Tuesday, July 13, 2010

Lumbar facet pain & facet pain in Osteoarthritis of lumbar spine

Lumbar facet pain (1):

Lumbar facet joints are a well recognized source of low back pain and referred pain in the lower extremity in patients with chronic low back pain. Conventional clinical features and other non-invasive diagnostic modalities are unreliable in diagnosing lumbar zygapophysial joint pain.
However with invasive diagnostic technique the chance of false positive result may be up to 47% but these controlled diagnostic studies have shown the prevalence of lumbar facet joint pain in 27% to 40% of the patients with chronic low back pain without disc displacement or radiculitis.

Facet joint surface area in LBA (2):

Facet joint surface area is an important parameter for understanding facet joint function and pathology. Otsuka et al investigated lumbar facet joint surface area in relation to age and the presence of chronic low back pain.
In this invivo study the following things are found:
1. The lumbar facet area was significantly greater at the inferior lumbar levels and also increased with age.
2. There is age-related increase in the facet joint surface was observed more in the low back pain subjects compared with asymptomatic subjects.
3. The increase in the area of the facet joint surface is probably secondary to increased load-bearing in the lower lumbar segments and facet joint osteoarthritis.

Facet joint dimension in OA of lumbar spine (3):

The FJ play an important role in load transmission; they provide a posterior load-bearing helper, stabilizing the motion segment in flexion and extension and also restricting axial rotation.
The capsule of the FJ, subchondral bone, and synovium are richly innervated and can be a potential source of the low back pain.
Degenerative changes: Degenerative changes in the FJ comprise cartilage degradation that leads to the formation of focal and then diffuse erosions with joint space narrowing, and sclerosis of the subchondral bone.
Risk factors for lumbar FJ osteoarthritis include advanced age, relatively more sagittal orientation of the FJ, and a background of intervertebral disk degeneration.

Facet joint tropism (dissimilar facing and/or size of a vertebra's zygapophyseal joints) in facet joint OA (4):

One cross sectional study tried to find out association between lumbar facet joint osteoarthritis (OA), degenerative spondylolisthesis (DS) and facet orientation and tropism which remains unclear. This study found:
1. Facets with OA were more sagittally oriented than those without OA, which is significant observed at L4-L5 spinal level.
2. Facet tropism did not show an association with facet joint OA at any spinal level.
3. Facet orientation was significantly associated with DS, however, facet tropism showed no association with DS.
This study confirms a significant association between sagittal orientation and OA of the lumbar facet joints at L4-L5 and DS. Facet tropism was not associated with occurrence of facet joint OA or DS.

Does osteoarthritis of the lumbar spine cause chronic low back pain of facet origin? (5)

According to may authorities OA it self is a painless condition which is readily exemplified in hip joint. However, according to Borenstein Osteoarthritis of the lumbar spine does cause low back pain.
The lumbar spine is a common location for osteoarthritis. The axial skeleton demonstrates the same classic alterations of cartilage loss, joint instability, and osteophytosis characteristic of symptomatic disease in the appendages.
Despite these similarities, in our discussion’s context, questions remain regarding the lumbar spine facet joints as a source of chronic back pain.
The facet joints undergo a progression of degeneration that may result in pain. The facet joints have sensory input from two spinal levels that makes localization of pain difficult. Radiographic studies describe intervertebral disc abnormalities in asymptomatic individuals that are associated with, but not synonymous for, osteoarthritis.
Low back pain is responsive to therapies that are effective for osteoarthritis in other locations.


1. Dutta S et al; Pain Physician. 2009 Mar-Apr;12(2):437-60. (Systematic assessment of diagnostic accuracy and therapeutic utility of lumbar facet joint interventions.)

2. Otsuka Y et al; Spine (Phila Pa 1976). 2010 Apr 15;35(8):924-8. (In vivo measurement of lumbar facet joint area in asymptomatic and chronic low back pain subjects.)

3. Kalichman L et al; Semin Arthritis Rheum. 2007 Oct;37(2):69-80. Epub 2007 Mar 26.
4. Kalichman L et al; Spine (Phila Pa 1976). 2009 Jul 15;34(16):E579-85. Facet orientation and tropism: associations with facet joint osteoarthritis and degeneratives.

