Low back pain (LBP) is one of the most common reasons for missed playing time in professional athletics, as well as a leading reason for healthcare provider visits. When evaluating patients with LBP, lumbar disc problems should be considered (see image below).
Poor training technique and overtraining are frequent causes of disc herniation. Activities that involve chronic combined flexion and rotation with compression can lead to radial tears of the annulus fibrosis and gradual posterior disc bulging. Chronic changes such as calcification and osteophyte formation of the vertebrae can also lead to disc problems.
See Back Pain: Find the Cause, Watch for the Comeback, a Critical Images slideshow, to help diagnose and manage this common problem.
At-risk sports for lumbar disc problems include activities that require frequent flexion, extension, and rotation of the spine. An example is gymnastics, in which disc degeneration is seen in up to 75% of participants that present with back pain.[1] Disc degeneration is significantly more common in elite athletes (75%) compared with nonathletes (31%).[2]
Lumbar disc herniation accounts for only 4% of back pain cases[3] ; symptomatic disc herniations are more common in adults (48%) than adolescent athletes (11%). Acute disc herniations commonly occur in individuals between the ages 30 and 55 years[4] ; however, athletes between ages 20 and 35 years are at the greatest risk for disc injury,[5] and the L4-L5 and L5-S1 levels are most commonly affected.
A study by Morimoto et al found that the most common cause of LBP among Japanese professional baseball players in their 20s was lumbar disc herniation (57%). Additionally, the incidence of lumbar intervertebral disc degeneration was significantly higher among players in their 30s (91%) than among those in their 20s (14%).[6]
In another Japanese study, Enoki et al reported that the prevalence of lumbar intervertebral disc degeneration among male pole vaulters was 38%. All of the athletes in the study had a history of LBP.[7]
The vertebrae are separated by vertebral discs that are composed of a gel substance (nucleus pulposus) surrounded by outer collagen fibers, which are arranged in a crossed manner (annulus fibrosis). These discs are further supported by the anterior and posterior longitudinal ligaments. Together, the vertebral disc complex resists spinal compression.
During axial rotation of the spine, the annular fibers are placed at a mechanical disadvantage. Furthermore, in forward flexion, the anterior vertebral endplates approximate, increasing the pressure of the disc posteriorly. The most common disc herniation is directed posteriorly toward the foraminal window, where the nerve roots exit the spinal canal. As such, a common mechanism of herniation in athletes is combined flexion, rotation, and compression of the spine. Football, wrestling, hockey, gymnastics, tennis, and golf are some sports in which this injury mechanism commonly occurs.
In the presence of a disc herniation, forward flexion worsens the herniation. In extension, the opposite occurs. The posterior vertebral endplates approximate, forcing the disc anteriorly, to reduce the herniation.
The anatomic structures that have been implicated as pain generators include the vertebral discs, nerve roots, ligaments, zygapophysial joints (z-joints), sacroiliac joints, and the musculature. Some studies suggest that discogenic pain secondary to annular disruption is the most common cause of LBP[8] ; vascularized granulation tissue with innervation along a torn annulus fibrosis is thought to be the cause. Inflammatory factors caused by the leakage of nuclear material from annular tears can delay intradiscal tissue healing. These factors include matrix metalloproteinases (MMPs), phospholipase A2 (PLA2), cyclooxygenase (COX), prostaglandins, nitric oxide (NO), cytokines, interleukins, and macrophages.
Disc protrusion describes a bulged annulus that has not ruptured. In this scenario, there is no contact between the nucleus and the extradiscal space.
Disc extrusion describes a ruptured annulus with some expelled nucleus that remains attached to the disc.
Sequestered disc or complete prolapse describes a nucleus that is expelled from the disc and is no longer attached.
In cycling, an incorrect seat position may predispose an individual to disc herniation. Running can cause wear and tear to the vertebral discs secondary to the repetitive trauma that is involved. Well-cushioned shoes and more forgiving training surfaces are thought to protect against disc injury.
