Arm and Neck Pain

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Chapter 29 Arm and Neck Pain

Evaluation of the patient with arm and/or neck pain is based on a careful history and clinical examination. Diagnosis of the common causes and a treatment plan can almost always be accomplished in the office before laboratory investigation, but further study may be required if the patient fails to improve or has other specific indications for imaging or electrical studies.

A useful approach is to consider the diagnosis in terms of pain-sensitive structures in the neck and upper limbs. These structures may be part of the nervous system or may involve joints. Neurological causes should be considered in terms of the innervation of the neck and arm, and non-neurological causes are based on dysfunction of the other anatomical structures of the arm or neck. Because nerve root irritation generates neck muscle spasm, this type of pain is usually lumped into the “neurological” category. Some essentially non-neurological conditions have neurological complications and are grouped in this chapter as “in-between” disorders.

Clinical Assessment

History

Neurological Causes of Pain

Plexus Pain

Peripheral pathology may involve the brachial plexus (Fig. 29.1) or individual nerves extending to the hand. Infiltrative or inflammatory lesions of the brachial plexus produce severe brachialgia radiating down the upper limb and also spreading to the shoulder region. Radiation to the ulnar two fingers suggests that the origin is in the lower brachial plexus, and radiation to the upper arm, forearm, and thumb suggests an upper plexopathy. Patients with a thoracic outlet syndrome complain of brachialgia and numbness or tingling in the upper limb or hand when working with objects above the head.

image

Fig. 29.1 Brachial plexus: schema.

(Netter illustration from www.netterimages.com © Elsevier Inc. All rights reserved.)

Examination

The physical examination is designed to localize a neurological deficit related to spinal cord, nerve roots, or peripheral nerves. Evaluation for non-neurological pathology is required because rheumatological problems often complicate a primarily neurological problem. A detailed knowledge of motor and sensory neuroanatomy is required for accurate localization.

Motor Signs

The examination begins with inspection. Particular attention is paid to atrophy of muscles of the shoulders, arms, and the small muscles of the hands. Fasciculations are often due to anterior horn cell disease, but they may be part of the neurology of cervical spondylosis and radiculopathy. Significant sensory signs would argue against anterior horn cell degeneration.

Muscles in the various myotomes must be tested individually. When there is unilateral weakness, the contralateral side can act as a control, but some standard measure of strength is necessary for accurate evaluation when bilateral weakness is present. If one can overcome the action of a patient’s muscle by resisting or opposing its action close to the joint it moves, using an equivalent equipotent muscle of the examiner (fingers test fingers, whole arm tests biceps), then that muscle in the patient is, by definition, weak. The degree of weakness can be graded, and the 5-point (Medical Research Council [MRC]) grading scale is often used. Grade 5 represents normal strength. Grade 4 represents “weakness” somewhere between normal strength and the ability to move the limb only against gravity (grade 3). Grade 4 covers such a wide range of weakness that it is usually expanded. One simple expansion is into “mild, moderate, or severe.” When the muscle can move the joint with the effect of gravity eliminated, it is graded at 2, and grade 1 is just a flicker of contraction.

The lower limbs must always be examined, even when the patient complains of symptoms only in the upper limbs. Evidence of a myelopathy as evidenced by the finding of sensory or motor dysfunction in the lower limbs, when combined with the presence of radicular signs in the upper limbs, indicates a spinal cord lesion in the neck.

The distribution of weakness is all important in localizing the problem to nerve root, plexus, peripheral nerve, muscle, or even upper motor neuron (central weakness). It is useful to use a simplified schema of radicular anatomical localization when evaluating nerve root weakness because overlap of segmental innervation of muscles can complicate the analysis (Table 29.1).

Table 29.1 Segmental Innervation Scheme for Anatomical Localization of Nerve Root Lesions

Segment Level Muscle(s) Action
C4 Supraspinatus First 10 degrees of shoulder abduction
C5 Deltoid Shoulder abduction
  Biceps/brachialis/brachioradialis Elbow flexion
C6 Extensor carpi radialis longus Radial wrist extension
C7 Triceps Elbow extension
C7 Extensor digitorum Finger extension
C8 Flexor digitorum Finger flexion
T1 Interossei Finger abduction and adduction
  Abductor digiti minimi Little finger abduction

The thoracic outlet syndrome, or brachial plexus entrapment, is an overdiagnosed condition. Maneuvers designed to test for compromise of the neurovascular structures passing through the thoracic outlet are often difficult to interpret. In these maneuvers, the arm is extended at the elbow, abducted at the shoulder, and then rotated posteriorly. The examiner palpates the radial pulse while listening with a stethoscope over the brachial plexus in the supraclavicular fossa. The patient takes a deep inspiration and turns the head to one or the other side. Many normal individuals lose their radial pulse, but the emergence of a bruit does suggest at the least vascular entrapment (Adson test). The patient then exercises the hands held above the head with extended elbows—numbness, pain, or paresthesias, often with pallor of the hand, support the diagnosis (Roos test).

