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There are two major types for the therapist to consider, compressive and entrapment.
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Appropriate therapist classification of patients into one of two types is imperative to providing appropriate treatment.
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Therapist management requires a comprehensive evaluation to determine the level and tissue involvement.
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Therapy is guided by patient classification and three phases of intervention: control, restorative and rehabilitative.
This chapter focuses on painful conditions in the upper extremity related to the brachial plexus, otherwise known as brachial plexus neuropathies (BPN). Other peripheral neuropathies of the involved upper extremity and cervical spine pathology can complicate the diagnosis. The existence of one type of BPN is referred to as thoracic outlet syndrome (TOS) and remains controversial. , As this pain syndrome becomes more ingrained within the central nervous system, accompanying alterations in the neural biomechanics of the brachial plexus and peripheral nerves occur, making diagnosis and treatment more difficult. It is the intent of this chapter to communicate a clearer understanding of brachial plexopathy and its varied manifestations, allowing the clinician to develop a logical sequence of evaluation, assessment, and treatment.
Major Types
Compressive Brachial Plexus Neuropathies
Two major types of brachial plexopathy are discussed. The first, compressive brachial plexus neuropathy (CBPN), is classically described as TOS. This implies that compression on the neurovascular structures is occurring as they pass through the thoracic inlet as a result of a reduction in the diameter of this potential space. The mechanism for this compression could be anatomic anomalies, muscular hypertrophy or adaptive shortening of surrounding fascia, or space-occupying lesions. Postural dysfunction is a major component of both types of brachial plexopathies. , Alterations in posture, especially longstanding ones, may result in the narrowing of spaces necessary for the neurovascular structures to freely traverse the thoracic inlet. Longstanding forward head posture can potentially create space limitations in shape and size secondary to adaptive shortening of tissues of the scalene triangle, costoclavicular, or axillary interval.
Brachial Plexus Entrapment Syndrome
The second type of brachial plexopathy, brachial plexus entrapment syndrome (BPES), is less understood. The term may often be used synonymously with the diagnosis of neurogenic TOS (NTOS). More recently this has been referred to as cervical brachial pain syndrome (CBPS). A result of a traction injury to the brachial plexus, , whiplash injuries, or other compressive neuropathies in the upper extremity, BPES impairs neural tissue mobility and tolerance to tension as a result of intraneural or extraneural fibrosis from direct trauma, local pathology within the cervical or thoracic spine, , or longstanding compression or overuse. This limitation in the nerve’s adaptability or compliance is referred to as adverse neural tension (ANT), , or, more recently, neural tension dysfunction (NTD). As a result of NTD movement of the patient’s involved extremity beyond the limits of the nervous system’s compliance creates abnormal tension in the peripheral nervous system (traction) further exacerbating the patient’s symptoms.
Anatomic Relationships in Brachial Plexus Neuropathies
Several anatomic relationships are important to the therapist’s evaluation and management of BPN. The first relationship is at the level of the cervical spine between the exiting nerve roots of the brachial plexus and the prevertebral fascia. The trunks of the brachial plexus enter the thoracic inlet through the scalene triangle. An important distinguishing feature at this level is the relationship of the subclavian artery as it accompanies the trunks of the brachial plexus through the scalene triangle. In comparison, the subclavian vein enters the thoracic inlet anterior to the scalene triangle. Clinically this may explain why patients present with neurogenic and classic arterial symptoms without venous symptoms ( Fig. 55-1 ).
