Tuesday, December 6, 2011

Baastrup disease: Lumbar interspinous bursitis

This disease is named after Danish radiologist (1855 - 1950) Christian Ingerslev Baastrup.

Introduction & Epidemiology:
It is claimed that Baastrup disease is responsible for intractable LBA (1). Though it is reported in mostly lumbar spine it’s cervical spine variant is also reported (2). Gardella called Baastrup disease as spinous process syndrome (3). It is reported in many occupational areas such as miners (4) & heavy vehicle drivers (8). Among of much debate now it is considered mostly a case of aging related problem. Let us discuss in little more detail:

The Baastrup disease is characterized by the development of abnormal contact between adjacent spinous processes of the lumbar spine that results in rubbing against each other producing a bursitis which further result in focal midline pain and tenderness relieved by flexion and aggravated by extension.

It tends to be more common in the elderly. According to Maes et al (5) the prevalence of Baastrup disease is 8.2% (44 of 539) of the study population. In this study the lumbar spine was studied. This study also revealed that Baastrup disease is associated with age (P = 0.001), central canal stenosis (P = 0.0013), disc bulging (P = 0.0341), and anterolisthesis (P = 0.0429). There were no associations between Baastrup disease and disc degeneration, disc herniation, endplate findings, retrolisthesis, scoliosis, lordosis, or gender.
According to Kwong et al (6); Baastrup disease occurs with high frequency among the elderly. This study suggests that Baastrup disease develops with increasing age and is part of the expected degenerative changes in the aging spine. According to these researchers (6) in their CT scan based study of 1008 patients evidence of Baastrup disease was found in 413 patients (41.0%). A decade-on-decade increase in frequency was found with a peak of 81.3% among patients older than 80 years. As many as five spinal levels were found to be affected in some patients (4.1% of 413), but in most patients (35.4%), one level was affected. Baastrup disease was most common at L4-L5. Associated degenerative changes were found at almost all affected levels (899/901). Hence Kwong et al urged the clinicians that because of the nearly universal association with other degenerative changes, caution must be taken before diagnosing Baastrup disease as the cause of back pain.
According to Hanger (8) prevalence rate of this disease in a group of heavy automotive vehicles drivers is 13% of the test population.

Patients with Baastrup disease may experience pain owing to irritation of the periosteum or adventitial bursae between abutting spinous processes. This process can result in a degenerative hypertrophy, inflammatory change and even a pseudarthrosis with bursa formation. This interspinous bursa may extend between the ligamentum flavae in the midline forming an epidural cyst and further contributing to the already existing canal stenosis.
This condition is usually seen patients with excessive lordosis of the lumbar spine. Often Baastrup lesions of the lumbar spine are located at L3-L4 and L4-L5 segments (8).

I myself employ the following technique to find a Interspinous bursa is swollen or not.
First the spinous processes are palpated. The gap between the spinous process (Interspinous area) is located and palpating finger (usually the thumb) is slided on the slope following a parallel path way to that of laminas. Reaching on to the area between the spinous process from the side is easy & if Baastrup disease is present then obviously high degree of tenderness is elicited.This palpation also gives us the idea if the crowding of (kissing of ) spinous process as compared with other interspinous spaces & further it may reveal the tissue texture of the local tissue. Inflammed bursa with cyst may impart a "bouggy" feeling to the palpating hand. 

Radiographic features (9)
Plain film and CT
 •    often shows close approximation and contact of adjacent spinous processes (kissing spines)
•    there is resultant enlargement, flattening and reactive sclerosis of apposing interspinous surfaces.

May demonstrate interspinous bursal fluid and a postero-central epidural cyst(s). MRI can be very helpful in determining whether there is resulting posterior compression of the thecal sac.

Baastrup's sign: Also known as kissing spine, is an radiographic sign. It is characterized by posterior spinous processes 'kissing' and touching one another on sagittal plane.

Treatment (9)
Both conservative and surgical options are available for treatment. Local steroid injection into the interspinous processes will often ease the back pain. Surgical options include interspinous process decompression devices (e.g, Wallis system, X STOP), and steroid / local anaesthetic injection into the bursa.


