TOSs) are a group of etiologically and clinically distinct disorders with 1 feature in common: compression of 1 or more neurovascular elements as they traverse the thoracic outlet. The medical literature reflects 5 TOSs: arterial; venous; traumatic neurovascular; true neurogenic; and disputed. Of these, the first 4 demonstrate all of the features expected of a syndrome, whereas disputed TOS does not, causing many experts to doubt its existence altogether. Thus, some categorize disputed TOS as a cervicoscapular pain syndrome rather than as a type of TOS. To better understand these disorders, their distinctions, and the reasoning underlying the categorical change of disputed TOS from a form of TOS to a cervicoscapular pain syndrome, a thorough understanding of the pertinent anatomy, pathology, pathophysiology, and the electrodiagnostic manifestations of their pathophysiologies is required. This review of the TOSs is provided in 2 parts. In this first part we address information pertinent to all 5 TOSs and reviews true neurogenic TOS. In part 2 we review the other 4 TOSs. Muscle Nerve 55: 782-793, 2017.

Neurogenic thoracic outlet syndrome: Are anatomical anomalies significant?

BACKGROUND: Thoracic outlet syndrome (TOS) is one of the most poorly understood syndromes. Neurogenic TOS is found in 95% of cases. The described anatomical spaces transform and evolve into 'entrapment spaces'. The aetiology is unclear. This study was based on the observation by a single surgeon that there appeared to be a high incidence of anatomical abnormalities in patients with neurogenic TOS. OBJECTIVE: To attempt to clearly define anatomical anomalies causing TOS. METHODS: The records from a prospectively maintained computer database of 219 patients submitted for surgery over a 10-year period (1999-2009) were reviewed. A substudy was done on the patients operated on over the last 4 years (n=63) in whom details of the intraoperative anatomical findings were meticulously recorded. RESULTS: Over the last 4 years, the surgical findings in the last 63 patients (67 operations) revealed a significant number of anatomical abnormalities believed to be responsible for the nerve compression. Brachial plexus anomalies were found in 99% of the patients--the majority comprised the postfixed configuration. In addition, 58% had a soft-tissue anomaly, 27% had a bony anomaly and 3% had other abnormalities. The majority had combinations of these abnormal findings. CONCLUSION: These findings strongly suggest that there is usually an identifiable anatomical cause, typically the brachial plexus, for the symptoms of TOS. We strongly recommend that the supraclavicular approach be used in order to define anatomical aberrations. Brachial plexus configuration anomalies causing TOS have not been emphasised previously. Further detailed recordings of these findings may help us better understand the aetiology of this poorly defined syndrome.

Thoracic outlet syndrome in 3T MR neurography-fibrous bands causing discernible lesions of the lower brachial plexus.

OBJECTIVES: To investigate whether targeted magnetic resonance neurography (MRN) of the brachial plexus can visualise fibrous bands compressing the brachial plexus and directly detect injury in plexus nerve fascicles. METHODS: High-resolution MRN was employed in 30 patients with clinical suspicion of either true neurogenic thoracic outlet syndrome (TOS) or non-specific TOS. The protocol for the brachial plexus included a SPACE (3D turbo spin echo with variable flip angle) STIR (short tau inversion recovery), a sagittal-oblique T2-weighted (T2W) SPAIR (spectral adiabatic inversion recovery) and a 3D PDW (proton density weighted) SPACE. Images were evaluated for anatomical anomalies compressing the brachial plexus and for abnormal T2W signal within plexus elements. Patients with abnormal MR imaging findings underwent surgical exploration. RESULTS: Seven out of 30 patients were identified with unambiguous morphological correlates of TOS. These were verified by surgical exploration. Correlates included fibrous bands (n = 5) and pseudarthrosis or synostosis of ribs (n = 2). Increased T2W signal was detected within compressed plexus portion (C8 spinal nerve, inferior trunk, or medial cord) and confirmed the diagnosis. CONCLUSIONS: The clinical suspicion of TOS can be diagnostically confirmed by MRN. Entrapment of plexus structures by subtle anatomical anomalies such as fibrous bands can be visualised and relevant compression can be confirmed by increased T2W signal of compromised plexus elements. KEY POINTS: • MR neurography (MRN) can aid the diagnosis of thoracic outlet syndrome (TOS). • Identifiable causes of TOS in MRN include fibrous bands and bony anomalies. • Increased T2W signal within brachial plexus elements indicate relevant nerve compression. • High positive predictive value allows confident and targeted indication for surgery.