5. Borenstein D; Curr Pain Headache Rep. 2004 Dec;8(6):512-7. (Does osteoarthritis of the lumbar spine cause chronic low back pain?)

Monday, July 12, 2010

Facet pain: Short falls of inteventional & non-interventional conservative management

How facet joint pain manifests?
Facet or zygapophysial joints are considered to be common sources of chronic spinal pain. In addition to causing localized spinal pain, facet joints may refer pain to adjacent structures. Cervical facet joint pain may radiate to the head, neck, and shoulders. Thoracic facets may produce paraspinous mid-back pain with neuralgic characteristics; and lumbar facet joints may refer pain to the back, buttocks, and proximal lower extremities.
Referred pain may assume a pseudoradicular pattern, making the underlying diagnosis difficult to confirm, without the use of diagnostic blocks.
Joint innervation:
Facet joints are well innervated by the medial branches of the dorsal rami. Neuroanatomic, neurophysiologic, and biomechanical studies have demonstrated free and encapsulated nerve endings in facet joints, as well as nerves containing substance P calcitonin gene-related peptide; facet joint capsules contain low-threshold mechanoreceptors, mechanically sensitive nociceptors and silent nociceptors ; and lumbar and cervical facet joint capsules can undergo high strains during spine loading.
Prevalence of facet pain in different areas of spine:
Consistent with criteria established by the International Association for the Study of Pain, facet joints may be a source of chronic pain in 15% to 45% of patients with chronic low back pain; 36% to 60% of the patients with chronic neck pain; and 34% to 48% of the patients with thoracic pain.

Difficulties associated with diagnosis & treatment of facet joint pain:

1. Clinically:
There is no definitive study to support that clinically facet joint pain can be diagnosed. Extension is the most incriminated movement to imply facet joint involvement. According to Van Eerd et al Clinically rotation and retroflexion (extension) are frequently painful or limited.
2. Investigations for facet joint are non-correlative: Direct correlation between degenerative changes observed with plain radiography, computerized tomography, and magnetic resonance imaging and pain has not been proven.
3. Short falls in non-interventional conservative approach: Conservative treatment options for cervical facet pain such as physiotherapy, manipulation, and mobilization, although supported by little evidence, are frequently applied before considering interventional treatments.
4. Short falls in interventional conservative approach: Facet joint pain may be managed by intraarticular injections, medial branch blocks, and neurolysis of medial branch nerves.

Evidence level:

a. Bogduk: A recent narrative review by Bogduk suggested that intraarticular facet joint injections were no better than placebo for chronic lumbar spine pain.
b. Slipman et al: Review of the evidence for the use of zygapophysial injections and radiofrequency denervation in the treatment of low back pain, found limited evidence for intraarticular injections in the lumbar spine and moderate evidence for radiofrequency neurotomy in the lumbar spine.
c. Boswell et al: Systematic review of therapeutic facet joint interventions for 3 regions of the spine, showed moderate evidence for lumbar intraarticular facet joint injections for short-term improvement, but only limited evidence for long-term improvement. The evidence was negative for cervical intraarticular facet joint injections. The evidence was moderate for cervical and lumbar medial branch blocks with local anesthetics and steroids. The evidence for pain relief with radiofrequency neurotomy of medial branch nerves was moderate to strong for cervical and lumbar regions.
d. European guidelines for the management of chronic nonspecific low back pain: (Analysis of data from January 1995 to November 2002) Concluded that intraarticular facet joint injections were ineffective in managing chronic low back pain. In this limited literature review, they showed no significant effectiveness of medial branch blocks.
The European guidelines concluded that there was conflicting evidence that radiofrequency denervation of the facet joints is more successful than placebo for eliciting short-term or long-term improvements in pain or functional disability in mechanical chronic low back pain. They also indicated that there was limited evidence that intraarticular denervation of the facet joints is more effective than extraarticular denervation.
e. Geurts et al: Concluded that there was moderate evidence that radiofrequency lumbar facet denervation was more effective for chronic low back pain than placebo, and there was only limited evidence for effectiveness of radiofrequency neurotomy for chronic cervical zygapophysial joint pain after flexion/extension injury.
f. Manchikanti et al: Evaluated medial branch neurotomy for the management of chronic spinal pain utilizing the Agency for Healthcare Research and Quality (AHRQ) criteria with inclusion of randomized and observational reports, and concluded that there was strong evidence for short-term relief and moderate evidence for longterm relief of facet joint pain.
g. Niemisto et al: in a systematic review of radiofrequency denervation for neck and back pain within the framework of Cochrane Collaboration Back Review Group, concluded that there was limited evidence that radiofrequency denervation had a positive short-term effect on chronic cervical zygapophysial joint pain, and a conflicting short-term effect on chronic low back pain.