No references are there about physiotherapy. However electro-analgesia & thermo-analgesia are quite effective. SWD, PSWD, MWD & FIR exert powerful anti-inflammatory effect with thermo-analgesia. IFT gives anti-inflammatory effect with electro-analgesia. UST in pulsed mode directed appropriately to the focal tissue is both anti-inflammatory & analgesic.
Manual mobilization techniques are tried once the local tenderness is less. Contrast heat in acute inflammation & Hot fomentation thrice a day is also very effective in long standing cases which should be used as a home remedy. Egronomic corrective methods & postural awareness are of utmost importance as they may be primary factor that produced such a disorder. Manual therapists well versed with soft tissue & fascial techniques should try out techniques that may lengthen the thoracolumbar fascia.
The outcome of physiotherapy is so satisfactory that author opine on his clinical experience, steroid infiltration & surgery are rarest of rare probabilities to be employed. 

1. FERNANDEZ DE LA MELA I; Medicamenta (Madr). 1951 Dec 10;9(210):404-5.[Lumbar interspinal nearthrosis (Baastrup disease) as responsible for some intractable backaches].

2. VIALLET P J Radiol Electrol Arch Electr Medicale. 1950;31(3-4):206-7. [Two cases of cervical localization of Baastrup disease].

3. GARDELLA G; Ann Radiol Diagn (Bologna). 1952;24(4):260-74.[Spinous process syndrome (Baastrup disease)].

4. Gajdek D; Chir Narzadow Ruchu Ortop Pol. 1976;41(2):171-4. Polish. No abstract available. [Baastrup syndrome of the lumbar spine in miners].

5. Maes R et al; Spine (Phila Pa 1976). 2008 Apr 1;33(7):E211-5. [Lumbar interspinous bursitis (Baastrup disease) in a symptomatic population: prevalence on magnetic resonance imaging.]

6. Kwong Y et al AJR Am J Roentgenol. 2011 May;196(5):1156-9. MDCT findings in Baastrup disease: disease or normal feature of the aging spine?

7. Pinto PS et al Clin Imaging. 2004 May-Jun;28(3):219-22. [Spinous process fractures associated with Baastrup disease.]

8. Hagner W; Med Pr. 1988;39(1):65-70. [Baastrup's disease of the lumbar segment of the spine among drivers of heavy motor vehicles].

9. http://radiopaedia.org/articles/baastrup_syndrome

Monday, December 5, 2011

Classification of spinal cord injury: ASIA classification Vs Frankel classification

Clinicians have long used a clinical scale to grade severity of neurological loss in SCI. First devised at Stokes Manville before World War II and popularized by Frankel in the 1970's, the original scoring approach segregated patients into five categories.

Frankel classification:Grade A:  no function
Grade B: sensory only
Grade C: some sensory and motor preservation
Grade D: useful motor function
Grade E: normal function

ASIA classification:Grade A:  Complete. No motor or sensory function preserved in the sacral segments (S4-S5)
Grade B: Incomplete. Sensory function is preserved but motor function is affected below the neurological level & includes the sacral segments (S4-S5)
Grade C: Incomplete. Motor function is preserved below the neurological level, and more than half of the key muscles below the neurological level have a muscle grade less than 3.
Grade D: Incomplete. Motor function is preserved below the neurological level, and more than half of the key muscles below the neurological level have a muscle more than 3.
Grade E: Normal. Motor & sensory functions are normal.

5-Clinical syndromes in incomplete SCI by ASIA classification:1. Central cord syndrome 2. Brown-Sequard syndrome 3. Anterior cord syndrome 4. Conus medullaris syndrome 5. Cauda equina syndrome
The ASIA committee also classified incomplete spinal cord injuries into five types. A central cord syndrome is associated with greater loss of upper limb function compared to the lower limbs. The Brown-Sequard syndrome results from a hemisection lesion of the spinal cord. Anterior cord syndrome occurs when the injury affects the anterior spinal tracts, including the vestibulospnal tract. Conus medullaris and cauda equina syndromes occur with damage to the conus or spinal roots of the cord.

Advantages of ASIA impairment scale:
1. First, instead of no function below the injury level, ASIA A is defined as a person with no motor or sensory function preserved in the sacral segments S4-S5. This definition is clear and unambiguous.
The new ASIA A categorization turns out to be more predictive of prognosis than the previous definition where the presence of function several segments below the injury site but the absence of function below a given level could be interpreted as an "incomplete" spinal cord injury.
2. ASIA B is essentially identical to Frankel B but adds the requirement of preserved sacral S4-S5 function. It should be noted that ASIA A and B classification depend entirely on a single observation, i.e. the preservation of motor and sensory function of S4-5.
3. The ASIA scale also added quantitative criteria for C and D. The original Frankel scale asked clinicians to evaluate the usefulness of lower limb function. This not only introduced a subjective element to the scale but ignored arm and hand function in patients with cervical spinal cord injury. To get around this problem, ASIA stipulated that a patient would be an ASIA C if more than half of the muscles evaluated had a grade of less than 3/5. If not, the person was assigned to ASIA D.
4. ASIA E is of interest because it implies that somebody can have spinal cord injury without having any neurological deficits at least detectable on a neurological examination of this type. Also, the ASIA motor and sensory scoring may not be sensitive to subtle weakness, presence of spasticity, pain, and certain forms of dyesthesia that could be a result of spinal cord injury. Note that such a person would be categorized as an ASIA E.

