Friday, December 3, 2010

Autonomy and the future of physiotherapy.

Link:

http://www.thefreelibrary.com/Autonomy+and+the+future+of+physiotherapy.-a0181366670

Either follow the link. If the link is not working properly then copy the above link in a web browser.

Then type search.

I assure you this is a topic to ponder.

Friday, October 22, 2010

Respiratory muscle stretch gymnastics (RMSG) a review of PUBMED from 1996-2002


Preamble:
RMSG can be called an exclusive Japanese contribution to our knowledge pool. First invented & later on further researched by Japanese researchers only. We found 6 papers by search of PUBMED with the search word “Respiratory muscle stretch gymnastics”. Abstract plus search categories found 3 full articles out of 6 mentioned journals listed in PUBMED. This article is a small review of those 6 articles.

What is RMSG?

RMSG is a group of stretching exercises sequentially performed to stretch specific muscles involved in respiration. There are 5 different muscle groups targeted in RMSG.
Respiratory Muscle Stretch Gymnastics RMSG was designed to be easy to learn and to perform at home on a daily basis, and to stretch either the inspiratory intercostal muscles during inspiration or the expiratory intercostal muscles during expiration, in attempt to reduce chest wall stiffness.

Who devised it first?

Yamanda M et al of Japan devised it first time in 1996 and they applied it on 13 COPD patients for 4 week duration whose mean FEV1 is 1.24 liters.

What was the initial report of Ymanda et al?

Out of above mentioned 13 patients 12 completed the 4 week schedule. They practiced the stretching thrice a day for 4 weeks. They claimed that Respiratory muscle stretch gymnastics is useful in pulmonary rehabilitation.

They found following changes in the spirometry based & non-spirometry based parameters after the training:

1. FRC, TLC & RV (residual capacity): Significantly decreased
2. 6- min walk distance: Increased
3. Dyspnoea after 6- min walk: Significantly decreased
4. Quality of Life (QOL): Significantly improved (Measured with the Chronic Respiratory Disease Questionnaire of Guyatt, et al)

Further studies on RMSG:

2nd published study – 1998

Onodera A et al applied a group of exercises including RMSG for chronic respiratory failure due to pulmonary emphysema. The entire group consist of pursed lip breathing, diaphragmatic breathing, respiratory muscle stretch gymnastics, and walking with synchronized breathing.

15 inpatients completed the study for 3 weeks. The dependant variables measured changed in the following way
1. VAS measured dyspnea at the end of a 6-minute walk before and after the program: Decreased significantly
2. Functional exercise capacity measured by 6-minute walking distance: Increased significantly
But maximal exercise capacity, endurance time measured by incremental treadmill test did not improve.
3. TLC & RV: Decreased significantly

This study concluded that
This combined program relieves dyspnea, increases functional exercise capacity, and decreases TLC and RV on patients with chronic respiratory failure due to pulmonary emphysema.

3rd published study – 1999

Ito M et al applied diaphragmatic breathing (DB) & RMSG separately on 16 elderly COPD patients and studied the immediate changes by them. The intervention was in the flowing order DB was performed for 10 minutes in supine position. For RMSG, 5 patterns were repeated 10 times each.

Following respiratory variables are studied after 20 minutes of gap between the end of the exercises & measurement.
1. Expiratory time: After RMSG there was a significant overall prolongation in expiratory time which was not marked after DB.
2. Minute ventilation (MV), CO2 output, respiratory gas exchange ratio, end tidal O2 fraction, end tidal CO2 fraction and tidal diaphragmatic volume: After DB there is over all decrease in the above said parameter but not seen after RMSG.
This study concluded that RMSG may have a beneficial effect on the respiratory pattern but DB may provoke post-hyperventilation hypoxemia.

4th published study – 2000

Miyahara et al studied the impact of RMSG and cycle ergometer exercise training on 18 COPD inpatients in a before-after study. The pulmonary rehabilitation program was carried out 5 days per week for 3 weeks.
Dependant variables included: PFT (Pulmonary function tests), incremental ergometer exercise test 6-min walking test, and a quality of life assessment by the Chronic Respiratory Questionnaire.

The changes are as follows:
1. VO2max (indicator of maximal exercise capacity)- No increase. But 6-min walking distance (indicator of functional exercise capacity)- increase significantly.
2. QOL improves significantly in terms of dyspnea, fatigue, and emotional state.
This study reveals a combined RMSG and cycle ergometer exercise training even for a 3-week program may be beneficial for COPD patients to increases in functional exercise capacity without an increase in maximal exercise capacity, are helpful for reducing dyspnea and improving QOL in patients with COPD.

5th published study – 2002

Minoguchi et al did a cross over trial between RMSG and inspiratory muscle training (IMT) patients with chronic obstructive pulmonary disease (COPD) to know which one is a better pulmonary rehabilitation method.
They concluded RMSG may have clinically significant benefits, which may be somewhat different from the benefits of IMT, in patients with COPD.
The compared dosages
IMT = 2 sessions of 10 minutes of training at 30% of PImax, daily × for 4 weeks and RMSG = 3 sessions of 5 RMSG patterns 4 times each, daily × for 4 weeks
* cases ware assigned in randomized order
* for cross over 4 week wash out period was given

This study found following effects of RMSG & IMT
1. PImax : RMSG has no effect on PImax but IMT increases PImax
2. Chest expansion (CE): Both IMT & RMSG show similar increases in CE.
3. FRC: Significantly decreased (by 158 ml) with RMSG, but not with IMT.
4. VC, FEV1, PEF &arterial blood gases: No significant changes.
5. 6-min walking distance: more significantly increased with RMSG than with IMT.

6th published study – 2002

Aida M et al are the first authors who tried to implement RMSG to alleviate pain in post coronary artery bypass patients. Earlier authors tried to implement RMSG mostly in COPDs.
This study is a randomized control trial with sample size 16 grouped in to 2. All of them exhibited rib cage dominant breathing after median sternotomy for coronary artery bypass grafting (CABG). One group was treated with conventional treatment and another with SMSG.

The finding ware as follows:
1. Expected decrease of spirometric measures like MIP (maximum inspiratory pressure), MEP (maximum expiratory pressure), FRC, FEV1 was small in the group treated with RMSG.
2. RMSG group had significantly reduced pain around both scapulas at discharge.
3. Overall ADL- Increased significantly in RMSG group
4. Profile of mood states (POMS)/Vigor scores, POMS/Tension-Anxiety scores: Scores at discharge for RMSG group were significantly smaller than those preoperatively.
5. 6-minutes walk distance: Significantly increased

RMSG specifically fashioned for post CABG patients approached with mid-sternotomy improves patient participation in exercise therapy and increases exercise capacity by reducing post operative pain, relieving anxiety and tension, and improving ADL.

