A 57-year-old woman presents to the Physical Medicine and Rehabilitation (PM&R) clinic with a history of neck pain. She describes her pain as constant. She experiences pain on movement of the neck. This pain has been present for about 4 to 5 months and is progressively worsening. She takes an occasional Tylenol which seems to help but temporarily. There is numbness of the upper left arm; she is unable to sleep because of this pain. She has not seen any other physician nor had any workup.
Past medical history: She has history of hypertension (HTN) for which she is on Losartan, 25 mg. O.D. for the past 10 years. She is postmenopausal.
Social history: She works as a school teacher, lives with family in an apartment with elevator on the fourth floor. She has two children aged 18 and 16 years.
Past surgical history: None
Medications: Losartan, 25 mg O.D., occasional Tylenol
BP: 140/70 mmHg, RR: 14/min, PR: 75 pm, Temp: 97° F, Ht: 5’5, Wt: 130 lbs, BMI: 22 kg/m 2
Well-developed (WD), well-nourished (WN) lady in moderate distress.
Head, ears, eyes, nose and throat (HEENT): Extraocular movement (EOM)’s full, no ptosis.
General: She is alert, oriented and in mild to moderate distress because of L sided neck pain.
Extremities: No edema, no skin rashes, no surgical scars, no fasciculations seen
Musculoskeletal examination: Range of motion (ROM) of neck—complete in all directions.
Right upper extremity (RUE) all groups 5/5 left upper extremity (LUE) 3/5 deltoid, biceps, and brachioradialis.
All other muscles were 5/5.
There was some wasting of deltoid and biceps muscles.
Deep tendon reflex (DTR)-1+ in biceps, brachioradialis on L 2 and + on R
Sensory examination: Dull to light touch in lateral forearm on the LUE intact in all dermatomes on the RUE.
Gait was within normal limits (WNL) without any deviations.
Tone was normal.
Labs: White blood cell (WBC) 7000, cell/mL; hemoglobin 12.0 g/dL.
General approach to neck pain. The approach to a patient with subacute onset neck pain is uniquely different from that of acute pain. The initial focus should be to differentiate neurologic disorders from musculoskeletal conditions. The points to focus in the physical examination are muscle wasting of deltoid and biceps. Weakness of muscle supplied by the C5‒C6 roots and depressed reflexes in the C5‒C6 distribution. Sensory loss also conforms to this distribution.
Differential diagnosis should include:
Discogenic pain —acute disc herniation at cervical spine intervertebral joints can lead to nerve root compression.
Symptoms depend upon the level of compression. A herniated nucleus pulposus (HNP) at C4‒C5 will be compressing C5 root causing arm pain, tingling, and root burning that may radiate to fingertips. Muscles supplied (diagram C spine, nerves by root) C5 nerve, that is, deltoid. Therefore a patient with HNP at C4‒C5 will have neurologic symptoms affecting C5 nerve root. Biceps, brachioradialis, and coracobrachialis will be affected ( Fig. 1.1 ).
Compression fracture —history of trauma usually precedes. Examination reveals pain and tenderness at spine level worsening with flexion. Compression fracture can be caused by traumatic or nontraumatic causes.
Strains and strains —diffuse neck pain following a motor accident vehicle usually referred to as “whiplash.” Examination is positive for neck tenderness diffusely, usually no neurologic symptoms exist.
Osteoarthritis/spondylosis —refer to generalized osteoarthritis (OA) in an elderly patient, usually pain is worse with activity. Flexion may cause more pain than extension. Neurologic symptoms are seen in the distribution of nerve root that is compromised.
Connective tissue disease— multiple joint arthralgia, fever, weight loss, fatigue and other systemic symptoms are seen. Examination reveals spinous process tenderness and other joint tenderness.
Inflammatory spondylarthropathies —present as neck pain with intermittent pain, morning stiffness worsening with activity.
Malignancy —constant pain, worsen in supine position. Systemic manifestation, such as weight loss, may accompany.
Vertebral discitis —constant pain, often no fever, normal blood count but C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are frequently elevated.
