Treatment of these nerve injuries requires a thorough examination of the shoulder complex and electrophysiologic testing to identify the location and extent of nerve injury.
Therapy plays a primary role in both surgical and nonoperative management of common shoulder injuries.
Treatment plans for therapy should address scapular dysfunction and prevention of a frozen shoulder.
Diagnosis and Management
The shoulder is a complex joint with complicated kinematics that rely on muscle function and balance for mobility and stability. Nerve injury that affects the function of these muscles will significantly alter this balance. Shoulder problems overall are common. Nerve injuries about the shoulder are relatively uncommon but are a commonly undiagnosed cause of shoulder dysfunction. The presenting signs or symptoms may be attributed to a structural problem (e.g., rotator cuff tear, shoulder instability) but will not improve with standard treatment for these conditions. The symptoms of local abnormalities of the shoulder may also present distally in the arm and forearm, complicating diagnosis.
The spectrum of nerve injuries involving the shoulder includes both acute and chronic conditions. These problems coexist with other more common injuries. Nerve injuries may be primary, from pathology arising within the nerve, or secondary, from other ongoing processes within the shoulder resulting in compression or traction neuropathy. Injury to the neurologic system can arise at many anatomic locations, including cervical roots, brachial plexus, and peripheral nerves innervating the shoulder. Cervical spine pathology can lead to nerve injury at the root or spinal cord level. Existing systemic conditions (e.g., multiple sclerosis, malignancy, enthesopathies) may also make diagnosis difficult. For all these reasons, nerve injuries about the shoulder are often difficult to diagnose and manage.
The injury level and/or primary nerve pathology can be localized from the results of a detailed history and physical examination. Other diagnostic modalities, including electromyography (EMG), nerve conduction studies, spinal cord or cortical evoked potentials, magnetic resonance imaging (MRI), myelography, and computed tomography, are useful in confirming the clinical diagnosis and help guide treatment.
The goal of management is early correct diagnosis. Only after the correct diagnosis is made can appropriate treatment be instituted to avoid atrophy and/or contracture and to restore stability and mobility to the shoulder.
The neurologic elements of the upper extremity originate from the cervical portion of the spinal cord. The upper extremity receives contributions from cervical roots C5, C6, C7, and C8 and thoracic root T1. The brachial plexus is formed by the junctions of the ventral rami of these five roots. Occasionally, there may be contributions from C4 and less commonly from T2. The five cervical roots unite just above the clavicle, forming three trunks: the upper, consisting of roots C5 and C6; the middle trunk, consisting of root C7; and the lower trunk, consisting of roots C8 and T1 ( Fig. 57-1 ). Just below the clavicle, each trunk divides into an anterior and posterior division. The anterior division of the upper and middle trunks forms the lateral cord. The anterior division of the lower trunk forms the medial cord, and the posterior divisions from the upper, middle, and lower trunks form the posterior cord. Note that the cords surround the subclavian artery and are named by their position relative to the artery. The lateral cord branches include the lateral pectoral nerve, musculocutaneous nerve, and median nerve. The medial cord branches include the medial pectoral nerve, medial brachial and antebrachial cutaneous nerves, and median and ulnar nerves. The posterior cord branches include the upper and lower subscapular nerves, the thoracodorsal, axillary, and radial nerves.
Other branches arise more proximally either from the cords, trunks, or roots to supply the shoulder girdle musculature. The dorsal scapular nerve, supplying the rhomboid muscles, arises directly from the C5 nerve root. The suprascapular nerve, supplying the supraspinatus and infraspinatus muscles, is a branch arising from the upper trunk. The long thoracic nerve, supplying the serratus anterior muscle, arises from contributions of the C5, C6, and C7 nerve roots ( Table 57-1 ).
|Long thoracic||C5, C6, C7—from roots|
|Dorsal scapular||C5—from root|
|Suprascapular||C5, C6—from upper trunk|
|Upper subscapular||C5—posterior cord|
|Lower subscapular||C5, C6—posterior cord|
|Thoracodorsal||C7, C8—posterior cord|
|Lateral pectoral||C5, C6, C7—lateral cord|
|Medial pectoral||C8, T1—medial cord|
|Medial brachial cutaneous||C8, T1—medial cord|
|Medial antebrachial cutaneous||C8, T1—medial cord|
|Axillary||C5, C6—posterior cord|
|Radial||C6, C7, C8—posterior cord|
|Median||C5 through T1—medial and lateral cords|
|Musculocutaneous||C5, C6—lateral cord|
|Ulnar||C8, T1—medial cord|
Types of Nerve Injury
Nerve injury can occur by laceration, traction, or compression. Laceration occurs by direct trauma through penetrating injury or as a result of a fracture or its treatment. Traction is a common mechanism that occurs with blunt trauma. A shoulder dislocation can result in a traction injury to the brachial plexus. A fall onto the shoulder with lateral deviation of the neck will result in a traction injury to the upper trunk of the brachial plexus. An injury with traction on the arm pulled in abduction will place traction on the lower plexus. Compression occurs either from a perineural scar or fracture callus in a post-trauma case or from an extrinsic lesion such as a ganglion or tumor.
