Wednesday, October 14, 2009

The flexion relaxation phenomenon


I. Lumbar erector spinae flexion-relaxation phenomenon (FRP):

A number of studies have shown differences in the FRP between patients with chronic low back pain and healthy individuals. Presence of the FRP during trunk flexion represents myoelectric silence (1).

This leads to increased load sharing on passive structures and further these tissues have been found to fail under excessive loading conditions and are a source of low back pain. Persistent activation of the lumbar erector spinae musculature among patients with back pain may represent the body's attempt to stabilize injured or diseased spinal structures via reflexogenic ligamentomuscular activation thereby protecting them from further injury and avoiding pain (1). However, flexion relaxation phenomenon (FRP) is an interesting model to study the modulation of lumbar stability (2).

II. Presence of fatigue of the erector spinae (ES) muscles modifies the FRP

Descarreaux et al studied to identify the effect of erector spinae (ES) muscle fatigue and spine loading on myoelectric silence onset and cessation in healthy individuals during a flexion-extension task. Trunk and pelvis angles and surface EMG of the erector spinae (ES) L2 and L5 were recorded during flexion-extension task.

They found:

1. Onset of myoelectric silence during the flexion motion appeared earlier after the fatigue task + cessation of myoelectric silence was observed later during the extension after the fatigue task.

2. Persistence of erector spinae (ES) myoelectric activity in flexion during the load condition.

These findings indicate presence of fatigue of the erector spinae (ES) muscles modifies the FRP. This study also confirmed earlier findings that superficial back muscle fatigue seems to induce a shift in load-sharing towards passive stabilizing structures. The loss of muscle contribution together with or without laxity in the viscoelastic tissues may have a substantial impact on post fatigue stability (2).

III. FRP in seated forward flexion or slumped postures: differences in thoracic & lumbar levels

Callaghan et al did SEMG on 22 subjects (both males & females) to examine the myoelectric activity of the erector spinae muscles (thoracic and lumbar) of the back if the FRP occurs in seated forward flexion or slumped postures.

The study shows:

1. Slumped sitting posture yield FRP of the thoracic erector spinae muscles, whereas the lumbar erector spinae muscle group remained at relatively constant activation levels regardless of seated posture.

2. Thoracic erector spinae silence occurred at a smaller angle of lumbar flexion during sitting than the flexion relaxation angle observed during standing flexion relaxation.

Hence myoelectric activity of the lumbar erector spinae did not increase, in seated forward flexion or slumped postures. This indicates that the passive tissues of the vertebral column were loaded to support the moment at L4/L5. Ligaments contain a large number of free nerve endings which act as pain receptors and therefore could be a potential source of low back pain during seated work.

This study has a great relevance as examination of flexion relaxation during seated postures may provide insight into the association between low back pain and seated work.

IV. FRP in lifting

During the full flexion phase of the back lift movement the lumbar part of the erector spinae muscle exhibits a reduced activity level (flexion relaxation).

But the question is how the required extension torque in the lumbo-sacral joint (L5/S1 joint) is balanced during the period in which apparently the lumbar erector spinae ceases to take its share?

Toussaint et al reported:

1. While flexion it is true that there is flexion relaxation but this coincide with a 25% increase in lumbar length. The change in length-force relationship & passive tissue strain provide part of the required extension torque.

2. With lifting of barbell there is a significant increase in EMG level of the thoracic part of the erector spinae occurr just before the flexion relaxation at the lumbar level. Apparently, the extensor function of the lumbar part is then taken over by the thoracic part of the erector spinae muscle.

3. This suggests that an intricate coordinating mechanism operate that apportions the load to be balanced over active--(lumbar and thoracic part of the erector spinae) and passive structures (post vertebral ligaments).

V. Repeated spinal flexions modulate FRP

Repeated flexion causes muscular fatigue, creep of passive tissues and diminished protective reflexes.

Dickey et al reported:

1. Majority of people show flexion-relaxation throughout the repeated trunk flexion.

2. With flexion-relaxation and maximum flexion angles increase.

3. The flexion-relaxation angle relative to the maximum flexion angle also increases. This effect depended on the load condition; the flexion-relaxation and maximum flexion angles show a greater increase in the unloaded than loaded condition.

Dickey et al concluded that FRP change due to repeated trunk flexions because of changes to the neuromuscular control system. The deactivation of the erector muscles near full flexion angle result in a greater spinal flexion following repeated spinal flexion. This may be related to the increased risk of injury associated with repeated flexion.

