Dynamic neuromusculoskeletal ultrasound documentation of brachial plexus/thoracic outlet compression during elevated arm stress testing

Background

The diagnosis and validation of thoracic outlet syndrome/brachial plexopathy (TOS) remains a difficult challenge for surgeons, neurologists, and radiologists. This is due to the fact that the responses of standard elevated arm stress tests can be considered somewhat subjective and can vary. Therefore, non-vascular TOS cases are presently diagnosed clinically, and any objective diagnosis has been controversial.

Methods

This is a technique paper describing the use of dynamic neuromusculoskeletal ultrasound to assist in the diagnosis of thoracic outlet/brachial plexus pathology. We propose a new way to observe the brachial plexus dynamically, so that physical verification of nerve compression between the anterior and middle scalene muscles can be clearly made at the onset of clinical symptoms. This gives a way to objectively identify clinically significant brachial plexus compression.

Results

Dynamic testing can add objective analysis to tests such as the elevated arm stress tests and can correlate the onset of symptoms with plexus compression between the anterior and middle scalene muscles. With this, the area of pathologic compression can be identified and viewed while performing the dynamic testing. If compression is seen and the onset of symptoms ensues, this is a positive confirmatory test for the presence of TOS and a clinically significant disease.

Conclusions

This paper offers a simple, objective, and visual diagnostic test that can validate the presence or absence of brachial plexus compression during arm elevation in patients with brachial plexus injury and thoracic outlet syndrome.     

Documentation of brachial plexus compression in the thoracic inlet with quantitative sensory testing

This study evaluated the cutaneous pressure threshold of subjects with and without a clinical diagnosis of brachial plexus compression in the thoracic inlet, usually termed thoracic outlet syndrome (TOS). Sixty-one subjects (102 arms) made up the control population; 11 subjects 120 arms) made up the TOS population. Assessment by two upper-extremity specialists preceded the testing. The one-point cutaneous pressure threshold was measured with the Pressure-Specifying Sensory Device (PSSD) on the pulp of both the index and little finger (upper and lower brachial plexus distributions) with the arm in the unprovoked (adducted) and provoked (abducted 180 degrees) positions. In the control subjects, there was no significant change in the cutaneous pressure threshold between unprovoked and provoked positions. In contrast in patients with TOS, there was a significant increase in the cutaneous pressure threshold at both sites (p < .0001 ) between the unprovoked and the provoked positions. Furthermore, the cutaneous pressure threshold for patients with TOS was significantly higher in both positions than it was in the controls (p < .0001 ). It was concluded that measurement of changes in the cutaneous pressure threshold with the PSSD in distal sensory targets of the upper and lower trunk can identify patients symptomatic for compression, when the brachial plexus is provoked as part of the testing sequence.     

Anomalous vasculature as direct cause of upper brachial plexus thoracic outlet syndrome

Direct vascular etiologies of upper plexus thoracic outlet syndrome (TOS) other than the subclavian vessels are exceptional. This is a unique case of an anomalous artery and its accompanying vein causing direct compression to the upper brachial plexus causing TOS. All symptoms resolved after successful treatment consisting of ligation and resection of the vessels. This case demonstrates that although direct vascular etiologies causing upper plexus TOS are extremely uncommon, they should be considered in the differential diagnosis.     

An osteopathic approach to conservative management of thoracic outlet syndromes

Thoracic outlet syndromes (TOS) are a group of disorders in which there is compression of the brachial plexus or the subclavian artery or vein or both as they pass through the thoracic outlet. Most patients have neurologic symptoms of the arm and hand. These syndromes are generally named according to the site of compression or the compressing structures. There are many factors that predispose patients to the development of TOS. The differential diagnosis includes many diseases that can add to or imitate TOS symptoms. Diagnosis is based mainly on the findings of the history and physical examination. Most patients respond well to a conservative care regimen, which should be tailored to the individual patient's needs. In most instances, surgery should be reserved as a treatment of last resort.     

Complete cervical rib. Possible neurovascular implications of the upper limb

The thoracic outlet syndrome (TOS) is caused by compression of the brachial plexus or subclavian artery or vein in the region of the neck and shoulder girdle. The neurovascular bundle may be compressed at multiple sites: costoclavicular space, interscalene triangle, insertion of the pectoralis minor into the coracoid process. More than 90% of the patients present with neurologic symptoms: pain, paraesthesias or arm and hand weakness and 10% also have vascular problems. The diagnosis of TOS is always difficult and depends on careful clinical study of patients. For the neurological type of TOS, electromyograms, arteriograms and venograms are not helpful. The value of Doppler study and of arteriography is demonstrated in the present case of a woman with a five month history of pain and paraesthesias of the arm and hand, who shoved sudden occlusion of left humeral artery. Roentgenograms showed the presence of a well developed left cervical rib. Doppler study and arteriography showed the compression of subclavian artery with the arm abduction manoeuver. After first rib resection and humeral artery thrombectomy there was a complete return of humeral artery flow and of all neurologic functions. Thus the role of first cervical rib or other bone and muscular structures must be emphasyzed both in the brachial and in the subclavian artery or vein compression. Embolization of the axillary or humeral artery should be corrected as soon as possible when the cervical rib is corrected.     