Composition of RMSG

Five patterns have been used routinely by the clinicians. A brief description of the movements is given below. On the starting day of RMSG rehabilitation, patients learn the 5 patterns by watching a demonstration and by using a pamphlet. At home, the patients performed the 5 stretch patterns 4 times following a order from 1-5.

Pattern 1. Elevating and pulling back the shoulders
As you slowly breath in through your nose, gradually elevate and pull back both shoulders. After taking a deep breath, slowly breathe out through your mouth, relax and lower your shoulders.

Pattern 2. Stretching the upper chest
Place both hands on your upper chest. Pull back your elbows and pull down your chest while lifting your chin and inhaling a deep breathe through your nose. Expire slowly through your mouth and relax.

Pattern 3. Stretching the back muscle
Hold your hands in front of your chest. As you slowly breathe in through your nose, move your hands front wards and down, and stretch your back. After deep inspiration, slowly breathe out and resume the original position.

Pattern 4. Stretching the lower chest
Hold the ends of a towel with both hands outstretched at shoulder height. After taking a deep breath, move your arms up while breathing out slowly. After deep expiration, lower your hands and breathe normally.

Pattern 5. Elevating the elbow
Hold one hand behind your head. Take a deep breath through your nose. While slowly exhaling through your mouth, stretch your trunk by raising your elbow as high as is easily possible. Return to the original position while breathing normally. Repeat the process using the alternate hand behind the head.

Modified RMSG used by Aida M et al for post CABG pain patients:

1. Whole body relaxation
Position: Either lying down on bed or sitting on a chair.
Do: Contract muscles of face, shoulder, back, hand and feet for several seconds, then exhale deeply to relax all the muscles of the body.

2. Bending the neck forward & to both the sides
Position: Sitting on a chair.
Do:
a.Raise the shoulder for 5 seconds, then exhale deeply to relax totally.
b. While pursing the lips- exhale and bend the neck to Rt side to stretch the sternomastoid, then inhale while bringing the neck back to it’s original position. Exhale deeply to relax totally.
c. Repeat the stretch to Lt hand side.

3. Rotating the shoulder (include pectoralis major & trapezius muscles)
Position: Sitting on a chair.
Do:
Gradually rotate the shoulders & scapulas forwards few times, then exhale deeply to relax totally.

4. Stretching the shoulder girdle & tricep brachaii muscle
Position: Sitting on a chair.
Do:
Extend the arms forwards as far as possible and retain the position for 5 seconds.
While exhaling return the arms to the original position and relax totally.

5. Stretching the tricep brachaii & serratus anterior muscles
Position: Sitting on a chair.
Do:
a. While using one hand to protect the wound (of mid sternotomy used for CABG), place the other hand on the the same side shoulder bending it at elbow
b. while inhaling, slowly raise the elbow vertically to extend the serratus anterior muscle under the arm pit.
c. while exhaling deeply, return the arm to the original position and relax totally.
d. Repeat the above said procedures by changing the sides.

Limitation of above said studies:
1. Inadequate sampe size & study duration.
2. Target muscles in stretches described by Aida M seem dubious.
3. Carry over effects not discussed.

References:

1. Aida N et al; J Med Dent Sci. 2002 Dec;49(4):157-70. (Respiratory muscle stretch gymnastics in patients with post coronary artery bypass grafting pain: impact on respiratory muscle function, activity, mood and exercise capacity).
2. Minoguchi H et a; Intern Med. 2002 Oct;41(10):805-12. (Cross-over comparison between respiratory muscle stretch gymnastics and inspiratory muscle training).
3. Miyahara N et al; Acta Med Okayama. 2000 Aug;54(4):179-84. (Effects of short-term pulmonary rehabilitation on exercise capacity and quality of life in patients with chronic obstructive pulmonary disease).
4. Ito M et al; Intern Med. 1999 Feb;38(2):126-32. (Immediate effect of respiratory muscle stretch gymnastics and diaphragmatic breathing on respiratory pattern. Respiratory Muscle Conditioning Group).
5. Onodera A et al; Nihon Kokyuki Gakkai Zasshi. 1998 Aug;36(8):679-83. (Effects of a short-term pulmonary rehabilitation program on patients with chronic respiratory failure due to pulmonary emphysema).
6. Yamada M et al; Nihon Kyobu Shikkan Gakkai Zasshi. 1996 Jun;34(6):646-52. (Clinical effects of four weeks of respiratory muscle stretch gymnastics in patients with chronic obstructive pulmonary disease).




Friday, October 15, 2010

Anticipatory postural adjustment (APA) & Posture



Objective of this review: To provide the reader basic idea of the anticipatory postural adjustments with spinal disorders. Understanding this topic will lead to appreciate the kinetic chain concepts through understanding of basic postural system operation.

Posture & Poise: Posture is a term to describe shape whether good or bad. Poise is either present or absent at any moment so to describe poise as good or bad is to misunderstand its meaning. The term posture is generally accepted to relate to the dynamic relationship of the body segments in activity. Poise is a state; an ability to maintain appropriate muscle tension at all times in both movement and static positions.

A well-balanced structure is supported and mobilised by gravitational forces with minimal effort. Correct posture is considered vital for health and functioning of the internal organs and all bodily functions. A poorly balanced structure requires inappropriate muscular activity to maintain position and initiate movement. This constant state of activity leads to unnecessary contraction to hold a position and impedes functioning. For example, tight muscles around the torso restrict movement of the ribcage and prevent natural breathing.

Ideal ‘plumb-line’ correct posture can also have poor movement patterns. This is because it is not the shape that is important but how it is maintained. A 'correct posture', i.e, one that looks right, can be achieved with totally inappropriate muscular activity. Physiologist Charles Sherrington once described our systems for maintaining posture as the ‘most uncertain and untrustworthy of all’. This is not encouraging when all corrective methods for improving posture rely on the very systems that are the cause of the problem. The fact that posture can deteriorate suggests the fallibility of the controlling mechanisms.

Core muscles (muscles towards the axis of the movement) have significant impact on postural stability on which movements are superimposed by the dynamic movers that lie in a layer(s) over the core muscle(s).
Anticipatory postural adjustments are a part of any movement, hence let us understand APA.

