10 Although patients were somewhat less satisfied with reassurance and an education booklet (the third group in that study this group fared no worse than the groups receiving therapy. Acute lumbosacral Radiculopathy The initial treatment of the patient with lumbosacral radiculopathy presenting with sensory symptoms and pain without significant neurologic deficits is not different from the approach for the patient with uncomplicated low back pain. However, such patients require observation for possible worsening of their neurologic status. Acute radiculopathy with neurologic Deficits The treatment plan should fit the severity of the symptoms and signs. The management approach for radiculopathy covers the gamut from avoidance of heavy lifting to laminectomy and fusion. In acute radiculopathy, the goals of treatment should be the reduction of pain and the stabilization or amelioration of neurologic deficits. Even patients with neurologic deficits such as segmental distributions of weakness, segmental loss of sensation, and reflex changes are likely to have significant spontaneous recovery.
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Because there is seldom a recognizable structural cause, treatment regimens tend to be nonspecific. Patient education is important, and part of art the good therapeutic effort should include patient education about the nature of the condition, the likelihood of a good outcome, and the approach to be taken to speed recovery and minimize the risk of recurrence. Once these approaches to management have been undertaken, if there is no meaningful response to treatment, it is necessary to explore the possibility that psychosocial issues underlie the symptoms. Acute nonspecific Back pain There is general agreement that patients with acute nonspecific spine pain or nonlocalizable lumbosacral radiculopathy (without neurologic signs or significant neurologic symptoms) require only conservative medical management. Patients should abstain from heavy lifting or other activities that aggravate the pain. Bed rest is not helpful and has been shown to delay recovery. 9 Bed rest may be recommended for the first few days for patients with severe pain with movement. Recommended medications include nonsteroidal anti-inflammatory drugs such as ibuprofen or aspirin. If there are complaints of muscle spasm, muscle relaxants such as cyclobenzaprine may be used in the acute phase of pain. Narcotic analgesia should be avoided, in general, but it can be prescribed in cases of severe acute pain. A study by Cherkin and coworkers compared standard physical therapy maneuvers and chiropractic spinal manipulation for the treatment of acute low back pain and found that both provide small short-term benefits and improve patient satisfaction, but they increase the cost of medical care and.
Treatment The initial management of acute spine pain writings must be directed toward determining if a serious neurologic condition exists. If there is a history of recent trauma or serious underlying medical illness, more-aggressive evaluation is warranted. The presence of acute and progressive neurologic dysfunction is an urgent medical problem. This is especially so when there is clinical evidence of bilateral neurologic dysfunction, increasing the likelihood of involvement of the spinal cord or cauda equina. Manifestations include bilateral leg weakness and sensory symptoms, and loss of bowel or bladder control. Such symptoms should trigger an urgent workup that includes mri studies and possibly neurosurgical consultation. Acute low Back pain Acute spine pain is very common, and the likelihood of spontaneous recovery is in the range of 80. Prolonged inactivity prolongs recovery.
Electrodiagnostic tests (nerve conduction studies and needle electromyography emg) are most useful in the presence of a motor deficit on neurologic examination. Nerve conduction studies are indicated primarily to exclude other neuromuscular disorders that can mimic radiculopathy, such as peripheral polyneuropathy and mononeuropathies. The h-reflex can be a useful nerve conduction study when assessing for the presence of an S1 radiculopathy. The needle electrode examination is most likely to be useful in the presence of clinical weakness. This procedure will help distinguish weakness due to spinal nerve root damage from other causes of weakness identified on the physical examination, such as other neuromuscular disorders, central nervous system disorders, and non-neurologic causes of weakness (pain, malingering). The needle electrode examination should be performed only after at least 3 weeks have passed since the onset of weakness because fibrillation potentials (the major manifestation of acute denervation) do not reliably develop before that time. Electrodiagnostic testing may be of value in the assessment of patients owl with postsurgical deficits, multisegmental neurologic deficits, or multilevel intraspinal structural changes. Such patients present with complicated clinical and neuroimaging evidence, and electrodiagnostic book testing might clarify issues of the location, activity, and severity of spinal nerve root disease.