Thoracic outlet syndrome: a neurological and vascular disorder.

Thoracic outlet syndrome (TOS) is a condition arising from compression of the subclavian vessels and/or brachial plexus as the structures travel from the thoracic outlet to the axilla. Despite the significant pathology associated with TOS, there remains some general disagreement among experts on the specific anatomy, etiology, and pathophysiology of the condition, presumably because of the wide variation in symptoms that manifest in presenting patients, and because of lack of a definitive gold standard for diagnosis. Symptoms associated with TOS have traditionally been divided into vascular and neurogenic categories, a distinction based on the underlying structure(s) implicated. Of the two, neurogenic TOS (nTOS) is more common, and typically presents as compression of the brachial plexus; primarily, but not exclusively, involving its lower trunk. Vascular TOS (vTOS) usually involves compression of the vessel, most commonly the subclavian artery or vein, or is secondary to thrombus formation in the venous vasculature. Any anatomical anomaly in the thoracic outlet has the potential to predispose a patient to TOS. Common anomalies include variations in the insertion of the anterior scalene muscle (ASM) or scalenus minimus muscle, the presence of a cervical rib or of fibrous and muscular bands, variations in insertion of pectoralis minor, and the presence of neurovascular structures, which follow an atypical course. A common diagnostic technique for vTOS is duplex imaging, which has generally replaced more invasive angiographic techniques. In cases of suspected nTOS, electrophysiological nerve studies and ASM blocks provide guidance when screening for patients likely to benefit from surgical decompression of TOS. Surgeons generally agree that the transaxillary approach allows the greatest field of view for first rib excision to relieve compressed vessels. Alternatively, a supraclavicular approach is favored for scalenotomies when the ASM impinges on surrounding structures. A combined supraclavicular and infraclavicular approach is preferred when a larger field of view is required. The future of TOS management must emphasize the improvement of available diagnostic and treatment techniques, and the development of a consensus gold standard for diagnosis. Helical computed tomography offers a three-dimensional view of the thoracic outlet, and may be valuable in the detection of anatomical variations, which may predispose patients to TOS. This review summarizes the history of TOS, the pertinent clinical and anatomical presentations of TOS, and the commonly used diagnostic and treatment techniques for the condition.

Modified transmanubrial approach for complicated type 1 cervical rib resection requiring subclavian artery reconstruction.

The transmanubrial musculoskeletal sparing approach (TMA) is commonly used for resecting apical lung tumours with vascular involvement. Non-neoplastic conditions which might require surgical exploration of the thoracic outlet include the 'cervical rib', a clinical condition consisting of an additional rib forming above the first rib and growing from the base of the neck just above the clavicle. Type 1 cervical rib-when a complete cervical rib articulates with the first rib or manubrium of the sternum-is the most challenging scenario where the subclavian artery can be damaged by continuous compression due to the narrow space between clavicle, first rib and supernumerary cervical rib, requiring prosthetic reconstruction of the involved tract. Here, we describe a modified TMA in which the incision in the neck is conducted posteriorly to the sternocleidomastoid muscle, thus allowing safe dissection of the superior and middle trunk of the brachial plexus.

MRI findings in thoracic outlet syndrome.