APA- Anticipatory postural adjustment

When a task to perform a fast, focal voluntary movement coexists with a task to maintain equilibrium in the field of gravity or posture of a limb, feedforward adjustments in the activity of apparently postural muscles are used to counteract the expected perturbing forces. These reactions are generated by the central nervous system in anticipation of a perturbation, and, therefore, they have been termed "anticipatory postural adjustments" (for a review see Massion 1992).

Anticipatory adjustments have been studied in a variety of experimental procedures, including voluntary foot movements (Alekseev et al. 1979; Dietz et al. 1980), trunk movements (Oddsson and Thorstensson 1986), and arm movements in standing subjects (Belenkiy et al. 1967; Bouisset and Zattara 1981; Cordo and Nashner 1982; Friedli et al. 1984, 1988; Riach et al. 1992; Aruin and Latash 1995), as well as in tasks restricted to upper extremities that did not involve maintenance of the vertical posture (Dufosse et al. 1985; Struppler et al. 1994).

Preceding all voluntary movements, no matter how small, a pre-emptive adjustment occurs to prepare for a change of position, known as postural preparation or anticipatory postural adjustment.

We do not start to attempt the act until we have first set up the conditions we associate with the movement, even if unsuitable. You will be generally unaware of these preparatory actions and continue to apply them for every move. The affect of unsuitable preparations on movement can be likened to applying the brake on a car before driving off. Your habit of getting set to lift, run or play a shot could be reducing performance. If you are already in a state of unbalance before you move due to poor employment of muscle, the ensuing preparations for movement will be inappropriate leading to inefficient actions.

Study 1:

CNS uses the same organization of the motor command for the control of both APA (segmental control) & CPA - corrective postural adjustments (whole body posture). But APA can be non-efficient in segmental postural control. CNS use anticipatory postural muscle activities (APMA) in synergy where gravity plays a crucial role.

Chabran et al (2001) in one study concluded central nervous system (CNS) uses the same organization of the motor command for the control of both segmental and whole-body posture: APA and corrective postural adjustments (CPA), which are based on well-organized anticipatory postural muscle activities (APMA), except that APA can be non-efficient in segmental postural control.

Further this study suggests that the CNS uses a sequence of APMA: a postural muscle synergy which is predetermined as a function of the intended direction of the movements and modulates the gain towards certain muscles, in accordance with the gravitational effects, and supports reaction changes.

Study 2:

Separate control of abdominals.

A study by Hodges et al (1999) reveal that transverse abdominal (a core muscle) is separately controlled than other abdominals. APA of Tr Abd do not vary with lower limb movement but co-vary with the other abdominal muscles. Hence TrA may be controlled independently of the motor command for limb movement in contrast to the other abdominal muscles.

Study 3:

Inertia associated with APA, when the time comes, balance the inertia forces due to the movement of the mobile limb therefore counteracting the disturbance to postural equilibrium.

Bouisset et al tried to find out whether APAs are programmed or not & biomechanical consequence of APA. They found APA like others (Chabran et al) corresponds to dynamic phenomena which are centrally preprogrammed. The inertia forces associated with APA may, when the time comes, balance the inertia forces due to the movement of the mobile limb therefore counteracting the disturbance to postural equilibrium.

Hence it is suggested that posturo-kinetic programming could result from a differential sensitivity of the CNS to two biomechanical factors, a linear and a rotational one, which can characterize the perturbation associated with voluntary movement.

Study 4:

Chabran et al (2002) studied whether fatigue of postural muscles influence the coordination between segmental posture and movement or not. They found postural fatigue induced by a low-level isometric contraction has no effect on voluntary movement and requires no dramatic adaptation in postural control.

Study 5:

CNS can also suppress APA

Alexander et al (1998) found in their study in conditions of high stability demands; the central nervous system may suppress APAs as a protection against their possible destabilizing effects. These effects are more pronounced when the direction of an expected perturbation is in the plane of instability.

Study 6:

APAs are less efficient in chr. low back pain (LBA)

According to Mosley & Hodges (2006) sustained decrease in the variability of anticipatory postural adjustments (APAs) occurs when performing cued arm raises following acute, experimentally induced low back pain (LBP). Jesse et al (2009) found people with chronic LBP may be less capable of adapting their APAs to ensure postural stability during movement.

Attempts to postural improvement:

Postural correction is one of the primary interventions of many physiotherapeutic interventions.
By now we are aware that postural muscles reactions start in anticipation of movement whose inertia helps to counteract the perturbing force to equilibrium. One may see the poised & coordinated segmental posture & movements notoriously in the presence of fatigue of the postural muscles because CNS can suppress APAs.

At this point of our discussion, famous physiologist Charles Sherrington’s description our systems for maintaining posture as the ‘most uncertain and untrustworthy of all’ sounds very true. This is not encouraging when all corrective methods for improving posture rely on the very systems that are the cause of the problem.

The fact that posture can deteriorate suggests the unreliability of the controlling mechanisms. Hence to take corrective methods following problems need to be understood & addressed:

(1) functional organization of the postural system
(2) localization of postural functions in the mammalian CNS
(3) postural networks
(4) impairment of postural control caused by different deficits such as vestibular, prorioceptive, kinesthetic etc.

Core stability & posture:

Core stability is the ability of the lumbopelvic hip complex to prevent buckling and to return to equilibrium after perturbation. Although static elements (bone and soft tissue) contribute to some degree, core stability is predominantly maintained by the dynamic function of muscular elements.

Dangers of not having proper core stability:

There is a clear relationship between trunk muscle activity and lower extremity movement. Current evidence suggests that decreased core stability may predispose to injury and that appropriate training may reduce injury. Core stability can be tested using isometric, isokinetic, and isoinertial methods.

A unique approach: Core integration to lengthen myofascia to improve posture

Postural organization is controlled by the central nervous system in conjunction with the skeletal, muscular, and fascial systems. DellaGrotte et al (2008) described a neuromotor re-education intervention for static and dynamic postural misalignment. This DellaGrotte et al (2008) approach is leads to lengthening of myofascia & core integration that leads to improved postural organization.

Appropriate intervention directed for core stability & integration may not only result in decreased rates of back and lower extremity injury but also in postural improvement.