1. van Eerd M et al; Pain Pract. 2010 Mar;10(2):113-23. Cervical facet pain.
2. Boswell MV et al; Pain Physician 2007; 10:229-253

Monday, July 5, 2010

Facet pain: Prevalence, diagnosis & features

Clinical examination is not an efficient method of diagnosis of spine pain!!!

Pain emanating from various structures of the spine is a major cause of chronic pain problems. Linton et al estimated the prevalence of spinal pain in the general population as 66%, with 44% of patients reporting pain in the cervical region, 56% in the lumbar region, and 15% in the thoracic region. Manchikanti et al reported similar results. Despite the high prevalence of spinal pain, it has been suggested that a specific etiology of back pain can be diagnosed in only about 15% of patients with certainty based on clinical examination alone (2).

Prevalence of facet joint pain & Z joint pain:
In the 1990s precision diagnostic blocks were developed, including facet joint blocks, provocative discography, and sacroiliac joint blocks. Facet joints have been implicated as a cause of chronic spinal pain in 15% to 45% of patients with chronic low back pain, 48% of patients with thoracic pain, and 54% to 67% of patients with chronic neck pain (2).

Out of 500 screened patients by Manchikanti et al (2004) the prevalence of facet joint pain in patients with chronic cervical spine pain was 55%, with thoracic spine pain was 42%, and in with lumbar spine pain was 31%.

Based on the literature, in the United States, in patients without disc herniation, lumbar facet joints account for 30% of the cases of chronic low back pain, sacroiliac joints account for less than 10% of these cases, and discogenic pain accounts for 25% of the patients (1).

Based on the literature available in the United States, cervical facet joints account for 40% to 50% of cases of chronic neck pain without disc herniation, while discogenic pain accounts for approximately 20% of the patients (1).

The Z (zygapophysial) joint pain:
Facet joints are entertained first in spine pain diagnosis because of their commonality as a source of chronic low back pain followed by sacroiliac joint & disc as the last step (1).

Bogduk noted that a reductionist approach to chronic low back pain requires an anatomical diagnosis. Bogduk identified 4 factors necessary for any structure to be deemed a cause of back pain:

1. nerve supply to the structure
2. ability of the structure to cause pain similar to that seen clinically in normal volunteers
3. structure's susceptibility to painful diseases or injuries
4. demonstration that the structure can be a source of pain in patients using diagnostic techniques of known reliability and validity

The facet or zygapophysial joints of the spine are well innervated by the medial branches of the dorsal rami. Facet joints have been shown capable of causing pain in the neck, upper and mid back, and low back with pain referred to the head or upper extremity, chest wall, and lower extremity in normal volunteers. They also have been shown to be a source of pain in patients with chronic spinal pain using diagnostic techniques of known reliability and validity. Conversely, the reliability of physical examination & medical imaging provides little useful data in identifying facet joint pain diagnosis.
Summary of symptoms of facet pain may include the following:

1. Acute episodes of lumbar and cervical facet joint pain are typically intermittent, generally unpredictable, and occur a few times per month or per year.
2. Most patients will have a persisting point tenderness overlying the inflamed facet joints and some degree of loss in the spinal muscle flexibility (called guarding).
3. Typically, there will be more discomfort while leaning backward than while leaning forward.
4. Low back pain from the facet joints often radiates down into the buttocks and down the back of the upper leg. The pain is rarely present in the front of the leg, or rarely radiates below the knee or into the foot, as pain from a disc herniation often does.
5. Similarly, cervical facet joint problems may radiate pain locally or into the shoulders or upper back, and rarely radiate in the front or down an arm or into the fingers as a herniated disc might.