Moving laterally, the neurovascular bundles converge and traverse the costoclavicular interval, inferior to the clavicle and superior to the first rib. Continuing laterally, the neurovascular bundle enters the upper extremity through the axilla. At the costoclavicular interval, the patient may present with neurologic symptoms related to the anterior and posterior divisions of the brachial plexus. At the axilla the symptoms may follow a cord distribution. Figure 55-1 further illustrates these relationships. Clinically, each of these could present with differing neurologic complaints and pain distribution. The final relationship to consider is muscular. Machleder and colleagues and Sanders and coworkers described histologic changes of the scalene muscles in patients presenting with a diagnosis of BPN. These changes include increased type I collagen and type II muscle fiber atrophy within the scalene muscles. These histologic changes support the theory that longstanding cervicobrachial pain may be an underlying cause and pathology for BPN. The increased percentage of connective tissue within the scalene muscles compared with normal muscle tissue may indicate a “stiffening” of the scalene triangle, resulting in a decrease in compliance of these muscles, placing the neurovascular structures at greater risk.
Potential Anatomic Spaces (Intervals) of Involvement
There are three potential spaces for CBPN or the development of BPES within the thoracic inlet. The first and most medial space is the interscalene triangle located within the boundaries of the posterior cervical triangle. The presence of a prefixed or postfixed brachial plexus along with other anatomic anomalies may add to poor neurovascular mobility and tension attenuation. Injury to the shoulder girdle or repetitive trauma may lead to symptoms and pathology. As previously discussed, the second potential space is the costoclavicular interval. The third potential space moving laterally is the axillary interval. In this area of the anterior structures, the deltopectoral fascia, pectoralis minor, and coracoid have all been implicated as potential sources of compression of the neurovascular structures.
Incidence of Brachial Plexopathy
BPN occurs more often in women, usually between the fourth and the sixth decades of life. Brachial plexopathies have also been associated with a history of cervical, thoracic, or shoulder trauma , ; arthritis ; bad posture; and repetitive motion disorders. Brachial plexopathies can include symptoms that are related to the venous, arterial, neurologic, or autonomic systems. The symptoms associated with multiple system involvement are often extremely variable, making the diagnosis of CBPN or BPES predominantly a clinical diagnosis made by a process of exclusion rather than specific objective signs or diagnostic tests. Therefore careful and meticulous evaluation and hypothesis formulation are necessary to identify the potential causes of the multiple problems that may coexist in many of these patients.
Diagnosis and Classification
Diagnosis
The diagnosis and classification of these patients continues to remain controversial. Arguments have been put forth to support and refute the existence of brachial plexopathy, especially those labeled as TOS. , The classification and diagnosis of brachial plexopathy centers on four types, based on symptoms: vascular–arterial, vascular–venous, true (specific) neurogenic, and false (nonspecific) neurogenic TOS. The problem is that the term TOS is often used as a diagnosis for other neuropathologies that include the brachial plexus. This confused diagnostic scheme makes it difficult for the treating clinician to develop an appropriate treatment strategy. Either way, brachial plexopathy needs to be considered as upper quarter neuropathic pain. This requires the therapist to have a clear understanding of pain. The reader is referred to Chapter 113 for further information on pain mechanisms and Chapter 114 for additional information on pain assessment and management.
Cuetter and Bartoszek classified thoracic outlet and brachial plexopathy into four categories. They identified two vascular components, arterial and venous, and believed that these were undisputed because diagnostic tests are available to confirm occlusion or changes of either vascular system. In addition, specific clinical examination techniques, discussed later in this chapter, may further support the presence of vascular involvement. The remaining two classification categories are neurogenic. Sanders and associates also identified three types: arterial, venous, and neurogenic. These have been identified as true (nondisputed) or false (disputed) NTOS. , Four criteria for true NTOS are (1) the presence of a cervical rib on radiograph, (2) intrinsic wasting of the hand, (3) sensory changes, and (4) pain or paresthesia over the lower trunk distribution implicating lower trunk involvement. , LeForestier and colleagues also included a fifth criterion: positive electrodiagnostic findings. However NTOS may also exhibit symptoms related to the upper plexus. Approximately 5% of neurovasculopathies within the thoracic inlet are true neurogenic or vascular. , The remaining 95% are classified as false NTOS , and may be more appropriately classified as BPES as will be discussed later. Within this classification, false NTOS symptoms are identical to those found in true NTOS; however; these cases lack the four criteria. Ribbe and coworkers developed a TOS index of signs and symptoms in an attempt to establish clear criteria for the diagnosis of TOS. The index included positive symptoms provoked by arm elevation, paresthesia over the ulnar nerve or lower trunk distribution, tenderness of the brachial plexus over the supraclavicular fossa, and a positive Roos’ test. The lack of a standardized classification system clouds the identification or diagnosis of BPN and hinders the development of a logical treatment approach.