A distribution of weakness that does not conform to a clearly defined anatomical distribution of a single peripheral nerve in the upper limb suggests plexopathy. Upper plexus lesions cause mainly shoulder abduction weakness, and lower plexus lesions will affect the small muscles of the hand.

Pathology and Clinical Syndromes

Spinal Cord Syndromes

Extramedullary Lesions

Extramedullary lesions may result in any combination of root, central cord, and long-tract signs and symptoms. The most common cause of extrinsic nerve root and spinal cord compression is cervical spondylosis. This is a degenerative disorder of the cervical spine characterized by disc degeneration with disc space narrowing, bone overgrowth producing spurs and ridges, and hypertrophy of the facet joints, all of which can compress the cord or nerve roots. Hypertrophy of the spinal ligaments, with or without calcification, may contribute to compression. Hypertrophic osteophytes are present in approximately 30% of the population, and the incidence increases with age. The presence of such degenerative changes does not indicate that the patient has symptoms due to these changes; astuteness in diagnosis is necessary. Furthermore, the degree of bony change does not always correlate with the severity of the signs and symptoms it produces. This degenerative process is sometimes referred to as hard disc as opposed to an acute disc herniation or soft disc in which the onset is acute with severe neck pain and brachialgia. Patients with cervical spondylosis often awake in the morning with a painful stiff neck and diffuse nonpulsatile headache that resolves in a few hours. The lesion is most commonly at C5/6 and C6/7, and focal signs are likely to be at these levels. Wasting and weakness of the small muscles of the hands, particularly weakness of abduction of the little finger, is also frequently seen. These signs localize to lower segmental levels, but there may be no observable anatomical change at those levels, and then they are referred to as false localizers. Restricted neck movement is always present with significant cervical spondylosis. Bladder dysfunction, indicated by frequency, urgency, and urgency incontinence or the finding of long-tract signs or symptoms, indicates the need for imaging of the cervical spine both to exclude other pathology and to define the severity of the spinal cord compression. Immobilization in a cervical collar often helps with the symptoms and signs of cervical spondylosis. The role of surgery in treatment is discussed in Chapter 75.

Extramedullary compression in the extradural space is usually due to primary or metastatic tumors. Of the primary tumors commonly encountered, a schwannoma produces signs and symptoms related to the nerve root on which it arises, and as it enlarges, progressive myelopathic dysfunction occurs. Plain radiographs of the cervical spine may demonstrate an enlarged intervertebral foramen, but MRI is diagnostic. A meningioma may present in a somewhat similar fashion but is more frequent in the thoracic region.

Epidural spinal cord compression due to metastatic malignancy presents initially with spine pain in over 90% of patients. Malignant bone pain is usually localized to the vertebra involved, and percussion tenderness is a good localizing sign, even in the neck. As the pathology spreads to the epidural space, radicular pain appears. Plain radiographs of the cervical spine may show bony pathology with preservation of disc spaces, and again, the imaging modality of choice is MRI. The whole spinal column should be scanned because the pathology is often at multiple sites and may be subclinical. Spinal cord compression due to metastatic disease is a neurological emergency requiring treatment with immediate high-dose steroids and local irradiation. Occasional patients are referred for surgery.

Epidural infection (abscess) may be either acute and pyogenic or more chronic when the organism is mycobacterial or fungal. Pyogenic epidural abscess usually presents acutely with fever, severe pain localized to a rigid neck, radicular pain, and rapidly progressing root and myelopathic signs. Sometimes the presentation is more subacute with less systemic evidence of infection. Imaging will usually reveal early destruction of the disc, with spread into the epidural space; only later is there spread to bone, with vertebral collapse. Optimal therapy is surgical decompression and evacuation combined with 6 to 12 weeks of appropriate antimicrobial therapy for pyogenic infections and more prolonged treatment for tuberculosis.