VI. FRP in relation to load & speed

The relative spine motion time differ depending on the direction of movement, being longer during trunk flexion and shorter during extension. Sarti et al (6) tried to find out whether variable speed and loading during trunk flexion-extension.

They found:

1. Increase in speed of movement increase the relative lumbar flexion time and significantly reduced the relative lumbar extension time.

2. Increased speed delays the appearance of the electrical silence or the flexion relaxation.
Adding FRP in assessment of LBA

The studies that show differences in the presence of the FRP among patients and control subjects are encouraging for this type of clinical assessment and suggest that assessment of the FRP is a valuable objective clinical tool to aid in the diagnosis and treatment of patients with low back pain (1).

References

1. Colloca CJ et al, The biomechanical and clinical significance of the lumbar erector spinae flexion-relaxation phenomenon: a review of literature; J Manipulative Physiol Ther. 2005 Oct;28(8):623-31.
2. Descarreaux M et al, Changes in the flexion relaxation response induced by lumbar muscle fatigue; BMC Musculoskelet Disord. 2008 Jan 24;9:10.
3. Callaghan JP et al, Examination of the flexion relaxation phenomenon in erector spinae muscles during short duration slumped sitting; Clin Biomech (Bristol, Avon). 2002 Jun;17(5):353-60.
4. Toussaint HM et al, Flexion relaxation during lifting: implications for torque production by muscle activity and tissue strain at the lumbo-sacral joint; J Biomech. 1995 Feb;28(2):199-210.
5. Dickey JP et al, Repeated spinal flexion modulates the flexion-relaxation phenomenon; Clin Biomech (Bristol, Avon). 2003 Nov;18(9):783-9.
6. Sarti MA et al, Response of the flexion-relaxation phenomenon relative to the lumbar motion to load and speed; Spine (Phila Pa 1976). 2001 Sep 15;26(18):E421-6.


Tuesday, October 6, 2009

Long thoracic nerve injuries: new theories to consider



The long thoracic nerve supplies the Serratus anterior, whose root value is (C5-C7) but the root from C7 may be absent.

Anatomic path: The roots from C5 and C6 pierce the Scalenus medius, while the C7 root passes in front of the muscle. The nerve descends behind the brachial plexus and the axillary vessels, resting on the outer surface of the Serratus anterior. It extends along the side of the thorax to the lower border of that muscle, supplying filaments to each of its digitations (finger-like projections).

Long thoracic nerve injuries in sports: Due to its long, relatively superficial course, it is susceptible to injury either through direct trauma or stretch. Injury has been reported in almost all sports, typically occurring from a blow to the ribs underneath an outstretched arm.

Also injuries to the nerve can result from carrying heavy bags over the shoulder for a prolonged time. Symptoms are often minimal – if symptomatic, a posterior shoulder or scapular burning type of pain may be reported.

A lesion of the nerve paralyses the serratus anterior to produce scapula winging, which is most prominent when the arm is lifted forward or when the patient pushes the outstretched arm against a wall. However, even winging may not be evident until the trapezius stretches enough to reveal an injury several weeks prior.

Long thoracic nerve palsy from a possible dynamic fascial sling cause:

Following is an review by Hester P et al

Long thoracic nerve palsy can result from sudden or repetitive external biomechanical forces. This investigation describes a possible dynamic cause from internal forces.

Six fresh cadaveric shoulders (3 female, 3 male, 4 left, 2 right) with full range of motion were systematically dissected to evaluate the anatomic course of the long thoracic nerve. In all specimens a tight fascial band of tissue arose from the inferior aspect of the brachial plexus, extended just superior to the middle scalene muscle insertion on the first rib, and presented a digitation that extended to the proximal aspect of the serratus anterior muscle.`

With progressive manual abduction and external rotation, the long thoracic nerve was found to "bow-string" across the fascial band. Medial and upward migration of the superior most aspect of the scapula was found to further compress the long thoracic nerve. Previous investigations have reported that nerves tolerate a 10% increase in their resting length before a stretch-induced neuropraxia develops. Previous studies postulated that long thoracic nerve palsy resulted from the tethering effect of the scalenus medius muscle as it actively or passively compressed the nerve; however, similar neuromuscular relationships occur in many other anatomic sites without ill effect.

We propose that the cause of long thoracic nerve palsy may be this "bow-stringing" phenomenon of the nerve across this tight fascial band. This condition may be further exacerbated with medial and upward migration of the superior aspect of the scapula as is commonly seen with scapulothoracic dyskinesia and fatigue of the scapular stabilizers. Rehabilitation for long thoracic nerve palsy may therefore benefit from special attention to scapulothoracic muscle stabilization.