These changes in the ASIA scale significantly improved the reliability and consistency of the classification. Although it was more logical, the new definition of "complete" injury does not necessarily mean that it better reflects injury severity.

Friday, December 2, 2011

Shoulder: Bankart surgery rehabilitation

Bankart surgery:
Bankart lesion is an injury of the anterior (inferior) glenoid labrum due to repeated (anterior) shoulder dislocation. Repeated dislocation forms a pocket at the front of the glenoid that allows the humeral head to dislocate into it. It is often accompanied by a Hill-Sachs lesion (damage to the posterior humeral head seen as a depression on X-ray). A bony bankart is a Bankart lesion that includes a fracture in of the anterior-inferior glenoid cavity.
Bankart lesion warrants surgery. In Bankart surgery the anterior (inferior) glenoid labrum is reattached to the glenoid. Generally there is a anterior approach to this shoulder operation. Rehabilitation is the key to successful reinstitution of functional activities. As it is a very common injury in sports like javelin throwing return to sports is heavily dependant on post operation physiotherapy. The following is an sample schema of physiotherapy & rehabilitation approach to the Bankart surgery.    


Restrictions up to 4 weeks: (To protect the reattached anterior capsule & labrum)
1. Shoulder extension (backwards) past the plane of the body
2. Shoulder external rotation (arm rotation outwards) greater than 0° (straight in front); extensive repairs may require more restrictions

For posterior repairs (To protect the reattached posterior capsule & labrum)

1. Avoid any shoulder internal rotation (turning in) past the body i.e. hand behind back.

Restrictions up to 3 months:
No passive forceful stretching into external rotation/extension following an anterior repair and into internal rotation for a posterior repair.


- Good posture is critical throughout the rehabilitation process to improve healing and decrease the risk of developing poor mechanics

- Aerobic conditioning throughout the rehabilitation process

- MD follow-ups Day 1, Day 8 - 10, 1 month, 4 months, 6 months and 1 year post-op

- All active exercises should be carefully monitored to minimize substitution or compensation

1 - 5 Days Post-op

1. Use of arm sling
2. Ice pack for first 3 - 5 days. (Apply over the dressing but should not sip into the dressing)
3. Postural education & sleeping posture advice (semi-reclined is most comfortable) 
4. Other general exercises: Stationary bike, stair machine etc
5. Codmann’s Pendulum exercise to reduce muscular spasms, Scapulothoracic stabilizer training, elbow flexion/extension, wrist and forearm strengthening, gentle passive/active assistive exercises of the arm in flexion (front) keeping below the level of the shoulder & finally cervical muscle stretching.

* Surgeon’s check up to change dressing etc.

5 - 14 Days Post-op

1. To reduce pain: IFT or TENS/ massage / contrast heat etc
2. Russian current for strengthening
3. Increase PROM and active assistive (AAROM) exercises as tolerated (from flexion out into the scapular plane) up to 90° unless otherwise indicated
4. Soft tissue therapy to developing scar as appropriate.
5. Scapulothoracic mobilization
6. General conditioning as tolerated (include trunk flexion & extension exercises)

2 - 4 Weeks Post-op

1. Now at this stage passive and active assisted flexion out to scaption (plane of the scapula) as tolerated.
 2. Sub-maximal isometrics (as dictated by pain) & Isotonic wrist, forearm.
 3. Resisted exercises using theraband are started from this phase onwards.
a.    Theraband resisted pull-downs from the front and the scapular plane
b.    Theraband resisted elbow flexion (high reps and low resistance)
4. Active scapular elevation, depression, and retraction exercises
5. Light weight bearing exercises

