Differential Diagnosis of Upper Extremity Disorders (Neck and Arm Pain)

Laith Al-Shihabi, MD

Howard S. An, MD

Dr. An or an immediate family member has received royalties from U & I and Zimmer; serves as a paid consultant to Bioventis and Stryker; has stock or stock options held in Articular Engineering LLC, Medyssey, Spinal Kinetics, and U & I; has received research or institutional support from Medyssey and Spinalcyte; and serves as a board member, owner, officer, or committee member of the American Journal of Orthopedics and Spine. Neither Dr. Al-Shihabi nor any immediate family member has received anything of value from or has stock or stock options held in a commercial company or institution related directly or indirectly to the subject of this article.

Introduction

By virtue of their frequently overlapping symptoms and examination findings, pathologies of the cervical spine and upper extremity often present a diagnostic challenge to the treating physician. Understanding the differential diagnosis of neck and arm pain can lead to great confusion among many specialists. Making an accurate diagnosis is critical to getting an athlete back on the field of play. Complaints affecting this portion of the body are common in the offices of spine surgeons, sport medicine specialists, and hand surgeons alike. Some patients may find themselves being evaluated by all three, speaking to both the variety of pathologies affecting the upper extremity and the potential difficulty in accurately distinguishing them. Symptoms may result from isolated or combined mechanisms, be acute or chronic in nature, and can be due to causes near to or far from the affected area. This diagnostic challenge is especially true in athletes, who at once may be attuned to subtle extremity dysfunction from one pathology while accepting and tolerating other injuries that do not impair performance. The key to making the correct diagnosis is starting with a broad initial differential diagnosis and then narrow it down with the history and physical examination (H&P). A well-done H&P is the cornerstone of the patient workup and is sufficient to establish the diagnosis in most cases. When it does not, additional tests—including imaging, injections, laboratory studies, and advanced neurologic studies—can be invaluable.

The Patient History

Beginning with the presenting complaint, the patient history is used to gather information on the onset, chronicity, and severity of the patient’s symptoms. With athletes, the relationship between the symptoms and athletic performance must also be determined. It is important to establish whether the patient is experiencing only one symptom, such as isolated pain, or a constellation of many, such as pain with weakness and numbness. In considering the various etiologies of pain, sensory disturbance, and weakness affecting the upper extremity, an effort should be made to differentiate between potential neurologic versus non-neurologic causes for the patient’s symptoms. Although the focus of this chapter is on the differential diagnosis of neurologic upper extremity pathologies, non-neurologic injuries may present similarly or concurrently and should also be considered. A table of commonly encountered injuries to the neck and arm are reviewed in Table 9-1.

Neuropathic Pain

Neuropathic pain can result from a traumatic nerve injury, central or peripheral nerve entrapment, or noncompressive mono- or polyneuropathy.

Symptoms are classically described as burning or electrical in nature¹^,² and occur in a predictable distribution of affected spinal or peripheral nerves.

TABLE 9-1 Commonly encountered diagnoses in the differential of neck versus arm and shoulder pain in athletes

Diagnosis	Primary Complaint	Associated Symptoms	Pertinent Negatives	Examination Findings and Keys	Clinical Example
Cervical sprain or strain	Paraspinal soreness and tightness Often follows a traumatic event	Pain to anterior cervical muscles or intrinsic and extrinsic cervical muscles	Neurologic symptoms typically absent	Muscular tenderness ROM limited by pain Normal neurologic examination results	“Whiplash” to neck in collision or motor sport athlete
Cervical facet dislocation	New-onset torticollis and loss of motion after high-energy trauma	Neurologic symptoms often present	No extremity tenderness in the absence of extremity injury	Spinal tenderness with asymmetric loss of motion Perform full neurologic exam or MRI before reduction	Rotational injury after “facemask” tackle in American football
Cervical DJD or DDD	Axial neck pain Worst at extremes of motion	Stiffness often present Neurologic symptoms are variably present	Minimal paraspinal tenderness No extremity tenderness	Axial symptoms outweigh radicular symptoms	“Spear tackler’s spine” in athlete with a history repetitive axial load to the cervical spine
Cervical radiculopathy	Radiating neurologic pain, numbness, paresthesias, or weakness Pain worsens with distinct movements or positions of the neck	Neck pain may also be present if associated with DDD	Palpation of the symptomatic area does not reproduce pain	Radicular symptoms outweigh axial symptoms Myelopathic signs should be absent in pure radiculopathy Extremity pain improved with shoulder abduction	Radicular symptoms with or without an inciting event May be exacerbated by cervical rotation and upward gaze (e.g., with a tennis serve)
Peripheral nerve injury	Extremity neurologic pain, numbness, paresthesias, or weakness	May be exacerbated by extremity position	No neck pain No exacerbation with neck motion	See Table 9-5	Ulnar neuropathy associated with elbow MCL insufficiency in a pitching athlete
Rotator cuff tear or tendinitis	Shoulder pain and weakness	Pain may radiate to neck	Absence of neurologic symptoms	Symptoms worsen with shoulder abduction Subacromial anesthetic injection improves pain and may improve weakness	Subacromial impingement resulting in rotator cuff tendinitis in an overhead athlete
Glenoid labrum injury	Pain with abduction/external rotation (anterior labrum), adduction or loading (posterior labrum), or overhead activity (superior labrum)	Glenohumeral instability or apprehension with certain arm positions	Absence of neurologic symptoms	Neck pain is infrequent Symptoms maximal when in an “at-risk” position for the shoulder	Shoulder instability after glenohumeral dislocation
Glenohumeral DJD	Shoulder pain or grinding, with or without stiffness	Pain may radiate to neck Pain-limited weakness	Absence of neurologic symptoms	Symptoms are worst at the extremes of shoulder motion Glenohumeral injection improves pain and strength	Accelerated joint wear caused by upper extremity weight bearing in a wheelchair athlete or weight lifter
DDD = degenerative disk disease, DJD = degenerative joint disease, MCL = medial collateral ligament, ROM = range of motion.

