Upper Extremity Nerve Entrapment
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GENERAL PRINCIPLES OF UPPER EXTREMITY NERVE ENTRAPMENT
The most common nerve entrapment is the carpal tunnel syndrome (CTS). Its occurrence is 3.46 cases per 1,000 person years. Female-to-male ratio is about 3.1 (23). The next highest incidence is entrapment of the ulnar nerve at the elbow. Krivickas and Wilbourn (25) studied 180 athletes with sports injuries in the electrodiagnostic (EDX) laboratory, of whom 23% had median nerve injuries, 22% stingers, 10.5% radial nerve lesions, 10.5% ulnar nerve compression syndromes, 12% axillary nerve problems, and 7.8% entrapment of the suprascapular nerve (SSN) only.
Nerve entrapment occurs when a nerve passes through a tight space, placing it at risk for mechanical compression as well as ischemia secondary to pressure on the vasa nervorum. Persistent compression results in predictable, progressive degrees of nerve damage, as classified by Seddon: neurapraxia, axonotmesis, and neurotmesis (23).
Neurapraxia (conduction block) is reversible. Demyelination may result.
Large myelinated fibers are most vulnerable. Duration of compression determines degree of damage (may last minutes to months).
Axonotmesis specifies axonal damage, with endoneurium and perineurium intact. Wallerian degeneration ensues. Preservation of endoneurial tubes provide a guide for regeneration of axons. Recovery can take months.
Neurotmesis represents complete disruption of axons, endoneurium, and perineurium. Poor functional outcome. Surgery usually indicated.
Narrowed space in bony and/or muscular tendinous/fibrous canals/tunnels.
Examples: thoracic outlet, quadrilateral space, Struthers ligament, anomalous bone spurs, muscles or fibrous bands, cubital tunnel, radial tunnel, carpal tunnel, Guyon canal, excessive callous formation after (especially malunited) fracture
Acute: compression, stretch, percussion
Chronic: repetitive motion, excessive pressure from equipment
Paralysis of cervical/thoracic muscles secondary to myelopathy
Medical conditions: endocrine problems (pregnancy, hypothyroidism), compartment syndrome, peripheral neuropathy
Symptoms and Signs
Pain, paresthesias, and weakness in distribution of affected nerve
Lesions of pure motor nerves (anterior/posterior interosseous, suprascapular, and long thoracic nerves) cause weakness and/or muscle atrophy.
Special tests: Tinel’s, Phalen’s, Spurling’s, Adson’s maneuver, pectoralis minor and costoclavicular maneuvers, and stress-abduction test that may or may not be positive
Persistent minor pain due to entrapment may cause a regional pain syndrome — reflex sympathetic dystrophy (RSD).
Electromyography (EMG) and nerve conduction studies (NCS) are significant factors in establishing the correct diagnosis of entrapment syndromes. Typical findings include the following.
EMG shows decreased recruitment, increase in polyphasic waves, action potential durations and amplitudes, and in more severe cases, fibrillations and positive sharp waves. Complex repetitive discharges (CRDs) denote chronicity. EMG demonstrates the severity of the abnormality, especially if there is evidence of denervation, which has considerable impact on treatment decisions.
Conduction delay across the site of compression; reduced amplitudes due to blocking or axonal loss (with normal duration) or secondary to demyelination (with increased duration)
Major diagnoses to be ruled out with EMG and NCS are:
Plexopathy, including neuralgic amyotrophy (brachial plexitis), myopathy, and malingering
SPECIFIC NERVE ENTRAPMENTS OF THE UPPER EXTREMITY
Major differential diagnosis in all entrapment syndromes. However, it also is subject to its own compression and entrapment (C7 > C6 > C8).
Entrapment is caused by pressure on a spinal nerve as it exits the spine. Primary anterior compression (disc herniation) may selectively affect motor fibers. It may spare the dorsal ramus, sparing sensation. Posterior compression may selectively affect sensory fibers. Compression of the nerve root can occur from any direction within the intervertebral foramen but most commonly occurs due to posterolateral disc herniation or facet degeneration.
Cervical disc herniation
Prior cervical spine trauma or surgery
Symptoms and Signs
Weakness and reflex changes in root distribution
Provocative maneuvers often positive
Muscle, sensory, and reflex examination
Provocative maneuver: Spurling — pressure on laterally and posteriorly tilted head reproduces symptoms in the affected root distribution
Indications for immediate surgical referral are as follows:
Progressive neurologic deficit, bowel or bladder dysfunction, and severe pain refractory to other approaches
Surgery usually includes nerve root decompression, discectomy if needed, and possible cervical fusion.