4 - 6 Weeks Post-op

1. By 4-6 weeks resting pain is substantially less.
2. Continue with passive and AAROM exercises (cane exercises, wall walking, table slide) from flexion & scaption out to abduction as tolerated
3.  Maximal isometrics
4. Active exercises from flexion into the scapular plane against gravity as tolerated
5. No resistance until able to perform 30 reps at limb weight with perfect mechanics
6. Rested internal rotation 0° to the body. (Only light resistance)
7. Add proprioceptive training exercises. (Alphabet writing, fine motor skills, work/sport specific exercises)

6 - 8 Weeks Post-op

1. Increase AROM exercises as tolerated (serratus anterior, upper, and lower trapezius).
2. Eccentrics exercises are added into protected ranges 
3. From this phase onwards begin LIGHT stretching into external rotation
4. GHJ joints play + mobilizations as tolerated
5. Increase proprioceptive training (prone on elbows, quadruped position ("on all four's") for rhythmic stabilization
6. Okay to begin jogging, road cycling, and standing arm resistance exercises in the pool

8 - 12 Weeks Post-op

Emphasis on regaining strength and endurance

1. PNF patterns (proprioceptive neuromuscular facilitation) can be started safely
2. AROM exercises: internal rotation and external rotation as motion allows
3. AROM exercises: lateral raises and supraspinatus isolation
4. Rower with a high seat, decline bench press, military press in front of body
5. Running, road or mountain biking, no activities with forceful, ballistic arm movement

3 - 6 Months Post-op

1. Aggressive stretching.
2. Start strenuous resistive exercises
3. Add light throwing exercises with attention to proper mechanics

6 Months Post-op

1.  Increase throwing program with focus on return-to-throwing sports as mechanics
2.  Sports conditioning with all of the normal shoulder movements

NB: Progression is based on individual patient presentation, which is assessed throughout the treatment process. People well versed with soft tissue & fascial tissue manipulations can appropriately employ them from 2nd week onwards.

Monday, November 21, 2011

Diagnosis of knee instability

According to Rossi et al, for knee; clinicians should have own series of exams with whom he is more confident and on whom he relies on for diagnosis. Usually, three sets of series are used:

1. One for patello-femoral/extensor mechanism pathologies
2. Another for meniscal and chondral (articular) lesions
3. The other one for instability evaluation

Among the above said to assess the 3rd category is difficult to diagnose. Often the diagnosis becomes more difficult because there are more than one tissue involved.

Following are clues to diagnose them:

1. Anerior medial instability (AMI):

AMI occurs due to: ACL + MCL + medial meniscus injury.

Test series to diagnose it are: valgus stress, anterior drawer, Lachman tests

2. Anterior lateral instability (ALI):

ALI occurs due to: ACL + lateral capsule + lateral meniscus injury.

Test series to diagnose it are: valgus stress, anterior drawer, Lachman, pivot shift tests

3. Posterior lateral instability (PLI):

PLI occurs due to: Injury to posterior lateral corner of the knee.

Test series to diagnose it are: external rotation, dial, recurvatum, posterolateral drawer tests

4. Posterior medial instability (PMI):

PMI occurs due to: MCL + ACL + Posterior medial corner.

Test series to diagnose it are: valgus stress, posterior drawer, Lachman tests

5. AMI + ALI instability:

Occurs due to: ACL + MCL + lateral capsule ( But PCL is intact)

Test series to diagnose it are: anterior drawer, Lachman, pivot shift, valgus stress
6. PMI + PLI instability:

Occurs due to: ACL + MCL + lateral capsule (But PCL is intact)

Test series to diagnose it are: anterior drawer, Lachman, pivot shift, valgus stress, varus stress tests


Rossi et al. Sports Medicine, Arthroscopy, Rehabilitation, Therapy & Technology 2011, 3:25 (http://www.smarttjournal.com/content/3/1/25)

Sunday, November 20, 2011

Type of SLAP lesions & The dead arm syndrome

The SLAP lesions:
Superior labrum tears were first described by Andrews. Further SLAP lesions as described by Snyder are subdivided into 4 types (I-IV) & this classification is according to their severity of tear. For best diagrams of the SLAP lesions refer to the following site:


Type I SLAP lesion:
This is a partial tear and degeneration to the superior labrum, where the edges are rough and fray along the free margin, but the labrum is not completely detached.
Type II lesion:
Type II is the comonest type of SLAP tear. The superior labrum is completely torn off the glenoid, due to an injury (often a shoulder dislocation). This type leaves a gap between the articular cartilage and the labral attachment to the bone. Type 2 SLAP tears can be further subdivided into (a) anterior (b) posterior, and (c) combined anterior-posterior lesions.
Type III lesion:
A Type III tear is a 'bucket-handle' tear of the labrum, where the torn labrum hangs into the joint and causes symptoms of 'locking' and 'popping' or 'clunking'. 