Former elite weight lifters and soccer players have been noted to have a higher incidence of degenerative disc disease (DDD)—as noted on magnetic resonance imaging (MRI) studies—but these findings have not been correlated with increased pain in the affected athletes.[5]
(See also the Medscape Drugs & Diseases articles Lumbar Degenerative Disk Disease [in the Physical Medicine and Rehabilitation section], Degenerative Disk Disease [in the Orthopedic Surgery section], and Degenerative Lumbar Disc Disease in the Mature Athlete [in the Sports Medicine section].)
About 95% of athletes have symptom resolution within 4 weeks, and 95% of those with lumbar disc problems return to play fully recovered.
A history of LBP is the greatest predictor for future episodes by up to a 3-fold increased risk; active LBP increases the risk of recurrence by 6 fold.
Complications of lumbar disc problems include prolonged or permanent nerve symptoms, chronic pain, and inability to return to sports.
Coaches, trainers, gym classes, pamphlets, and team and/or primary care physicians should provide education on how to avoid lumbar disk injuries.
For excellent patient education resources, see eMedicineHealth's patient education articles Slipped Disk and Back Pain.
The following symptoms should be noted with regard to the patient's pain:
Intensity (The severity of pain does not always correlate with the extent of the herniation.)
Character or quality (eg, sharp, dull, achy, or burning)
Location (Before irritation of the nerve root occurs, pain may be limited to the lower back without radicular symptoms.)
Percentage of back to leg pain
Onset (ie, sudden or insidious)
Duration
Exacerbating and relieving factors (eg, sitting, standing, lying, ambulating, or during Valsalva maneuver)
Radiation (eg, dermatomal pattern)
Morning stiffness (This is usually limited to 20-30 min with discogenic pain vs 2-3 h with arthritis.[4] )
Constitutional symptoms (eg, weight loss, fever, or nausea)
Remote or recent trauma
Recent change in training routine
It is imperative to ask the patient about any “red flags,” which are grounds for prompt specialist referral. These red flags include:
Younger or older patients (younger than age 20 y or older than 50 y)
History of previous malignancy
Fever/chills
Weight loss
Night symptoms
History of intravenous/injection (IV) drug use
Immunosuppressed patients
Saddle anesthesia (eg, possible cauda equina syndrome)
Recent bowel or bladder dysfunction, particularly urinary retention
Severe progressive neurologic deficit
Pediatric patients with vertebral disc pathology usually present with localized back pain as opposed to the radicular patterns more often seen in adults.[9] These young patients may describe back stiffness, paraspinal muscle spasm, and buttock or hip pain. They may also present with a history that resembles a chronic hamstring strain in the absence of an acute hamstring injury.
Typical symptoms of nerve root compression are pain and paresthesias that follow a dermatomal pattern, and findings may include lower-extremity muscle weakness.
Cauda equina syndrome can occur in the presence of significant central disc herniation. This is considered a surgical emergency, and patients should be referred for evaluation without delay.
(See also the Medscape Reference articles Cauda Equina and Conus Medullaris Syndromes [in the Emergency Medicine section] and Cauda Equina and Conus Medullaris Syndromes [in the Orthopedic Surgery section].)
It is important to observe the patient's ambulation, posture, affect, gait, and need of assistive devices. Asymmetries in the patient's neck, shoulders, back, hips, and legs can also be helpful in the evaluation of LBP. Lumbar shift (ie, list) is commonly seen with disc herniation, and the list is usually away from the side of the pain.[4]
The spinous process and interspinous ligaments should be palpated, and any step-off deformity should be noted.
Range-of-motion assessment should include the following:
Flexion – This motion tends to produce pain with disc herniation and ligamentous injury.
Extension – This motion tends to produce pain with facet disease, spinal stenosis, spondylolysis, and DDD. (See also the Medscape Reference articles Lumbar Facet Arthropathy, Spinal Stenosis, Lumbar Spondylolysis and Spondylolisthesis [in the Physical Medicine and Rehabilitation section]; Lumbosacral Facet Syndrome [in the Sports Medicine section]; and Spondylolisthesis, Spondylolysis, and Spondylosis [in the Orthopedic Surgery section].)