References:

1. Chabran E et al; J Electromyogr Kinesiol. 2002 Feb;12(1):67-79.
2. Chabran E et al; Exp Brain Res. 2001 Nov;141(2):133-45.
3. DellaGrotte J et al; J Bodyw Mov Ther. 2008 Jul;12(3):231-45. Epub 2008 Jul 9.
4. Bouisset et al; Journal of Biomechanics, Volume 20, Issue 8, 1987, Pages 735-742 (Biomechanical study of the programming of anticipatory postural adjustments associated with voluntary movement)
5. Alexander et al; Electroencephalography and Clinical Neurophysiology/Electromyography and Motor Control Volume 109, Issue 4, August 1998, Pages 350-359 (Anticipatory postural adjustments in conditions of postural instability )
6. Willson JD et al; J Am Acad Orthop Surg, Vol 13, No 5, September 2005, 316-325.
© 2005 the American Academy of Orthopaedic Surgeons. (Core Stability and Its Relationship to Lower Extremity Function and Injury)
7. Hodges et al; Neuroscience Letters Volume 265, Issue 2, 16 April 1999, Pages 91-94 (Transversus abdominis and the superficial abdominal muscles are controlled independently in a postural task).
8. Jesse V et al; Behav Neurosci. 2009 April; 123(2): 455–458 (People with chronic low back pain exhibit decreased variability in the timing of their anticipatory postural adjustments).
9. Deliagina TG et al; Physiol Behav. 2007 Sep 10;92(1-2):148-54. Epub 2007 May 21. (Nervous mechanisms controlling body posture).





Friday, September 17, 2010

Neck pain due scapular origin




Various scapular connections:

Following group of muscles are essential for proper shoulder functioning:
1. Scapulo-humeral group (Supra & infraspinatus, Subscapularis)
2. Cervico-scapular group (Levator scapulae, Upper trapezius)
3. Thoraco-scapular group (Ex: Rhonboids, middle trapezius)
4. Other muscle like latissimus dorsi etc

Shoulder is one of the most active joints of human body & upper limb function is heavily dependant on optimal shoulder joint function. However, the shoulder function is in turn heavily dependant on the scapular stability & mobility. Among various attachments of the scapula, scapular position is also dependant on the Cervico-scapular & other muscles described above. Various scapular conjugate movements with shoulder joint function demands heavy stress on all of it’s attachments. Specific shoulder tasks demands specific static & dynamic scapular positions.

Scapular positional faults & shoulder pain:

Rhomboids dominance: This scapula is rotated on the frontal plane downwards (see the figure). This scapular positioning may lead to premature contact of Gt & acromion that can lead to impingement pain. Hence it is clear that scapular position affect shoulder function.

Brian Mulligan: has explained components of specific scapular positional faults associated with painful shoulder conditions. (Ref: 5th edition of his book)

Scapular positional faults & neck pain:

1. Cervico-scapular focus

Our focus in this topic is scapular positioning & it’s effect on neck. Changes in the alignment of either the scapulae or the cervical spine can potentially influence the biomechanics of the other by altering the tension at the cervicoscapular muscles (1).

Altered scapular alignment is proposed to be related to neck dysfunction and pain. Among the recent occupation related hazards extensive computer use amongst office workers has lead to an increase in work-related neck pain. Aberrant activity within the three portions of the trapezius muscle and associated changes in scapular posture have been identified as potential contributing factors (2). During the typing task people with neck pain generate greater activity in the middle trapezius and less activity in the lower trapezius.

Andrade et al (1) compared the active cervical rotation range of motion (ROM) between healthy young subjects with a neutral vertical scapular alignment and subjects with scapular depression. They also examined the influence of modifying the vertical position of the scapulae on active cervical rotation ROM.

Cervical rotation ROM was assessed for two equal groups out of total 58 college age students ware segregated into neutral vertical scapular alignment or depressed scapular alignment. Cervical rotation ROM was assessed either in resting scapular position or neutral vertical scapular position with forearms supported.

Results suggest that in a young healthy population the vertical scapular alignment does not influence cervical rotation ROM. Supporting the upper limbs, however, results in a significant and similar increase in cervical rotation ROM for both groups.

Van Dillen et al (3): examined the effect of elevating the scapulae on symptoms during neck rotation during physical examination. They obtained data in 2 scapulae positions: a patient-preferred scapulae position and a passively elevated scapulae position. They found in patient-preferred positions, 63% of the 46 patients reported an increase in symptoms with neck rotation in at least one direction. But in passively elevated scapulae position significant percentage of patients reported a decrease in symptoms with neck rotation both in left & right direction.

Passive elevation of the scapulae resulted in a decrease in symptoms with right and left neck rotation in the majority of patients. These findings are important because they indicate that neck symptoms can be immediately improved within the context of the examination. Such information potentially can be used to assist in directing intervention (3).

Levator scapulae syndrome: In an anatomic-clinical study involving 22 alive subjects & 30 cadavers, Menachem et al (4) have reported the following features & reason to this syndrome:

a. Pain over the upper medial angle of the scapula almost always (82%) on the side of dominant shoulder radiating to the neck and shoulder but rarely to the arm.
b. Movements that stretched the levator scapulae on the affected side aggravated symptoms.
c. Radiographs and bone scans of the shoulders and cervical spine were negative. However digital thermographic imaging showed increased heat emission from the upper medial angle of the affected shoulder in 60% of the patients.

Possible explanation for this syndrome was found by anatomic dissection of cadavers. Possible causes are
a. Great variability in the insertion of the levator.
b. A bursa was found between the scapula, the serratus, and the levator in more than 50% of the shoulders.

This study suggests that this syndrome, leading to bursitis and pain, may be caused by anatomic variations of the insertion of the levator scapulae and origin of the serratus anterior. This may explain the constant trigger point and crepitation as well as the increased heat emission found on thermography.

2. Thoraco-scapular focus:

Wegner et al (influence of thoraco-scapular muscles on neck pain): Wegner et al in a recently published study utilized sEMG of the three portions of the trapezius in healthy controls (n=20) to a neck pain group with poor scapular posture (n=18) during the performance of a functional typing task. Again they introduced a scapular postural correction strategy to correct scapular orientation in the neck pain group and electromyographic recordings were repeated. Following correction of the scapula, activity recorded by the neck pain group was similar to the control group for the middle and lower portions.

These findings indicate that a scapular postural correction exercise may be effective in altering the distribution of activity in the trapezius to better reflect that displayed by healthy individuals.

3. The fascia focus:

Off late interesting properties of fascia have reveled that fascia is a independent organ with it’s innate contracting capabilities due presence of myofibroblasts. Misalignments in the body compromise the architectural integrity. At the tissue level, fascia shortens and thickens as the body engages in compensatory strategies to maintain itself upright; these changes are known as myofascial contractions.

In physical therapy, there are several methods by which practitioners treat neck dysfunction. According to James et al (5) Rolfing structural integration (RSI) is capable of significantly decreasing pain and increasing AROM in adult subjects, male and female, with complaints of cervical spine dysfunction regardless of age in 10 basic sessions.

