eMedicine Specialties > Physical Medicine and Rehabilitation > Plexopathy

Thoracic Outlet Syndrome

Author: Benjamin M Sucher, DO, FAAPMR, FAOCPMR, Medical Director, EMG Labs of AARA (Arizona Arthritis & Rheumatology Associates)
Contributor Information and Disclosures

Updated: Jul 1, 2009

Introduction

Background

Thoracic outlet syndrome (TOS) is a controversial topic in the literature; many proponents support the existence of the condition, but some strongly vocal opponents doubt the validity of TOS as a medical entity. Even the name itself has been questioned because the actual site of pathology is technically the thoracic "inlet," not the "outlet." The primary controversy seems to center around the lack of objective criteria for diagnosis and the confusion with multiple types or clinical presentations.

Since TOS involves proximal neurovascular structures (see image below and Image 1), symptoms often are confused with various distal compression neuropathies or cervical radiculopathies. In addition, surgical treatment has been known to have devastating complications, which further fuels debate with the opponents of recognition of this entity. Conservative treatment appears to be the most universally accepted approach, with even surgeons recommending a prolonged trial before any operative procedure.

Pathophysiology

Thoracic outlet syndrome (TOS) involves compression, injury, or irritation to the neurovascular structures at the root of the neck or upper thoracic region, bounded by the anterior and middle scalenes; between the clavicle and first rib (with possible enlargement/hypertrophy of the subclavius); or beneath the pectoralis minor muscle. Some authors define the thoracic outlet as an opening bordered by the first rib laterally, the vertebral column medially, and the claviculomanubrial complex anteriorly. The syndrome of compression at this site could be primarily neurologic, involving the brachial plexus, most often the lower trunk or medial cord; alternatively, it could involve compression of the subclavian artery and/or vein.^1,2 Thrombosis, embolus, or aneurysm of these vessels is a less likely possibility.

One proposed classification system has broken TOS into the following 3 categories:

• True neurogenic TOS: The brachial plexus is injured in these cases as documented by electromyography (EMG) and/or nerve conduction studies.
• True vascular TOS: The subclavian artery and/or vein is damaged or thrombosed, as documented by arteriogram or venogram.^1,2
• Nonspecific or disputed TOS: Patients have symptoms, but there are no abnormal tests to document the lesion clearly. This category is by far the most common type of TOS seen in the clinical setting.

Many authors have discovered accessory cervical ribs associated with TOS³ ; however, they have noted tough fibrous bands coming off the accessory ribs that are believed to be more responsible for the pathology. There have even been reports of bony fusion of variant cervical ribs, resulting in bifid ribs with attached fibrous bands.⁴ The bands cause tethering of the brachial plexus, which results in traction and, therefore, symptoms. Other authors report compression or irritation of the neurovascular bundle more distally under the pectoralis minor muscle or from anterior displacement of the humeral head.

Additionally, clavicle fractures can result in plexopathy from expanding hematomas or pseudoaneurysms that compress the plexus, with variable latent periods following the fracture. Delayed onset of symptoms may suggest exuberant callus from the healing fracture site. Nonunion of the fracture site also can result in direct compression by the lateral fragment, which is pulled inferiorly.

Trapezius weakness due to spinal accessory nerve injury (following cervical lymph node biopsy) also has been implicated as a cause of TOS. This results in "droopy shoulder" with secondary compression of the neurovascular bundle, which is particularly aggravated with arm elevation (abduction).⁵

Frequency

United States

The inability to make a definitive and accurate diagnosis makes determination of the exact prevalence of this condition impossible. The prevalence of nonspecific thoracic outlet syndrome (TOS) has been reported as high as 23% of soft-tissue injuries of the cervical spine. TOS is overlooked or misdiagnosed commonly, especially upon presentation to the emergency department. The true or classical neurogenic or vascular TOS incidence is considered rare, with only 1 case per million population estimated for the neurogenic type. Some believe that TOS is the most common cause of acute arterial occlusion in the upper limbs of adults younger than 40 years. It is more common with occupations or activities that involve prolonged posturing of the neck, such as secretaries, cashiers, machine operators, surgeons, truck drivers, and overhead work or lifting. There is no increased incidence in athletes.

Mortality/Morbidity

No known mortality is associated directly with thoracic outlet syndrome (TOS). Morbidity often encompasses debilitating functional loss of the involved upper extremity, loss of livelihood or occupation, especially if the work involves overhead activity (eg, hairdressing, carpentry, painting). True neurogenic TOS causes neurologic deficit. Depending on the amount of nerve injury, there usually is weakness of the hand and sensory deficits in the lower trunk distribution. Devastating complications, usually to the brachial plexus, have been reported from surgical treatment for TOS.

Sex

Females are diagnosed more commonly with thoracic outlet syndrome than males, with some reports of a 9:1 female-to-male ratio. The shape of the chest wall is believed to predispose women by encouraging closure of the thoracic outlet. Large, pendulous breasts have been particularly implicated, with these adding to the anterior forces on the chest, leading to drooped shoulder posturing and further closing the outlet.⁵

Age

Age of onset of thoracic outlet syndrome is from the second to the eighth decade, with a peak occurring in the fourth decade. In the younger age group, there appears to be a greater likelihood of anatomic or structural abnormality, such as cervical rib variants and fibrous bands.