Cervical myelopathy —present in 90% of individuals by the seventh decade and is the most common form of spinal cord dysfunction in people over 55 years of age. Upper motor neuron signs and symptoms.
Referred pain: lung cancer—both small cell and adenocarcinoma can metastasize to cervical spine and cause epidural or extradural metastasis, likewise breast cancer can metastasize to cervical spine.
Cervical myeloradiculopathy —believed to occur because of spondylosis and repetitive compression damage to C-spinal cord and roots. Anterior spondylitic spurs, posterior longitudinal ligament in folding can also cause compression. Acute flexion extension injuries can initiate compression of an already compromised C-spine because of spurs, osteophytes, and thickening of ligaments.
Signs and symptoms are characterized by weakness in lower extremities, gait disturbances. Spasticity and upper motor neuron changes caused by corticospinal and spinocerebellar tract dysfunction. Additional sign and symptoms, such as pain in upper C-spine, tingling, numbness and paresthesia in fingers, and sensory changes, can also manifest. Occasional bowel and bladder changes can be seen depending on compression level.
Myeloradiculopathy: combination of myelopathy and radiculopathy, a clinically complex clinical presentation. Typically, patients present with radicular symptoms, that is, pain and weakness in the arms combined with myelopathy symptoms in the legs, that is, gait disturbance, loss of position, and vibration sense and spasticity. Sometimes signs and symptoms overlap.
Referred pain because of bony metastasis— many cancers can metastasize to cervical vertebrae. The prime examples are lung cancer both small cell and adenocarcinomas, thyroid, breast, prostate. Both epidural and extradural compressions are possible and cause symptoms of cord compression.
Motor neuron diseases (MND)—term used to describe a group of sporadically acquired and familial disorders that affect the anterior horn cells. This group includes spinal muscular atrophy (SMA), amyotrophic lateral sclerosis (ALS), primary lateral sclerosis (PLS), progressive muscular atrophy (PMA), and progressive bulbar palsy (PBP). ALS is by far the most common with a prevalence rate of 5 to 7 per 100,000. It most commonly affects people between the age of 50 and 60 years. This disease can show signs and symptoms of both upper motor neuron (UMN) and lower motor neuron (LMN) involvement. Depending upon whether the presentation is primarily UMN, LMN, bulbar, or mixed UMN and LMN involvement, clinically patients may have weakness of upper extremity (UE), bulbar muscle weakness, that is, speech and swallowing deficits, and generalized weakness. Physical examination findings include weakness of UE muscles, hyperreflexia, fasciculations, and pathologic reflexes as Babinski and Hoffman. Tongue may also show fasciculations and atrophy.
Neck tension syndrome —a patient with this syndrome usually complains of aching discomfort at the base of the neck and upper back. Headaches may be reported if suboccipital and trapezius are involved. Referred pain may also be felt in upper arms, elbows, and forearms. Physical usually is negative. Skilled palpation techniques may help to identify the areas of trigger points. Postural biomechanics is the mainstay of management.
Our patient describes indolent development of symptoms over a few months suggesting chronicity. Existence of pain with numbness in C5‒C6 dermatomes, combined with weakness of deltoid, biceps, brachioradialis, and triceps muscles along with reduced reflexes, points to neurologic involvement. Therefore our focus should be on those conditions that lead to probable compression of the C5‒C6 and possibly C7 roots, such as discogenic disease, spondylosis, spondylarthropathies, space occupying lesions, and metastatic compression fractures leading to nerve root compression.
Vertebral discitis is probably not a possibility because ESR and CRP are normal, likewise inflammatory arthropathies and connective tissue disorders are unlikely because the complaints are focal and multijoint involvement is not there.