Type IV lesion:
The Type IV SLAP tear is one where the tear of the labrum (bucket handle tear) extends into the long head of biceps tendon.

Dead arm syndrome (DAS) &; Type II SLAP lesion:

Now the most important part of the article is which of the SLAP lesion presents with “Dead arm syndrome”.
Dead arm syndrome is clearly a subjective phenomenon (see the definitions below). The sufferer is mostly an athlete whose work involves lot of throwing for example base ball or cricket. The athlete will often say "I just can't throw anymore, and / or the shoulder just doesn't feel right". This type of injury tends to progress gradually over time, slowly creeping up on the overhead athlete until severe pain and subjective instability limits his or her ability to perform.

Dead arm syndrome: Definition

1. Sensory diminution or loss in the arm after anterior shoulder dislocation or subluxation. (Stedman's medical dictionary)

2. The Dead Arm Syndrome has been defined as the inability to throw, spike or serve at pre-injury level secondary to subjective pain and instability.

Description & progression of DAS:

Dead arm syndrome starts with repetitive motion and thus force exerted on the posterior capsule of the shoulder. Overuse can lead to posterior capsule hypertrophy. The next step is tightness of the posterior capsule called posterior capsular contracture. This reduces the shoulder internal rotation. If shoulder activities are still continued then over time, with enough force, a tear may develop in the labrum. The shoulder is unstable and dislocation may come next. Dead arm syndrome won't go away on its own with rest—it must be treated. If there's a SLAP lesion, then surgery is needed to repair the problem. If the injury is caught before a SLAP tear, then physical therapy with stretching and exercise can restore it. Before hand how to know then a SLAP lesion or a dead am syndrome may occur? The answer is shoulders at risk for the dead arm syndrome have a marked loss of internal rotation caused by contracture of the posteroinferior capsule such that less than a 180 degrees arc of rotation is achieved with the arm abducted 90 degrees (the 180 degrees rule).

What is the cause of DAS?
According to Buckhart et al root cause of the dead arm syndrome is the Type II SLAP lesion.
Type 2 SLAP lesions that cause the dead arm syndrome in overhead-throwing athletes are most likely acceleration injuries that occur in late cocking rather than deceleration injuries in follow-through.

More about Type II SLAP lesions form Buckhart et al’s article:

Clinical presentations of all 3 types of Type II SLAP lesion are different. Following are few points to remember about them.
1. Posterior and combined Type 2 SLAP lesions can be disabling to overhead-throwing athletes because of posterosuperior instability and anteroinferior pseudolaxity.
2. The Jobe relocation test is positive with posterosuperior pain in patients with posterior or combined anterior-posterior Type 2 SLAP lesions and is negative in patients with anterior Type 2 SLAP lesions.
3. Rotator cuff tears are frequently associated with posterior or combined anterior-posterior SLAP lesions, are lesion-location specific, and typically begin from inside the joint as undersurface tears.
4. The peel-back mechanism is a likely cause of posterior Type 2 SLAP lesions.

•    Two categories
o    Aware of subluxation
o    Unaware of subluxation
•    Often misdiagnosed as other shoulder pathology or cervical lesion

Associations with other diseases
•    Thoracic Outlet Syndrome
o    30% of patients had coexistent TOS
o    Due to altered kinetics of the Scapulothoracic Joint
o    Resultant neurovascular compromise

Treatment of DAS:

A. Surgical:
1. Repair of posterior SLAP lesions can return overhead-throwing athletes to full overhead athletic functioning.
2. To securely repair the posterosuperior labrum to resist torsional peel-back, suture anchors must be placed posterior to the biceps at the corner of the glenoid. The repair must be protected against external rotation past 0 degree for 3 weeks to avoid undue premature torsional stresses on the repair from the peel-back mechanism.

B. Physiotherapy:
Rehabilitation of athletes with the dead arm syndrome must include the entire kinetic chain.

1. Burkhart SS et al;  Clin Sports Med. 2000 Jan;19(1):125-58.
2. Wikipedia
3. http://www.shoulderdoc.co.uk/article.asp?article=1027
4. http://www.orthofracs.com/adult/elective/shoulder/dead-arm-syndrome.html

Friday, November 18, 2011

What is metabolic fitness (MF)?

