Updated: Jul 15, 2009
Patellofemoral syndrome (PFS) is characterized by a group of symptoms that are easily diagnosed and often respond to simple management. The common presentation is knee pain in association with positions of the knee that result in increased or misdirected mechanical forces between the kneecap and femur.1 Ironically, as simple as its presentation is, lack of consensus on the fundamental factors associated with PFS remains. Accordingly, synonyms for the syndrome go in and out of fashion. No agreement exists on the exact pathophysiology, but significant work is being completed on the extent and direction of the associated forces on the patella, as well as on the tracking and alignment of the patella.
While theories regarding the pathophysiology of patellofemoral syndrome vary, identification of the resultant forces involved in dynamic and static knee positions has been fundamental to the research on this syndrome. Factors believed to contribute to production of retropatellar pain include impairments affecting the patellofemoral joint interface. Such impairments may be a consequence of an unbalanced muscle pull, malalignment between the joint surfaces, excessive knee valgus (ie, increased Q-angle) resulting in increased lateral forces, and quadriceps contractures causing production of excessive leverage forces on the patellofemoral joint surface. Excessive use of the joint, either in frequency of loading or excessive loading, also contributes to the symptoms.
Patellofemoral syndrome is common in the United States, especially among physically active persons.
Patellofemoral syndrome has an estimated prevalence rate of 20% in student populations.
Morbidity associated with patellofemoral syndrome is directly proportional to the activity level of the patient. Curtailing physical activities that place unnecessarily stressful demands upon the patellofemoral articulation may be necessary (preferably while substituting other activities into the exercise program).
No racial predilection has been identified for patellofemoral syndrome.
Patellofemoral syndrome more frequently affects females than males.
Patellofemoral syndrome occurs most frequently in adolescents and young adults.
Physical examination of a patient with patellofemoral syndrome should include examination of the musculoskeletal system, including the following2 :
The potential causes of patellofemoral syndrome remain controversial and are therefore more appropriately referred to as associated factors.1 Overuse, overloading, and misuse of the patellofemoral joint seem to be the cornerstone factors on which most authors agree.
Patellofemoral Arthritis
Prepatellar Bursitis
Referred pain from hip
Osgood-Schlatter syndrome
Sindling-Larsen-Johansson syndrome
Neuroma
Patellar tendonitis
Plica syndromes of the anterior knee
Radicular pain
Infection of the knee joint
Tumor (eg, knee joint, femur)
Histologic findings are dependent on the extent to which the cartilage surfaces have been compromised. Shearing stresses may result in changes in subchondral bone and dysplasia of the cartilage surface. More severe cartilage changes have been identified in persons with patellofemoral syndrome that has been refractory to conservative measures.
The basic exercise principles for management of patellofemoral syndrome (PFS) are restoring muscle balance within the quadriceps group, improving range of motion, and restricting the offending physical activity. Quadriceps strengthening traditionally is performed while the knee is flexed 0-30°. Controversy remains regarding the extent to which the individual muscle groups making up the quadriceps can selectively be strengthened. Usually, the lateral forces of the vastus lateralis need to be countered better by the vastus medialis. This goal is accomplished best by strengthening all of the quadriceps.
Stretching of the quadriceps should be of long duration (20-30 seconds) and performed with low force. This technique allows for overcoming neural and connective tissue barriers to lengthening. Exercises to stretch the iliotibial band, hip, hamstring, and calf also are important for patients with PFS. Manual stretching of the lateral retinaculum may be used as a conservative approach, partially mimicking the effect of lateral retinacular release. Physical therapists should educate patients about home exercise programs that include stretching and strengthening exercises.
Patellar taping techniques are used in patients with PFS to reduce the friction on the patella. Many physical therapists are trained in the McConnell method of taping of the knee. Some patients report reduction of pain when wearing the tape. Some individuals report that the taping allows them to complete more functional quadriceps-strengthening activities without anterior knee pain. If successful, the physician or physical therapist can teach the patient self-taping techniques to use at home.
Proper footwear also is important for individuals with PFS. The physical therapist can evaluate the patient's biomechanics and recommend proper shoes and orthoses, which in turn can lessen knee pain.
Foot orthoses are often of benefit in returning the subtalar joint to a nearly neutral position; this reduces foot pronation, thereby decreasing rotational forces in the tibia that affect tracking of the patella during locomotion.8 Improvement in quality of life measures has been demonstrated following provision of custom orthoses to individuals with PFS and excessive foot pronation.
One study compared the effectiveness of off-the-shelf foot orthoses in the treatment of PFS pain with that of either flat inserts or physical therapy; the report also investigated whether the combined use of orthoses and physical therapy is more effective than the employment of physical therapy alone.8 The prospective, single-blind, randomized trial utilized 179 patients (including 100 women) between ages 18 and 40 years.
