There is no single test or examination finding that establishes the diagnosis of neurogenic TOS. Rather, the clinical diagnosis is based on the history, physical examination findings, and objective tests, such as electrodiagnostic studies of the peripheral nerves, that are used to rule out other more distal compression neuropathies. Chest and neck x-rays are obtained routinely to look for cervical ribs or other bony abnormalities. Paresthesias in the upper extremity may be the result of either compression at the brachial plexus or compression more distally. The pain associated with TOS usually results from a muscle imbalance in the cervical, thoracic, and scapular regions.2 Patients with TOS-related pain often assume an abnormal posture with forward position of the head and neck, thoracic kyphosis, and scapulae abduction (Fig. 142-3). This posture results from a weakness of the lower scapular stabilizers (i.e., middle and lower trapezius and serratus anterior) that leads to overuse and hypertrophy of other muscle groups (e.g., levator scapulae, upper rhomboids and trapezius, and scalene muscles). Upper extremity activities (e.g., arm abduction or elevation) often exacerbate the symptoms. The onset of symptoms is usually insidious without a defined traumatic event.
Abnormal posterior and muscle imbalance associated with neurogenic TOS results in shortened and hypertrophied scalene, sternocleidomastoid, and pectoralis minor muscles anteriorly. The back muscles (i.e., levator scapulae, upper rhomboid, and trapezius) become overdeveloped to compensate for the weakened serratus anterior and middle and lower trapezius muscles, pulling the head forward.
Chronic nerve compression is associated with a continuum of symptoms. Initially, the patient may complain of aching in the muscles innervated by the compressed nerve. Later, the patient complains of muscle weakness and, finally, muscle atrophy. With sensory nerve compression, patients complain first of intermittent paresthesias, then persistent paresthesias, and eventually numbness. Clinical sensory testing follows a similar continuum; therefore, not all sensory tests are equally effective for detecting nerve compression at all stages of TOS. Initially, patients may have symptoms only with positional changes or provocative maneuvers. Sensory testing in a resting position will be normal, only becoming abnormal when the patient is tested in positions of provocation (e.g., with the arms elevated). With continued nerve compression, axonal involvement, and wallerian degeneration, the innervation density of the sensory receptors decreases, and sensory testing with two-point discrimination is abnormal.
It has been hypothesized that proximal compression of a nerve increases its susceptibility to compression injury more distally. Thus, in treating upper extremity neuropathic symptoms, it is important to identify and treat all sites of compression.3 Distal sites of nerve entrapment, for example, the elbow, forearm, and wrist, should be evaluated carefully and managed conservatively. Clinical evaluation using pressure and positional provocative testing is key to making the diagnosis because electrodiagnostic studies usually do not detect these dynamic sites of nerve compression.4 Conservative treatment often effectively relieves these distal symptoms, but when surgical intervention is required, surgery at the carpal or cubital tunnel levels is usually more effective than surgical decompression of the thoracic outlet for complete relief of hand paresthesias and numbness. Overlapping symptoms from the cervical disc level or the shoulder are common.
Loss of radial pulse with arm movement on physical examination forms the basis of several clinical tests designed to detect vascular insufficiency, although not effective for the evaluation of neurogenic TOS. In Adson test, the patient is asked to turn his or her head toward the affected side, extend the neck, and inspire deeply. Obliteration of the radial pulse suggests compression. In Roos test, the subject elevates his or her arm to 90 degrees of shoulder abduction and then rotates the arm externally and flexes the elbow for 3 minutes. The patient then is asked to rapidly open and close the hand. A positive test will reproduce the patient's symptoms.
The physical examination of patients with TOS should include documentation of pinch and grip and two-point discrimination, as well as examination of the upper extremity for other compression issues. The cervical spine and rotator cuff are examined as well as the muscles of the parascapular area. Standard tests performed at the wrist are used to assess carpal tunnel syndrome, including Tinel sign, the pressure provocative test, and Phalen test. Care is taken to keep the forearm in a neutral position during testing because extreme supination of the forearm will cause median nerve compression at the pronator teres and lead to a false-positive result. The elbows also must remain extended so as not to provoke signs of cubital tunnel syndrome. One test for median nerve compression in the proximal forearm is to maximally supinate the forearm with pressure applied just proximal to the pronator teres while keeping the wrist in neutral position. If this maneuver produces paresthesias in the distribution of the median nerve, it suggests median nerve compression in the proximal forearm. The radial sensory nerve is provoked by extreme forearm pronation and wrist ulnar deviation. A Tinel sign between the tendons of the extensor carpi radialis longus and the brachioradialis indicates radial sensory nerve compression in the forearm.
The evaluation for cubital tunnel syndrome or ulnar nerve compression at the elbow involves elbow flexion and pressure over the ulnar nerve at the cubital tunnel. The wrist and the forearm are kept in neutral position so as not to provoke median nerve symptoms. Brachial plexus compression in the region of the thoracic outlet is tested by elevating the arms over the head while keeping the wrist neutral, the elbows extended, and the forearms neutral. The examiner evaluates for change in pulse and color while the patient reports any new or increased sensory disturbance in the upper extremity.
Patients with neurogenic TOS typically have an associated muscle imbalance in the cervical scapular area. To evaluate these muscles, the examiner stands behind the patient while the patient slowly elevates the arms above the head. Elbows are kept extended, and the shoulders are forward flexed. The arms then are lowered to the sides from this forward-flexed, elevated position while the examiner observes for winging of the scapula. Winging of the scapula suggests weakness of the serratus anterior muscle. Middle and lower trapezius muscle function is tested by abducting the shoulders with the extremities extended while the arms are elevated above the head from an abducted position. Once again, the arms are lowered slowly to the side. Winging of the scapula suggests a weakness of the middle and lower trapezius muscles. Patients with muscle imbalance in the scapular areas typically have abducted scapulae. Instead of rotating normally with movement of the arms, the scapulae tend to move “up and down” on the back because of overuse of the upper trapezius muscle.
We have described a new test, the scratch collapse test, that can be used to identify areas of nerve irritation and/or muscle weakness. To perform this maneuver, the examiner scratches the patient's skin lightly over the area of nerve compression while the patient performs sustained resisted movement of both arms. If the patient has allodynia owing to compression neuropathy, a brief loss of muscle resistance will be elicited. The patient can be scratched lightly at the multiple levels in the neuromuscular pathway to elicit the collapse. When the culprit area is scratched, the muscle collapses. Patients with TOS-related muscle weakness will respond if the examiner just touches along the posteromedial border of the scapula. This test does not rely on patient report and hence is a more objective evaluation method than most clinical tests for nerve compression.5
We also rely on a pain questionnaire to assess each patient's symptoms. The questionnaire consists of visual analog scales of pain, questions for patients to describe their pain, and a body diagram for the patient to indicate the location(s) of pain. Responses are considered positive if more than three descriptors are chosen, the body diagram does not follow an anatomic pattern, or if the questionnaire score exceeds 20. Patients who score positive in more than two of these areas are referred for psychological assessment and are not offered immediate surgical intervention. An example of this questionnaire is provided in Table 142-1.6
Table 142-1Tos Patient Questionnaire
Specific physical therapy protocols that address postural abnormalities, neural mobility, and muscle imbalance relieve the neurologic and muscular symptoms of most neurogenic TOS patients.3 In our experience, few patients require surgical decompression. When one is evaluating a patient who has “failed” physical therapy, it is important to review the physical therapy regimen. In our experience, a faulty physical therapy program actually can exacerbate the patient's symptoms.