In previous years, fitness was commonly defined as the capacity to carry out the day’s activities without undue fatigue. These days, physical fitness (PF) is considered a measure of the body’s ability to function efficiently and effectively in work and leisure activities, to be healthy, to resist hypokinetic diseases, and to meet emergency situations.

Physical fitness comprises two related concepts: general fitness (for the purpose of health), and specific fitness (a task-oriented definition based on the ability to perform specific aspects of sports or occupations). Physical fitness is generally achieved through correct nutrition, exercise, and enough rest.

PF can be measured as an out come of physical activity and also as a moderator on morbidity and mortality. Physical fitness for purposes of health, is best defined by the specific components that relate to improved health or reduced disease. The components of Health-Related Fitness are:
–    Morphological
–    Muscular
–    Motor
–    Cardiorespiratory
–    Metabolic
For the discussion of our topic metabolic fitness is more important. Metabolic fitness is the newest component if fitness.

Metabolic fitness:

Physical inactivity is strongly associated with an increased risk of premature disease and death, and the falling level of physical activity. Both aerobic fitness (maximum oxygen uptake) and metabolic capacity of the muscles are important in this matter. The role of the metabolic capacity/fitness of muscle, appears to be especially critical for the development of metabolic-related diseases and thus for the health of the individual.

Definition: A definition of metabolic fitness is proposed as the ratio between mitochondrial capacity for substrate utilisation and maximum oxygen uptake of the muscle.
Indirect means of determining metabolic fitness is Glucose tolerance, blood lipid & cholesterol profiles (especially HDL & triglyerisdes) & finally lipid oxidation.

Skeletal muscle is an extraordinarily plastic tissue and metabolic capacity/fitness changes quickly when the level of physical activity is altered. High metabolic fitness includes an elevated use of fat at rest and during exercise. The capacity for glucose metabolism is also enhanced in trained muscle.

There are many adaptations to physical activity. Exercise-induced activation of genes coding for proteins involved in metabolism is described as an underlying mechanism for some of these adaptations. The increased gene expression is of relatively short duration, which implies that a certain regularity of physical activity is required to maintain high metabolic fitness. Thus, metabolic fitness is directly related to how much the muscle is used, but even low levels of physical activity have a beneficial effect on metabolic fitness and the overall health of the individual.
Subcomponents of metabolic fitness include:
–    Glucose Tolerance
–    Blood Lipid and Cholesterol Profiles
–    Lipid Oxidation

Glucose Tolerance
1. Regular exercise can be used to treat glucose intolerance in Type II diabetics.
2. Effects of exercise include normalizing insulin and glucagon production by the liver, increasing insulin sensitivity by the exercising muscle, thus enhancing glucose uptake.

Blood Lipid and Cholesterol Profiles
1. Exercise decreases total blood cholesterol, increases HDL-Cholesterol, and decreases blood triglycerides.

Lipid Oxidation
1. High lipid oxidation alters cholesterol metabolism and reduces body fat to reduce risk of cardiovascular disease. Thus, chronic aerobic exercise spares glucose stores and uses more fat oxidation for fuel.

Assessment of metabolic fitness:
The direct measurement of metabolic fitness and/or aerobic demand is the means that can be used as an index of the efficacy of an exercise training program or other therapeutic intervention; as medical risk factor for predicting the risk of cardiovascular disease, diabetes, death or other health outcome; or as an aid to pharmaceutical companies for drug discovery in the area of metabolic fitness, deconditioning, and oxidative biology.

1. Ugeskr Laeger. 2002 Apr 15;164(16):2156-62.
2. Kennedy RA et al; Journal of Sports Science and Medicine (2007) 6, 448-454

Saturday, November 12, 2011

Clinical classification of Erb’s palsy & it’s physiotherapy

Narakas classified babies with obstetric palsy into four groups
I. Upper Erb's palsy (C5, C6 injury)
II. Extended Erb's (C5, C6, C7 injury)
III. Total palsy (C5, C6, C7, C8 & T1 injury)
IV. Total palsy with Horner’s syndrome (C5, C6, C7,C8 & T1 injury)

Clinically however Narakas Group II can be sub-classified into two groups according to this 'early recovery of wrist extension.'

II a. recovery of Gr 3 wrist extension before 2 months of age.
II.b. recovery of Gr 3 wrist extension after 2 months of age.

II a recovers the UL function much faster than the II b group.