By 6 weeks, patients using orthoses had experienced greater improvement than had persons using flat inserts, but the orthotic group had experienced no significant difference in improvement over patients treated with physical therapy or with a combination of orthoses and physical therapy. By 52 weeks, a significant improvement in patellofemoral pain had occurred in all of the patient groups.
Soft knee braces may also be of benefit to patients with PFS. Bracing involves control of the tracking position of the patella and restriction of full knee flexion. Braces vary in the manner in which the patella is restricted (eg, patellar window, patellar bar, patellar horseshoe), but they accomplish the same theoretical result. Braces that are tightly applied directly over the patella should be avoided, because they actually increase patellofemoral pressures and may exacerbate the condition.
Recommend a change in activity level or the ergonomics of the offending activity until the symptoms of patellofemoral syndrome are under control. Activities that require repetitive squatting are a good example. The task or sport may need to be modified to reduce the frequency of squatting, or the patient may need to choose an alternate occupation or recreational activity. Occupational therapists can be of assistance when reviewing the ergonomics of the environment in which symptoms occur with individual patients.
Introducing alternative recreational pursuits and means of fitness may be of benefit in alleviating symptoms of patellofemoral syndrome when conservative measures are not effective. Modifications in recreational pursuits may need to be only temporary measures if other conservative measures are effective.
Most symptoms of patellofemoral syndrome resolve with simple measures. As with many exercise routines, patients often fail to adhere to the exercise prescription, producing treatment results that appear to be refractory but which are actually caused by the fact that the therapeutic approach has not been given a fair trial. Follow-up studies suggest that more than 95% of persons who are compliant with treatment have results that are acceptable or better.
Surgical intervention for patellofemoral syndrome usually is in the form of arthroscopic evaluation followed by release of the lateral attachments of the patella. Most authors agree that surgical treatment rarely is indicated. Arthroscopy has been cited as assisting the physician with clinical diagnoses; however, the visualization procedure, in and of itself, does not significantly help the symptoms of patellofemoral pain.9
Management of patellofemoral syndrome overlaps many specialties. When necessary, consider consultation to answer specific questions regarding refractory response to treatment or optimization of treatment approaches.
Knee pain secondary to defined degenerative changes may be relieved by injecting the joint with steroid or synthetic hyaluronic acid. Such management of patellofemoral syndrome is rare. Injection may be used when many symptoms result from disruption of the joint surface and when all other reasonable measures have failed.
Two approaches to medicating symptoms of patellofemoral syndrome are recognized. These approaches are administration of analgesic medication and administration of nonsteroidal anti-inflammatory drugs (NSAIDs). Analgesics commonly are restricted to acetaminophen or aspirin. The choices of NSAIDs available for management of joint pain are expanding continuously. Consider tolerance of medication (which may result in epigastric distress), prior history of gastric ulceration, renal disease, possible interaction with other medications, and cost. The NSAIDs all have similar efficacy, but changes in formulation have been made to reduce the frequency of adverse effects. Selective cyclooxygenase 2 (COX-2) inhibitors have fewer gastrointestinal adverse effects.
No NSAID has been found to be more effective in treating symptoms of patellofemoral syndrome than any other, although tolerances of NSAIDs vary between individuals. Listed below are the commonly used NSAIDs. These NSAIDs are used predominantly in the adult population. Except for the COX-2 NSAIDs, most have similar adverse effect profiles, and most have the same effect on prostaglandins.
Inhibits prostaglandin synthesis by decreasing activity of enzyme cyclo-oxygenase, which in turn decreases formation of prostaglandin precursors.
25 mg PO bid/tid; if well tolerated, increase by 25 or 50 mg at weekly intervals until satisfactory response is obtained or total daily dose of 150-200 mg is reached; higher doses generally do not increase effectiveness
<12 years: Not established
>12 years: Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; do not administer into CNS; patients with peptic ulcer disease, recent GI bleeding or perforation, or renal insufficiency; those at high risk of bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; low white blood cell counts occur rarely and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if persistent leukopenia, granulocytopenia, or thrombocytopenia occurs
Inhibits prostaglandin synthesis by decreasing activity of the enzyme cyclo-oxygenase.
The decreased activity of cyclo-oxygenase results in decreased formation of prostaglandin precursors, which in turn results in reduced inflammation.
200-400 mg PO q6-8h prn; not to exceed 1200 mg/d
Not established
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; do not administer into CNS; patients with peptic ulcer disease, recent GI bleeding or perforation, or renal insufficiency; those at high risk of bleeding
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; low white blood cell counts occur rarely and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if persistent leukopenia, granulocytopenia, or thrombocytopenia occurs
May inhibit cyclo-oxygenase enzyme, which in turn inhibits prostaglandin biosynthesis.
These effects may result in analgesic, antipyretic, and anti-inflammatory activities.
200-300 mg/d PO divided bid/qid
Not established
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Category D in third trimester of pregnancy; acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug
DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
200-400 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d
<6 months: Not established
6 months to 12 years: 4-10 mg/kg/dose PO tid/qid
>12 years: Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy
Rapidly absorbed. Inhibits prostaglandin synthesis. Metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation.