Axial rotation and lateral bending
The neurologic examination should include sensory, motor, and reflex assessments.
Through light touch and pinprick testing of the medial (L4), dorsal (L5), and lateral or plantar (S1) aspect of the foot, the most likely affected nerve roots are tested. Most herniations occur medial to the dorsal root ganglion (DRG), which is a bipolar neuron. Therefore, it is possible for distal sensory testing to remain normal despite abnormal motor testing.
Motor testing includes having the patient squat, as well as walk on the heels and toes. Manual muscle testing is commonly measured according to the Oxford scale, as follows:
0 – No movement
1 – Trace contraction without joint movement
2 – Joint motion with gravity eliminated
3 – Joint movement against gravity
4 – Movement against gravity and some resistance
5 – Normal strength
Repeat testing can fatigue the muscles and may allow the clinician to distinguish subtle weakness(es) on examination. The muscles to be tested include the following:
Iliopsoas (L2-L3)
Quadriceps (L3-L4)
Hamstring (L5-S1)
Tibialis anterior(L4-L5)
Extensor hallucis longus (L5)
Posterior tibialis (S1-S2)
The following reflexes should be tested and compared with the contralateral side:
Patellar (L3-L4)
Medial hamstring (L5) – Perform with the patient prone.
Achilles (S1) – This reflex may be difficult to elicit. The calf must be relaxed and the foot slightly dorsiflexed. A diminished Achilles reflex is a common finding of radiculopathy.
Upper motor neuron testing is performed through Babinski and clonus testing.
The straight-leg raise (SLR) is performed with the patient supine as the examiner elevates the lower extremity. This test is considered to be positive if the patient's symptoms are reproduced between 30-70º of elevation. Pain at 60º is 95% sensitive for an L5-S1 radiculopathy.[4] Pain at greater than 70º of elevation is more consistent with lumbar facet or sacroiliac pain.[4] Performing a seated SLR gives fewer false-positive results,[10] and the test is more commonly positive in adults relative to children. (See also the Medscape Reference article Sacroiliac Joint Injury.)
The distribution of pain with SLR testing can predict anatomic location of a lesion 88.5% of the time.[11] The majority of lesions (95%) occur at the L4-L5 or L5-S1 disc space, affecting primarily the L5 and S1 nerve roots. S1 typically produces more leg pain than back pain and travels down the buttock region, posterior thigh, along posterolateral calf and heel, and into the lateral foot, and fourth and fifth toes. L5 typically affects the lateral aspect of the leg, the medial dorsal aspect of the foot, and the plantar aspect of the great toe.
The crossed straight-leg raise (CSLR) test is an SLR test performed on the asymptomatic limb. The CSLR is considered positive if it reproduces pain that radiates down the symptomatic extremity. This test is less sensitive (25%) than the SLR, but it is more specific (90% vs 40%). A positive CSLR is suggestive of a large herniation and predicts minimal improvement with nonoperative treatment.[4]
The slump test is performed with the patient seated at the edge of the examination table. The cervical, thoracic, and lumbar spine is flexed as the examiner passively extends the patient's leg. If pain occurs, the patient is asked to extend the neck. Relief of pain with cervical extension suggests neural tension radiculopathy; if the pain is not relieved, it suggests the cause of the pain is from stretching muscle fibers.
The femoral nerve tension sign (femoral stretch test) evaluates higher lumbar disc radiculopathy (L2-L3). The test is performed with the patient in the prone position; the physician flexes the patient's knee to 90º, as well as extends the hip while keeping the patient's pelvis on the examination table. Although the validity of this test has not been well documented,[4] it is thought that tension on the femoral nerve can reproduce anterior thigh radicular symptoms.
A hip examination is necessary because disc herniation may present with radicular symptoms to the anterior thigh and groin. These pain findings may be falsely attributed to L1-L3 nerve impingement. Hip range of motion should be evaluated, particularly internal rotation testing, which commonly elicits pain in cases in which there is intra-articular hip pathology.