Proposed Therapist’s Classification
Compressive Brachial Plexus Neuropathy, or Thoracic Outlet Syndrome
As a result of this lack of consensus, I found it necessary to develop a clinical classification dividing brachial plexopathies into two major types. The contrast between these two types is found in Table 55-1 . The first type of brachial plexopathy is classic TOS or which I classify as CBPN, a compressive vasculopathy or neuropathy of the brachial plexus. Classic TOS, as described in the literature, has six identifiable components. (1) Posture appears to play a role in the patient’s symptoms. (2) The onset of discomfort is usually described as insidious with transient symptoms. (3) These symptoms are usually associated with extremity position, posture, or particular motions described by the patient such as overhead work or extended periods of static upper extremity positioning. (4) After the offending posture or activity is corrected, symptoms usually subside. These same symptoms may be transiently provoked during treatment. (5) The TOS provocative tests, discussed later, may be more reliable in identifying the potential anatomic interval of compression. (6) Finally, most of these patients present with minimal resting pain, minimal sleep disturbance, low pain scores (verbal reporting or visual analog pain scales), rapid recovery when symptoms are provoked, less mechanical tissue sensitivity to physical examination, with rapid resolution of symptoms once the offending clinical examination is terminated, and the knowledge needed to relieve their symptoms, indicating low tissue irritability .
| TOS (CBPN) | BPES | |
|---|---|---|
| Posture | Offending posture = ↑ Symptoms | Antitension postures = ↓ Symptoms |
| Onset | Insidious | Trauma-related (cervical/shoulder) |
| Repetitive strain injury (RSI) | ||
| Irritability | Low | High |
| Symptoms | Transient often posture/activity | Continuous (features of neuropathic-dependent pain) |
| Special Tests | ↑ Number positive tests = ↑ Sensitivity | Poor sensitivity—diffuse symptoms |
| Adson’s | Scalene triangle | |
| Wright’s | Axillary interval | |
| Halsted’s | Retroclavicular space | |
| Neurodynamic Tests | Low symptom response | High symptom response |
| Mild limitation of motion | Significant limitation of motion | |
| Treatment: Soft/Neural Tissue Mobilization | Transient symptom provocation | Protracted symptom provocation |
Brachial Plexus Entrapment Syndrome
The second type of brachial plexopathy is brachial plexus entrapment syndrome (BPES), often associated with trauma , that involves either a traction injury directly or indirectly to the brachial plexus, or local soft tissue inflammation resulting in a compromise of adequate blood flow to the brachial plexus or intraneural or extraneural fibrosis. This fibrosis compromises brachial plexus neural excursion and its ability to attenuate tensile forces placed across the plexus from upper limb or combined cervical motion. These patients typically report delayed onset of their intractable pain that can occur several days, weeks, or months after their injury. It is theorized that the delay in onset of the symptoms is explained by the normal course of biologic healing and the development of neuropathic pain. Mature scar formation eventually compresses the neurovascular structures or limits brachial plexus mobility, creating neural tension dysfunction. Under these conditions, upper quarter motion results in repetitive traction to the neural tissues and development of symptoms. In these patients, the reliability of the TOS provocative tests for determining the interval of involvement is poor and may easily provoke symptoms by placing traction on the neural or surrounding tissues, creating a false positive result. Treatment that might be used for the classic TOS patient may provoke symptoms in patients with BPES at the time of treatment, or the response may be delayed by several hours to a day. Often these patients report a significant increase in symptoms at the next follow-up appointment. Finally, the tissue response in patients with BPES tends to be much more irritable . Symptoms are easily provoked with minimal movement of the upper quarter, and patients often report spontaneous bursts of pain and other features of neuropathic pain. The reader is referred to Chapters 113 and 118 for further discussions on neurogenic pain. In addition, additional concomitant dysfunction, such as myofascial trigger points, shoulder pathology, or cervicothoracic spine involvement, may accompany the brachial plexus symptoms.