The mechanism of injury is determined from the patient history. The degree of injury for each mechanism is determined by physical examination and electrophysiologic testing. The degree of nerve injury is characterized as one of three types based on the classification of Seddon and Sunderland.
Neurapraxia: A minimal nerve injury characterized by a temporary, fully reversible nerve conduction block, with good prognosis
Axonotmesis: A moderate nerve injury characterized by a disruption of the axons and myelin sheath with the epineurium left intact to guide regeneration; has a fair prognosis
Neurotmesis: A severe injury characterized by complete destruction of the nerve with poor prognosis for regeneration
Another nerve injury classification system with more categories of nerve injury is described by Sunderland. The rate of nerve regeneration is about 1 inch per month, which must be considered when assessing nerves recovering various distances to muscles or skin.
Examination for nerve injuries should be a part of every routine physical examination. The patient should be carefully observed with the trunk and upper extremities disrobed so that the normal side can be compared with the symptomatic side. Subtle areas of atrophy, deformity, discoloration, or swelling should be noted. The active and passive range of motion of the neck, shoulders, elbows, wrists, and hands should be measured and these joints tested for stability. The motor evaluation is one of the most important components of the neurologic examination. Each of the muscles of the shoulder should be tested, including those that move and stabilize the scapula. A comprehensive motor assessment can often define the site of a neurologic lesion. The nerve innervation of the muscles of the shoulder is outlined in Table 57-2 .
|Peripheral Nerve||Muscle Innervated|
|Long thoracic||Serratus anterior|
The strength of each muscle should be recorded using the muscle grading system of Sunderland ( Table 57-3 ). Sensory deficits can occur in either a dermatomal (nerve root) distribution ( Fig. 57-2 ) or along the distribution of peripheral nerves. If spinal cord lesions are suspected, a detailed evaluation of all sensory functions (pain, hot/cold, vibration, and position sense) is mandatory.
|5 Normal||Able to withstand full resistance|
|4 Good||Able to withstand some resistance|
|3 Fair||Move against gravity—no resistance|
|2 Poor||Move with gravity eliminated|
|1 Trace||Muscle contraction without movement|
|0 Zero||No muscle contraction|
Electrophysiologic examination remains the most commonly performed test for evaluation of neurologic injury. This test has two components: an electromyogram and a nerve conduction velocity (NCV) study. The combination of NCV and EMG allow localization of the nerve injury, assess the age and degree of injury, and provide evidence of nerve recovery. Chapter 15 provides detailed information on this diagnostic tool, but it is briefly reviewed in this chapter.
EMG is performed by placing a recording needle into the muscle being studied and observing the nature of the electrical activity in the muscle. A normal muscle is electrically silent at rest and produces a well-defined single-peaked recording when the muscle is contracted voluntarily (motor unit potential [MUP]). A nerve with an acute injury with denervation will produce spontaneous electrical signals at rest recorded as fibrillation potentials or positive sharp waves. The MUP will be altered or nonexistent, depending on the degree of axonal injury. These electrical changes in an acute injury do not become detectable by EMG until 3 weeks after injury. As regeneration occurs, the fibrillation potentials disappear. Intact motor nerves sprout to innervate denervated motor units, producing a polyphasic MUP with multiple peaks. The presence of polyphasic potentials indicate that the nerve injury is more than 3 months old.
EMG can detect the effects of denervation caused by a lower motor lesion. EMG cannot define the location of the lesion between the spinal cord and muscle, unless multiple muscles are individually tested to map the location of the nerve injury. EMG can determine whether the pathologic process involves more than one peripheral nerve. It can also identify whether the observed pathology is part of a generalized peripheral neuropathy or chronic myopathy (e.g., muscular dystrophy).
The NCV is a direct measurement of nerve conduction through the extremity. Myelin is the insulating material for the nerve axons. As myelin is lost as a result of compression or injury, the conduction across the injured segment will decrease. This test helps to define areas of compression or injury along a peripheral nerve. These measurements are obtained by direct stimulation of a nerve proximally in the extremity and measurement of the time required for impulse conduction to a point in the nerve more distal in the extremity. The measurement is recorded in meters per second. Abnormal values (decreased conduction velocity) are determined by comparison with the uninvolved extremity or published normal standards. Nerve conduction can also be measured by stimulating the nerve at a fixed distance from an anatomic landmark and tracking (from a distal muscle) the time from stimulation to recording of a MUP. This measurement is a motor latency and is recorded in milliseconds. A sensory latency is measured by stimulating the fingertip and recording from the nerve at a fixed distance proximally. These measurements, if prolonged, imply abnormal nerve conduction in the anatomic region being studied.
Spinal Accessory Nerve
The spinal accessory nerve is the 11th cranial nerve and the primary motor nerve to the trapezius and sternocleidomastoid muscles. It is susceptible to injury because of its superficial course through the subcutaneous tissues on the floor of the posterior cervical triangle. This anatomic structure is bound by the trapezius, sternocleidomastoid, and clavicle ( Fig. 57-3 ). Injury occurs from blunt trauma directly to the nerve, traction injury to the nerve from a force depressing the shoulder while the head is forced in the opposite direction, or iatrogenic injury from surgical procedures in the posterior cervical triangle, most commonly cervical node biopsy. Injury to the spinal accessory nerve results in paralysis of the trapezius muscle.