To explore the fascia connections of scapula on needs to read the extra-thoracic fascia. This is present else where in this blog.

References:


1. Andrade GT et al; J Orthop Sports Phys Ther. 2008 Nov;38(11):668-73. (Influence of scapular position on cervical rotation range of motion.)
2. Wegner S et al; Man Ther. 2010 Jul 21. (The effect of a scapular postural correction strategy on trapezius activity in patients with neck pain.)

3. Van Dillen LR et al; lin J Pain. 2007 Oct;23(8):641-7. (The immediate effect of passive scapular elevation on symptoms with active neck rotation in patients with neck pain.)

4. Menachem A et al; Bull Hosp Jt Dis. 1993 Spring;53(1):21-4. (Levator scapulae syndrome: an anatomic-clinical study.)
5. James H et al; J Bodyw Mov Ther. 2009 Jul;13(3):229-38. Epub 2008 Sep 13. (Rolfing structural integration treatment of cervical spine dysfunction.)

Tuesday, August 31, 2010

Shoulder joint functional alteration during arm elevation with impingement syndrome & latent trigger points

Justify FullShoulder elevation mechanics in impingement syndrome:

Both glenohumeral and scapulothoracic kinematics are altered during impingement syndrome. Normal & altered mechanics during shoulder elevation is discussed below.

Normal mechanics:

Functions of Trapezius muscle: Upper trapezius produces clavicular elevation and retraction. The middle trapezius is primarily a medial stabilizer of the scapula. The lower trapezius assists in medial stabilization and upward rotation of the scapula.

Functions of serratus anterior muscles: The middle and lower serratus anterior muscles produce scapular upward rotation, posterior tilting, and external rotation.

Pectoralis minor: The pectoralis minor is aligned to resist normal rotations of the scapula during arm elevation.

Rotator cuff: The rotator cuff is critical to stabilization and prevention of excess superior translation of the humeral head, as well as production of glenohumeral external rotation during arm elevation.

Alterations of shoulder muscle functions in impingement syndrome:

Alterations in activation amplitude or timing have been identified across various investigations of subjects with shoulder impingement. These include
1. Decreased activation of the middle or lower serratus anterior and rotator cuff,
2. Delayed activation of middle and lower trapezius
3. Increased activation of the upper trapezius and middle deltoid.

* Subjects with tight pectoralis minor exhibit altered scapular kinematic patterns similar to those found in persons with shoulder impingement.

Scapular tipping and serratus anterior muscle function are important to consider in the rehabilitation of patients with symptoms of shoulder impingement (3).

Impact of Latent myofascial trigger point in upward scapular rotator muscles (upper and lower trapezius and serratus anterior).

What are latent myofascial trigger points ?: These lesions are not pain producers but present as nodules in the muscle bulk. Commonly in shoulder upper and lower trapezius and serratus anterior hosting Latent Myofascial Trigger Points.

Lucas et al found presence of Latent Trigger Points in upward scapular rotators alters the muscle activation pattern during scapular plane elevation. This potentially predisposes to overuse conditions including impingement syndrome, rotator cuff pathology and myofascial pain.

Lucas et al found
1. In normal condition there is a relatively stable sequence of muscle activation.
2. The sequence is significantly different in timing and variability in the subjects with Latent Trigger Point group in all muscles except middle deltoid.
3. The Latent Trigger Point group muscle activation pattern under load was inconsistent, with the only common feature being the early activation of the infraspinatus.

Hence latent trigger points should be searched for treatment when it is even not producing non-segmental pain as it is known to produce.

References:

1. Phadke V et al; Rev Bras Fisioter. 2009 Feb 1;13(1):1-9. (Scapular and rotator cuff muscle activity during arm elevation: A review of normal function and alterations with shoulder impingement.)
2. Lucas KR et al; Clin Biomech (Bristol, Avon). 2010 Oct;25(8):765-70. Epub 2010 Jul 27. (Muscle activation patterns in the scapular positioning muscles during loaded scapular plane elevation: the effects of Latent Myofascial Trigger Points.)
3. Ludewig PM et al;Phys Ther. 2000 Mar;80(3):276-91. (Alterations in shoulder kinematics and associated muscle activity in people with symptoms of shoulder impingement.)


Tuesday, August 24, 2010

Composition of different treatments in subacromion bursitis: Evidence from a recent study.


Tate AR et al recently tried to define the dosage and specific techniques of manual therapy and exercise for rehabilitation for patients with subacromial impingement syndrome in a case series. 10 patients (age range, 19-70 years ware treated with a standardized protocol for 10 visits over 6 to 8 weeks.

More about this program:

1. Strengthening rotator cuff and scapular muscles (3-phase progressive strengthening program)
2. Manual stretching
3. Manual therapy aimed at thoracic spine (Both thrust and nonthrust manipulation)
4. Manual therapy aimed at and the posterior and inferior soft-tissue structures of the glenohumeral joint (Both soft & bony. Bony manipulation: Both thrust and nonthrust manipulation)
5. Other components of this program: Activity modification and a daily home exercise program of stretching and strengthening.

Result of this program: This case series describes a comprehensive impairment-based treatment which resulted in symptomatic and functional improvement in 8 of 10 patients in 6 to 12 weeks and appeared to be successful in the majority of patients.

LEVEL OF EVIDENCE: Therapy, level 4.

Reference:
Tate AR et al; J Orthop Sports Phys Ther. 2010 Aug;40(8):474-93. (Comprehensive impairment-based exercise and manual therapy intervention for patients with subacromial impingement syndrome: a case series.)


Tuesday, August 17, 2010

Condensing osteitis of clavicle: Presenting with sternoclavicular pain & swelling


What is Condensing osteitis of clavicle?

Osteitis condensans of the sternoclavicular joint was first described by Brower et al in 1974 (5). Till 1989 only 16 cases ware reported in world medical literature (6).

Definition: Condensing osteitis of the clavicle is a benign idiopathic entity that is probably degenerative or mechanical in etiology manifesting by variably painful and tender swelling over the medial end of the clavicle.

There is no clinical or laboratory evidence of infection in all cases of Condensing osteitis.

Where else Condensing osteitis is also marked?

Condensing osteitis is also marked at ilium, and pubis (4).

The etiopathogenesis of this rare benign clinico-radiologic entity remains unknown (7). However Berthelot et al have proposed a pathogenic hypothesis for condensing osteitis of the clavicle, ilium, and pubis. According to their observation joint aspects spared by the sclerosis are covered with hyaline cartilage but occurs in bone overlaid by fibrocartilage.