Muscles paralysed in Group I are: Biceps, Deltoid, Brachialis, Brachioradialis, partly supraspinatus, infraspinatus, Supinator.

Extended erbs palsy involves the elbow & wrist

Intrinsic muscles of hand & ulnar flexors are paalysed in total palsy

Horner’s syndrome comprise of: Ptosis, Miosis, Anhydrosis, Enopthalmus, Loss of ciliospinal reflex.

Sensory loss in Gr I & II may be in little area over deltoid.

Physical therapy approach in nut shell:

Therapy is the cornerstone in the management of the symptoms of a child with BPP brachial plexus palsy. Popular or conventional physiotherapy approaches include exercise therapy, tactile stimulation, soft tissue manipulation techniques and functional splinting. Recently functional stimulation is found better than common electrical stimulation (2).

Galvanic stimulation to the paralysed muscles. Libile method is used with faradic stimulation.

Exercise therapy:
A comprehensive program that includes stretching exercises, safe handling and early positioning techniques, developmental and strengthening activities, and sensory awareness should be developed and updated as needed.
For the first 2 weeks, the child may have some pain in the affected shoulder and limb, either from the injury or from an associated clavicular or humeral fracture. The arm can be fixed across the child's chest by pinning of his/her clothing to provide more comfort. However, some authors have discouraged this pinning in favor of immediate institution of gentle ROM exercises. Parents should be instructed in techniques for dressing the child to avoid further traction on the arm.
A comprehensive therapy program should consist of ROM exercises, facilitation of active movement, strengthening, promotion of sensory awareness, and provision of instructions for home activities. Overall goals should focus on minimizing bony deformities and joint contractures associated with BPP, while optimizing functional outcomes.

Splinting & taping:
Often a wrist extension splint is necessary to maintain proper wrist alignment and reduce the risk of progressive contractures even at 2 weeks period.
Static and dynamic splinting of the arm is useful to reduce contractures, prevent further deformity, and in some cases, assist movement. Commonly prescribed splints include resting hand and wrist splints, elbow extension splints, dynamic elbow flexion and supinator splints. Careful selection and timing of splint use is essential to optimization of the desired effect.

Taping techniques may be used by the therapist to control scapular instability and hence to promote improved shoulder mobility.

Contractures &stretching:
Severe contractures should be avoidable with consistent therapeutic exercises, including passive and active stretching, flexibility activities, myofascial release techniques, and joint mobilization.

Over time, these contractures can lead to progressive bony deformity and shoulder dislocation. Early and consistent stretching of internal rotators should minimize the risk of this problem. External rotation, performed with the shoulder adducted alongside the chest and with the elbow flexed to 90°, provides maximum stretch of internal rotators (specifically, the subscapularis) and the anterior shoulder capsule.
The scapula should be stabilized while stretching shoulder girdle muscles to maintain mobility and preserve some scapulohumeral rhythm. Early development of flexion contractures at the elbow is common and can be exacerbated by radial head dislocation caused by forced supination. Aggressive forearm supination, therefore, should be avoided.

Sensory awareness:
Sensory awareness activities are useful for enhancing active motor performance, as well as for minimizing neglect of the affected limb. Use of infant massage and drawing visual attention to the affected arm can be incorporated easily into play and daily activities. Weight-bearing activities with the affected arm in all positions not only provide necessary proprioceptive input but also can contribute to skeletal growth.


1. Al-Qattan MM et al; J Hand Surg Eur Vol. 2009 Dec;34(6):788-91. Epub 2009 Sep 28.
2. Okafor UA et al; Nig Q J Hosp Med. 2008 Oct-Dec;18(4):202-5.
3. http://emedicine.medscape.com/article/317057-treatment

Friday, October 28, 2011

Implications of Physiotherapists as indipendent mecine prescriber

Hi all physiotherapists. Time is changing rapidly for us. Our services at different areas of medicine has brought credit to us. As a result of that

In USA: We are trying to get into 1st hand practice where clinical entry level DPT and many such advancements are noted.

In UK: Recently in BBC news it was flashed that "Physiotherapists may get independent medicine prescription rites". Already physios have injection rights in UK.

In AUS: Physiotherapists are trying to persuade legislators to allow physiotherapists for minor surgeries "wound suturing", injection rights, independent prescription writes.     