We discuss MRI findings in patients with thoracic outlet syndrome (TOS). A total of 100 neurovascular bundles were evaluated in the interscalene triangle (IS), costoclavicular (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 subclavian artery (SA) and vein (SV) in abduction were obtained. If there is compression on the vessels, MRA and MRV of the subclavian vessels were repeated in neutral. Seventy-one neurovascular 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 compressed 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 bundle. Severe cervical spondylosis was noted in 14%, contributing 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 cervicothoracobrachial region are mandatory.

[Diagnosis of patients with thoracic outlet syndrome (TOS) using physiological measures of the medial antebrachial cutaneous nerve].

The diagnosis of thoracic outlet syndrome (TOS) remains difficult; therefore, reliable and objective tests are required. We examined the process to diagnose TOS, and assessed the validity of measuring the medial antebrachial cutaneous nerve (MAC), also the ulnar nerve (UN) as a diagnostic tool. Between 2008 and 2011, 86 sides in 73 patients admitted to our hospital for the treatment of TOS were analyzed. In the process for the diagnosis as TOS, the narrow parts of the subclavian artery that was compressed by the anterior scalene muscle were confirmed with a three-dimensional CT angiography. All patients were taken a brachial plexus anesthesiological block to aim at both for diagnosis and treatment of TOS. For the diagnosis of TOS, measurements of latency (LT) and sensory nerve action potential (SNAP) of MAC and UN were analyzed between the TOS side and the non-TOS side and separated into traumatic type or disputed type. In our research, the LT of MAC and UN did not differ much between the TOS side and the non-TOS side; however, the amplitude of SNAP of MAC and UN were lower on the TOS side, especially in traumatic TOS. We concluded that comparison of the amplitude of SNAP of MAC on the injured or non-injured side was comparatively helpful for the diagnosis of TOS.

Anatomy and Embryology of the Thoracic Outlet.

The thoracic outlet is the space between the thorax and axilla through which the subclavian vein, subclavian artery, and brachial plexus travel from their central origins to their peripheral termini. Its bounds include the clavicle, first thoracic rib, insertion of the pectoralis minor muscle onto the coracoid process of the humerus, and the sternum. It contains three areas: the scalene triangle, the costoclavicular space, and the subcoracoid or pectoralis minor space. Aberrant anatomy is common in the thoracic outlet and may predispose patients to compression of the neurovascular bundle and development of clinical thoracic outlet syndrome (TOS). Much of this aberrancy is explained by the embryologic origins of the structures that comprise the thoracic outlet. A thorough understanding of this anatomy and embryology is therefore critical to the understanding of TOS.

Contemporary management of thoracic outlet syndrome.

PURPOSE OF REVIEW: The diagnosis and management of thoracic outlet syndrome (TOS) has been surrounded by controversy since this disorder was first recognized. Recent evidence from observational studies has helped us better understand the pathophysiology of different TOS subtypes and guide clinical decision making for this disorder. RECENT FINDINGS: The identification of anatomic anomalies involved with the cause of different TOS subtypes has been made easier by contemporary diagnostic techniques. This includes the injection of neuromuscular blocking agents into anterior scalene muscles to help confirm the diagnosis of neurogenic TOS. Surgical intervention by means of first rib resection and anterior scalenectomy is an effective treatment for patients diagnosed with neurogenic and venous TOS, resulting in a significant increase in quality-of-life measures for the majority of patients. Patients with acute and chronic venous TOS should be maintained on anticoagulation during the perioperative period and may not need thrombolysis prior to surgery. Finally, patients with arterial TOS should undergo cervical or first rib resection with or without arterial reconstruction to alleviate and prevent recurrence of symptoms. SUMMARY: The management of TOS requires a multidisciplinary approach with specific treatment algorithms for each TOS subtype. Appropriately selected patients with all different types of TOS may benefit from surgical intervention.

Brachial plexus and nerves about the shoulder.