Clinical features:
1. Pain at medial end of the clavicle or SC joint with shoulder joint movement specially with over head abduction or horizontal adduction.
2. Sex: Seen more in women of late child-bearing age.
3. Radiographs show sclerosis and slight expansion of the medial one-third of the clavicle.

Investigations: Radiologic, scintigraphic, and histologic features should be studied (2). Recognition of condensing osteitis of the clavicle may avoid the occasional unnecessarily aggressive diagnostic approach taken to search for a malignant tumor.

Radiological findings include sclerosis of the medial part of the clavicle and a normal sternoclavicular joint. Radiographic investigations reveal an increase in volume and a condensation of the median part of the clavicle, and scintigraphical studies revealed an intense incorporation of the radioisotope (7). According to Vierboom et al (9) magnetic resonance imaging is a useful non-invasive procedure for the diagnosis of condensing osteitis of the clavicle.

Diagnosis is usually confirmed by biopsy (5). Generally biopsy reveals an inflammatory exudate, and histochemical staining for Langerhans'-cell histiocytosis was negative (3). Histopathologic studies showed lamellar and spongious bone tissue, with a normal trabecular structure, although considerably thickened (7).

Differential diagnosis:
It can be mistaken for - Friedrich disease, bone island, osteoid osteoma, sternoclavicular osteoarthritis, and even a metastasis and osteosarcoma (2). Although malignant tumor of bone must be considered in the differential diagnosis, tests for a presumed primary malignant lesion are not recommended for most patients. It is recommended, however, that an excisional or (preferably) incisional biopsy be performed in all patients unless pain is insignificant and the clinical presentation strongly supports the diagnosis of condensing osteitis (1).
Shiv Sankar et al have suggested hypertrophic sclerosis causing painful enlargement of the medial end of the clavicle in isolation should be distinguished from condensing osteitis and chronic recurrent multifocal osteomyelitis.
However according to Baciu et al in the first place those concerning intra-sterno-clavicular hyperostosis, sterno-costo-clavicular arthrosis, chronic subacute osteitis, avascular necrosis of the clavicular epiphysis (Friedrich disease), and Tietze syndrome must be considered for differential diagnosis (7).

Treatment options:
Pain management can be challenging in these patients.Many patients who have slight pain do not need treatment. Anti-inflammatory medications are variably effective(1).

Multiple treatments have been described in the past including oral NSAIDS, physical therapy, radiation, surgical resection, and oral corticosteroids but have met with limited success. Galla et al described the novel utility of sternoclavicular joint steroid injections in treating a patient with Osteitis condensans of the clavicle after failed medical therapy. They also have advocated sternoclavicular joint injection under fluoroscopic guidance using a local anesthetic-corticosteroid injectate as a viable treatment option for pain associated with Osteitis condensans of the clavicle (5).Patients in whom the lesion is refractory respond well to excision of the medial one-third of the clavicle (1).

Course of the disease:
A report of self limiting nature of the disease is considered by Berthelot JM et al (4). According to a intermediate follow up (mean length of follow-up was 38 months - range, 9 to 77 months) by Sng KK et al (6) the severity of the pain appears to improve with time, although the clinical swelling over the medial clavicle does not resolve significantly.

References:

1. Kruger GD et al; J Bone Joint Surg Am. 1987 Apr;69(4):550-7. (Condensing osteitis of the clavicle. A review of the literature and report of three cases.)
2. Greenspan A et al; AJR Am J Roentgenol. 1991 May;156(5):1011-5. (Condensing osteitis of the clavicle: a rare but frequently misdiagnosed condition.)
3. Shiv Shanker V et al; J Pediatr Orthop B. 1999 Jan;8(1):48-9. (Hypertrophic osteitis of the medial end of the clavicle.)
4. Berthelot JM et al; Pain Physician. 2009 Nov-Dec;12(6):987-90. Rev Rhum Engl Ed. 1995 Jul-Sep;62(7-8):501-6. (Osteitis condensans of the clavicle: does fibrocartilage play a role? A report of two cases with spontaneous clinical and roentgenographic resolution.)
5. Galla R et al; Pain Physician. 2009 Nov-Dec;12(6):987-90. (Sternoclavicular steroid injection for treatment of pain in a patient with Osteitis condensans of the clavicle.)
6. Sng KK et al; Ann Acad Med Singapore. 2004 Jul;33(4):499-502. (Condensing osteitis of the medial clavicle--an intermediate-term follow-up.)
7. Baciu CC et al; Rev Chir Oncol Radiol O R L Oftalmol Stomatol Chir. 1989 Sep-Oct;38(5):381-6. (Condensing osteitis of the middle third of the clavicle)
8. Noonan PT et al; Skeletal Radiol. 1998 May;27(5):291-3. (Condensing osteitis of the clavicle in a man.)
9. Vierboom MA et al; Ann Rheum Dis. 1992 Apr;51(4):539-41. (Condensing osteitis of the clavicle: magnetic resonance imaging as an adjunct method for differential diagnosis.)



Thursday, August 12, 2010

Coccygodynia (Tail bonepain): Causes




What is a dynia?

The "dynias" are a group of chronic, focal pain syndromes with a predilection for the orocervical and urogenital regions. They include glossodynia, carotidynia, vulvodynia, orchidynia, prostatodynia, coccygodynia, and proctodynia. In some cases, the dynias occur secondarily, but more often, despite an exhaustive evaluation, no etiology is found and in these remaining cases, the cause of the pain remains enigmatic. The controversy that surrounds this group of disorders, which ranges from questioning their existence to suggesting that they are purely psychosomatic, is counterbalanced by an extensive literature attesting to their organicity (1).

What is coccygodynia? & Causes of coccygodynia:

The three most common functional disorders causing anorectal and perineal pain are levator ani syndrome, coccygodynia and proctalgia fugax. However, Alcock's canal syndrome is also responsible for pain in these areas (3).
A review of Mayo clinic records Physical Medicine and Rehabilitation from 1970 through 1975 with pelvic floor myalgia (pyriformis syndrome, coccygodynia, levator ani spasm syndrome, proctalgia fugax, or rectal pain) is associated with poor posture, deconditioned abdominal muscles, and generalized muscle attachment tenderness. The most effective therapeutic regimen was a combination of rectal diathermy, Thiele's massage, and relaxation exercises (20).
Local pain in the area of coccyx (tail bone) is called coccygodynia. Chronic coccygodynia is a difficult problem diagnostically and therapeutically (2). According to Dr. Cyriax (Father of orthopedic medicine) there are 4 different causes of coccygodynia.
1. Trauma by direct blow to the coccyx
2. Sprain of sacro-coccygeal & Ilio-coccygeal ligament
3. Sprain of muscle fibers attached to the over lying sacro-coccygeal & Ilio-coccygeal ligaments

Coccyx disc disorder in common idiopathic coccygodynia: Coccygodynia are usually attributed to soft tissue injuries or psychologic disturbances. However Maigne et al (13) in 1994 has hypothesized that the source of coccygodynia as a lesion of the coccygeal disc. Basing on discography study Maigne et al (13) found Common coccygeal pain could come from the coccygeal disc in approximately 70% of cases.

