Harrison’s Manual of Medicine



Low Back Pain
Neck and Shoulder Pain


Local pain—caused by activation of local, pain-sensitive nerve endings near affected part of the spine (i.e., tears, stretching).

Pain referred to the back—abdominal or pelvic origin; back pain unaffected by spine movement.

Pain of spine origin—restricted to the back or referred to lower limbs. Diseases of upper lumbar spine refer pain to upper lumbar region, groin, or anterior thighs. Diseases of lower lumbar spine refer pain to buttocks or posterior thighs.

Radicular pain—radiates from spine to leg in specific nerve root territory. Coughing, sneezing, lifting heavy objects, or straining may elicit pain.

Pain associated with muscle spasm—diverse origin; accompanied by taut paraspinal muscles.
EXAMINATION   Include abdomen, pelvis, and rectum to search for visceral sources of pain. Inspection may reveal scoliosis or muscle spasm. Palpation may elicit pain over a diseased spine segment. Pain from hip may be confused with spine pain. Manual internal/external rotation of leg at hip (knee and hip in flexion) may reproduce the pain. Straight-leg raising (SLR) sign—elicited by passive flexion of leg on abdomen with knee extended; pt in sitting or supine position; maneuver stretches L5/S1 nerve roots and sciatic nerve passing posterior to the hip; SLR is positive if maneuver reproduces the pain. Crossed SLR sign—positive when SLR on one leg reproduces symptoms in opposite leg or buttocks; nerve/nerve root lesion is on the painful side. Reverse SLR sign— passive extension of leg on trunk with the knee extended and pt prone or standing; maneuver stretches L2-L4 nerve roots and femoral nerve passing anterior to the hip. Neurologic exam—search for focal atrophy, weakness, reflex loss, diminished sensation in a dermatomal distribution. Findings with radiculopathy are summarized in Table 5-1.

Table 5-1 Lumbosacral Radiculopathy—Neurologic Findings

LABORATORY STUDIES   “Routine” laboratory studies and lumbar spine x-rays—rarely needed for acute LBP but indicated when risk factors for serious underlying disease are present (Table 5-2). MRI and CT-myelography are tests of choice for anatomic definition of spine disease.

Table 5-2 Risk Factors for Possible Serious Causes of Acute LBP

ETIOLOGY   Lumbar Disk Disease   Common cause of low back and leg pain; usually at L4-L5 or L5-S1 levels. Dermatomal sensory loss, reduction or loss of deep tendon reflexes, or myotomal pattern of weakness more informative than pain pattern for localization. Usually unilateral; bilateral with large central disk herniations compressing multiple nerve roots—may cause cauda equina syndrome. Five possible indications for lumbar disk surgery: (1) progressive motor weakness from nerve root injury, (2) progressive motor impairment by EMG, (3) abnormal bowel or bladder function, (4) incapacitating nerve root pain despite conservative treatment, and (5) recurrent incapacitating pain despite conservative treatment. The latter two criteria are controversial.
Spinal Stenosis   A narrowed spinal canal producing back and bilateral leg pain induced by walking or standing and relieved by sitting. Unlike vascular claudication, symptoms are provoked by standing without walking. Unlike lumbar disk disease, symptoms are relieved by sitting. Focal neurologic deficits common; severe neurologic deficits (paralysis, incontinence) rare. Stenosis results from acquired (75%), congenital, or mixed acquired/congenital factors. Symptomatic treatment adequate for mild disease; surgery indicated when pain interferes with activities of daily living or focal neurologic signs present. Surgery successful in 65–80%; 25% develop recurrent stenosis within 5 years.
Trauma   Low back strain or sprain used to describe minor, self-limited injuries associated with LBP. Vertebral fractures from trauma result in wedging or compression of vertebral bodies; burst fractures involving anterior and posterior spine elements can occur. Neurologic impairment common with vertebral fractures; early treatment produces better outcome. Most common cause of nontraumatic fracture is osteoporosis; others are osteomalacia, hyperparathyroidism, hyperthyroidism, multiple myeloma, or metastatic carcinoma; glucocorticoid use may predispose vertebral body to fracture. Clinical context, exam findings, and spine x-rays establish diagnosis.
Spondylolisthesis   Slippage of anterior spine forward, leaving posterior elements behind; L4-L5 > L5-S1 levels; can produce LBP or radiculopathy/cauda equina syndrome.
Osteoarthritis   Back pain induced by spine movement. Increases with age; radiologic findings do not correlate with severity of pain. Facet syndrome— radicular symptoms and signs, nerve root compression by unilateral facet hypertrophy. Foraminotomy and facetectomy—long-term pain relief in 80–90%. Loss of intervertebral disk height reduces vertical dimensions of intervertebral foramen; descending pedicle can compress the exiting nerve root.
Vertebral Metastases   Back pain most common neurologic symptom in patients with systemic cancer. Metastatic carcinoma, multiple myeloma, and lymphomas frequently involve spine. LBP may be presenting symptom of cancer; pain typically unrelieved by rest. MRI or CT-myelography demonstrate vertebral body metastasis; disk space is spared.
Vertebral Osteomyelitis   LBP unrelieved by rest; focal spine tenderness, elevated ESR. Primary source of infection (lung, urinary tract, or skin) found in 40%; Staphylococcus species most common. Destruction of the vertebral bodies and disk space common. Lumbar spinal epidural abscess presents as back pain and fever; exam may be normal or show radicular findings or cauda equina syndrome; abscess extent best defined by MRI.
Lumbar Arachnoiditis   May follow inflammatory response to local tissue injury within subarachnoid space; fibrosis results in clumping of nerve roots, best seen by MRI; treatment is unsatisfactory.
Immune Disorders   Ankylosing spondylitis, rheumatoid arthritis, Reiter’s syndrome, psoriatic arthritis, and chronic inflammatory bowel disease. Ankylosing spondylitis—typically male <40 years with nocturnal back pain; pain unrelieved by rest but improves with exercise.
Osteoporosis   Loss of bone substance resulting from hyperparathyroidism, chronic steroid use, immobilization, or other medical disorders. Sole manifestation may be LBP exacerbated by movement.
Visceral Diseases (Table 5-3)   Pelvis refers pain to sacral region, lower abdomen to lumbar region, upper abdomen to lower thoracic or upper lumbar region. Local signs are absent; normal movements of the spine are painless. Up to 20% of patients with contained rupture of abdominal aortic aneurysm have isolated LBP.