25-50 mg PO bid/tid
75 mg SR PO bid; not to exceed 200 mg/d
1-2 mg/kg/d divided PO bid/qid; not to exceed 4 mg/kg/d or 150-200 mg/d
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; GI bleeding or renal insufficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur (discontinue if persistent leukopenia, granulocytopenia, or thrombocytopenia occurs)
For relief of mild to moderate pain and inflammation. Small dosages initially are indicated in small and elderly patients and in those with renal or liver disease.
Doses over 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient for response.
25-50 mg PO q6-8h prn; not to exceed 300 mg/d
<3 months: Not established
3 months to 12 years: 0.1-1 mg/kg PO q6-8h
>12 years: Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy
Nonacidic NSAID rapidly metabolized after absorption to a major active metabolite that inhibits cyclo-oxygenase enzyme, which in turn inhibits pain and inflammation.
1-2 g PO qd
Not established
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; active peptic ulceration, hepatic impairment
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Category D in third trimester of pregnancy; elderly may require lower doses; caution in those with hepatic and renal impairment
For relief of mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase, which results in a decrease of prostaglandin synthesis.
500 mg PO followed by 250 mg q6-8h; not to exceed 1.25 g/d
<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Category D in third trimester of pregnancy; acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug
For relief of mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase, which is responsible for prostaglandin synthesis.
600-1200 mg PO qd; not to exceed 1800 mg/d
Not established
Increases toxicity of anticoagulants, aspirin, and diuretics
Documented hypersensitivity; history of GI disease, cardiac failure, renal or hepatic dysfunction, or bleeding disorders
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Category D in third trimester of pregnancy; may cause dizziness, indigestion, nausea, and abdominal cramps
Decreases activity of cyclo-oxygenase, which in turn inhibits prostaglandin synthesis. These effects decrease formation of inflammatory mediators.
10-20 mg/d PO qd
0.2-0.3 mg/kg/d PO qd; not to exceed 15 mg/d
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; active GI bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur (discontinue if persistent leukopenia, granulocytopenia, or thrombocytopenia occurs)
Decreases activity of cyclo-oxygenase, which in turn inhibits prostaglandin synthesis. Results in a decreased formation of inflammatory mediators.
150-200 mg PO bid or 300-400 qd; not to exceed 400 mg/d
Not established
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; patients in whom aspirin, iodides, or other NSAIDs induce hypersensitivity; GI bleed; renal insufficiency
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in preexisting renal disease or compromised renal perfusion; low white blood cell counts occur rarely and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if persistent leukopenia, granulocytopenia, or thrombocytopenia occurs; caution in those with anticoagulation defects and in those receiving anticoagulant therapy
Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is clearly less with COX-2 inhibitors than with traditional NSAIDs. Ongoing analysis of cost avoidance of GI bleeds will further define the populations that will find COX-2 inhibitors the most beneficial.
Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme, induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus GI toxicity may be decreased. Seek lowest dose of celecoxib for each patient.
200 mg/d PO qd; alternatively, 100 mg PO bid
Not established
Coadministration with fluconazole may cause increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration of celecoxib with rifampin may decrease celecoxib plasma concentrations
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Category D in third trimester of pregnancy; may cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, conditions predisposing to fluid retention, severe heart failure, and hyponatremia because celecoxib may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in the presence of existing controlled infections; evaluate symptoms and signs suggesting liver dysfunction
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patellofemoral syndrome, knee pain, patella, patellofemoral, knee cartilage, patellofemoral pain syndrome, pain behind knee, patellofemoral joint, kneecap pain, patella femoral, patella pain, patella femoral syndrome, PFPS, anterior knee pain, chondromalacia patella
Patrick J Potter, BSc, MD, FRCP(C), Associate Professor, Physical Medicine and Rehabilitation, The University of Western Ontario; Consulting Staff, Department of Physical Medicine and Rehabilitation, St Joseph's Health Care Centre
Patrick J Potter, BSc, MD, FRCP(C) is a member of the following medical societies: American Paraplegia Society, Canadian Association of Physical Medicine and Rehabilitation, Canadian Medical Association, College of Physicians and Surgeons of Ontario, Ontario Medical Association, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.
Keith AJ Sequeira, MD, Associate Director of Spinal Cord Medicine, Assistant Professor, Department of Physical Medicine and Rehabilitation, Parkwood Hospital, University of Western Ontario
Disclosure: Nothing to disclose.
Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM, President and Director, Georgia Pain Physicians, PC; Clinical Associate Professor, Department of Physical Medicine and Rehabilitation, Emory University School of Medicine
Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, American Medical Association, International Association for the Study of Pain, Physiatric Association of Spine, Sports and Occupational Rehabilitation, and Texas Medical Association
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD, FAAPMR, FAAEM is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.
Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.
Consuelo T Lorenzo, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Alegent Health Care, Immanuel Rehabilitation Center
Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.
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