The Waddell test maneuvers are a series of maneuvers (total flexion, extension, lateral flexion, palpation, supine SLR test, bilateral active SLR, active sit-up) that help the to clinician differentiate between those patients with LBP who have significant structural deformities (including fractures, surgical scars) or permanent neurologic deficits and those who do not.
The Waddell tests should be employed when nonorganic causes of pain are suspected in cases that include the following:
Tenderness that is out of proportion to the examination
Contradictory findings between the seated and supine SLR tests
Pain with maneuvers that normally do not cause pain, such as light axial pressure to the cervical spine or gentle axial rotation
Reduced pain response with distraction
Disturbance that is not correlated with dermatomal distribution
Overreaction during the examination
In 2014, the North American Spine Society (NASS) released evidence-based guidelines for lumbar disk herniation with radiculopathy. Recommended tests for diagnosis and imaging included[12] :
Manual muscle testing, sensory testing, supine straight leg raise, Lasegue sign, and crossed Lasegue sign.
Supine straight leg raise, compared with the seated straight leg raise is suggested
MRI
CT scan, myelography, and/or CT myelography
Cross-sectional imaging considered the diagnostic test of choice; electrodiagnostic studies only to confirm comorbid conditions.
The non-surgical and surgical treatments recommended included[12] :
A limited course of structured exercise for patients with mild-to-moderate symptoms
Spinal manipulation for symptomatic relief
Contrast-enhanced fluoroscopy to guide epidural steroid injections (ESIs) and improve the accuracy of medication delivery
Transforaminal ESI for short-term (2–4 weeks) pain relief
Interlaminar ESIs may be considered
Insufficient evidence to make a recommendation for or against the effectiveness of one injection approach over another
Endoscopic percutaneous discectomy for carefully selected patients to reduce early postoperative disability and reduce opioid use compared with open discectomy
Automated percutaneous discectomy may be considered
There is an insufficient evidence to make a recommendation for or against the use of automated percutaneous discectomy compared with open discectomy
Lumbosacral Spondylolisthesis
A complete blood cell (CBC) count may demonstrate evidence of infection or malignancy.
The erythrocyte sedimentation rate (ESR) level is elevated in the presence of infection.
Alkaline phosphatase is a marker of bone destruction (among other diseases) and may be elevated in cases in which there are tumors or infection.
Imaging studies should be interpreted with caution and correlated with the patient’s symptoms because abnormalities are commonly noted in asymptomatic populations. Imaging modalities for the evaluation of LBP include radiographs, MRI, computed tomography (CT) scanning, nuclear bone scanning, and discography.
Anteroposterior (AP), lateral, and oblique views are commonly obtained.
Radiographs are limited for the evaluation of disc herniations, but they may demonstrate disc space narrowing (see image below).
Radiographs are best utilized to view:
Fractures
Osseous lesions
Sacroiliitis
Infection
Overall bony architecture
Radiographs are not routinely needed in the first 4-6 weeks of symptoms, but radiography should be performed in the presence of trauma or any red flags (see History).
MRI is the gold standard for visualization of herniated discs (see image below) and should be performed in patients who have neurologic symptoms such as bowel/bladder incontinence and sexual dysfunction, as well as in those who have a history of lumbar spinal stenosis with neurologic deficit.
MRI is a good method to evaluate vertebral discs, nerve root compression, and spinal cord impingement.
Evidence of disc degeneration is present in 35% of patients aged 20-39 years, and in nearly 100% of subjects aged 60-80 years.[13] Therefore, patient symptoms should be well corroborated with MRI findings. Note: Radicular symptoms alone are not an indication for an MRI scan, and the study should not be ordered unless the results are likely to change the patient’s management.
CT scanning is better utilized to evaluate bony pathology that involves cortical bone, trabecular bone, lateral recesses, foramina, and the central spinal canal.
Single photon emission CT (SPECT) scanning is the most sensitive test to evaluate for spondylolysis.
CT myelography can be used if MRI and electromyography (EMG) are nondiagnostic, if patients have a contraindication for MRI, or for preoperative planning.
Disadvantages of this modality include its high level of ionizing radiation exposure, its invasive nature, and its limited ability to evaluate the neuroforaminal and extraforaminal areas.