This theory of differentiating TOS from BPES was explored by Jordan and associates in the development of a Cervical Brachial Symptom Questionnaire. They identified several factors that predicted responsiveness to treatment in a group of 85 patients treated for TOS and compared the TOS treatment-responsive group ( N = 59) and nonresponsive group ( N = 26). The authors identified this latter group as suffering from treatment-resistant cervical brachial pain syndrome (CBPS). The results indicated the TOS treatment-responsive group was less likely to have comorbidities, fewer surgeries, fewer widespread sensory symptoms, and was less likely to have weakness extending beyond the lower trunk distribution. In comparison, the CBPS group had sensory and strength complaints extending beyond the lower trunk distribution, greater history of non-TOS-related surgeries, and greater comorbidities, such as complex regional pain syndrome and fibromyalgia.
Differential Therapy Diagnosis
In addition to classifying these cases, it is also essential for the therapist to consider differential diagnoses of other potential conditions that may mimic the symptoms associated with brachial plexopathy. Major ones are listed in Box 55-1 . Myofascial trigger points, as indicated by Travell and Simons, can mimic the distribution of brachial plexopathy involvement. Table 55-2 contains common myofascial trigger points that may mimic brachial plexopathy symptomatology. Glenohumeral joint pathology or dysfunction may also provoke symptoms that are similar in nature to the brachial plexopathies referred to as the dead arm syndrome. As reported by Upton and McComas and others, the presence of double- or multiple-crush syndromes may also disguise the involvement of the brachial plexus. Eurroll and Hurst, MacKinnon, and Seror reported that these associated double crushes could include carpal tunnel syndrome, ulnar nerve involvement, or anterior interosseus syndrome. The presence of these disorders and others may help explain treatment failure. Therapists must also consider visceral causes such as an apical lung tumor encroaching on the brachial plexus or coronary pathology.
Cervical dysfunction/pathology
Glenohumeral joint pathology
Myofascial trigger points
Visceral pathology
Multiple/double crush
| Muscle | Area of Referral |
|---|---|
| Trapezius | Face and interscapular region |
| Scalene | Posterolateral arm/radial three digits |
| Supraspinatus | Lateral arm/forearm |
| Infraspinatus | Lateral arm/forearm and radial half of hand |
| Latissimus dorsi | Posteromedial arm, forearm, and ulnar half to hand |
| Pectoralis | Anterior shoulder, medial arm, and ulnar two digits |
| Subscapularis | Posteromedial arm and wrist |
| Serratus | Medial arm, forearm, and ulnar half of hand/digits |
Therapist’s Management
Examination
History
To classify an upper quarter compression neuropathy, a careful and thorough examination is essential. This examination starts with a detailed inquiry about the mechanism of the problem and the specific distribution and qualitative attributes of the patient’s symptoms. As previously discussed, the distribution of symptoms can vary greatly. The history also provides insightful information about particular positions, postures, or activities that relieve, accentuate, or aggravate the symptoms. This helps the therapist determine the tissue or anatomic space involved. Figure 55-2 is an example of the presentation of symptoms related to the upper and lower trunks of the brachial plexus. The neurogenic symptoms are classically distributed over the lower trunk , but may also include the upper trunk, middle trunk, and cords of the brachial plexus. With upper trunk plexopathies (C5-C6 distribution), the pain may tend to be more proximal in nature. This proximal pain may be distributed over the anterior and lateral aspect of the cervical region, portions of the face, and the scapular and interscapular region of the involved side. Distal paresthesia and pain may be distributed over what appears to be the median or ulnar nerve distribution (or both) or the C5-C6 dermatomal region. In contrast, lower trunk (C8-T1) plexopathy symptoms of pain and paresthesia are distributed mostly distal. The paresthesia may be located over the medial aspect of the arm, the forearm, and the ulnar aspect of the hand, appearing to be ulnar nerve-related. If involvement of the brachial plexus occurs at a more lateral position, such as the division or cord level, the variability of the symptom distribution may be even more pronounced. The use of a body diagram to represent symptom distribution may provide further insight, to which the Cervical Brachial Symptom Questionnaire previously alluded.