Associated sensory disturbance or weakness within the same spinal or peripheral nerve distribution also indicates a neurologic cause of symptoms.
Activities that place the nerve in tension or compression may exacerbate symptoms.

Non-Neuropathic Pain

Fractures and dislocations are associated with the acute onset of sharp pain and deformity (if displaced) relative to a traumatic event. Secondary neurologic injury may also occur, however, as the displacement and energy of the fracture or dislocation increases.
Inflammatory or degenerative arthritis is characterized by deep-seated aching or painful motion of the affected joint, with the former often improving with activity and the latter worsening. Concomitant swelling and stiffness of the affected joint may also be present.
Tendinitis, tendinopathy, and tenosynovitis cause a sharp, activity-related pain brought on by resistance against the associated muscle–tendon unit. Palpation the affected tissue should also reproduce the patient’s pain complaints. Immobilization of the affected tendon improves symptoms.
Vascular dysfunction may cause acral pain through either activity-related claudication, chronic ischemia, or reperfusion (as with Raynaud disease). It is frequently associated with cold intolerance and changes or asymmetry in skin temperature.

Neuropathic Weakness

Traumatic nerve injuries resulting from compression, traction, laceration, or ischemia lead to a disruption in nerve conduction by severing one or more structural components of the nerve.³^,⁴
Acutely, patients experience loss of some or all active motor function of the innervated muscles. Chronic denervation leads to muscle wasting and potential joint contractures due to a loss of balanced motors around the joint.
Mononeuropathy is most often from nerve compression, either at the spine (following a nerve-root pattern) or peripherally in the extremity. Sensory or motor dysfunction can occur either in isolation or in tandem and should follow the anatomic course of the affected nerve.
Polyneuropathy is usually secondary to a systemic cause, and etiologies can be genetic, metabolic, infectious, inflammatory, or iatrogenic. Nerve dysfunction can follow a predictable (e.g., stocking-and-glove) or unpredictable pattern and by definition affects multiple extremities or nerve patterns.

Non-Neuropathic Weakness

A tendon or intrasubstance muscle rupture is usually associated with a discrete traumatic event, such as with eccentric overload of a muscle, or with atraumatic attritional wear. In both cases, patients report a sudden, isolated inability or weakness with performing a specific joint motion. Numbness and paresthesias are absent, and pain is often minimal in the subacute or chronic presentation.
Tendinopathy or tenosynovitis often results in pain-limited weakness, in which the onset of pain prevents full force exertion or motion. It can be distinguished from other forms of weakness by restoration of strength with elimination of pain, such as with an anesthetic injection around the tendon.
Rhabdomyolysis may result from overexertion, causing pain and swelling of the affected muscle belly in association with weakness. Aggressive hydration to prevent renal injury is critical in the acute phase.
Myopathy or myositis secondary to an infectious, genetic, metabolic, iatrogenic, or other systemic cause may also produce weakness, typically affecting multiple muscles simultaneously.

Sensory Disturbance

Subjective numbness or paresthesias to the extremity indicate nerve dysfunction at some level. The history should elicit the exact nature and distribution of symptoms and whether they are constant, intermittent, or activity related.
Whereas bilateral complaints should raise the suspicion of a spinal cord etiology, unilateral symptoms more often indicate a nerve root–level or peripheral cause of nerve dysfunction.