Pain medications, nonsteroidal anti-inflammatory drugs (NSAIDs)
Antispasmodics, antiepileptics, and antidepressants
Physical therapy modalities: cervical traction
Strengthening exercises, biomechanical mobilization
Alignment techniques as indicated
Transcutaneous electrical nerve stimulation (TENS) and biofeedback
Epidural steroid injections may help facilitate physical therapy.
Spinal Accessory Nerve: Cranial Nerve XI
The trapezius, the major muscle supplied by the spinal accessory nerve, is a significant scapular stabilizer and thereby critical for the maintenance of efficient shoulder function (18).
It originates on the occipital protuberance, the ligamentum nuchae, and spinous processes of C7-T12. The upper portion inserts at the lateral clavicle and the acromion (upward rotation of the scapula), the middle portion inserts in the spine of the scapula (retracts the scapula), and the lower portion inserts in the root of the spine of the scapula (depresses and upward rotates the scapula).
Nerve supply is through the spinal component of cranial nerve (CN) XI. It originates from the anterior horn cells of the cervical spinal cord (C1-C5). Fibers enter the skull through the foramen magnum. The cranial component of the accessory nerve arises from the caudal part of the nucleus ambiguous. It is closely related to the vagus nerve (CN X). The cranial and spinal components, together with CN X, leave the skull through the jugular foramen and then separate again.
An important fact of the central connections is that the corticobulbar tract from the midbrain eventually terminates in the brainstem, where the fibers to the trapezius muscle are crossed (therefore, central lesions cause contralateral deficit), whereas the corticobulbar fibers to the sternocleidomastoid muscle are either uncrossed or, more likely, double decussate (therefore, lesions are ipsilateral). These deficits help to locate the site of a lesion (12).
In the neck, the spinal component of the accessory nerve passes through the posterior triangle (anterior border: sternocleidomastoid; posterior: trapezius; and inferior: clavicle). The roof is the platysma, and the floor is the splenius capitis, levator scapulae, and medial and posterior scalenus muscles.
The triangle is subdivided by the traversing omohyoid. The superior space is the occipital triangle and below is the supraclavicular triangle.
The contents of the occipital triangle are as follows:
Superior trunk of brachial plexus between scalenus anticus and medius
Branches of C5, C6, and C7
Dorsal scapular nerve (supplies levator scapulae and rhomboids)
Long thoracic nerve (innervates serratus anterior)
The accessory nerve also passes through this space, after giving off a branch to supply the sternocleidomastoid muscle. It then supplies the trapezius muscle. This location is vulnerable for injury and compression. (Also space for nerve stimulation and conduction studies.)
The contents of the supraclavicular triangle are as follows:
Middle trunk of brachial plexus
SSN (supplies the supraspinatus and infraspinatus muscles)
Nerve to subclavius muscle
Lower trunk of brachial plexus (C8)
External jugular vein descends across sternocleidomastoid muscle to drain into subclavian vein.
Intracranial: head injuries (especially basal skull fracture)
Intraspinal cord: posttraumatic syrinx
Percussion or compression of the accessory nerve in the posterior triangle in sports (football, ill-fitting shoulder pads)
Blows to the shoulder with a hockey stick
Backpack straps and shoulder dislocations
Mild to moderate (rarely severe) lesions result such as stingers/burners and occasionally involve nerve roots (26).
Traumatic penetrating neck injuries
Atraumatic, iatrogenic lesions, acute or delayed, mainly after radical neck dissections or lymph node biopsies
Cannulation of internal jugular vein or after carotid endarterectomies (due to hemorrhages, hematomas, malpositioned suction drainage, infection, or scarring)
Deep tissue massage
Spontaneous accessory nerve lesion (trapezius weakness) (16)
Must rule out neuropathic or myopathic diseases
Symptoms and Signs
Shoulder syndrome: consists of shoulder drooping, acromion prominence, limited lateral abduction, and impaired forward shoulder flexion
Aberrant scapular rotation, abnormal scapulohumeral rhythm (8)
Abnormal EDX findings
Significant pain and tenderness over trapezius, exacerbated by shoulder movement
Feeling of heaviness in the affected arm may be present.