Taking the patient history also includes investigating past injuries or medical problems to determine prior upper quarter trauma or symptoms (e.g., a previous motor vehicle accident with cervical spine injury, or blunt trauma directly over the superior aspect of the shoulder and upper trapezius region). Prior injury might suggest preexisting mobility problems of the plexus. The medical history also provides valuable information about contributory medical conditions such as diabetes mellitus, hyperthyroidism or hypothyroidism, arthritis, or other systemic neurologic disease. It is also important to note the length of time the symptoms have been present. There is a tendency for secondary tissue dysfunctions to develop the longer the symptoms have persisted; knowing the duration of symptoms assists in developing an accurate prognosis. In general, symptoms that are more diffuse or have persisted for a longer period require extended therapy and are less likely to completely resolve. Specific questioning about occupational or avocational activities that could compromise the neurovascular structures within the thoracic inlet is also essential.
Symptoms
Neurogenic Symptoms
Information regarding symptom distribution and previous history leads to more specific questions about the qualitative nature of the symptoms. Symptoms with neurogenic features involve the motor, sensory, or autonomic nervous system, such as specific muscle performance deficits, alterations in sensibility, and vasomotor instability. These may be intertwined in the pain as associated sensory disturbances of paresthesia and numbness over the same distribution. Accompanying these early neurologic symptoms may be autonomic nervous system complaints such as hyperhidrosis and burning pain over the same distribution. Raskin and coworkers and others reported that headache was present in 26 of 30 patients diagnosed with TOS. Validation of the diagnosis was based on relief of symptoms after first rib resection. Utilizing an isokinetic testing technique, Ozcakar and associates were able to confirm and quantify the weakness and fatigue often reported by the patients.
Late neurogenic symptoms can include complaints of pain; sensory changes; and paresthesia distributed over the posterior lateral cervical region, anterior shoulder, and posterior lateral aspects of the humerus. More evident intrinsic muscular weakness of the hand with lower trunk involvement, reflex changes, and actual sensory loss may be present. These sensory changes may also manifest with pencil pointing of the digits for the involved nerve distribution. The most common complaints are listed in Box 55-2 .
Headache ipsilateral side
Neck pain
Shoulder/arm pain: Intermittent (TOS) or neuropathic features (BPES)
Shoulder/arm paresthesia: Intermittent (TOS) or continuous (BPES)
Arm/hand fatigue (arterial)
Arm heaviness (venous)
Pain/paresthesia with lifting/carrying: Brachial plexus traction
Pain/paresthesia with overhead activities
Tinel’s sign over the brachial plexus: Neural hyperalgesia
BPES, brachial plexus entrapment syndrome; TOS, thoracic outlet syndrome.
Vascular Symptoms
Venous symptoms include reports of distal edema, especially after activity and pain described as a dull ache over a nonspecific distribution. The patient may also report a sensation of heaviness in the involved extremity. , With more significant venous involvement, cyanosis may also be present. Arterial symptoms can include descriptions of fatigue, ischemia-like pain, coldness in the distal part of the extremity, and Raynaud’s phenomenon. , The complaint of ischemic pain may be diffuse or specific to a localized area over the distal extremity. Although rarely seen, late arterial signs could include distal thrombosis or embolization with ischemia changes. Clinical signs of vascular involvement include loss or a decrease in the quality of distal pulses when performing provocative stress tests; vascular involvement may also be detected with an arteriogram.