Ultrasound (US) and MR imaging have been shown able to detect in-depth features of brachial plexus anatomy and to localize pathological lesions in disorders where electrophysiology and physical findings are nonspecific or nonlocalizing. High-end gradient technology, phased array coils, and selection of an appropriate protocol of pulse sequences are the main requirements to evaluate the brachial plexus nerves with MR imaging and to distinguish between intrinsic and extrinsic pathological changes. A careful scanning technique based on anatomical landmarks is required to image the brachial plexus nerves with US. In traumatic injuries, MR imaging and myelographic techniques can exclude nerve lesions at the level of neural foramina and at intradural location. Outside the spinal canal, US is an excellent alternative to MR imaging to determine the presence of a lesion, to establish the site and the level of nerve involvement, as well as to confirm or exclude major nerve injuries. In addition to brachial plexus injuries, MR imaging and US can be contributory in a variety of nontraumatic brachial plexopathies of a compressive, neoplastic, and inflammatory nature. In the thoracic outlet syndrome, imaging performed in association with postural maneuvers can help diagnose dynamic compressions. MR imaging and US are also effective to recognize neuropathies about the shoulder girdle involving the suprascapular, axillary, long thoracic, and spinal accessory nerves that may mimic brachial plexopathy. In this article, the clinical entities just listed are discussed independently, providing an overview of the current status of knowledge regarding imaging assessment.

Supernumerary subclavius muscle in Thais: predisposing cause of thoracic outlet syndrome.

OBJECTIVE: To demonstrate and classify the variation of the subclavius muscle according to its insertion in the Thais. MATERIAL AND METHOD: One hundred and twenty eight upper limbs were dissected out to expose the scapular region. The attachments of subclavius muscles were examined and recorded. RESULTS: The subclavius muscle was categorized into 4 types according to its insertion. There are 64.06% of type I, 17.96% of type II, 15.62% of type III and 2.34% of type IV. The insertion of subclavius muscle is gradually extended from the shallow groove on the inferior surface of the clavicle towards the conoid ligament and corocoid process, to the superior transverse scapular ligament and to the superior border of the scapula adjacent to the insertion of inferior belly of omohyoid muscle. CONCLUSION: The present study prevailed 64% normal subclavius muscle and other 36% of varied supernumerary subclavius muscle. The presence of supernumerary subclavius muscle could be a predisposing causative factor of thoracic outlet syndrome.

Case reports: unusual cause of shoulder pain in a collegiate baseball player.

The objective of reporting this case was to introduce a unique cause of shoulder pain in a high-level Division I NCAA collegiate baseball player. Various neurovascular causes of shoulder pain have been described in the overhead athlete, including quadrilateral space syndrome, thoracic outlet syndrome, effort thrombosis, and suprascapular nerve entrapment. All of these syndromes are uncommon and frequently are missed as a result of their rarity and the need for specialized tests to confirm the diagnosis. This pitcher presented with nonspecific posterior shoulder pain that was so severe he could not throw more than 50 feet. Eventually, intermittent axillary artery compression with the arm in abduction resulting from hypertrophy of the pectoralis minor and scalene muscles was documented by performing arteriography with the arm in 120 degrees abduction. MRI-MR angiographic evaluation revealed no anatomic abnormalities. The patient was treated successfully with a nonoperative rehabilitation program and after 6 months was able to successfully compete at the same level without pain.

Iatrogenic thoracic outlet syndrome secondary to vertical expandable prosthetic titanium rib expansion thoracoplasty: pathogenesis and strategies for prevention/treatment.