Table 5-3 Visceral Causes of Low Back Pain

Other   Chronic LBP with no clear cause; psychiatric disorders, substance abuse may be associated.

Acute Low Back Pain (ABP) Pain of ❤ months’ duration; full recovery occurs in 85%. Management controversial; few well-controlled clinical trials exist. Algorithms presented in Fig. 5-1 and Fig. 5-2. Entry begins with adults having < 3 months’ activity intolerance due to ABP or back-related leg symptoms. Medical history and physical exam used to search for “risk factors” (Table 5-2); if absent, initial treatment is symptomatic and no diagnostic tests necessary (Fig. 5-1). Spine infections, fractures, tumors, or rapidly progressive neurologic deficits require urgent diagnostic evaluation. Patients with no risk factors and no improvement over 4 weeks are subdivided by the presence/ absence of leg symptoms (Fig. 5-2) and managed accordingly.

FIGURE 5-1. Low back pain management: first 4 weeks. (1) Adults £18 years old, symptoms <3mos. (2) Excluding heavy manual labor.

FIGURE 5-2. Low back pain management: 4–12 weeks.

Clinical trials do not show benefit from bed rest >2 days. Possible benefits of early activity—cardiovascular conditioning, disk and cartilage nutrition, bone and muscle strength, increased endorphin levels. Studies of traction fail to show benefit. Proof lacking to support acupuncture, ultrasound, diathermy, transcutaneous electrical nerve stimulation, massage, biofeedback, or electrical stimulation. Self-application of ice or heat or use of shoe insoles is optional given low cost and risk; benefit of exercises or posture modification uncertain. Spinal manipulation may lessen pain and improve function; treatment >1 month or in radiculopathy is of unknown value and carries risk. Temporary suspension of activities known to increase mechanical stress on the spine (heavy lifting, straining at stool, prolonged sitting/bending/twisting) may relieve symptoms. Value of education (“back school”) in long-term prevention is unclear.
Pharmacologic treatment of ABP includes NSAIDs, acetaminophen, muscle relaxants, and opioids. NSAIDs and acetaminophen are superior to placebo. Muscle relaxants provide short-term benefit (4–7 days), but drowsiness limits use. Opioids are not superior to NSAIDs or acetaminophen in the treatment of ABP. Epidural anesthetics, steroids, opioids, or tricyclic antidepressants are not indicated as initial treatment.
Chronic Low Back Pain (CLBP) Pain lasting >3 months; differential diagnosis includes most conditions described above. Management is complex and not amenable to a simple algorithmic approach. Treatment based upon identification of underlying cause; when specific cause not found, conservative management necessary. Pharmacologic and comfort measures similar to those described for ABP. Exercise (“work hardening”) regimens effective in returning some pts to work, diminishing pain, and improving walking distances.
CLBP causes can be clarified by neuroimaging and neurophysiologic (nerve conduction velocity/EMG) studies; diagnosis of radiculopathy secure when results concordant with findings on neurologic examination. Surgical intervention based upon neuroimaging alone not recommended: 25% of asymptomatic young adults have a herniated lumbar disk by CT or MRI.

