Cervical angina

Cervical angina

Patricia Wells

Cervical angina is an uncommon entity that may explain the presence of chest pain despite a negative cardiac work-up. Patients with cervical nerve root compression can present with angina-type pain in association with nausea, diaphoresis and shortness of breath. When a complete cardiac work-up reveals no evidence of coronary artery disease, diagnoses ranging from Prinzmetal’s angina to psychosomatic causes may be ascribed to these patients. When these diagnostic alternatives seem unsatisfactory because of a lack of other supporting symptoms, a diagnosis of cervical disc disease should be considered.[1]

Illustrative Case

A 48-year-old woman initially presented to her cardiologist complaining of classic angina-type symptoms, including crushing substernal left anterior chest pressure radiating from her left sternum around to her left scapula and going down into her left arm. She reported some nausea and shortness of breath with the episodes but denied emesis and diaphoresis. The episodes would come on suddenly and last a few seconds to minutes, often leaving her feeling drained. These attacks had started approximately two weeks before presentation.

Her medical history was significant only for a distant hepatitis B infection without residual effects. She denied neck trauma. Her surgical history included a total abdominal hysterectomy with bilateral salpingo-oophorectomy. Her family history was noncontributory. She denied tobacco use but reported intake of one glass of wine approximately every other day. She had no known drug allergies, and her only medication was conjugated estrogens (Premarin) in a dosage of 0.625 mg per day.

After an apparently benign physical examination, the cardiac work-up (electrocardiogram, exercise treadmill test, resting echocardiogram and stress echocardiogram) revealed no evidence of cardiac disease. The patient’s chemistry panel revealed a total cholesterol level of 265 mg per dL (6.85 mmol per L); however, the ratio of total cholesterol to high-density lipoprotein was 3.08. The values for the rest of the chemistry panel, as well as the complete blood count, thyroid panel and posteroanterior and lateral chest radiographs, were within normal limits. Having found no cardiologic basis for the patient’s disease, the cardiologist referred the patient for a primary care evaluation.

This time, on physical examination, the patient’s chest pain was reproduced by left lateral tilt of her head. Her left triceps reflex was slightly decreased (1+) compared with her right reflex. The remainder of the neurologic examination was normal, as were her cardiac and pulmonary examinations.

Magnetic resonance imaging (MRI) of the cervical spine showed a slight anterior indentation of the thecal sac due to minimal disc bulging at the C4-5 level. At the C5-6 level, a right lateral disc herniation was causing minimal right-sided indentation of the thecal sac and narrowing of the neural foremen. At the C6-7 level, a left-sided disc herniation was causing an anterior and left-sided extradural defect of the thecal sac (Figure 1). The C7-T1 level showed minimal bulging with no evidence of disc herniation. Cervical levels C1-2, C2-3 and C3-4 were normal.

[Figure 1 ILLUSTRATION OMITTED]

Based on the patient’s pain distribution, the reflex changes that were consistent with a C-7 radiculopathy, the reproduction of symptoms with head tilt and the imaging studies, the diagnosis of cervical angina was made.

The patient was treated with nonsteroidal anti-inflammatory drugs (NSAIDs), physical therapy and intermittent cervical traction. Two months after initial diagnosis, she was responding well to conservative treatment, and her pain was reduced by 70 to 80 percent.

Pathophysiology

The pathogenesis of cervical angina can be explained by the fact that cervical neural roots from C-4 to C-8 contribute to the sensory and motor innervation of the anterior chest wall. It has been shown that neural root compromise at the cervical foramina can produce several symptoms, including radicular pain.[2] Often, however, the pain is not clearly radicular but is less discrete, and it may be referred to a muscle innervated by the cervical myotomes, resulting in precordial pain. Patients with true cervical angina are more likely to have disease at the C-6 and/or C-7 level.

Anatomically, a clear demarcation exists between the dorsal sensory roots and the ventral motor roots. This predisposes patients to compromise of only one root or the other. The larger dorsal roots are more often affected, because they are closely associated with the facet joints that form the posterior aspect of the neural foramina.