Clinical

History

• Pain, numbness and/or tingling, and heaviness of the involved upper extremity are common complaints reported by a patient with thoracic outlet syndrome (TOS). Often, the symptoms are vague and generalized. The entire extremity may be involved; additionally, neck pain and headaches are reported concomitantly.
• Symptoms may begin insidiously after repetitive or stressful activity, such as prolonged computer keyboard use or mechanical and overhead work. Trauma, such as an automobile accident with occurrence of a whiplash injury, also has been associated with onset of TOS with a frequency of up to 23%. Sports activities, especially throwing and swimming, have been implicated as well; symptoms may be similar to those of a clavicular fracture, with a delayed onset from hours to weeks.
• Autonomic phenomena (eg, cold hands, blanching, swelling) also may be reported. The proximity of the stellate ganglion to the first rib articulation, which is often dysfunctional or restricted in TOS, has been postulated as a cause.

Physical

A careful neurologic and musculoskeletal examination is essential to diagnose thoracic outlet syndrome (TOS) adequately. Often, the most important aspect of the physical examination is to diagnose or rule out other problems of the neck and arm.^6,7

• The mainstay of the physical examination diagnosis of TOS involves the so-called stress tests (or provocative maneuvers) (see images below and Images 2-3). The sensitivity and specificity of these tests have been low in the studies on TOS completed to date. Different techniques for performing and interpreting these tests are discussed in the literature and vary even more in the bedside clinical situation.
  • The most common tests are the Adson maneuvers, where the head is placed in extension and side bending while the patient takes a deep breath and holds it, followed by rotation to stretch or tether the plexus and/or artery by the anterior and middle scalenes. The maneuver is held for 15-30 seconds while the clinician observes for onset of symptoms and obliteration of the pulse. Symptoms have been reported to the side of bending and, more commonly, to the side away from bending. If the symptoms are reported on the side of bending, then this finding overlaps with the Spurling sign, commonly used to assist in the diagnosis of cervical radiculopathy. Some examiners ask the patient to pull the head forward while maintaining the test position, causing the anterior scalene to contract against the plexus to enhance the stress effect.
  • Hyperabduction of the involved arm also can be used to stress the outlet; however, this maneuver often causes symptoms and loss of pulse even in normal individuals and may be misleading. The area of compression with this maneuver is considered more distal and frequently located at the anterior humeral head and plexus, with tethering under the pectoralis minor muscle.
  • Costoclavicular bracing (military maneuver) closes the space between the clavicle and first rib and may reproduce symptoms.

• Focal stress tests involve applying pressure directly to the anterior scalene or upper segment of the pectoralis minor. These tests are considered positive if symptoms are reproduced within 15-30 seconds. In addition, some authors have noted a positive Tinel sign (percussing over the plexus) as diagnostic for TOS.
• The elevated arm stress test has been noted to be highly sensitive for TOS. The upper extremity is held in the "stick-'em-up" position with the arms abducted and elbows flexed (both at 90°) for 3 minutes, while the patient simultaneously and vigorously flexes and extends the fingers (grasp and release). This test is considered positive if the patient cannot complete the full 3 minutes. Unfortunately, this test is challenging even for individuals without neurovascular symptoms to complete; thus, it may have limited practical usefulness in most clinical situations. In one study, over 80% of patients with carpal tunnel syndrome presenting to an electrodiagnostic medicine laboratory had a positive elevated arm stress test results.
• Careful observation for asymmetry of the upper chest wall may reveal clavicular irregularity consistent with prior fracture. A nontender hard mass over the middle third of the clavicle often is noted. Deformity from displaced fracture (with or without nonunion) or exuberant callus could be responsible for direct compression of the plexus. Pressure on the clavicle can reproduce or aggravate symptoms, especially when nonunion is present; motion can be detected between the fragments.

Causes

Thoracic outlet syndrome (TOS) most likely has multiple causes. The primary cause is believed to be mechanical or postural. Stress, depression, overuse, and habit all can lead to the forward head, droopy shoulder, and collapsed chest posture that allows the thoracic outlet to narrow and compress the neurovascular structures (see image below and Image 1).⁵ Accessory ribs or fibrous bands also may be present, predisposing the site to narrowing and compression. Large breasts have been implicated as a contributing cause by pulling the chest wall forward (anterior and inferior); this theory has been supported by relief of discomfort following reduction mammoplasty. TOS has also been associated with breast implants, which may increase tension under the chest wall muscles and irritate the neurovascular tissue.

Primary vascular lesions, such as thrombus or aneurysm, may be present as well as secondary problems such as emboli. Tumors, such as upper lobe lung lesions (Pancoast tumor), are also possible causes.

• Many other problems may predispose an individual to TOS, some of which are classic perpetuators of myofascial pain syndrome, including the following:
  • Sleep disorder
  • Hormonal imbalance (estrogen, thyroid)
  • Inflammatory disorder (rheumatoid arthritis)
  • Fibromyalgia
  • Nutritional insufficiency (B vitamins, folate, vitamin C)
  • Anemia
  • Infection
  • Masses, tumors, axillary lymph nodes
  • Mechanical disorders (short leg, hyperlordosis, hypolordosis)
  • Psychologic (stress, depression)
  • Nerve entrapment/impingement (other sites)

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