Neurovascular compression in the thoracic outlet: changing management over 50 years.

SUMMARY BACKGROUND DATA: During the past five decades, significant improvements have been made in the diagnosis and treatment of thoracic outlet syndrome (TOS) secondary to sports activities, breast implants, or median sternotomy. METHODS, RESULTS, AND CONCLUSIONS: Of more than 15,000 patients evaluated for TOS, 3914 underwent primary neurovascular decompression procedures and 1221 underwent second surgical procedures for recurrent symptoms. Of 2210 consecutive patients, 250 had symptoms of upper plexus compression only (median nerve), 1508 had symptoms of lower plexus compression only (ulnar nerve), and 452 patients had symptoms of both. Ulnar and median nerve conduction velocities confirmed the clinical diagnosis. Transaxillary first rib removal alone for neurovascular decompression relieved both upper and lower plexus symptoms (without a combined transaxillary and supraclavicular approach). There are two reasons for this: most upper compression mechanisms attach to the first rib, and the median nerve is also supplied by C8 and T1 as well as C5, C6, and C7 nerve roots. Axillary subclavian artery aneurysm or occlusion was treated successfully in 240 patients. Dorsal sympathectomy was performed concomitantly in 71 patients for occlusion or embolectomy. It was combined with first rib resection in 1974 patients for sympathetic maintained pain syndrome and causalgia that did not improve with conservative therapy. Of 264 patients with effort thrombosis (Paget-Schroetter syndrome), 211 were treated by urokinase thrombolysis and prompt first rib resection with excellent long-term results. Recurrent TOS symptoms required a second procedure using the posterior approach in 1221 patients with brachial plexus neurolysis and dorsal sympathectomy. The use of hyaluronic acid significantly reduced recurrent scarring.     

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.     

胸廓出口综合征的诊断治疗进展

胸廓出口综合征(thoracic outlet syndrome,TOS)是指臂丛神经或者锁骨下动脉或者锁骨下静脉在胸廓出口受到卡压而出现的一些列症状。可分为神经型TOS、静脉型TOS和动脉型TOS,其中神经型TOS最为常见。TOS的临床表现非常多样,并且缺乏确诊性的检查方法,因此诊断应结合详细的病史、查体及相关的辅助检查。保守治疗和手术治疗均适用于TOS,并且都能获得较好的预后。神经型TOS首选保守治疗,对于有症状的血管型TOS和保守治疗失败的神经型TOS,应尽早手术。     

胸廓出口综合征的新认识——解剖学与临床观察

目的探讨胸廓出口综合征的病因。方法对３０具６０侧经福尔马林固定的成人尸体小斜角肌及前中斜角肌的起始部进行解剖研究;对５３例胸廓出口综合征手术患者（１９６６～１９９４年４５例,１９９６～１９９７年８例）随访情况进行总结分析。结果解剖研究发现小斜角肌的出现率为８８３％,Ｔ１神经根或其下干在小斜角肌近段起源的腱性组织上跨过;前中斜角肌在颈椎横突的前后结节均有起点,Ｃ５、Ｃ６神经根从前中斜角肌的交叉腱性起点中穿过。４５例１９６６～１９９６年手术者中,有颈肩痛症状者３４例,术后１７例颈肩痛症状仍存在,其中７例加重;８例１９９６～１９９７年手术者中,７例有颈肩痛,术中切断前中斜角肌在Ｃ５～６神经根旁的腱性纤维组织,术后仅有１例仍有颈肩部不适。结论小斜角肌的腱性纤维是臂丛神经下干或Ｔ１神经根受压的原因;前中斜角肌在Ｃ４～５横突前后结节的交叉腱性起点是压迫Ｃ５～６,有时包括Ｃ７神经根或臂丛神经上（中）干的原因     

Thoracic outlet syndrome

Thoracic outlet syndrome (TOS) is an often misdiagnosed cause of neck, shoulder, and arm disability. Neurovascular compression may be seen in the interscalene triangle, costoclavicular space, or posterior to the pectoralis minor, although any cause of abnormalities of shoulder girdle alignment may cause a localized area of brachial plexus compression. Nerve compression in this way may lead to upper extremity weakness, pain, paresthesias, and numbness. A careful and detailed medical history and physical examination are essential to proper identification of thoracic outlet syndrome, which remains primarily a clinical diagnosis. Diagnostic testing may differentiate other causes of pain or neurologic symptoms of the upper extremity from TOS. Clinical management is often challenging.     