Diagnostic Tests
Diagnostic tests can also be of assistance. Radiographs may indicate the presence of a cervical rib, other bony conditions, or a prominent C7 transverse process, which may suggest the presence of a rudimentary fibrous band that has the potential of occupying space in the scalene triangle. Arteriograms may indicate a possible blockage of subclavian or axillary vessels. The use of somatosensory evoked potentials, , nerve conduction velocities of the medial antebrachial cutaneous nerve, and electromyography studies are also helpful. All of these tests may provide additional information about the location and degree of the neuropathology and can rule out the presence of double- or multiple-crush syndromes.
The use of imaging techniques has been found to be more predictive when combined with the provocative testing positions. Gillard and colleagues confirmed vascular changes when visualized with sonography in 48 patients diagnosed with TOS, utilizing MRI in 29 patients and 12 healthy individuals as controls. Demirbag and associates determined there was a significant difference in MRI findings in the patient group when comparing neutral to provocative test positions and a significant difference in the positional change values in MRI between the groups. Although further studies are needed to demonstrate imaging’s usefulness, these studies show promise in bringing more objectivity to the diagnosis of CBPN (TOS).
Observation
While obtaining the history from the patient, the therapist should observe the patient’s standing and sitting postures. The therapist should look for any cervical asymmetry, thoracic kyphotic changes, or accessory breathing patterns. Examples of cervical postures are demonstrated in Figure 55-3 . As is evident from these photos, observing the posture strictly in the sagittal plane may result in incorrect or insufficient information. Figure 55-3B demonstrates the classic forward-head and rounded-shoulder posture in the sagittal plane, with a flattened upper thoracic kyphosis commonly seen in CBPN. In the frontal plane ( Fig. 55-3A ) cervical asymmetry is evident with rotation and lateral flexion of the cervical spine toward the affected side, accompanied by increased upper trapezius muscle tone. Through this observation alone, the therapist is able to hypothesize the patient’s level of irritability. This posture demonstrates the patient’s effort to decrease the tension on the brachial plexus by elevating the scapula via contraction of the upper trapezius and levator scapulae and rotating and laterally flexing the cervical spine toward the involved side. The therapist must also inspect for the presence edema in the supraclavicular fossa and any atrophy and trophic, temperature, or color changes in the extremity. The position of the upper extremity should also be noted to determine whether the patient is using distal joints to reduce neural tension by maintaining the elbow in flexion, the forearm in neutral, and the wrist and digits in flexion. , These components may exist separately or in combination, and each may vary in the amount it contributes to the patient’s position and pain.
Upper Quarter Screening
Details of the upper quarter screen are presented in Chapter 10 , but in regard to upper quarter neuropathies, the cervical spine’s active range of motion (ROM) is assessed to determine limitations in motion and the presence of mechanical spine pain, which may be provoking the patient’s pain. Special tests, including Spurling’s test for foraminal encroachment and the vertebral artery test, are executed to determine nerve root or vascular involvement. Myotome scanning and reflex testing provide further information on neural conduction. Tinel’s test in the supraclavicular fossa, in the axilla, and along the peripheral nerves allows identification of neural hyperalgesia or other peripheral nerve pathology in the upper extremity. Ide and associates reported that in 111 patients diagnosed with combined compression and stretch TOS, 103 patients had a positive Tinel’s sign over the supraclavicular fossa. Finally, the supraclavicular fossa and axilla should be auscultated for the presence of a bruit.
Careful sensory evaluation is undertaken using vibrometry and monofilament cutaneous pressure sensation testing. These threshold tests are reported to be more sensitive than other forms of sensibility testing for early detection of peripheral neuropathies. , Sensory evaluation should be carried out to investigate: (1) dermatomal distribution, to rule out possible cervical root involvement; (2) peripheral nerve distribution, to rule out the possible local peripheral nerve compressive neuropathies; and (3) sensory disturbance related to the brachial plexus and its divisions. On completion of the general upper quarter screen, assessment for active motion dysfunction is undertaken. This process is explained in Chapter 118 . The purpose of active dysfunction testing is to determine whether imparting tension on the peripheral nervous system in various locations alters active motion of the cervical spine or upper extremity. The presence of active motion dysfunction assists the therapist in identifying the nervous system’s role in the presenting complaints.
