Physical Medicine and Rehabilitation for Thoracic Outlet Syndrome 

  • Author: Benjamin M Sucher, DO, FAAPMR, FAOCPMR; Chief Editor: Robert H Meier III, MD   more...
 
Updated: Oct 18, 2011
 

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 the image below), symptoms often are confused with various distal compression neuropathies or cervical radiculopathies.

Progressive postural decompensation with neurovascProgressive postural decompensation with neurovascular compression. A: Normal resting posture. B: Shoulder protraction beginning; the sternomastoid muscles are shortening, drawing the head anteriorly and inferiorly. C: Advanced deformity with adaptive shortening of scalene and pectoralis minor muscles. Also note narrowed costoclavicular space (ribs 1-5 have been relatively elevated). Neurovascular compression is evident at all 3 sites.

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.

A review of the pathomechanics and dysfunctional body habitus associated with this type of presentation suggests that the term "postural TOS" may be more appropriate, particularly when no neurologic or vascular abnormality is documented (or testing results are inconclusive).[1]

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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.[2, 3] Thrombosis, embolus, or aneurysm of these vessels is a less likely possibility.

In addition, imaging with diagnostic ultrasound has been able to identify deformation of the pectoralis minor in TOS that may be related to the pathophysiology, due to excessive tightness or shortening of the muscle that impinges on the neurovascular bundle.[4]

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.[2, 3]
  • 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 TOS[5] ; 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.[6] 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).[7]

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Epidemiology

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.[7]

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.

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Contributor Information and Disclosures
Author

Benjamin M Sucher, DO, FAAPMR, FAOCPMR  Medical Director, EMG Labs of AARA (Arizona Arthritis & Rheumatology Associates)

Benjamin M Sucher, DO, FAAPMR, FAOCPMR is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Osteopathic Association, and American Osteopathic College of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Specialty Editor Board

Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM  President and Director, Georgia Pain Physicians, PC; Clinical Associate Professor, Department of Physical Medicine and Rehabilitation, Emory University School of Medicine

Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, American Medical Association, International Association for the Study of Pain, and Texas Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Patrick M Foye, MD  Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School

Patrick M Foye, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society

Disclosure: Nothing to disclose.

Kelly L Allen, MD  Medical Director, Medevals

Disclosure: Nothing to disclose.

Chief Editor

Robert H Meier III, MD  Director, Amputee Services of America; Active Medical Staff, Presbyterian/St Luke's Hospital, Spalding Rehabilitation Hospital, Select Specialty Hospital; Consulting Staff, Kindred Hospital

Robert H Meier III, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Association of Academic Physiatrists

Disclosure: Nothing to disclose.

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Progressive postural decompensation with neurovascular compression. A: Normal resting posture. B: Shoulder protraction beginning; the sternomastoid muscles are shortening, drawing the head anteriorly and inferiorly. C: Advanced deformity with adaptive shortening of scalene and pectoralis minor muscles. Also note narrowed costoclavicular space (ribs 1-5 have been relatively elevated). Neurovascular compression is evident at all 3 sites.
Scalene focal (left) and regional (right) stress tests for thoracic outlet syndrome. Both tests can be easily combined to enhance the stress effect (may be helpful in mild cases).
Pectoral focal (left) and regional (right) stress tests for thoracic outlet syndrome.
Stretching technique for the pectoralis minor muscle. Left: The patient has taken the slack out of the muscle. Center: He then rotates the body away from the side being stretched, increasing traction. Right: Maximum rotation and stretch effect are achieved slowly. Image courtesy of The Journal of the American Osteopathic Association
Sagittal plane posture of patient with thoracic outlet syndrome before (left) and after (right) treatment. Notice the release of the pelvis that occurred with the reduction in hyperlordosis, which allowed the shoulder girdle to drop back and open the thoracic outlet. Image courtesy of The Journal of the American Osteopathic Association
Myofascial release technique for the scalene muscles. Left: Side-lying approach. Right/top: Supine approach with pillow under thorax. Right/bottom: Supine approach with head extended off the table and supported by the operator's knees. Image courtesy of The Journal of the American Osteopathic Association
Stretching technique for the scalene (anterior and middle) muscles. Left: The arm on the side to be stretched is secured down (hooked under the seat) to allow more control and effective stretch. Center: The opposite hand wraps partially around the head for good control to assist with the stretch. Right: After proceeding as far as tolerated, the patient leans the whole trunk away from the side being stretched, creating additional traction (downward) on the muscle by the arm that is secured. Image courtesy of The Journal of the American Osteopathic Association
Algorithm for the treatment of nonprogressive thoracic outlet syndrome (TOS). Anti-inflammatory medication, muscle relaxants, and activity modifications all are used as indicated and tolerated in all cases. Values for very severe TOS are greater than those for severe TOS, and the patient probably should be referred for surgical evaluation.
 
 
 
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