The differential diagnosis of a very rapidly progressing painful epidural lesion includes spinal epidural abscess and spinal subarachnoid, subdural, or epidural hemorrhage. The latter are usually associated with some form of coagulopathy or anticoagulant therapy and sometimes with vascular anomalies or trauma. The sudden onset of severe pain in the neck, with or without radicular pain, may be due to hemorrhage. Reversal of the coagulation deficit, if present, should be followed by decompression.

The sudden onset of pain at the back of the neck with associated posterior fossa signs suggests vertebral artery dissection. The diagnosis is easily made with MRI and fat suppression sequences.

Repetitive sudden shooting pains radiating from the occipital region to the temporal areas or vertex suggests the diagnosis of occipital neuralgia. There may be local tenderness over the greater or lesser occipital nerve, and a local injection of corticosteroid plus local anesthetic is both diagnostic and therapeutic. Failure to respond suggests that the craniovertebral junction area should be imaged.

Brachial Plexopathy

Brachialgia and signs not respecting a single nerve root, associated with tenderness to palpation in the supraclavicular notch, should arouse suspicion of a brachial plexopathy.

Thoracic Outlet Syndrome

Brachial plexus involvement as an entrapment syndrome in the thoracic outlet is rare. The very existence of this entrapment remains open to debate, partly because it is rare and difficult to diagnose, and partly because it has been used as a disability issue, often in the absence of proven pathology. Consequently, questions remain about diagnosis and the efficacy of surgical treatment. Entrapment may involve the plexus, the subclavian artery, or both. Sagging musculature with postural abnormalities including droopy shoulders and a long neck contribute to the predisposition for thoracic outlet syndrome.

A supernumerary cervical rib or simply an elongated transverse process of the seventh cervical vertebra may be seen on plain radiographs. The rib may articulate with the superior surface of the first true rib, or a fibrous band may extend from its tip or the tip of the abnormal transverse process connecting to the first true rib. The abnormal structure compresses the plexus, particularly when the upper limb is elevated above head level. Pain and paresthesias radiate to the ulnar side of the hand and fingers, and weakness of the intrinsic muscles of the hand secondary to lower plexus compression may be evident. Thoracic outlet maneuvers described earlier are generally considered to be unreliable but do raise suspicion. The examination may be normal, or there may be weakness of abductor digiti minimi and hypothenar sensory loss. Occasionally, the abductor pollicis brevis is particularly atrophic and weak.

The diagnosis is often one of exclusion; imaging of the cervical spine is normal, and nerve conduction studies below the clavicle are also normal. Venous and arterial anatomy can be studied by catheter angiography, Doppler flowmetry, or MR angiography and venography. Electrophysiological studies that show partial denervation of the small muscles of the hand and a decreased sensory nerve action potential amplitude from digit 5 are compatible with the diagnosis of thoracic outlet syndrome.

In all cases, a conservative approach should be tried initially. Postural exercises and thoracic outlet muscle strengthening exercises, instructions in proper sitting at work, and correction of unusual sleep positions should provide relief in 50% to 90% of patients, usually within 6 weeks. Failure of conservative treatment prompts consideration of a surgical opinion.

Suprascapular Nerve Entrapment

The suprascapular nerve may be entrapped or injured as it passes through the suprascapular notch (see Chapter 76). It is occasionally cut in the process of lymph node biopsy. The branch to the infraspinatus muscle can be entrapped at the spinoglenoid notch by a hypertrophied inferior transverse scapular ligament. The patient complains of deep pain at the upper border of the scapula, aggravated by shoulder movement, and there may be atrophy and weakness of the supra- and more commonly the infraspinatus muscles. The supraspinatus muscle accounts for the first 10 degrees of shoulder abduction, and the infraspinatus muscle externally rotates the arm.

Carpal Tunnel Syndrome

Carpal tunnel syndrome, the most common entrapment neuropathy, is more frequent in females. It is now accepted as an occupational hazard secondary to repetitive stress and occasionally is the presenting symptom of underlying systemic disease. The nerve is entrapped in the bony confines of the carpal tunnel, which is roofed by the transverse carpal ligament.

Pregnancy, diabetes, rheumatoid arthritis, hypothyroidism, sarcoidosis, acromegaly, and amyloid infiltration of the ligament are possible predisposing factors, and appropriate screening studies should be performed on all patients with carpal tunnel syndrome.

Numbness or pain radiates to the thumb, index, and middle fingers and often wakes the patient at night. At times there is diffuse brachialgia. Atrophy of the abductor pollicis brevis muscle may be marked, but the motor deficit is rarely the cause of disability. Significant sensory loss in median nerve distribution can be a handicap because of poor feedback when using the hand out of sight.