Nerve ischemia secondary to impaired vascular inflow may also produce sensory disturbances.⁵^,⁶

The Physical Examination

As with the history, the physical examination is performed in a systematic manner that identifies and grades all components of the patient’s symptoms. In this way, one or few leading diagnoses are determined, and competing diagnoses can be excluded. Whether the examination is performed by region or by system is
unimportant as long as all components of upper extremity function are tested. To facilitate the examination, patients are asked to either change into an examination gown or remove their shirts. The examination begins with a visual inspection of the patient’s spine and extremity. With a recent trauma, the examiner should look for signs of injury such as bruising or deformity. The presence and distribution of skin lesions or any asymmetry in the quality of the skin should be noted (Table 9-2). If the patient reports either preferential or obligate positioning of the neck or extremity, this should be noted along with the reasons why. Any asymmetry in muscle bulk or tone is also noted. Cervical spine position and motion is tested along with active and passive motion of the upper extremity joints. Any discrepancy in active and passive range of motion (ROM) of a joint must be investigated further. Preserved passive ROM with an absence of active ROM after an acute injury speaks to a disruption in the motors around that joint, either caused by paralysis of or damage to the motor–tendon unit. A chronic injury, on the other hand, may lead to joint contracture and loss of passive motion. Conversely, increased passive motion indicates dysfunction of either the passive stabilizers (bone, ligament) or dynamic stabilizers (muscles, tendons) surrounding a given joint.

Painful areas of the upper extremity are assessed next. In attempting to reproduce the patient’s symptoms, it is important to establish whether or not the painful area is directly tender or not. As a general rule, pain originating from neural compression at the cervical nerve root or brachial plexus will not cause tenderness within the extremity even if it causes pain. Similarly, a peripheral nerve may be tender at its site of injury or entrapment but not distally within its territory even if the patient experiences pain there. Spurling’s test for cervical nerves or compression, tension, or palpation of a peripheral nerve may cause shooting pain distally; this does not occur with non-neurologic injuries. Instead, with somatic injuries, patients are most often maximally tender at the same location where they experience maximal pain. Specific maneuvers to produce soft tissue impingement or isolate and test specific tendons, ligaments, and other periarticular structures as pain generators are also used to help identify sources of pain in the extremity.

TABLE 9-2 Commonly encountered skin lesions and their diagnostic implications

Skin Findings	Potential Associated Pathology
Bruising, edema	Fractures, muscle or ligament rupture or contusion, joint dislocation or subluxation
Chronic sores or ulcerations	Loss of protective sensation, vascular insufficiency
Color or temperature changes	Complex regional pain syndrome, cellulitis Raynaud’s disease
Hair or nail overgrowth	Complex regional pain syndrome
Vesicles	Herpes zoster, herpes gladiatorum, impetigo
Anhidrosis	Horner syndrome (associated with brachial plexus injury)
Hyperhidrosis	Complex regional pain syndrome

TABLE 9-3 Tests for myelopathy of the cervical spinal cord

Myelopathic Tests
Test	Level	Pathologic Findings
Jaw-jerk reflex	Cranial nerve V (proximal to foramen magnum)	Hyperactive masseter reflex
Scapulohumeral reflex	C3	Scapular elevation or humeral abduction
Biceps reflex	C5	Hyperactive biceps reflex
Brachioradialis reflex	C5–C6	“Inverted” reflex with diminished brachioradialis and hyperactive finger flexor contraction
Hoffman sign	No specific level	Thumb IP or index finger DIP flexion with flicking of the long finger DIP joint
Finger escape sign	No specific level	Inability to maintain extension and adduction of the ulnar digits
Grip-and-release test	No specific level	Early fatigue or slowness with repetitive opening and closing of the hand
DIP = distal interphalangeal, IP = interphalangeal. Adapted from An HS, Al-Shihabi L, Kurd M: Surgical treatment for ossification of the posterior longitudinal ligament in the cervical spine. JAAOS 2014;22:420–429.

A thorough neurologic examination is critical in the assessment of upper extremity complaints, both to distinguish neurologic from somatic diagnoses and to accurately identify the manifestations of neurologic injury when present. Our preference is to begin centrally and work peripherally in an attempt to identify the location, level, and symptoms of potential neurologic dysfunction. As such, signs of myelopathy are tested for first and correlated to the level of spinal cord compression (Table 9-3). It is important to note that patients may experience dysfunction of
muscles innervated by nerve roots distal to the level of compression and that the severity of myelopathic findings present on examination may be asymmetric. Neurologic pain is often absent in a “pure” myelopathy but can present if there is concomitant exiting nerve root compression.

TABLE 9-4 Testable myotomes, dermatomes, and reflexes for the cranial and cervical nerve root contributions to upper extremity innervation

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