Of the two modalities, mri resolution for neural structures is superior. In the absence of motor, sensory, or autonomic deficits, and in the absence of significant trauma, infection, or malignancy, the American Academy of neurology guideline recommends nonsurgical therapy before these techniques are used in patients with uncomplicated acute low back pain of less than. 8 Patients with acute neurologic deficits associated with low back pain should be considered for mri or ct of the lumbosacral spine unless surgery and invasive therapeutic options are not indicated. Computed tomographic myelography ct myelography employs traditional myelography (intrathecal instillation of a radiocontrast agent, followed by routine spinal radiographs) followed by ct of the spine. It may be of value when mri studies are inconclusive, especially in the assessment of the relation between spinal nerve roots and the bony neural foramina. Although this technique involves an invasive procedure, it is the study of choice when there are absolute contraindications to the use of mri (presence of an implanted electronic device such as cardiac pacemaker or metal object in the inner ear, eye, or brain, such. Electrodiagnosis Electrodiagnostic tests assess the neurophysiologic function of peripheral nerves and can identify the presence of various forms of nerve fiber damage.
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6 Box 3 Signs on the Physical Examination Indicating Nonorganic causes of Low Back pain Superficial tenderness over the lumbar region to light touch Nonanatomic tenderness Exacerbation of pain by applying wallpaper a few pounds of pressure with the hands to the top of the head. Diagnosis The appropriate evaluation and management of low back pain rest on a few basic principles. First, it is necessary to determine whether the symptoms are caused by nerve root involvement. Second, it is necessary to determine whether the acute or chronic spine pain is related to a serious underlying medical illness that is manifesting itself as spine pain. After an initial assessment of the likely cause of the symptoms, the spine pain can then be treated. A number of diagnostic tests can help pinpoint the cause of low back pain. Which test is selected depends on a host of factors uncovered during the history and physical examination.
The diagnostic tests are described next. Routine radiographs of the Spine routine spine radiographs are of limited value because they visualize only bony structures. Guidelines from the. Agency for health Care policy and Research (ahcpr) indicated value of routine spine radiographs for acute low back pain in the following settings: acute major trauma, minor trauma associated with risk of osteoporosis, risk of spinal infection, pain that does not respond to rest. 7 They may also be of value in assessing spinal alignment and rheumatologic disorders of bone. Computed Tomography and Magnetic Resonance Imaging Computed tomography (CT) and magnetic resonance imaging (MRI) are sensitive tools for evaluating neural structures such as spinal nerve roots and the spinal cord, and they can visualize soft tissue structures within the spinal canal.
These include advanced age, history of cancer, unexplained weight loss, use of injected drugs, chronic infection, prolonged duration of pain, pain that does not respond to rest or recumbency, and failure to respond to previous therapy. Box 1 reviews these factors. Box 1 Warning Signals of Systemic Disease Underlying Back pain. Cancer, prior history of malignancy, advanced age, unexplained weight loss no pain relief with bed rest pain duration greater than 4 to 6 weeks failure to respond to standard therapies Spinal infection History of intravenous drug use Urinary tract infection skin infection Compression fracture Advanced. 5 These are reviewed in Box. Box 2 Historical Symptoms Suggesting Nonorganic causes of Back pain pain at the tip of the tailbone Whole-leg pain in global distribution Whole-leg numbness in a global distribution Sudden give-way weakness of the leg Absence of even brief periods of relative pain relief failure.
Bmj (Clin Res Ed) 1984:289:739-741. Examination A general examination should be performed to identify potential systemic disorders, such as rheumatologic disease, skin disease, or bone deformities. The spine should be inspected for alignment, curvature, range of motion, focal tenderness, and overlying skin abnormalities such as a tuft of hair or pore. Mechanical maneuvers to elicit radicular and hip-joint symptoms should be considered, including straight-leg raising, reverse straight-leg raising, patricks test, and Lasègues sign. A careful neurologic examination should be undertaken to exclude motor and sensory deficits. Muscle strength in the L2 through S1 myotomes should be examined. The sensory examination should include soft-touch and pain sensation in the same segmental distributions. Muscle stretch reflexes should be elicited at the knee for the L3 to L4 segment and at the ankle for the S1 segment, and they can also be performed in the posterior thigh at the tendinous insertion of internal hamstrings for the L5 segment. Waddell and colleagues have also described a number of findings on the physical examination that point to nonorganic causes for low back pain, predicting delayed recovery and suggesting the need for a multidisciplinary approach to treatment ( Box 3 ).