References: 1. Manchikanti L et al; Pain Physician. 2009 Jul-Aug; 12(4):E225-64. (An algorithmic approach for clinical management of chronic spinal pain.) 2. Manchikanti L et al; BMC Musculoskeletal Disorders 2004, 5:15doi:10.1186/1471-2474-5-15. (Prevalence of facet joint pain in chronic spinal pain of cervical, thoracic, and lumbar regions.)

Friday, July 2, 2010

Anterior Knee Pain & It's primary treatment

I. Introduction
o other causes of anterior knee pain, besides primary PF pain
o differential diagnosis may be more difficult than anticipated owing to interrelationships
o realize that more than one problem may exist concurrently
o a small acute injury may stir up an underlying mechanical anomaly that had previously been painfree; daily activity with a malalignment may be enough to perpetuate symptoms

II. Plica
o embryologically the knee is formed by the fusion of three synovial compartments and the intervening synovial tissues resorbed. The plicae are synovial remnants of these synovial tissues
o intrapatellar plica (ligamentus mucosum) most common and runs parallel to the ACL; it has no clincial significance
o suprapatellar second most common: acts as a tethering band in the superior portion of the quadriceps bursa and may separate it into two separate segments
o medial plica least common, but probably produces the most symptoms; runs distally along the medial aspect of the knee from the level of the superior pole of the patella to insert into the medial fat pad
o incidence of medial plica ranges from 9.1-50%
o as knee is passively flexed form 30-60°, this plica can be seen to slide over the MFC beneath the patella; ER of tibia causes wedging of the plica between the medial facet and the MFC
o generally tender one fingerbreadth proximal to the distal pole of the patella, medially
o symptoms increased with repetitive activities

o painfree stretching
o LE strengthening, avoiding repetitive activities
o work in painfree range
o occasional injection and/or surgical resection

III. Prepatellar bursitis
o common in wrestlers
o cause: either acute trauma from a single blow or chronic irritation
o if acute, often the result of small blood vessel rupture, resulting in aspiration of blood
o if chronic, likely the result of chronic inflammation, and aspiration will not contain blood
o in wrestlers, probably a combination of chronic and acute onset
o chronic bursitis much more difficult to treat; has a high recurrance rate; surgery reveals a thickened bursal wall
o high incidence of septic bursitis (>95% in Myshnyk's series); staphylococcus aureus most common cause
o repeated aspiration of chronic bursitis discouraaed owing to the high rate of infected bursae
o swelling is superficial to patella
o blood workup not particularly helpful in making diagnosis of septic bursitis

o cortisone injection not helpful in most cases
o aspiration (limited)
o consider HVPC
o maintain CV, ROM
o maintain quad strength without increasing swelling
o consider pool therapy
o kneepad when returning to kneeling activity

IV. Iliotibial band friction syndrome
o commonly seen in runners, bikers
o symptoms can be seen at hip, knee or both
o hip pain generally over the greater trochanter, and involves both the TFL and gluts
o knee pain is over LFC
o at 0°, ITB is anterior to LFC; as the knee passes 30° of flexion, it passes across the LFC to become posterior
o diagnosis is made on history, palpation and special test at knee
o must assess alignment and treat underlying cause; varus or valgus knee alignment, and pronation can predispose to symptoms at knee
o tight ITB (+ Ober test) and tight hamstrings are diagnostic and form basis for treatment program
o assess patella for related problems

o ice
o activity modification
o treat malalignment
o flexibility
o strength, posture, predisposing habits (running surface)
o surgery used for chronic cases unresponsive to conservative management; consist of making a "window" in ITB in area of irritation

V. Fat pad impingement
o rare problem, generally not painful
o may be related to patellar malalignment (AP tilt)
o correct underlying cause
o tender medial and/or lateral to patellar tendon on fat pad
o quad setting (screw home mechanism) hurts
o thickening of fat pad produces additional irritation as problem progesses
o can be chronic or acute

o correction of underlying cause
o ice
o HVPC, ionto/phonophoresis
o cortisone injection (NOT into the tendon)
o surgical resection