References:
Hester P et al; J Shoulder Elbow Surg. 2000 Jan-Feb;9(1):31-5.
http://en.wikipedia.org/wiki/Long_thoracic_nerve




Monday, October 5, 2009

Scapular Dyskinesia



Abnormal scapular motion is called scapular dyskinesis. Tennis players with scapular dyskinesia present a smaller subacromial space than non-athletes. Silva RT et al reported in Br J Sports Med (2008 Apr 8) that tennis players with scapular dyskinesia present a smaller subacromial space than control subjects. Additionally, when the shoulder was analyzed dynamically, moving from neutral abduction to 60 degrees of elevation, the tennis players with scapular dyskinesia presented a greater reduction in the subacromial space compared to unaffected athletes.

Hence it seems logical that scapular dyskinesis is one causative factor in over-head athletic injuries. However the causal relationship between scapular dyskenesia & shoulder injuries has not been reported. Moreover reliable and valid clinical methods for detecting scapular dyskinesis are lacking.

Let us discuss more on this issue on this subject & understand what exactly is scapular dyskenesia & how to test it.

Following definitions are taken from Journal of Athletic Training 2009; 44(2):160–164 g by the National Athletic Trainers’ Association, Inc (Philip M et al)

Operational Definitions

The movement that is studied:

Shoulder flexion and frontal-plane abduction (5-repeatations). (see the figure above)


Normal scapulohumeral rhythm: The scapula is stable with minimal motion during the initial 30 to 60 degrees of humerothoracic elevation, then smoothly and continuously rotates upward during elevation and smoothly and continuously rotates downward during humeral lowering. No evidence of winging is present.

Scapular dyskinesis: Either or both of the following motion abnormalities may be present.

Dysrhythmia: The scapula demonstrates premature or excessive elevation or protraction, non-smooth or stuttering motion during arm elevation or lowering, or rapid downward rotation during arm lowering.

Winging: The medial border and/or inferior angle of the scapula are posteriorly displaced away from the posterior thorax.

The Rating Scale for scapular dyskinesia:

Each test movement (flexion and abduction) rated as

a) Normal motion: no evidence of abnormality

b) Subtle abnormality: mild or questionable evidence of abnormality, not consistently present

c) Obvious abnormality: striking, clearly apparent abnormality, evident on at least 3/5 trials (dysrhythmias or winging of 1 in [2.54 cm] or greater displacement of scapula from thorax)

Final rating is based on combined flexion and abduction test movements.

Normal: Both test motions are rated as normal or 1 motion is rated as normal and the other as having subtle abnormality.

Subtle abnormality: Both flexion and abduction are rated as having subtle abnormalities.

Obvious abnormality: Either flexion or abduction is rated as having obvious abnormality.

The relationship of Scapular dyskinesia to that of Shoulder injuries

Source: Journal of Athletic Training 2009;44(2):165–173 g by the National Athletic Trainers’ Association, Inc (Angela R et al)

Angela et al reported that presence of scapular dyskinesis was not related to shoulder symptoms in athletes engaged in overhead sports.



Friday, October 2, 2009

Complete frozen shoulder lookout


Classification of FSS (Frozen shoulder syndrome)

1. Primary (Idiopathic) Frozen Shoulder

2. Secondary Frozen Shoulder

1. Systemic
1. Diabetes mellitus
2. hypothyroidism
3. hyperthyroidism
4. Hypoadrenalism

2. Extrinsic
1. Cardiopulomonary disease
2. Cervical Disc
3. CVA
4. humerus fractures
5. Parkinson's

3. Intrinsic
1. RTC Tendinitis
2. RTC Tears
3. Biceps tendinitis
4. Calcific tendinitis
5. AC arthritis

*from Coumo, F. Diagnosis, Classification, and Management of the Stiff Shoulder. In: Disorders of the Shoulder: Diagnosis and Management. Iannotti, JP and Williams GR (eds). 1999

Description of pain in primary FSS (Frozen shoulder syndrome):

The onset: After a period of pain, localized mostly in the shoulder and / or upper arm, begins the onset of severe limitation of movement of the glenohumeral joint in all directions.

Cause: Movement limitation is caused by the retraction of the glenohumeral joint capsule and adhesions of the subdeltoid bursa. Due to this condition of the glenohumeral joint the arm is not able to be elevated forward, actively or passively, more than 90 degrees. This movement is made possible by rotation of the scapula and forced posterior movement of the clavicle.