Complete blood count—WNL
Complete metabolic panel—WNL
Complete chest x-ray (CXR)—negative for infiltrates, or any other lesions
X-ray of spine—degenerative disc, disease C4‒C5 and C5‒C6 disc spaces with lateral canal narrowing at C6‒C7 levels, no fracture or dislocation was seen. No sclerotic or lytic lesion are seen
Magnetic resonance imaging (MRI) of C-spine—spinal root compression at C5, C6, C7 with no signal abnormality or evidence of cord compression
Electromyography (EMG) showed acute radiculopathy involving C5‒C6 with preservation of motor units
The aforementioned laboratory and imaging data are helpful to further narrow down the differential diagnosis. Because basal ESR and metabolic panel are normal, infection processes and discitis could be eliminated. Imaging did not reveal any lytic or blastic lesions, therefore metastatic disease can be ruled out. Also imaging was helpful to rule out traumatic involvement of C-spine, such as acute fractures and dislocation. Likewise, cord compression can be eliminated because no signal changes are seen on MRI. Clinically myelopathy was low on the suspicion index because the patient did not present with any UMN signs or symptoms, such as increased tone, positive Hoffman sign, ataxia, bladder bowel compromise, or hyperactive reflexes.
The objective data are notable for x-ray and MRI findings of disc degenerative disease at multiple levels. The C5 root compression leads to weakness of deltoid. C6 root compression is causing her weakness in biceps, brachioradialis, and decreased biceps and BR reflexes. EMG nerve conduction data are consistent with the clinical suspicion of cervical radiculopathy involving C5 and C6 roots.
Review of Proposed Pathology and Pathobiomechanics
Myelopathy, radiculopathy, and myeloradiculopathy involve structural abnormalities and lead to problems with movements. Disc height loss because of degenerative changes and dehydration lead to reduction of space both at the central canal where spinal cord is situated and lateral canal recesses where the nerve root exits. Structural changes at the discs ligaments and capsule lead to viscoelastic changes and movement abnormalities. According to Wilson, flexion and extension movement cause a variety of neurologic abnormalities in severe degenerative conditions.
Because of the enfolding ligaments during extension, spinal canal shortens and causes canal encroachment; disc may bulge posterity, further reducing space. Reduction in ROM of spine and symptoms of root compression and pain ensue.
Cervical myelopathy on the other hand is hallmarked by multilevel stenosis and encroachment of spinal cord leading to upper motor neuron findings. This encroachment is from sagittal narrowing of the canal, often by (1) osteophytes, secondary to degeneration of intervertebral joints, (2) stiffening of connective tissue, such as ligamentum flavum, (3) degeneration of intervertebral disc with bony changes, or (4) other degenerative connective tissue changes.
Structural based conditions as syringomyelia, or arachnoid cysts, tumor or epidural lipomatosis may also be associated, although not as common.
Cervical radiculopathy in our patient is caused by nerve root compression leading to nerve root distortion, intraneural edema, and focal nerve ischemia. This leads to a localized inflammatory response, chemical mediators within the disc stimulate production of inflammatory cytokines, substance P, bradykinin, tumor necrosis factor alpha, and prostaglandins. , The membrane surrounding the dorsal root ganglion becomes more permeable, allowing a local inflammatory response that further contributes to radiculopathy. The most common cause of cervical radiculopathy leading to compression is herniated disc. The disc materials are extruded from its normal space and impinge upon the exiting nerve root posterolaterally or intraforaminally.
Degeneration of spine components, that is, osteophytes, facet joint hypertrophy, and ligament hypertrophy, , can cause decrease in disc height, leading to a “hard disc” bulging with compressive elements.
As far as location, anterior causes (soft or hard disc herniation) and osteophytes from uncinate process are most common causes of radicular symptoms compared with ischemia, trauma, postradiation therapy, neoplasia, and spinal infectious congenital disorders.
Cervical myeloradiculopathy can occur during chronic spondylosis and repetitive compressive changes to the cervical spinal cord and roots and also acutely as a result of flexion and extension injuries. ,
Anterior spondylitic spurs and posterior unfolding ligaments can cause chronic compressive changes and lead to demyelination, vascular compromise, and inflammation of nerve roots.
Clinical Signs and Symptoms of Radiculopathy
Neurological symptoms consists of pain, motor weakness and sensory deficits, and reflexes changes ( Table 1.1 ). , Depending on the nerve root, concurrent symptoms occur in the neck, shoulder, upper arm, and forearm. Pain can vary from dull ache to severe burning. Pain may not be localized because of overlap from multiple roots.