Difficulty with overhead activities, heavy lifting, prolonged writing, or driving
Possible impingement pain secondary to inability to rotate scapula, thereby causing the greater tuberosity to abut the acromion (3)
Late onset of pain is mostly due to adhesive capsulitis, a common sequela of spinal accessory nerve injury.
Test trapezius strength by resistance to lateral abduction of the arm from about 100-180 degrees with arm internally rotated and hand pronated (18); check endurance. Isolation of trapezius must be assured since shoulder elevation can also be accomplished with the levator scapula and the rhomboids.
Test strength of sternocleidomastoid muscles by resisting head turning, opposite to the side of the muscle tested. Also test tilting. Resistance to head flexion tests both sternocleidomastoid muscles at the same time.
Lateral scapular winging is not as pronounced as with a long thoracic nerve lesion. The scapula is laterally translocated with medial rotation of the inferior angle. Shoulder winging caused by trapezius weakness is most pronounced by arm abduction, whereas weakness secondary to long thoracic nerve lesion is most pronounced by arm flexion (pushing upper extremity against a wall).
EDX testing may be helpful (EMG looking for denervation or other neurogenic changes).
NCS from posterior triangle to trapezius may be abnormal.
Posttraumatic focal shoulder elevation dystonia (9)
Motor neuron disease
Physical therapy: range of motion (ROM) exercises to prevent contracture; resistive exercises to restore strength. If not successful, surgery may be considered if neurologic deficits are present (EMG confirmed).
The anterior rami (motor) and the posterior rami (sensory) of C5-T1 combine to form the brachial plexus. The C5-C6 roots together become the upper trunk, the C7 alone the middle trunk, and C8-T1 the lower trunk. Under and slightly below the clavicle, the trunks divide into three anterior and 3 posterior divisions. The anterior upper and middle divisions join to become the lateral cord, and the lower division forms the medial cord. All divisions participate to develop the posterior cord (position under the pectoralis minor). The cords divide into the major nerves of the upper extremities. (Terminal branches are median, ulnar, radial, axillary, and musculocutaneous nerves.)
Compression, stretch, or a combination of both
Excessive pressure on the plexus after prolonged anesthesia, post-median sternotomy, coronary bypass surgery, jugular vein cannulation
Difficult deliveries (Erb palsy)
Symptoms and Signs
Pain in shoulder and/or arm or hand
Weakness of upper extremity, in one or multiple muscles
Numbness, tingling, coldness
Horner syndrome (ptosis, apparent enophthalmos, decreased sweating in affected side of face, miosis) possible with C8-T1 lesions such as tumors, radiculopathy (often root avulsion)
Test ROM and strength in all muscle groups of the upper extremity
Sensory examination (pinprick, light touch, temperature, and position sense)
Nerve conduction tests and EMG
If necessary, magnetic resonance imaging (MRI) or sonography
Rotator cuff lesions
Lesions secondary to radiation
Pain medication: NSAIDs; antiseizure medications (phenytoin, carbamazepine, gabapentin, tricyclic antidepressants) may be helpful to reduce stabbing pains
After reinnervation, strengthening exercises
If no significant progress after 6 months (mostly if root avulsion is present), surgery should be considered
Upper Trunk Plexopathy
The upper trunk is formed from the combination of the C5 and C6 nerve roots/spinal nerves. From this region, the SSN and the nerve to the subclavius arise. The fibers to the musculocutaneous, axillary, median, and radial nerves pass through the upper trunk of the brachial plexus. An important landmark is Erb point. This location is about 2.5 cm above the clavicle, posterolateral to the sternocleidomastoid about the level of the sixth vertebra. This place is vulnerable to injury (compression, entrapment, stretch, or sharp disruption) and, in fact, is the area involved in the stinger/burner injury (13). At this point, the C5 and C6 roots, the SSN, and fibers of the musculocutaneous and axillary nerves can be electrically stimulated simultaneously, which can be helpful in correct diagnosis.
The mechanisms of injury considered are (28):
Nerve root compression in the neural foramina (lack of protective epineurium and perineurium at that site)
Brachial plexus stretch (traction injury)
Direct blow to the plexus (percussion, compression)
A combination of stretch and percussion/compression
Football (highest incidence in defensive backs)
Participants in other collision sports (ice hockey, field hockey, boxing)
Shoulder laxity (33)
Ill-fitting shoulder pads, neck rolls, or other equipment (26)
Faulty techniques (especially during tackling)
Carrying heavy loads for a long time including backpacks
High-risk child birth (forceps, breech delivery)
Symptoms and Signs
Burning pain and dysesthesia in affected arm on impact lasting seconds to hours, followed by mostly transient weakness and no sensory symptoms. At times, there is prolonged loss of strength (13).