True & pseudo coccygodynias: According to Traycoff et al (4) true coccygodynia consists of pain arising from the sacrococcygeal joint, whereas pseudococcygodynia consists of pain referred to but not arising from the coccyx. Coccygodnia can usually be distinguished from pseudococcygodynia by physical examination with the diagnosis being confirmed by injection of local anesthetic into the sacrococcygeal joint. The etiology of pain not relieved by intraarticular injection can be further defined by selective neuroblockade.

Differentiating traumatic and idiopathic coccygodynia:

Intercoccygeal angle: It is the angle between the first and last segment of the coccyx (11). According to Kim et al (11) intercoccygeal angle in the normal population is around 52.3 degrees. Intercoccygeal angle of the idiopathic (non-traumatic) coccygodynia is greater than that of the traumatic and normal population.Increased intercoccygeal angle can be considered a possible cause of idiopathic coccygodynia. The intercoccygeal angle was a useful radiological measurement to evaluate the forward angulation deformity of the coccyx.
According to Kim et al (11) the differences observed between traumatic & non-traumatic coccygodynia are
1. There is no difference between the traumatic and idiopathic coccygodynia groups in terms of age, male/female sex ratio, and the number of coccyx segments.
2. Significant differences between the traumatic and idiopathic coccygodynia groups are marked in terms of the pain score, the intercoccygeal angle, and the satisfactory outcome of conservative treatment.
a. If pain is compared in sitting then the pain in traumatic coccygodynia is more than non traumatic category.
b. If pain is compared on defecation then the pain in non traumatic coccygodynia is more than traumatic category.
c. Intercoccygeal angle is more in non traumatic coccygodynia than traumatic category.
d. Response to conservative treatment is better with non traumatic coccygodynia

Pregnancy & Coccygodynia: Coccygodynia appears to occur more in females. Coccydynia can result from a varying number of causes, parturition being one of them (6). Ryder et al (5) reviewed literature to find out coccydynia with specific reference to those cases of pregnancy and birth-related onset. They found there is little information about incidence, prevalence, pathophysiology, methods of differential diagnosis and efficacy of treatment for these women. No qualitative data from women with pregnancy or birth-related coccydynia were identified.
However according to a case report by Kaushal et al (6) strains and sprains of the ligaments attached to the coccyx is thought to be the usual cause for coccydynia occurring after childbirth, an intrapartum coccygeal fracture dislocation can result in the same. Similarly Jones et (12) reported a case of coccygodynia due to coccygeal fracture secondary to parturition.

Cyst in precoccygeal region as a cause of coccygodynia: Jaiswal et al in 2008 (7) reported for the first time a single case precoccygeal epidermal inclusion cyst presenting as a coccygodynia. This study suggests that patients with intractable coccygodynia should have a magnetic resonance imaging to rule out treatable causes of coccygodynia.
A few coccygodynia cases are attributed to so-called pericoccygeal glomus tumors. Pericoccygeal soft tissues normally contain numerous small glomus bodies and a larger one known as the glomus coccygeum, which can reach several millimeters in diameter. Most reported cases of alleged pericoccygeal glomus tumors represent normal, incidentally discovered coccygeal glomus bodies (14).
Intracoccygeal glomus tumor are also reported as a cause of coccygodynia. However, Pericoccygeal and intracoccygeal glomus bodies are normal findings in humans at all ages. They should not be mistaken for tumors, and their role in the pathogenesis of coccygodynia is questionable (14).
Ziegler et al (17) have reported a case of typical coccygodynia caused by a sacral nerve cyst. Relief of the pain by excision of the cyst occurred.
No case of arachnoid cyst causing coccygodynia has been found available in medical literature till Kepski A et al (18) reported a case of arachnoid cyst of cauda equina with severe chronic coccygodynia. Arachnoid cysts are often asymptomatic, by they may be responsible for coccygodynia and/or incomplete cauda equina syndrome (19).
Arachnoid cysts are called Tarlov’s cysts (perineurel meningeal cysts on the sacral nerve roots).It’s presence is suggested by the characteristics of the symptoms which are paroxysmal, exacerbated in standing position, relieved in dorsal position and revived by percussing the sacrum. Treatment is medical in most cases. The decision to operate depends on the persistence and intensity of pain and on whether signs of neurological defecit are present (19).
According to a single case study by Charpentier et al (21) ependymoma of the filum terminale caused the coccygodynia in that case. Similarly according to a single case study by Chateau et al (22) ependymoma of the filum terminale caused the coccygodynia in that case.

Association of depression with coccygodynia: Maroy B (15) investigated association of depression with coccygodynia in 1988. Out of 313 patients with signs of depression or spontaneous or evoked pain of coccygeal area were studied over six months. One hundred eighty (58 percent) had no spontaneous pain, 87 (28 percent) had moderate pain, and 46 (15 percent) a severe coccygodynia leading to consultation.

Association of jeans seam with coccygodynia: Stoshak ML (16) et al have tried to associate jeans seam with coccygodynia back in 1985.

Normal coccygeal movement during defecation don’t cause coccygodynia: Over view of coccygeal movement
An abnormal motion (laxity or hypermobility) of the coccyx that occurred in the sitting position and spontaneously was reducible when placed in the lateral decubitus position (13). According to a dynamic MRI study by Grassi R et al (2), coccyx is mobile during defecation and that it is possible to demonstrate coccygeal excursions by assessing the difference between its positions at maximum contraction and during straining-evacuation. This study also found there is no correlation between coccygeal movements and age, sex, parity, minor trauma and coccygodynia.
Dynamic radiography is a useful tool to differentiate posttraumatic from idiopathic coccygodynia (9).
Changes in post traumatic coccygodynia:
In an analysis of morphological changes associated with 23 different patients with post traumatic coccygodynia the following ware found by Brusko et al (8)
1. Coccyx cartilaginous tissue showed dystrophic changes of chondrocytes, destruction of the basic material with partial replacement of a fibrillar cartilaginous tissue with a hyaline cartilage were observed with a different degree of manifestation.
2. Vessels and sacrococcygeal nervous plexus were subjected to pathological changes.
3. Increased post-traumatic mobility, alterations in the process of ossification, deceleration of physiological joining of coccyx vertebras and sacrococcygeal joint alter biomechanical properties of coccyx at sitting.
Study by Brusko et also found that these above alterations lead to the long-lasting traumatization with degenerative - dystrophic changes, reinforcement of pain syndrome and manifestation of dysfunctions of organs of pelvis (8).