BACKGROUND: An innovative treatment for thoracic insufficiency syndrome involves a vertical expansion of the chest wall through a horizontal chest wall osteotomy maintained by a distraction device (vertical expandable prosthetic titanium rib or VEPTR). Upper-extremity neurovascular dysfunction has been reported after expansion. The purposes of this study are to identify potential etiologies for compression of the brachial plexus after expansion thoracoplasty and to suggest strategies to reduce the incidence of this complication. METHODS: A simulated VEPTR procedure was performed on 8 fresh cadaveric specimens. Manometric measurements were taken in the 3 anatomic regions of the thoracic outlet after thoracotomy and rib distraction were performed. Confirmation of the location of compression was performed by placing barium-impregnated putty along the course of the brachial plexus and evaluating the effect of expansion using video fluoroscopy. A midclavicular osteotomy was then performed and video fluoroscopy repeated. RESULTS: A 20% increase in pressure was seen in the costoclavicular region of the thoracic outlet after expansion. Constriction of the midclavicular region of the thoracic outlet between the first rib and clavicle was confirmed using the putty model. Midclavicular osteotomy alleviated this region of compression. CONCLUSIONS: Expansion thoracoplasty with the VEPTR procedure causes increased pressure in the costoclavicular region of the thoracic outlet. A midclavicular osteotomy may be one method to alleviate thoracic outlet narrowing after VEPTR procedure, although the short- and long-term effects of this is procedure is not known. CLINICAL RELEVANCE: Our model supports an iatrogenic thoracic outlet syndrome caused by expansion thoracoplasty. Based on our data as well as a review of the literature, we recommend intraoperative neurologic monitoring of the ipsilateral upper extremity during the VEPTR procedure.

Three muscles in the upper costovertebral region: description and clinical anatomy.

The aim of the study was to describe three small muscles in the upper costovertebral region that have close proximity to the ventral rami of the lower cervical and upper two thoracic spinal nerves. The study was performed using both anterior and posterior approaches to the costovertebral region. Twenty-five human cadavers, 15 males and 10 females with a mean age of 50 years and with normal spines, constituted the material of the study. Dissection revealed the presence of three triangular muscles that extended from the transverse processes of the seventh cervical through second thoracic vertebrae to the upper borders of the necks of the first through third ribs, respectively. The second and third muscles are described and reported for the first time. The ventral rami of the lower cervical and upper two thoracic spinal nerves emerged through narrow gaps between the described muscles and the bodies of seventh cervical and upper two thoracic vertebrae, respectively. The lateral branch of the dorsal ramus of the corresponding spinal nerve issued posteriorly between the muscle and the articular capsule of the zygapophyseal joint. It then curved round the posterior aspect of the muscle and passed through the gap between the muscle and the levator costarum, after supplying them both. We suggest that these three muscles were suggested to share a common embryogenesis with the intertransverse muscles. In addition, this study suggests that the three muscles described herein could be one of the potential causes of thoracic outlet syndrome.

[Thoracic outlet syndromes]. / Syndromes de la traversée cervico-thoracobrachiale.

Thoracic outlet syndromes (TOS) may induce neurologic signs, vascular pathology, and pain, but the clinical signs are often unclear. The relationship between a cervical bony abnormality is often unclear, and the investigations not always contributive. First-line treatment consists in physiotherapy. Surgery remains controversial, in both its indication as its modalities. However, well-adapted surgery gives a good result in 60-85% of cases.

Overview of venous pathology related to repetitive vascular trauma in athletes.