小斜角肌的应用解剖

目的：探讨小斜角肌与臂丛神经的解剖关系，为临床治疗臂丛神经血管受压征提供解剖学依据。方法：观察２４具成人固定尸体中小斜角肌的形态及其与臂丛、血管的关系。２具成人新鲜尸体作Ｍａｓｓｏｎ染色，了解小斜角肌腱性组织成分。结果：４８侧尸体中，４２侧有小斜角肌，出现率为８７．５％，其止点的主要成分为腱性结构，臂丛神经下干从其止点上方跨过。结论：小斜角肌存在广泛，是引起臂丛神经血管受压征的因素之一。在臂丛神经血管受压征的手术中，应在切断前、中斜角肌时，同时切断小斜角肌     

Compression and stretching of the brachial plexus in thoracic outlet syndrome: correlation between neuroradiographic findings and symptoms and signs produced by provocation manoeuvres

In order to investigate the mechanism of nerve irritation in thoracic outlet syndrome (TOS), we studied 150 patients who presented with symptoms of neurologic TOS between 1985 and 1999. They first performed various provocative physical manoeuvres and then underwent injection of contrast medium into the supraclavicular part of the brachial plexus. Several of the provocative manoeuvres were then repeated and radiographs were again obtained. Based on the neuroradiographs, we identified three subsets of patients; those with only compression (type 1 TOS, n=27, 18%), those with combined compression and stretching (type 2 TOS, n=111, 74%), and those with only stretching (type 3 TOS, n=12, 8%). We were able to correlate the neuroradiological subsets with symptoms elicited by pre-radiographic provocative manoeuvres; in 92 patients (61%) these were elicited by traction manoeuvres. We conclude that stretching is an important factor of nerve irritation in TOS.     

Diagnosis of thoracic outlet syndrome

Thoracic outlet syndrome (TOS) is a nonspecific label. When employing it, one should define the type of TOS as arterial TOS, venous TOS, or neurogenic TOS. Each type has different symptoms and physical findings by which the three types can easily be identified. Neurogenic TOS (NTOS) is by far the most common, comprising well over 90% of all TOS patients. Arterial TOS is the least common accounting for no more than 1%. Many patients are erroneously diagnosed as "vascular" TOS, a nonspecific misnomer, whereas they really have NTOS. The Adson Test of noting a radial pulse deficit in provocative positions has been shown to be of no clinical value and should not be relied upon to make the diagnosis of any of the three types. The test is normal in most patients with NTOS and at the same time can be positive in many control volunteers. Arterial TOS is caused by emboli arising from subclavian artery stenosis or aneurysms. Symptoms are those of arterial ischemia and x-rays almost always disclose a cervical rib or anomalous first rib. Venous TOS presents with arm swelling, cyanosis, and pain due to subclavian vein obstruction, with or without thrombosis. Neurogenic TOS is due to brachial plexus compression usually from scarred scalene muscles secondary to neck trauma, whiplash injuries being the most common. Symptoms include extremity paresthesia, pain, and weakness as well as neck pain and occipital headache. Physical exam is most important and includes several provocative maneuvers including neck rotation and head tilting, which elicit symptoms in the contralateral extremity; the upper limb tension test, which is comparable to straight leg raising; and abducting the arms to 90 degrees in external rotation, which usually brings on symptoms within 60 seconds.     

Thoracic outlet and pectoralis minor syndromes

Compression of the neurovascular bundle to the upper extremity can occur above or below the clavicle; thoracic outlet syndrome (TOS) is above the clavicle and pectoralis minor syndrome is below. More than 90% of cases involve the brachial plexus, 5% involve venous obstruction, and 1% are associate with arterial obstruction. The clinical presentation, including symptoms, physical examination, pathology, etiology, and treatment differences among neurogenic, venous, and arterial TOS syndromes. This review details the diagnostic testing required to differentiate among the associated conditions and recommends appropriate medical or surgical treatment for each compression syndrome. The long-term outcomes of patients with TOS and pectoralis minor syndrome also vary and depend on duration of symptoms before initiation of physical therapy and surgical intervention. Overall, it can be expected that >80% of patients with these compression syndromes can experience functional improvement of their upper extremity; higher for arterial and venous TOS than for neurogenic compression.     