Occasionally, the only objective change may be seen as postural abnormality (drooping of the shoulder, especially if the accessory nerve is also involved).
Weakness of shoulder muscles, especially supraspinatus and infraspinatus, deltoid, biceps
Check for positive Tinel sign at Erb point
Spurling test to rule in or out radiculopathy
More severe injuries may involve the middle and lower trunk. There also may be denervation, which can be identified with EMG (earliest 2 weeks after the injury).
Cervical cord neurapraxia (CCN)
Rotator cuff injury
Only treatment is prevention of recurrences (improved techniques, appropriate shoulder pads, neck rolls, orthoses).
In severe lesions, inactivity and slow return to strength and flexibility with gradually increasing collision work and improved tackling techniques are necessary before returning to contact sports.
Emphasis is placed on postural exercises with cervicothoracic stabilization training and resistive exercises to shoulder muscles (when there is no evidence of denervation).
The athlete may return to participation in contact sports on reestablishment of pain-free motion and full recovery of strength and functional status.
Contraindication for return to play is two or more episodes of transient CCN, cervical myelopathy, evidence of neurologic deficit, decreased ROM, and/or neck pain (35).
Lower Trunk Plexopathy
Position between clavicle and first rib. It carries sensory and motor fibers of C8-T1 distribution (median and ulnar nerves). The closeness of median motor and ulnar sensory fiber at this level has EDX significance.
The best known and most debated compression syndrome is thoracic outlet syndrome.
Thoracic Outlet Syndrome
Thoracic outlet clinically refers to the thoracic inlet, the anatomic structure of a bony ring (first thoracic vertebra, first pair of ribs, and the manubrium). The clavicle articulates with the manubrium, which represents the anterior border of the inlet. Several vital structures pass through that opening (brachial plexus, subclavian artery and vein). Thoracic outlet syndrome (TOS) is due to the impingement of the brachial plexus and/or subclavian artery in the region of the scalenus muscles (anterior and medial), the first rib, and the clavicle. The subclavian vein lies on top of the scalenus anticus but joins the nerve and artery before the tight area between the clavicle and first rib. Compression/entrapment can also occur a bit more inferior (pectoralis minor syndrome).
TOS is frequently caused by hyperextension injuries of the neck due to accidents, repetitive motion stress at work, and overhead activities like continued reaching for high-placed items. Muscles become tight (scar tissue has been found throughout the muscles by microscopic examination), or ligaments or bands press on the neurovascular structures, mostly just behind the collar bone.
Several TOS are identified by location:
Between the anterior and middle scalenus muscles
The scalenus anticus syndrome: Nerve entrapment between the insertion of the scalenus anticus, the clavicle, and the first rib (especially in the presence of a cervical rib) (1)
Costoclavicular syndrome: Nerve entrapment in the narrowed space between clavicle and first rib; prolonged downward and backward shoulder pressure as by heavy loads on the shoulder; worse with abnormal clavicle or malunion or nonunion of clavicle fracture
Pectoralis minor syndrome (between chest wall and pectoralis minor)
Classification by structures involved:
Neurogenic thoracic outlet syndrome (NTOS): most common; compression of brachial plexus (lower trunk)
Venous thoracic outlet syndrome (VTOS) (Paget-Schrötter syndrome): obstruction of the subclavian vein; presents with arm swelling, pain, and cyanosis, possible thrombosis
Arterial thoracic outlet syndrome (ATOS): 1% only; emboli arising from subclavian artery stenosis or aneurysm obstruct blood flow and cause ischemia; usually a cervical rib or anomalous first rib is present (27)
Clinical TOS without objective findings is very common. Identification as such depends on the diagnostician.
Cervical rib (with fibrous bands to the first rib) (36)
Slim, asthenic females (with long “swan neck” and droopy shoulders)
Accessory nerve lesion (weak trapezius muscle causing droopy shoulders)
Sternotomy (at risk for pectoralis minor syndrome, especially those with premorbid impaired shoulder motion)
Neoplasm (e.g., Pancoast tumor, bulky lymphadenopathy)
Klippel-Feil anomaly (24)
Swimmers and other sports using repeated overhead motion
Scalenus hypertrophy (1)
Symptoms and signs
Vague pain and fatigue (claudication)
Color change (pallor and/or cyanosis)
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