Some advantages include CT myelography's ability to evaluate abnormalities at the nerve root sleeve and to detect abnormalities not seen on MRI.
Nuclear bone scanning is useful for ruling out cancer, stress fractures, and osteomyelitis. (See also the Medscape Reference article Osteomyelitis in Emergency Medicine.)
The use of provocative discography remains controversial. This study is performed based on the principle that normal discs are not painful when injected at low pressures (with dye or saline). The goal of discography is to reproduce the patient’s clinical symptoms or to demonstrate leakage by injecting fluid into the disc. Some spine surgeons routinely order provocative discography before surgery.
Indications for discography include the following:
Several months of LBP of unclear etiology despite thorough evaluation
Equivocal findings on MRI or CT scans
No clinical improvement with nonoperative measures
Electromyography (EMG) and nerve conduction studies (NCSs) evaluate nerve root function, help in the presence of inconclusive imaging studies, and aid in the assessment of nonstructural causes of radicular symptoms (infection and infiltration). These studies locate the level of the lesion, determine acuity, and are used for preoperative planning.
Epidural steroid injections are performed under fluoroscopic guidance and are used for diagnostic or therapeutic purposes with varying results. Successful outcomes for steroid injections have been seen in up to 84% of nonathletes[4] ; however, their use in athletic populations has not been studied.
One study evaluated the efficacy of epidural corticosteroid injections for lumbar disk herniation in National Football League players and found them to be a safe and effective treatment option in this highly selective group of professional athletes, with a high success rate of return to play and no reported complications.[14]
Epidural steroid injections are indicated when other nonoperative measures have failed, and they are commonly administered before surgical intervention.
Physical Therapy
Patients should avoid prolonged bed rest to prevent joint stiffness, muscle wasting, bone mineral loss, pressure sores, and deep venous thrombosis. Two days or less of relative rest may be prescribed initially.
Cooke and Lutz described a staged approach to LBP as the following[15] :
Stage I involves early, protected mobilization with brief rest (48-72 h). Medications and therapeutic modalities including heat, ice, nonsteroidal anti-inflammatory drugs [NSAIDs], soft-tissue mobilization, and epidural injection are considered.
Stage II involves dynamic spinal stabilization exercises with co-contraction of the abdominal and lumbar extensors to stabilize the injured segment. Isometric exercises (muscle contraction without changing its length) retrain muscles to maintain a neutral postural position.
Stage III involves exercises to strengthen lumbar musculature beginning with extension exercises and progressing to flexion exercises. Flexion exercises are delayed due to their increased load on the disc.
Stage IV involves sports-specific exercises and plyometrics such as eccentric strengthening (resisted stretching of the muscle), followed by an explosive concentric contraction.
Stage V involves maintenance exercises (home program) to prevent recurrence.
Types of Surgical Intervention
Discectomy has been recommended for athletes with LBP because there is less anatomic disruption during the procedure, although some investigators argue that athletes have worse outcomes than the general population.[13] These less-favorable outcomes are believed to be secondary to return to play before complete recovery has occurred. In one large case series, pediatric patients made up 0.4% of patients that underwent discectomy.[5]
Percutaneous lumbar disc decompression is indicated in patients with LBP that is associated with radicular symptoms down a lower extremity. Patients should undergo provocative discography examination before surgery.
Criteria for spinal fusion include multiple recurrences of lumbar disc problems or vertebral instability, and at least 4-6 months of symptoms with failed nonoperative therapy. The patient's pain should correlate with imaging studies (MRI). Midline spinal tenderness should correspond to the level of disease.
Randomized, controlled clinical trials have not shown significant long-term benefit with spinal fusion relative to aggressive physical and cognitive rehabilitation protocols.[4] A disadvantage of spinal fusion includes loss of motion at the fused segment that leads to increased stress to the adjacent disc levels, which places the adjacent discs at risk of injury and degenerative changes.
Lumbar total disc replacement has been used in patients with purely discogenic symptoms secondary to DDD. There are, however, many contraindications and possible complications limiting the use of total disc replacement.