ETIOLOGY   Trauma to the Cervical Spine   Whiplash injury is due to trauma (usually automobile accidents) causing cervical musculoligamental sprain or strain due to hyperflexion or hyperextension. This diagnosis should not be applied to pts with fractures, disk herniation, head injury, or altered consciousness. One study found that 18% of pts with whiplash injury had persistent injury-related symptoms 2 years after the car accident.
Cervical Disk Disease   Herniation of a lower cervical disk is a common cause of neck, shoulder, arm, or hand pain. Neck pain (worse with movement), stiffness, and limited range of neck motion are common. With nerve root compression, pain may radiate into a shoulder or arm. Extension and lateral rotation of the neck narrows the intervertebral foramen and may reproduce radicular symptoms (Spurling’s sign). In young individuals, acute cervical nerve root compression from a ruptured disk is often due to trauma. Subacute radiculopathy is less likely to be related to a specific traumatic incident and may involve both disk disease and spondylosis. Patterns of reflex, sensory, and motor changes that accompany cervical nerve root lesions are listed in Table 5-4.

Table 5-4 Cervical Radiculopathy—Neurologic Features

Cervical Spondylosis   Osteoarthritis of the cervical spine may produce neck pain that radiates into the back of the head, shoulders, or arms; can also be source of headaches in the posterior occipital region. A combined radiculopathy and myelopathy may occur. An electrical sensation elicited by neck flexion and radiating down the spine from the neck (Lhermitte’s symptom) usually indicates cervical or upper thoracic spinal cord involvement. MRI or CT-myelography can define the anatomic abnormalities, and EMG and nerve conduction studies can quantify the severity and localize the levels of nerve root injury.
Other Causes of Neck Pain   Includes rheumatoid arthritis of the cervical apophyseal joints, ankylosing spondylitis, herpes zoster (shingles), neoplasms metastatic to the cervical spine, infections (osteomyelitis and epidural abscess), and metabolic bone diseases. Neck pain may also be referred from the heart in the setting of coronary artery ischemia (cervical angina syndrome).
Thoracic Outlet   The thoracic outlet is an anatomic region containing the first rib, the subclavian artery and vein, the brachial plexus, the clavicle, and the lung apex. Injury to these structures may result in posture- or task-related pain around the shoulder and supraclavicular region. True neurogenic thoracic outlet syndrome results from compression of the lower trunk of the brachial plexus by an anomalous band of tissue; treatment consists of surgical division of the band. Arterial thoracic outlet syndrome results from compression of the subclavian artery by a cervical rib; treatment is with thrombolyis or anticoagulation, and surgical excision of the cervical rib. Disputed thoracic outlet syndrome includes a large number of patients with chronic arm and shoulder pain of unclear cause; surgery is controversial, and treatment often unsuccessful.
Brachial Plexus and Nerves   Pain from injury to the brachial plexus or arm peripheral nerves can mimic pain of cervical spine origin. Neoplastic infiltration or postradiation fibrosis can produce this syndrome. Acute brachial neuritis consists of acute onset of severe shoulder or scapular pain followed over days by weakness of proximal arm and shoulder girdle muscles innervated by the upper brachial plexus; onset often preceded by an infection or immunization. Complete recovery occurs in 75% of pts after 2 years and in 89% after 3 years.
Shoulder   If signs of radiculopathy are absent, differential diagnosis includes mechanical shoulder pain (tendonitis, bursitis, rotator cuff tear, dislocation, adhesive capsulitis, and cuff impingement under the acromion) and referred pain (subdiaphragmatic irritation, angina, Pancoast tumor). Mechanical pain is often worse at night, associated with shoulder tenderness, and aggravated by abduction, internal rotation, or extension of the arm.

Symptomatic treatment of neck pain includes analgesic medications and/or a soft cervical collar. Indications for cervical disk and lumbar disk surgery are similar; however, with cervical disease an aggressive approach is indicated if spinal cord injury is threatened. Surgery of cervical herniated disks consists of an anterior approach with diskectomy followed by anterior interbody fusion; a simple posterior partial laminectomy with diskectomy is an acceptable alternative. The cumulative risk of subsequent radiculopathy or myelopathy at cervical segments adjacent to the fusion is 3% per year and 26% per decade. Nonprogressive cervical radiculopathy (associated with a focal neurologic deficit) due to a herniated cervical disk may be treated conservatively with a high rate of success. Cervical spondylosis with bony, compressive cervical radiculopathy is generally treated with surgical decompression to interrupt the progression of neurologic signs; spondylotic myelopathy is managed with anterior decompression and fusion or laminectomy.


For more detailed discussion, see Engstrom JW: Back and Neck Pain, Chap. 16, p. 79, in HPIM-15.


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