Provocative (Special) Tests
Specific provocative tests, described later in this chapter, are carried out only after the therapist has taken an adequate history and completed an upper quarter screening to develop an initial hypothesis about the level of irritability. These provocative positions can potentially place adverse tension on the peripheral nervous system or brachial plexus, exacerbating the patient’s symptoms and creating false positive results. These special tests were originally designed to determine the integrity of the vascular system and the brachial plexus.
Numerous authors have questioned the specificity, sensitivity, and reliability of these tests. Most of these studies examined asymptomatic subjects as to the frequency of positive tests defined as diminished or lost pulse. None of these studies compared normal subjects with a patient population or considered provocation of symptoms. Falconer and Weddell examined the specificity and sensitivity of the costoclavicular maneuver in four case studies—three vascular and one neurogenic—that had a positive costoclavicular maneuver. They confirmed the involvement of the costoclavicular interval surgically. In 100 normal subjects, 50 males and 50 females 19 to 47 years of age, the costoclavicular maneuver was positive for pulse changes in 25 males and 29 females. In 50% of the males and 60% of the females, either a positive Adson’s or costoclavicular maneuver was obtained. In contrast, Adson found 9 males and 11 females had a decrease or obliteration of pulse performing his provocative maneuver. In 1980, Gergoudis and Barnes investigated the reliability and validity of the provocative maneuvers. The authors used photoplethysmography to measure the changes in vascular status that occurred with Adson’s, costoclavicular, and Wright’s test in 130 normal subjects. They determined that 60% had an abnormal finding with at least one test, 27% with two tests, and less than 7% had an abnormal finding when all three tests were performed. It should be noted that the provocation of any kind of symptoms from a neurogenic standpoint was not measured. In 1987, Warrens and Heaton examined the validity of these provocative maneuvers by determining the frequency of false positive results and the role of photoplethysmography. In 64 normal volunteers, they found 17% were reporting some symptoms. They determined that complete obliteration of the pulse occurred in 58% of the population with at least one test, and 30% had bilateral findings. The incidence of positive findings was 27% for the costoclavicular maneuver, 15% for Adson’s test, and 14% for Wright’s test. Using photoplethysmography, at least one test was positive in 39% of the subjects. In only 2% of the population were all three tests positive.
In determining the prevalence of a positive elevated arm stress test (EAST) or Wright’s maneuver, Costigan and Wilbourn used two groups: 24 normal subjects and 65 patients diagnosed with carpal tunnel syndrome (CTS). They determined that the EAST was positive for 92% of the CTS patients and 74% of the controls. Novak and coworkers reported that in 65 of 115 patients with possible TOS, the EAST was positive in 94% of the 65 patients and in 100% of the 65 patients with confirmed TOS when direct pressure over the supraclavicular region was combined with the EAST. A positive result was symptom production, but not necessarily the exact symptoms reported by the patient. In 1995, Rayan and Jensen studied the prevalence of a positive response for three provocative maneuvers in a typical patient population of 100. The subjects were divided into two groups: those younger than 40 and those older than 40. They reported that 87 of 100 subjects had at least one positive test for vascular signs and that 41 of 100 had at least one positive test for a neurogenic response. Plewa and Delinger examined 50 healthy subjects and reported changes in pulse in 11% for both Adson’s and costoclavicular maneuver, 62% for Wright’s test, and 21% for supraclavicular pressure. Provocation of symptoms (pain or paresthesia) was positive for 11% with Adson’s maneuver, 15% with costoclavicular maneuver, and 36% with Wright’s test. They concluded that as the number of positive maneuvers increased in each subject, the specificity improved because only six subjects had all three tests positive. In 1999, Toomingas and colleagues examined the position of abduction/external rotation among male industrial and office workers. They determined the positive prevalence value was 24% of the population in 1987 and 15% in 1992. Distal symptoms were positive in 12% to 20% of the population, whereas proximal symptoms were present in 5% to 6%. It was their opinion that the symptoms of numbness in the hands had the highest specificity and sensitivity associated with decreased sensitivity to touch.