A study of outcomes of 87 National Hockey League (NHL) athletes who underwent either nonsurgical treatment (31), discectomy (48), or a single-level fusion (8) for the treatment of lumbar disk herniation found similar high rates for return to play (85%) in all treatment groups. For all players, regardless of treatment, there was a significant decrease in games played per season, points scored per game, and performance score. However, performance measures were not significantly different among the groups. The study data suggest that a lumbar fusion is compatible with a return to play in the NHL, which is in contrast to other professional sports, but this may be due to the small sample size.[16]
Consultations with specialists in primary care sports medicine, orthopedic surgery, neurosurgery, neurology, or physiatry should be sought as indicated.
Physical Therapy
Goals for physical therapy include pain reduction, reinforcement of a comfortable body position, core strengthening, and stabilization of the spine.
Tight musculature, including the hamstrings, hip flexors/rotators/extensors, and abdominals, should be stretched.
A home program should be tailored for performance on a lifelong basis.
Lifestyle modifications
Exercise is not beneficial for the acute symptoms of LBP, but it is beneficial for chronic LBP sufferers. Increased activity reduces pain as well as improves functional status.
Tobacco cessation improves outcomes for LBP.
Weight loss in overweight patients
If a patient continues to have pain in the back, buttock(s), and back of the thigh(s) without pain below the knee (true sciatica causes pain below the knee), then the diagnosis can be confusing in cases in which a disc herniation is present on MRI. A large percentage of patients have disk abnormalities on MRI without symptoms.
Considerations for surgical referral include the following:
Leg pain greater than back pain
Cauda equina syndrome
Progressive or profound neurologic deficit
Severe and disabling pain that is refractory to nonoperative treatment
Herniated disc (at least 4-6 wk)
Spinal stenosis (at least 8-12 wk)
Confirmation of the lesion on imaging studies
There are no data that prove surgical intervention restores neurologic deficit(s) more rapidly than natural history or nonoperative care.
Surgical complications include the following :
Infection
Bleeding
Nerve damage
Worsened pain
Recurrence of herniation
Paralysis
Idiosyncratic reaction
Anaphylaxis
Death
Surgical consultation is indicated in the presence of any red flags (see History).
Referral for epidural spine injection or EMG should also be considered, if indicated.
Primary care sports medicine, neurosurgery, orthopedic surgery, neurology, and physiatry are specialties that have expert clinicians who often treat lumbar disc problems.
Steroids may be injected into the epidural space of the spinal canal if the patient's sciatica persists even with bracing. Bracing may take as long as 4 months to be successful.
Physical Therapy
During the maintenance phase, the performance of exercise stimulates tissue growth, slows or possibly reverses degenerative conditions, and enhances nutrition to the disc. Increasing the strength and endurance in the major muscle groups (eg, quadriceps, hamstrings, hip, and abdominal muscles) is important. Spine flexibility has not been shown to reduce the risk of future injury. Hip flexibility and abdominal strength exercises, however, has been demonstrated to be important, as well as hip ROM stretching and strengthening activities and hamstring and quadriceps stretching and strengthening activities.
Muscle contraction with the spine in neutral position is the most successful exercise program. Sport-specific exercises may now be integrated, and lifelong activity and lifestyle modification should be maintained.
Other treatments include the following:
Intradiscal electrothermal therapy (IDET) – There have been anecdotal reports of high failure rates with IDET in athletes.[5] A randomized, double-blind control trial reported that IDET is a relatively safe procedure, but patients rarely experienced improvement and did not experience better results when compared to sham treatment.[17]
Transcutaneous electrical nerve stimulation (TENS) is not effective for chronic LBP.[5] Limited evidence supports the use of TENS, but this is a safe modality and could be utilized in the acute phase of LBP.
Acupuncture lacks controlled randomized studies to prove its efficacy. This therapy is generally safe, but it is not routinely recommended.
Conflicting evidence exists regarding spinal manipulation,[5] which is not routinely recommended, but it is generally a safe modality.