BACKGROUND: Athletes are generally young, high-functioning individuals. Pathology in this cohort is associated with a decrease in function and consequently has major implications on quality of life. Venous disorders can be attributed to a combination of vascular compression with a high burden of activity. OBJECTIVE: This article promotes increased awareness of these uncommon conditions specific to the athlete by summarizing pathophysiology, clinical features, investigation, and treatment protocols for use in clinical practice. Prognostic outcomes of these management regimens are also discussed, allowing for clinicians to counsel these high-functioning individuals appropriately. With the aim of providing an overview of sport-related venous pathology, a literature review was undertaken identifying articles that were independently reviewed by the authors. RESULTS: Lower limb venous thrombosis has been identified in young, high-functioning athletes attributed to both compression-related venous trauma, associated with repetitive movements resulting in intimal damage, and blunt trauma. The diagnosis and treatment follow the same protocols as for the general population. Of note, early ambulation is advocated, with an aim to return to premorbid (noncontact) function within 6 weeks. Athletes performing high-intensity repetitive upper limb movement, such as baseball players, are predisposed to upper limb deep venous thrombosis (DVT). Diagnosis follows the same protocols as for lower extremity DVT; however, the optimal treatment strategy remains debated. Current guidelines advocate the use of anticoagulation alone. A specific subset of primary upper limb DVT is effort thrombosis, where there is compression at the level of the thoracic outlet. Thrombolysis with first rib resection is indicated in the acute setting within 14 days. In cases of complete occlusion, surgical decompression with venous reconstruction may be required. Popliteal vein entrapment syndrome is also discussed. This entity has been identified as an overuse injury associated with popliteal vein compression. Duplex ultrasound examination is indicated as a first-line investigation, with conservative noninvasive options considered as an initial management strategy. Chronic venous insufficiency or persistent symptoms may require subsequent surgical decompression. CONCLUSIONS: Key conditions including upper extremity and lower extremity venous thrombosis, venous aneurysms, Paget-Schroetter syndrome (effort thrombosis), and popliteal vein entrapment syndrome are discussed. Further studies evaluating long-term outcomes on morbidity for current treatment regimens in upper extremity DVT, effort thrombosis, venous thoracic outlet syndrome, and popliteal venous entrapment syndrome are required.

Thoracic outlet syndrome: a review.

BACKGROUND: : Arterial and venous thoracic outlet syndrome (TOS) were recognized in the late 1800s and neurogenic TOS in the early 1900s. Diagnosis and treatment of the 2 vascular forms of TOS are generally accepted in all medical circles. On the other hand, neurogenic TOS is more difficult to diagnose because there is no standard objective test to confirm clinical impressions. REVIEW SUMMARY: : The clinical features of arterial, venous, and neurogenic TOS are described. Because neurogenic TOS is by far the most common type, the pathology, pathophysiology, diagnostic tests, differential and associate diagnoses, and treatment are detailed and discussed. The controversial area of objective and subjective diagnostic criteria is addressed. CONCLUSION: : Arterial and venous TOS are usually not difficult to recognize and the diagnosis can be confirmed by angiography. The diagnosis of neurogenic TOS is more challenging because its symptoms of nerve compression are not unique. The clinical diagnosis relies on documenting several positive findings on physical examination. To date there is still no reliable objective test to confirm the diagnosis, but measurements of the medial antebrachial cutaneous nerve appear promising.

First rib resection and scalenectomy for chronically occluded subclavian veins: what does it really do?

First rib resection and scalenectomy is an acceptable therapy for those with axillosubclavian vein thrombosis who have responded to lytic therapy and demonstrated subclavian vein patency. However, the treatment for those patients who present with a chronically occluded subclavian vein is controversial. We present four such patients who underwent first rib resection and scalenectomy and whose subclavian vein spontaneously opened within the first year following surgery while anticoagulated, as well as the ultrasound protocol we employ at our institution to identify such reopening. The average age of these patients was 20 (range 17-23) years; three were male and one was female. The average time interval prior to surgery when the initial thrombosis occurred was 25 (12-34) weeks. All patients were symptomatic and underwent a transaxillary first rib resection and scalenectomy with attention to incise the subclavius tendon. All were maintained on warfarin postoperatively and surveilled by duplex scan. In all four patients the subclavian vein subsequently opened after an average of 7 (2-11) months and anticoagulation was stopped. The resultant patent subclavian vein correlated with improvement in symptoms in all four patients. All patients were asymptomatic in the postoperative follow-up period at an average of 14 (2-33 months). In conclusion, selective symptomatic patients with subclavian vein occlusion can be aggressively treated with first rib resection and scalenectomy along with anticoagulation that will lead to recanalization and opening of vein over time. This treatment correlates with improvement of their symptoms.