Diagnosis of thoracic outlet syndrome by magnetic stimulation of the brachial plexus

The abductor pollicis brevis (APB) and abductor digiti minimi (ADM) compound muscle action potential (CMAP) latencies, and median and ulnar motor conduction velocities (MCVs), obtained by magnetic stimulation of the brachial plexus, were evaluated for the diagnosis of thoracic outlet syndrome (TOS). These measurements were compared in three groups of limbs: (1) the symptomatic limbs of patients with TOS (symptomatic group), (2) the asymptomatic con-tralateral limbs of these patients (asymptomatic group), and (3) the limbs of healthy control subjects (control group). Although no significant differences were observed in MCVs among the three groups, the APB CMAP latency in the sym-ptomatic group (12.0 ± 1.2 ms) was significantly prolonged compared with that in the control group (10.4 ± 0.64 ms; P < 0.01), and the ADM CMAP latency in the symptomatic group (11.0 ± 0.82 ms) was also significantly prolonged compared with that in the control group (10.1 ± 0.59 ms; P < 0.01). The possibility is suggested that the evaluation of APB and ADM CMAP latencies by magnetic stimulation of the brachial plexus may be helpful for the diagnosis of TOS. Received: March 14, 2001 / Accepted: October 9, 2001     

Reported in-hospital complications following rib resections for neurogenic thoracic outlet syndrome

While brachial plexus injury has been described as the most common complication following thoracic outlet syndrome (TOS) operation and case series have been reported, the exact incidence rate has not been described. We conducted a retrospective analysis of 5 years (1999-2003) of the Nationwide Inpatient Sample database. Neurogenic TOS patients, rib resections, brachial plexus injuries, and vascular injuries are identified by ICD-9 diagnosis codes or procedure codes. A total of 2,016 TOS operations were identified, ranging 317-468 per year, in this database. Mean age was 37.3 years, with 1,409 (70.2%) women and 1,270 (63.0%) Caucasians. These patients were treated in a total of 392 hospitals, with an average volume of 1.03 cases per hospital per year (range 0-114). Their mean hospital length of stay was 2.51 days (median 2), with a mean total hospital charge of $16,160 in inflation-adjusted year 2005 dollars (median $11,824). The majority (1,421, or 70.5%) was treated at a teaching hospital. There were 12 brachial plexus injuries (0.60%) and 35 vascular injuries (1.74%). The rate of vascular injuries was significantly lower among teaching hospitals (1.34% vs. 2.69%, P = 0.03) and in women (1.35% vs. 2.67%, P = 0.03). Vascular injury patients had significantly longer lengths of stay (7.7 vs. 2.4 days, P < 0.001) and higher total hospital charges ($53,373 vs. $15,507, P < 0.001), while no such difference was observed among brachial plexus injury patients. On hospital discharge, brachial plexus injury following rib resection for TOS occurs in <1% of cases, while vascular injuries occur in 1-2% of cases. The low complication rates suggest that the operation can be performed safely in all patients, especially at teaching hospitals, which had significantly lower rates of vascular injuries, shorter hospital lengths of stay, and lower hospital charges. The low incidence rates of these traditional clinical measures of outcome in TOS patients suggest that the appropriate measure for TOS patient outcome would be patient-reported quality of life or functional outcomes.     

Reoperation for thoracic outlet syndrome

The clinical history and operative findings in a group of 60 patients who underwent reoperation for thoracic outlet syndrome (TOS) are presented. The patients were severely disabled by arm, shoulder, and neck pain and presented with physical findings pointing to scar fixation of the brachial plexus in the neck (upper tract recurrence) or at the thoracic outlet (lower tract recurrence). The causes of recurrence of TOS as discovered at operation are outlined. Basic principles governing the surgical management of recurrent TOS are elimination of the known causes of recurrence, thorough neurolysis of the brachial plexus, and coverage of the nerves with healthy fat. The role of an expanded PTFE surgical membrane (Gortex) as an adjunct to prevent recurrent scarring is discussed. The surgeon who operates on patients with recurrent TOS must be capable of managing the potential intraoperative complications of severe nerve injury and life threatening bleeding.     