A study by Paige et al reviewed the effectiveness of spinal manipulative therapy for acute low back pain. The study reported that 15 randomized controlled trials that examined 1711 patients found moderate-quality evidence that spinal manipulation therapy led to improvements in pain and 12 trials that examined 1381 patients found moderate evidence of improvements in function.[18]
Prolotherapy attempts to treat pain through injection of irritant solutions. This therapy is not recommended for the treatment of disc herniation, and there are limited long-term safety data.[10]
Back school has been used for patients with chronic LBP and marked functional impairment. There is a question of whether or not back school is a cost-effective option.
Intradiscal methylene blue injection has been studied and reported to be effective in a prospective clinical trial by Peng et al.[8] Methylene blue has a neurotropic effect that results in blocking nerve conduction and destruction of nerve endings. These neurologic changes result in pain relief when the patient's pain is discogenic in nature.
Avoidance of injury can be achieved through proper education, use of proper body mechanics, and appropriate stretching and strengthening exercises. Smoking cessation, weight control, and maintaining an active lifestyle can also be helpful.
Percutaneous discectomy requires at least 2-3 months of postoperative rest.
Microdiscectomy requires 6-8 weeks of rest for noncontact sports, and at least 3 months of rest (typically 4-6 months) for contact sports. Athletes are less likely to return to play when multiple disc levels are affected. Return to play for single-level microdiscectomy has been reported to be 90%.[13]
Return to play after spinal fusion is controversial. Some authors suggest no return to play at the professional or collegiate level for contact sports after spinal fusion. Others utilize criteria for return to contact sports to include the following[13] :
At least 1 year following surgery
Evidence of solid fusion
Resolution of pain
Full strength
Pain-free ROM
Full endurance
NSAIDs are used to for LBP.
Muscle relaxants (eg, cyclobenzaprine) show some benefit in controlling LBP, but the use of these agents should be limited to the acute phase (ie, the first 4-7 d). Side effects such as drowsiness limit the use of muscle relaxants, but they may be helpful for patients with night symptoms.
Tramadol is effective for pain control in chronic LBP and can be safely used in combination with NSAIDs.
Acetaminophen is effective for pain control in chronic LBP, although NSAIDs may be superior. Acetaminophen may also be used as an adjunct to the analgesic properties of NSAIDs (not to exceed 4 g/d).
Narcotic medications may be helpful in severe cases that involve functional limitations, but long-term use should be avoided.
Selective serotonin reuptake inhibitors (SSRIs) may have a role in managing chronic radicular symptoms.
Tricyclic and tetracyclic antidepressants (TCAs) have shown moderate symptom reduction that is independent of the patient's depression status in chronic pain cases.
Oral steroids help reduce acute pain and swelling; however, no study has shown benefit over the potential harmful side effects of steroid use.
Because pain is usually the most debilitating symptom of lumbar disc disease, pharmacologic therapy is directed at alleviating the patient's pain.
DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, those with upper GI disease, or who are taking oral anticoagulants.
This class of medications provides analgesia to the low back and reduces inflammation surrounding a herniated nucleus pulposus.
DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
These agents are indicated for severe muscle spasms that are associated with LBP; little evidence exists to support universal use in lumbar disc disease.
Skeletal muscle relaxant that acts centrally and reduces the motor activity of tonic somatic origins that influence both alpha and gamma motor neurons.
Structurally related to tricyclic antidepressants and, thus, carries some of the same liabilities.
One of the least expensive and least addictive options in this class.
These agents are used in the treatment of depression.
Analgesic for certain chronic and neuropathic pain. Blocks reuptake of norepinephrine and serotonin, which increases concentrations in the CNS. Decreases pain by inhibiting spinal neurons that are involved in pain perception. Highly anticholinergic. Often discontinued because of somnolence and dry mouth.
Cardiac arrhythmia, especially in overdose, has been described; monitoring the QTc interval after reaching the target level is advised. Up to 1 mo may be needed to obtain clinical effects.
Inhibits ascending pain pathways, altering perception of and response to pain. Inhibits also reuptake of norepinephrine and serotonin.
Inhibits ascending pain pathways, altering perception of and response to pain. Inhibits also reuptake of norepinephrine and serotonin.