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Disk herniation through the apple annulus fibrosis does not in itself produce pain, but compression by disk of the dural lining estate around the spinal nerve root sleeve is one likely explanation for the back pain associated with acute disk herniation. This is also likely to contribute to the pain from spinal nerve root compression from arthritic spurs at degenerated facet and uncovertebral joints. Compression can directly stretch nociceptors in dura or nerve root sleeve tissues, but ischemia from compression of vascular structures, inflammation, and secondary edema is also likely to play a role in some cases. Signs and Symptoms, history and physical examination are critical to the diagnosis and thus to the formulation of a rational approach to management. The following briefly summarizes the major points. The medical history should focus on both triggering and alleviating factors, as well as on the character of the pain. Signs and symptoms such as increased pain with Valsalva maneuvers, straight-leg-raising symptoms, the tendency for the pain to radiate into the buttock or leg, the presence of weakness or sensory deficit, and bowel or bladder urgency or incontinence are associated with neurologic causes of low. The history should also explore factors that increase the likelihood of an underlying systemic disorder as a cause.
S1 radiculopathy is the next most common, followed by L3 to L4 radiculopathy. Pathophysiology, the pathophysiology of nonradicular low back pain is usually indeterminate. In fact, one of the defining features of this disorder is its nonspecific etiology. Pain can arise from a number of sites, including the vertebral column, surrounding muscles, tendons, ligaments, and fascia. Stretching, tearing, or contusion of these tissues can occur after sudden unexpected force applied report to the spine from events such as heavy lifting, torsion of the spine, and whiplash injury. Whether muscle spasm is a significant etiology of lumbar spine pain, either as cause or effect of back injury, has not been proved. The pathophysiology of radicular spine pain and lumbosacral radiculopathy is usually more obvious.
to upper respiratory illness as a cause for visiting a physician. 1, up to two thirds of the population has low back symptoms at some time in their lives. In 1995 there were about two workers compensation claims for low back pain for every 100 workers. Seventy-five percent of patients with acute low back pain are back to work within 1 month of the onset of symptoms, and only 5 are disabled for more than 6 months. 2, however, among those with continuing pain 6 to 10 weeks after onset, most still have some symptoms at 1 year. 3, among persons with chronic low back pain without neurologic deficits, a number of factors play a role in the length of disability. Recurrent low back pain and prolonged disability tend to correlate with prior history of low back pain, advancing age, job dissatisfaction, emotional distress, heavy or repetitive lifting and physical work, prolonged sitting or standing, and the presence of a workers compensation claim or pending litigation. 4, lumbosacral radiculopathy and radicular low back pain are less common than nonspecific low back pain. L5 radiculopathy is the most common lumbosacral radiculopathy, usually produced by disk herniation between the fourth and fifth lumbar vertebral bodies.
Table 1 for the differential diagnosis for low legs back pain. Table 1 Differential diagnosis of Low Back pain. Mechanical causes, nonmechanical causes, causes of Referred pain, idiopathic (sprain, strain). Malignancy, pelvic disease (prostatitis, endometriosis, pelvic inflammatory disease). Spondylosis (disk, annulus, facet infection, renal disease (kidney stones, pyelonephritis, perinephric abscess). Compression fracture, inflammatory spondyloarthropathy (ankylosing spondylitis, psoriatic spondylitis, reiters syndrome, inflammatory bowel disease). Aortic aneurysm, traumatic fracture, osteochondrosis, gastrointestinal disease (pancreatitis, cholecystitis, penetrating ulcer). Alignment disorders (kyphosis, scoliosis, spondylolisthesis pagets disease of bone 2002 The Cleveland Clinic foundation, low back pain accompanied by spinal nerve root damage is usually associated with neurologic signs or symptoms and is described as radiculopathy.
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Definition, low back pain can best be described in terms of specific accompanying features. Low back pain is acute if it has a duration of about 1 daddy month or less. Chronic low back pain is usually defined by symptoms of two months or more. Both acute and chronic low back pain can be further defined by the presence or absence of neurologic symptoms and signs. Nonspecific or nonradicular low back pain is not associated with neurologic symptoms or signs. In general, the pain is localized to the spine or paraspinal regions (or both) and does not radiate into the leg. In general, nonspecific low back pain is not associated with spinal nerve root compression. Nonspecific low back pain might or might not be associated with significant pathology on magnetic resonance imaging (MRI) and is often a result of simple soft tissue disorders such as strain, but it can also be caused by serious medical disorders arising in the bony.