Most recently the accuracy of the special tests has been examined using MRI and ultrasonography. Demirbag and associates, using MRI, measured various space size and anatomic relationships of the thoracic inlet and confirmed that the provocative tests of Adson, hyperabduction (Wright), and Halsted (costoclavicular) resulted in significant alteration of these measurements in a group of 29 patients. There was also a significant difference noted between the patient group and the control group of 12 for the Halsted and hyperabduction test. Gillard and associates reported mean sensitivity and specificity values of 72% and 53%, respectively, for the three primary tests alluded to earlier using ultrasonography. They also determined that combining more than one test improved sensitivity. Finally Ide and coworkers, using neuroradiographic techniques to examine 150 patients diagnosed with compressive, mixed compressive/stretch, and stretch TOS, determined that the “stretch test” (axial distraction of the upper extremity in neutral) and 90 degrees of abduction/external rotation position (Wright) resulted in greater sensitivity for the compression and mixed compression/stretch group of patients.
Provocative Test Application Techniques
The original proponents of provocative tests used them to delineate the location of compression of the neurovascular structures in the thoracic inlet. In the case of Adson, the proposed test implicated compromise at the scalene triangle. This test, described by Adson and Coffey in 1927, involves cervical rotation and extension to the tested side with the upper extremities supported in the patient’s lap. This is followed by a deep inspirational breath, which is held for 30 seconds while the examiner palpates for changes in the radial pulse. Obliteration or diminution of the pulse is a positive test. As discussed previously, the importance of the pulse remains in question. Of equal or greater importance is symptom provocation reported by the patient. The clinician is also reminded that this position may stress the contralateral scalene triangle and indirectly provoke symptoms.
The stress hyperabduction test (Wright’s test) described by Wright in 1945 implicates the axillary interval. This test is performed in two steps as the patient sits comfortably positioned with the cervical spine in neutral. The arm is passively positioned in 90 degrees of adduction and 90 degrees of external rotation for up to 1 minute while the clinician monitors the patient’s symptoms and the quality of the radial pulse. The maneuver may implicate the subclavian vessels and plexus as it is stressed across the coracoid pectoralis loop. A positive test is loss of pulse and implicates the axillary interval. When this test was performed on 150 normal young adults, 83.3% had obliteration of their radial pulse on the right and 82% on the left.
Halsted initially described, and Falconer and Weddell further researched and described the costoclavicular maneuver or military brace position for stressing the costoclavicular interval. This test is performed with the patient in the sitting position while the clinician helps position the patient into scapular protraction, elevation, retraction, and depression. The patient holds this position for 30 seconds. The patient’s arms remain comfortably supported on the thighs while the examiner simultaneously monitors for any pulse changes. The test is positive when radial pulse changes occur or symptoms are provoked.
In 1966, Roos and Owens described a provocative maneuver that uses exercise stress and positioning. No specific anatomic interval is tested. The patient sits in a neutral position, humerus abducted to 90 degrees, full external rotation, and elbows flexed to 90 degrees. The patient then performs repetitive finger flexion and extension that can be continued for up to 3 minutes. The examiner monitors for any evidence of dropping of the extremities, indicating possible fatigue and arterial compromise. The therapist also observes the color of the distal extremity, comparing left to right. According to Roos, this test stresses all three intervals and places the arterial, venous, and nervous system in tension. The test is considered positive when the patient is unable to maintain the elevation for 3 minutes because of fatigue or pain. Examples of these four maneuvers are depicted in Figure 55-4 .