Cineradiography of the primary frozen shoulder reveals:

Cineradiography of the primary frozen shoulder reveals that not only is the movement pattern of scapula and clavicle changed, but also the relationship between the coracoid process and the clavicle. Further forward elevation of the arm is made impossible due to obstruction of the coracoid process by the clavicle. This obstruction results in the compression of the tissues lying between these bones causing pain. Postmortem examination confirms this theory.

Guided by these observations it is thus illustrated that patients with a frozen shoulder suffer pain, not only from the primarily affected tissues around the shoulder, but also from the compression of the tissues between the coracoid process and the clavicle during forward elevation of the arm. (Stenvers and Overbeek 1978).

Change in the thinking of the approach to FSS:

Many researchers and clinicians believe the effectiveness of existing physical therapy interventions can be improved by targeting the provision of specific interventions at patients who respond best to that treatment. The key messages are that subgroups should be identified (Hancock et al).

Frozen shoulder is a vast entity. This syndrome is classified in to primary & secondary. Depending on acuteness & time course of presentation FSS (Frozen shoulder syndrome) has 4 distinct stages.

1. Stage 1: "Pre-adhesive Stage"
2. Stage 2: "Freezing Stage"
3. Stage 3 "Frozen Stage"
4. Stage 4: Thawing Stage

The pain resistance sequence pattern is conspicuous in different stages. Many different articles claim, there are secondary myofascial shortening & stiffness of thoracic spine in addition to capsular tightness. Hence the treatment advocacy is varied yet not streamlined. Treatment involves:

1. Shoulder mobilization
2. Shoulder mobilization + or - capsular stretching
3. Shoulder mobilization + or - capsular stretching + or -myofascial stretching +or - *
4. Shoulder mobilization + or - capsular stretching + or - myofascial stretching + or -**

* AC ± SC± ST ± joint mobilization
** AC ± SC± ST joint mobilization ±thoracic mobilization
*** All mobilization procedures are appropriately supplemented with strengthening

Research report about effectiveness of joint mobilization in FSS:

Bulgen et al (1984) performing a RCT comparing passive mobilization techniques (3 times per week for 6 weeks, intensity unknown) with intra-articular steroid injections, ice therapy followed by PNF, or no therapy, reported following-term (6 months) advantages of any of the treatment regimens over no treatment.

Yang et al (2007) compared the use of 3 mobilization techniques----in the management of 28 subjects with frozen shoulder syndrome. ERM and MWM (Mobilization with movement) were more effective than MRM in increasing mobility and functional ability.

Research report about effectiveness of multidirectional stretching in FSS:

The vast majority of patients who have phase-II idiopathic adhesive capsulitis can be successfully treated with a specific 4-direction shoulder-stretching exercise program. Patients with more severe pain and functional limitations before treatment had relatively worse outcomes. More aggressive treatment such as manipulation or capsular release was rarely necessary, and the efficacy of early use of these treatments should be further studied.

Content of the Pre-introduction class to shoulder techniques

Thursday, October 1, 2009

Be cautious while mobilizing stiff shoulder.


Current much acclaimed article of Vermeulen HM et al has changed the approach to frozen shoulder. End range mobilization is preferred over other techniques of mobilization. However, administering mobilization in shoulder is not out of danger.

Drakos MC et al (The Hospital for Special Surgery, 535 E 70th St, New York, NY 10021, USA) reported “Shoulder dislocation after mobilization procedures for adhesive capsulitis”. This study is published in Orthopedics. 2008 Dec;31(12). No abstract or text available in PUBMED.


Leon Chaitow’s recommendation of manual therapy for parkinsonism


1. Antero-posterior and lateral mobilization of the thoracic and lumbar spine (patient seated).

2. Myofascial release of the thoracic spine (patient seated).

3. Atlanto-occiptal release (patient supine; not manipulation).

4. Mobilization of the cervical spine (patient supine).

5. Muscle-energy technique (MET) release of cervical muscles (patient supine).

6. General mobilization of the shoulder joints including use of MET (patient side-lying).

7. Mobilization of the forearms (patient supine).

8. Mobilization of the wrists (patient supine).

9. Mobilization of the SI joint (patient supine).

10. MET to the hip adductors (patient supine).

11. MET to psoas muscles (patient supine).

12. MET to hamstrings (patient supine).

13. Mobilization of the ankles (patient supine).

14. MET to the ankle in dorsi and plantar flexion (patient supine).

Note: This sequence has to be performed in this order in 30 minutes.