VI. Osgood-Schlatter's disease
o originally described by Osgood & Schlatter in 1903
o tibial tuberosity apophysitis - result of tensile forces
o self-limiting problem with pain & enlargement of the tibial tuberosity
o incidence for those in sports = 21%, those uninvolved = 4.5% for an overall incidence of 12.9%
o Males:females = 1.5:1 to 4:1 (depending upon who you ask)
o common in athletes with a past history of Sever's disease
o average age of onset = 13.1
o bilateral in 56%
o etiology is likely the result of avulsion of a portion of the developing ossification center and overlying hyaline cartilage
o inflammatory changes occur seconday to micro-avulsion fractures of the tuberosity
o S&S: dull ache increased with running and jumping; local redness and point tenderness
o x-ray may demonstrate soft tissue swelling anterior to tibial tuberosity

o symptomatic
o ice
o stretching, strengthening
o activity modification
o rarely immobilize

Complication: tibial tuberosity fracture; rare, requires surgical fixation

VII. Sinding-Larsen-Johansson disease
o similar to Osgood-Schlatter, but symptoms present at the inferior pole of the patella
o age 10-13
o no history of trauma
o hypothesize that etiology is avulsion of the periosteum at inferior pole of the patella with resultant ossification
o seen with repetitive traction at the patellar tendon attachment site
o knee pain exacerbated by running, stairs and kneeling
o may have concomitant Osgood-Schlatter
o tender over inferior pole
o x-rays demonstrate irregular calcification at inferior pole

o similar to Osgood-Schlatter

VIII. Patellar tendinitis
o Blazina referred to patellar tendinitis and quadriceps tendinitis as "jumper's knee" in a classic 1973 article; this same paper described the "Blazina scale" of pain and functional impairment
o focus here on patellar tendinitis as quadriceps tendinitis is rare (usually over age 40)
o very difficult problem to treat; patients often wait until problem is advanced before seeking treatment
o specific point tenderness at distal pole of patella (must tip patella to get at distal pole)

Blazina's phases:
Phase I: Pain after activity only. No undue functional impairment.
Phase II: Pain during and after activity. Still able to perform at a satisfactory level.
Phase III: Pain during and after activity and more prolonged. Patient has progressively increasing difficulty in perfoming at a satisfactory level.

Stages of healing:
o cell mobilization
o ground substance proliferation
o collagen protein synthesis
o final organization

o controlled activity
o modalities
o medications
o exercise

Principles of eccentric exercise program:
o muscle length
o intensity
speed of contraction

Optimal loading:
o must try to mimick demands of their activity

About PACE

Progressively Accelerating Cardiopulmonary Exertion (PACE)
– A More Effective Alternative to Modern Exercise Prescriptions

This following is an article from a news letter from Dr. Al Sears (USA)

Ask a personal trainer, pick up a fitness magazine, or consult a medical organization and you will see the same fitness-training concepts. These modern exercise prescriptions will be cardiovascular endurance training (CVE) or “cardio” for short, “aerobic” exercises often given in hour-long group classes, and weight training on machines or with free-weights. These forms of exercise, while promoted by a majority of physicians and fitness professionals, fail to bring about the physiological adaptations necessary for a healthy and vital cardiopulmonary system and may leave patients at a heightened risk of mortality.