In advanced cases, examination reveals atrophy of the abductor pollicis brevis muscle, which produces a longitudinal furrow in the thenar eminence. There is weakness of thumb abduction. In theory there should also be weakness of the opponens, but patients recruit the long flexor tendons when testing opposition, so weakness is hard to identify. The palmar cutaneous nerve branch leaves the median nerve proximal to the flexor retinaculum and supplies the skin over the thenar eminence and proximal palm on the radial aspect of the hand. Hence, sensory loss secondary to dysfunction of the median nerve in the carpal tunnel, if present, is likely to involve the distal thumb, index, and middle fingers but not the thenar eminence, a diagnostic point helpful in localization of the lesion. The Phalen test is performed by holding the wrist in complete flexion, and the test is considered positive when numbness or tingling in a median nerve distribution is seen within 20 seconds, but the latency before the sensory symptoms occur can be up to a minute. Sensitivity is about 74% and the false-positive rate is about 25%. The Tinel sign, distal tingling on tapping the median nerve at the wrist, may be elicited. Confirmation of the diagnosis is provided by nerve conduction studies and electromyography (EMG); distal motor and sensory latencies are prolonged, and polyphasic reinnervation potentials are seen in the abductor pollicis brevis muscle. More extensive and expensive investigations are usually not warranted, but sonography and MRI have been utilized. Initial relief of the sensory symptoms can be obtained with the use of wrist splints, but patients with unremitting pain or significant motor and sensory signs, together with confirmatory nerve conduction studies, should be offered decompressive surgery. This is usually curative. The surgeon should always send the excised flexor retinaculum for histopathological examination to search for amyloid deposition.

Occasionally, carpal tunnel syndrome may be mimicked by entrapment of the median nerve more proximally at the elbow. Here it passes beneath the thick fascial band between the biceps tendon and the forearm fascia and then between the two heads of the pronator teres muscle. As the nerve passes between the heads of the pronator teres, it supplies that muscle as well as the flexor carpi radialis (which flexes and abducts the hand at the wrist) and the flexor digitorum superficialis (which flexes the fingers at the interphalangeal joints with the proximal phalanx fixed) muscles. After it passes between the two heads of the pronator teres muscle, it supplies the flexor pollicis longus muscle (which flexes the distal phalanx of the thumb with the proximal phalanx fixed), the flexor digitorum profundus muscle to the first and second digits (which flexes the distal phalanx with the middle phalanx fixed), and the pronator quadratus muscle (which pronates the forearm with the elbow completely flexed). Nerve conduction studies may localize the site of pathology, and the EMG precisely defines which muscles are involved.

Radial Nerve–Posterior Interosseus Nerve Syndrome

Having passed through the spiral groove of the humerus, the radial nerve pierces the lateral intermuscular septum to lie in front of the lateral condyle of the humerus between the brachialis and brachioradialis muscles. There it bifurcates to form the superficial branch, which provides sensory innervation to the lateral dorsal hand and the deep branch, referred to as the posterior interosseus nerve. This branch supplies the finger and thumb extensors and the extensor carpi radialis brevis muscle, which is of lesser importance for radial wrist extension (extensor carpi radialis longus is dominant, and its nerve supply comes off slightly more proximally, so radial wrist extension is spared in lesions of the posterior interosseus nerve). The deep branch passes through the fibrous edge of extensor carpi radialis muscle through a slit in the supinator muscle (arcade of Frohse). Entrapment of the posterior interosseous nerve produces symptoms similar to those of lateral epicondylitis—lateral arm pain or a dull ache in the deep extensor muscle area, which radiates proximally and distally and is increased with resisted active supination of the forearm. Extension of the elbow, wrist, and middle fingers against resistance increases the lateral elbow pain. Tenderness may be elicited over the posterior interosseous nerve just distal and medial to the radial head. Pain secondary to posterior interosseous entrapment is typically seen in manual laborers and occasionally in typists. The site of pathology is easily localized by EMG and nerve conduction studies, and surgical decompression is usually successful. Occasionally a neoplasm of the nerve causes the same symptoms, and some surgeons prefer MRI prior to surgery.

Complex Regional Pain Syndrome

Complex regional pain syndrome (CRPS) encompasses syndromes previously called reflex sympathetic dystrophy (RSD), causalgia, shoulder-hand syndrome, Sudeck atrophy, transient osteoporosis, and acute atrophy of bone (see Chapters 44, 76, and 77). By consensus, the syndrome requires the presence of regional pain and sensory changes following a noxious event. The pain is of a severity greater than that expected from the inciting injury and is associated with abnormal skin color or temperature change, abnormal sudomotor activity, or edema. Type I CRPS refers to patients with RSD without a definable nerve lesion, and type II CRPS refers to cases where a definable nerve lesion is present (formerly called causalgia). A soft-tissue injury is the inciting event in about 40% of patients, a fracture in 25%, and myocardial infarction in 12%.