Coccyx instability following post traumatic coccygodynia:
Coccyx instability is a fairly common phenomenon after trauma to this area. Mouhsine et al reported 15 posttraumatic coccygodynia with instability which was diagnosed with dynamic lateral radiography and magnetic resonance imaging (MRI) (9). Doursounian et al between 1993 and 2000 surgically treated 61 patients with instability-related coccygodynia using a single technique. Twenty-seven patients had hypermobility of the coccyx and 33 subluxation. In all cases, the unstable portion was removed through a limited incision directly over the coccyx.

Complications of coccygodynia:
Complications of coccygodynia are not many however coccygodynia out of Coccygeal fracture dislocation may result in introital dyspareunia and tension myalgia of the pelvic floor. Pain from this lesion may become recurrently symptomatic (6).

References:
1. Wesselmann U et al; Semin Neurol. 1996 Mar; 16(1):63-74. (The dynias)
2. Grassi R et al; Eur J Radiol. 2007 Mar;61(3):473-9. Epub 2007 Jan 16. Coccygeal movement: assessment with dynamic MRI.
3. Mazza L et al; Tech Coloproctol. 2004 Aug;8(2):77-83. (Anorectal and perineal pain: new pathophysiological hypothesis.)
4. Traycoff RB et al; Orthopedics. 1989 Oct;12(10):1373-7. (Sacrococcygeal pain syndromes: diagnosis and treatment.)
5. Ryder I et al; Midwifery. 2000 Jun;16(2):155-60. (Coccydynia: a woman's tail.)
6. Kaushal R et al; J Surg Orthop Adv. 2005 Fall;14(3):136-7. (Intrapartum coccygeal fracture, a cause for postpartum coccydynia: a case report.)
7. Jaiswal A et al; Singapore Med J. 2008 Aug;49(8):e212-4. (Precoccygeal epidermal inclusion cyst presenting as coccygodynia.)
8. Brusko AT, Fiziol Zh. 2004;50(6):114-7.( Morphofunctional changes of coccyx area in posttraumatic coccygodynia)
9. Mouhsine E et al; Spine J. 2006 Sep-Oct;6(5):544-9. Epub 2006 Jul 26. (Posttraumatic coccygeal instability.)
10. Doursounian L et al; Int Orthop. 2004 Jun;28(3):176-9. Epub 2004 Mar 13. (Coccygectomy for instability of the coccyx.)
11. Kim NH et al; Yonsei Med J. 1999 Jun;40(3):215-20. (Clinical and radiological differences between traumatic and idiopathic coccygodynia.)
12. Jones ME et al; Injury. 1997 Oct;28(8):549-50. (A case of coccygodynia due to coccygeal fracture secondary to parturition.)
13. Maigne JY et al; Spine (Phila Pa 1976). 1994 Apr 15;19(8):930-4. (Idiopathic coccygodynia. Lateral roentgenograms in the sitting position and coccygeal discography.)
14. Albrecht S et al; Surgery. 1994 Jan;115(1):1-6. (Intracoccygeal and pericoccygeal glomus bodies and their relationship to coccygodynia.)
15. Maroy B; Dis Colon Rectum. 1988 Mar;31(3):210-5. (Spontaneous and evoked coccygeal pain in depression.)
16. Stoshak ML et al; Pediatrics. 1985 Jul;76(1):138. (Jean seam coccygodynia.)
17. Ziegler DK et al; eurology. 1984 Jun;34(6):829-30. (Coccygodynia caused by perineural cyst.)
18. Kepski A et al; Neurol Neurochir Pol. 1978 Jan-Feb;12(1):109-12. (Arachnoid cyst of the cauda equina: a contribution to the etiology of coccygodynia)
19. Dehaine V et al; Rev Med Interne. 1990 Jul-Aug;11(4):280-4. (Coccygodynia disclosing Tarlov's cysts)
20. Sinaki M et al; Mayo Clin Proc. 1977 Nov;52(11):717-22. (Tension myalgia of the pelvic floor.)
21. Charpentier J et al; Rev Neurol (Paris). 1968 Feb;118(2):160-2. (Coccygodynia revealing an ependymoma of the filum terminale. Complete removal without sequelae)
22. Chateau R et al; Med Lyon. 1967 Apr 5;48(118):573-8. (Coccygodynia revealing a giant tumor of the cauda equine)

Interesting note by the author: The above picture of an MRI is taken in my center shows a coccyx fracture dislocation with no coccygodynia. The patient is a 32 year old lady.

Tuesday, August 3, 2010

Compensation for weak gluteus medius


1. Excessive lateral pelvic tilt (Trendelenburg):

Areas that may be affected due to compensation: Lumbar spine, sacroiliac joint (SIJ), greater trochanter bursa, insertion of muscle on greater trochanter, overactivity of piriformis and tensor fascia lata (TFL) .

2. Medial knee drift:

Areas that may be affected due to compensation: Lateral tibiofemoral compartment (via compression), patellofemoral joint, patella tendon and fat pad, pes anserinus, iliotibial band (ITB)

3. Lateral knee drift:

Areas that may be affected due to compensation: Medial tibiofemoral compartment (via compression), ITB, posterolateral compartment, popliteus

4. Same-sided shift of trunk (lateral flexion of trunk):

Areas that may be affected due to compensation: Lumbar spine (increased disc and facet joint compression), SIJ (increased shear)


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.

References:

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.

References:
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

Treatment:
o NSAID's
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

Treatment:
o RICE
o NSAIDs
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

Treatment:
o ice
o activity modification
o treat malalignment
o flexibility
o NSAIDs
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

Treatment:
o NSAIDs
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

Treatment:
o symptomatic
o ice
o stretching, strengthening
o activity modification
o rarely immobilize
o NSAIDs

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

Treatment:
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

Treatment:
o controlled activity
o modalities
o medications
o exercise
stretching
strengthening

Principles of eccentric exercise program:
o muscle length
o intensity
load
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.

LEARNING OBJECTIVES
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.

References:

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.