The key failing of both cardiovascular endurance training and aerobics classes is the focus on exercise duration at the expense of intensity. In order to achieve the recommended durational benchmarks (typically a minimum of 30 minutes), exercise participants are forced to reduce exercise intensity into the low to moderate range. Yet the data demonstrate an unequivocal advantage of exercise intensity over duration. For example, in a study published in the Archives of Internal Medicine, 8896 recreational runners were asked to report their average running duration and intensity. The results illustrated that increased intensity was significantly associated with lower blood pressure, lower triglycerides, lower CHOL/HDL ratios, lower BMIs, and lower waist, hip, and chest circumferences. Exercise duration had no effect on these parameters.1 Similarly, data from the Harvard Alumni Health Study demonstrated a significant inverse relationship between intense physical activity and mortality,2 with low-intensity exercise failing to decrease the risk of all-cause mortality. The Harvard data also revealed that long-duration exercise did not reduce the risk of coronary heart disease. High-intensity exercise, however, resulted in a decreased risk of CHD.3

In addition to failing to protect against all-cause mortality and CHD, non-vigorous durational exercise also fails to challenge the heart and lungs to achieve and maintain the capacity necessary to respond to sudden and unexpected increases in demand.4,5 This problem worsens with aging because both lung size and cardiac output decline with age. Of even greater concern is the evidence that repeated durational challenges with low-intensity exercise may actually reduce cardiac function.6 These findings are of paramount importance in light of the fact that even moderate reductions in cardiopulmonary capacity dramatically increase the risk of disease progression and mortality.7,8

As health-care professionals, we must recognize that exercise is not all one thing. Different types of exercise challenges produce different, even opposite, physiological adaptations. It is clear that exercise intensity is the key to promoting good cardiopulmonary capacity and in combating modern deconditioning and age-related losses. We must also recognize, however, that the average deconditioned patient is not capable of safely or effectively participating in most high-intensity training programs. We can find a solution to this problem and the key to optimal cardiovascular conditioning at any age in two concepts: Progressivity and Acceleration. Progressivity in exercise refers to a regular and consistent increase in the intensity of demands placed on the cardiovascular system. Progressivity takes into consideration the baseline fitness level of each patient and allows safe incremental increases in intensity, regardless of the current level of conditioning. Acceleration refers to training the cardiovascular system to respond more quickly to increases in demands, as well as reducing the amount of time it takes for the heart and lungs to recover from exertion. Primary research data will be presented suggesting that a program of Progressively Accelerating Cardiopulmonary Exertion (PACE) conditions the heart and lungs to build larger reserve capacities to respond adequately to large and sudden increases in demands. PACE is the first and only program to offer the benefits of improved cardiovascular capacity to patients of all ages and all fitness levels.

1) Understand how modern exercise programs fail to contribute to improved cardiopulmonary fitness and how they may be increasing the risk of mortality.
2) Understand the importance of cardiopulmonary capacity and how it relates to longevity.
3) Understand the key components of the PACE program and how it provides a safe and effective way to improve cardiopulmonary capacity and decrease cardiopulmonary aging and disease and subsequent mortality.


1 Williams P. Relationships of heart disease risk factors to exercise quantity and intensity. Arch Intern Med. 1998;158(3):237-245.
2 Lee IM, Hsieh, CC, Paffenparger, RS Jr. Exercise intensity and longevity in men. The Harvard Alumni Health Study. JAMA. 1995;273(15):1179-1184
3 Lee IM, Sesso HD, Paffenparger, RS Jr. Physical activity and coronary heart disease risk in men: does the duration of exercise episodes predict risk? Circulation. 2000;102(9): 981-986.
4 Baily S, Wilkerson DiMenna F, Jones A. Influence of repeated sprint training on pulmonary O2 uptake and muscle deoxygenation kinetics in humans. J Appl Physiol. 2009 Jun;106(6):1875-87.
5 Adachi H, Koike A, Obayashi T, et al. Does appropriate endurance exercise training improve cardiac function in patients with prior myocardial infarction? Eur Heart J. 1996 Oct;17(10):1511-21.
6 Oberman, A, Fletcher F, Lee J, et al. Efficacy of high-intensity exercise training on left ventricular ejection fraction in men with coronary artery disease (the Training Level Comparison Study). Am J Cardiol. 1995 Oct 1;76(10):643-7.
7 Schunemann H, et al. Pulmonary function is a long-term predictor of mortality in the general population: 29-year follow-up of the Buffalo Health Study. Chest. 2000 Sep;118(3):656-64.
8 Kannel WB, Seidman JM, Fercho W, Castelli WP. Vital Capacity and Congestive Heart Failure. The Framingham Study. Circulation. 1974;49(6):1160-1166.