Osteoarthritic degeneration can result in spur formation, which causes scarring of the roots. The ventral root, which lies deep to the dorsal root, is more protected and therefore less likely to be affected by osteoarthritic changes. However, anterior foraminal encroachment by a degenerative or herniated nucleus pulposus can selectively compromise the ventral root. This may result in a relatively painless paresis, loss of reflexes relating to the affected disc or even myalgia.[3]

Divisions of the anterior roots of C-5 to T-1 give origin to a number of individual nerves that supply motor, sensory and autonomic fibers to the upper thorax, shoulder and arm.[4] Autonomic symptoms, including nausea and diaphoresis, can occur and are mediated through the sympathetic nervous system, although the exact mechanism is not known.

History and Physical Examination

Useful clues obtained from the history include neck pain and/or stiffness, occipital headache and arm pain with sensory symptoms.[3] In addition to neck pain, symptoms that support the diagnosis of cervical disc disease may include nocturnal pain, pain with a change in posture or pain precipitated by sneezing or coughing.[2] A complaint of breast pain is often correlated with myalgia of the greater pectoral muscle.[5] The patient may or may not have neurologic deficits, depending on the severity and the chronicity of the discopathy. Often, passive and/or active cervical motion elicits “anginal” symptoms.

A useful diagnostic maneuver is the lateral head tilt. This maneuver involves extension and rotation of the cervical spine to the symptomatic side in combination with downward compression by the examiner. If the cause of the syndrome is truly cervical discopathy, the maneuver should reproduce the pain.

MRI studies can be used to diagnose cervical disc disease. However, some investigators recommend discography as the gold standard of diagnosis.[3]

Coexisting coronary artery disease must be ruled out. A complete work-up includes an electrocardiogram, a chest radiograph and at least a stress exercise test and an echocardiogram, if not cardiac catheterization.

Treatment

The treatment of cervical angina includes all of the measures that are used in the management of cervical disc disease. The combination of intermittent traction, isometric exercises, NSAIDs and muscle relaxants often relieves most of the symptoms. Many patients also benefit from wearing a hard cervical collar.

At least three months of conservative treatment are recommended in all but the most severe cases. The response to treatment depends on the severity of the underlying pathology. Conservative treatment should continue as long as the patient improves. Most acute attacks subside spontaneously with analgesics and immobilization of the neck by a cervical collar.[6]

If conservative treatment fails, anterior cervical discectomy with fusion can be considered.

Final Comment

Family physicians occasionally see patients who complain of ongoing chest pain for which no pathologic diagnosis can be established. Most of these patients have undergone extensive cardiologic work-ups without a definitive cause being identified as the source of the pain. Although often attributed to psychologic factors, the chest pain in such patients is rarely wholly psychosomatic. A careful history combined with a thorough physical examination, including the lateral head tilt, may lead to the provisional diagnosis of cervical angina.

Conservative treatment should be implemented to relieve symptoms, but a definitive diagnosis can be made with MRI or discography. Other causes must still be ruled out, since the patient may have coexistent pathology. If a three-month trial of conservative therapy fails, referral to a spine surgeon may be indicated.

REFERENCES

[1.] Mitchell LC, Schafermeyer RW. Herniated cervical disk presenting as ischemic chest pain. Am J Emerg Med 1991,9:457-60.

[2.] Brodsky AE. Cervical angina. A correlative study with emphasis on the use of coronary arteriography. Spine 1985,10:699-709.

[3.] Jacobs B. Cervical angina. N Y State J Med 1990;90:8-11 [Published erratum appears in N Y State J Med 1990,90:78].

[4.] Gilroy J. Basic neurology. 2d ed. New York: Pergamon Press, 1990.

[5.] Laban MM, Meerschaert JR, Taylor RS. Breast pain: a symptom of cervical radiculopathy. Arch Phys Med Rehabil 1979;60:315-7.

[6.] Rowland LP, ed. Merritt’s Textbook of neurology. 9th ed. Baltimore: Williams & Wilkins, 1995.

PATRICIA WELLS, M.D. is in private family medicine practice in Scottsdale, Ariz. Dr. Wells graduated from the University of California-San Diego School of Medicine. After serving a general surgical internship, she completed a residency in family practice at Scottsdale Memorial Hospital.

Address correspondence to Patricia Wells, M.D., Scottsdale Memorial Hospital, Suite 334, 3501 N. Scottsdale Rd. Scottsdale, AZ 85251.

COPYRIGHT 1997 American Academy of Family Physicians

COPYRIGHT 2004 Gale Group