The pathophysiology is unclear, but because many patients respond to sympathetic block and autonomic features are prominent, it has been suggested that there is an abnormal reflex arc that follows the routes of the sympathetic nervous system and is modulated by cortical centers. There is decreased sympathetic outflow to the affected limb, and autonomic manifestations previously ascribed to sympathetic overactivity are now thought to be due to catecholamine hypersensitivity. Significant emotional disturbances at the time of onset occur in many patients, and stress may be a precipitating factor.

Pain can be progressive, and three stages of progression have been described:

Motor impairment is not necessary to make the diagnosis, but weakness, tremor, or dystonia are sometimes present.

The diagnosis is essentially clinical. Diffuse, severe, nonsegmental pain with cyanosis or mottling, increased sweating and shiny skin, swollen nonarticular tissue, and coldness are characteristic. Hypersensitivity to pin prick may preclude precise sensory testing. There may be associated myofascial trigger points and tendonitis about the shoulder.

Autonomic testing may help with the diagnosis; the resting sweat output and quantitative sudomotor axon reflex test used together are 94% sensitive and 98% specific and are excellent predictors of a response to sympathetic block. Bony changes including osteoporosis and joint destruction may be seen. Bone scintigraphy is most sensitive in stage I and less useful in later stages. A stellate ganglion block may be useful both therapeutically and diagnostically (see Chapter 76).

These patients require a good deal of support as well as trials of symptomatic medication. Drugs that sometimes work are prazosin, propranolol, nifedipine or verapamil, guanethidine or phenoxybenzamine, and antidepressants. Bisphosphonates may prevent bone resorption and are also helpful with pain control. A trial of stellate ganglion block, which can be repeated if successful, is worthwhile. Sympathectomy has been used for progressive disease in patients who previously responded to sympathetic block.

“In-Between” Neurogenic and Non-Neurogenic Pain Syndrome—Whiplash Injury

“Whiplash is an acceleration-deceleration mechanism of energy transfer to the neck. It may result from rear-end or side impact motor vehicle collisions but can also occur during diving or other mishaps. The impact may result in bony or soft tissue injuries (whiplash injury), which in turn may lead to a variety of clinical manifestations (whiplash-associated disorders).” – Québec Task Force on Whiplash Associated Disorders (Spitzer et al., 1995).

Rear-end motor vehicle collisions are responsible for 85% of whiplash injuries, and about 1 million such injuries occur in the United States every year. Severe injuries can cause rupture of ligaments, avulsion of vertebral endplates, fractures, and disc herniations, often associated with cervical nerve root or spinal cord damage. The severity of injury can be graded:

The prognosis is related to the severity of injury:

The cause of persistent symptoms in patients with minor injuries is unknown, and little evidence exists for a structural basis for chronic whiplash pain in this group. The difference between a trivial injury and one of more significance should be based on the presence or absence of neurological signs.

About 20% of patients complain of cognitive symptoms after whiplash; cognitive dysfunction is likely to be functional or malingering.

The influence of compensation and legal action in whiplash-associated disorders remains controversial. Two studies from Lithuania, where only a minority of car drivers are insured for personal injury, demonstrated both retrospectively and prospectively significantly less symptomatology than for similar accidents in the United States; at 1 year, no significant difference existed between collision and control groups. The Québec Task Force emphasizes that whiplash is essentially a benign condition, with the majority of patients recovering, but it is the refractory minority that accounts for an inordinate proportion of the costs.

Support, physical therapy, muscle relaxants, and antidepressants are the main therapeutic options, but if neurological signs are present, imaging of the cervical spine with MRI is indicated. Persistence of pain for more than 6 weeks should indicate referral to a more specialized service; often a multidisciplinary team approach is best.

Non-Neurological Neck/Arm Pain Syndromes

Patients with non-neurological causes for acute, subacute, or chronic neck and arm pain are frequently referred for neurological opinion. They may have no focal deficits or have minor nerve root or peripheral nerve signs that are incidental to their main complaint. Usually the clue to diagnosis is to be found in the history, where a good story of movement aggravating or triggering the pain signposts the cause.

Tendonitis, Bursitis, and Arthritis

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