Documentation of brachial plexus compression (in the thoracic inlet) utilizing provocative neurosensory and muscular testing

Diagnosis and documentation of brachial plexus compression in the thoracic inlet, "thoracic outlet syndrome", remains difficult because the syndrome complex overlaps that of patients with cervical disc disease, intrinsic shoulder pathology, and peripheral nerve compression. While traditional electrodiagnostic testing can identify cervical radiculopathy and the rare isolated lower trunk compression, it cannot identify brachial plexus compression in the thoracic inlet. In 2000, neurosensory testing with the Pressure-Specified Sensory Device (PSSD) was applied to this diagnostic dilemma, demonstrating a significant increase in the one-point static touch cutaneous pressure threshold between controls and patients, when the index finger (upper trunk) and little finger (lower trunk) were tested with the hands at rest and after provoking the plexus by elevating the hands above the head. In the present study, this approach has been extended to include two-point static touch thresholds with the PSSD, and pinch and grip strength (Digit-Grip). Sixteen controls (mean: 34.2, range: 11 to 48 years) were tested and the 99 percent upper confidence limit calculated for percent change after elevation of the hands for 3 min. Forty-one patients symptomatic for brachial plexus compression (mean: 41.0, range: 21 to 62 years) were tested. The clinical severity of the plexus compression was dichotomized as either "severe" or "not severe" judged by the Roos and Tinel sign. Results demonstrated that when five or more of the eight possible neurosensory and motor test results were > 99 percent normal confidence limit for change, this testing has a sensitivity of 82 percent, a specificity of 100 percent, and a positive predictive value of 100 percent for the diagnosis of clinically severe brachial plexus compression. Seventeen patients who were in the "severe" category prior to surgery, were tested before and after plexus neurolysis and anterior scalenectomy. All 17 patients were clinically improved and in 16 of these patients, postoperative neurosensory and motor testing returned to a normal pattern (no significant increase in thresholds with hand elevation). It is concluded that neurosensory (PSSD) and motor testing (Digit-Grip) can help in the diagnosis and documentation of brachial plexus compression.     

Supraclavicular Approach for Thoracic Outlet Syndrome

The authors' experience with the supraclavicular approach for the treatment of patients with primary thoracic outlet syndrome (TOS) and for patients with recurrent TOS or iatrogenic brachial plexus injury after prior transaxillary first rib resection is presented. The records of 33 patients (34 plexuses) with TOS who presented for evaluation and treatment were analyzed. Of these, 12 (35%) plexuses underwent surgical treatment, and 22 (65%) plexuses were managed non-operatively. The patients who were treated non-operatively and had an adequate follow-up (n = 11) were used as a control group. Of the 12 surgically treated patients, five patients underwent primary surgery; four patients had secondary surgery for recurrent TOS; and three patients had surgery for iatrogenic brachial plexus injury. All patients presented with severe pain, and most of them had neurologic symptoms. All nine (100%) patients who underwent primary surgery (n = 5) and secondary surgery for recurrent TOS (n = 4) demonstrated excellent or good results. On the other hand, six (54%) of the 11 patients from the control group had some benefit from the non-operative treatment. Reoperation in three patients with iatrogenic brachial plexus injury resulted in good result in one case and in fair results in two patients; however, all patients were pain-free. No complications were encountered. Supraclavicular exploration of the brachial plexus enables precise assessment of the contents of the thoracic inlet area. It allows for safe identification and release of all abnormal anatomical structures and complete first rib resection with minimal risk to neurovascular structures. Additionally, this approach allows for the appropriate nerve reconstruction in cases of prior transaxillary iatrogenic plexus injury.     

Gilliatt-Sumner hand or true neurogenic thoracic outlet syndrome. A report on seven operated cases

Background and purpose

The clinical picture of hand atrophy related to a cervical rib or elongated C7 transverse process was well described in the modern literature by Gilliatt and Sumner; in 1970, they reported a series of nine patients whose motor status was stabilized following brachial plexus decompression. We report here seven patients suffering from thoracic outlet syndrome (TOS), who developed hand atrophy, sometimes because of diagnostic delay.

Methods

The patient's charts were analysed retrospectively.

Results

The seven patients were all female; the mean age was 43 years. The first complaints were arm pain and paresthesias lasting six months to 5 years. Three patients were treated with C56/C67 discectomy plus disc prosthesis (one patient), ulnar neurolysis at the elbow (the same patient), carpal tunnel release (one patient), and intravenous immunoglobulins (one patient) before TOS diagnosis. Hand atrophy, severe in five patients, was present at presentation. All patients underwent brachial plexus decompression by the anterior (four), posterior (two), or transaxillary (one) approach. This last approach was completed 18 months later by brachial plexus neurolysis via the anterior approach. Postoperatively, motor deficit was improved in two patients and stabilized in five patients.

Conclusions

Physicians’ unfamiliarity with TOS diagnosis or their reluctance to accept the diagnosis without electrical confirmation can lead to hand atrophy. Brachial plexus decompression at this stage usually stabilizes the deficit.