9thnrhc.ruralhealth.org.au/program/docs/papers/moore_D3.pdf  (Download)

2008 WHO classification of "Health workers" 

Please refer to the WHO (World health organization) classification (2008) of health workers which is an international standard classification where there are separate ISCO codes to physiotherapists & physiotherapy technician. Thankfully the classification is far more indicative this time.  

Physiotherapist: ISCO code- 2264  

Physiotherapy technician: ISCO code- 3255


Saturday, September 24, 2011

Implication of anterior drawer test, Lachman’s test, Pivot shift test to that of knee Instability

Lachman's vs. Anterior Draw Test

•    Lachman's test may be more difficult for clinicians to perform but tends to be more sensitive
•    In the anterior draw test knee is positioned so that the hamstrings have a mechanical advantage. Increased hamstring activity can inhibit tibial translation, causing a false negative test
•    A torn meniscus can act as a block to tibial motion, again causing a false negative while doing the anterior draw test

Anterior drawer test with tibia external rotation:

Anterior drawer test with tibia in neutral rotation demonstrates equal displacement of both condyles & this displacement is eliminated by internal rotation of the tibia, then both anteromedial and anterolateral rotary instability may be present.

Similarly positive anterior drawer test in neutral tibial rotation, that is accentuated when the test is repeated in 30 deg of external rotation and reduced when performed with the tibia in 15 deg of internal rotation indicates anteromedial rotary instability.

Pivot shift test is the test which indicates antrolateral instability (ALI) of the knee.

Research indicates antrolateral instability further increase with injury to LCL (lateral collateral ligament) & PCL (Posterior Cruciate ligament).  Broadly speaking ALI is also associated with injury to accuate complex that includes posterior 1/3 of lateral supporting structures i.e. LCL, arcuate ligament, & exension of popliteus.

It is also reminded to the reader that posterior 1/3 of the lateral ligamentous complex is reinforced by biceps, popliteus, & lateral head of gastrocnemius.

Wednesday, August 17, 2011

C6-C7 syndrome: My clinical experience & suggestions

Many confuse marked tenderness at the coracoid tip, lateral pectoral and medial elbow sites to be a variant of fibromyalgia however usually it comes along with tenderness at the C6-7 level in the cervical spine. A close look in to the history reveals in this group of patients lose tenderness at C5-6 and standard upper body sites with proper neck support during sleep, but remained symptomatic at coracoid tip, lateral pectoral, medial elbow and C6-C7.

Smythe HA (1994) have supported that mechanical factors determine patterns of symptoms and tenderness in this group. This implies that we are talking of segmental referred pain or referred tenderness rather than a pathologically ill-defined spectrum called “fibromyalgia”. If we differ on this front our treatment strategy is mislead. That’s why centrally acting medications or behavioral modifications are equally disappointing outcomes. To add to that tricyclic medications, stretch and spray or trigger point injections may be simply out of wrong terminology assigned to such a clinical entity.

Cyriax in his classical text book of orthopaedic medicine has elaborated how we get pain out of C6-C7 region & wry neck which is clinically better defined than the C6-C7 syndrome as we are talking of. We sleep 70% of our night in side lying positions. Most of the neck supports reach maximum up to caudal surface of vertebral body however with most we can reach adequately C5. Because of this C6-C7 segments sags towards the side on which we sleep with side flexion we also get a coupled rotation at the same site. That’s why people with Discogenic wry neck there is side-bend to the opposite side (same side bending is difficult) & restriction of the rotation to the painful side. However if there is strain to the facet joint structures we may get a pattern side-bend to the same side (opposite side bending is difficult) & restriction of the rotation to the non-painful side.

Physical strategies that have been helpful in such cases as far as my experience go is as follows:
1. Electro-analgesics: Pain reliving modalities in electrotherapy
2. Manual therapy:
Maitland: transverse glide to C6-C7 on the painful side progressing to central PA of C6- may be up to T2 as per the condition.
Mulligan: SNAGs to C6-C7 facets or spine as per the condition
McKenzie: Chin retraction (Chin tucking) with or without extension
Soft tissue therapy: I have found B/L rhomboids stretch to be very effective with digital ischemic pressures to tender points
Neural mobilization: As symptoms abate add neural mobilization program

N:B In my opinion C6-C7 syndrome is a mechanical derangement of minor grade due to repetitive positioning such as side lying.


1. Smythe HA; J Rheumatol. 1994 Aug;21(8):1520-6. (The C6-7 syndrome--clinical features and treatment response).
2. Walker JM, Helewa A (Physical therapy in arthritis): WB sounders & Company

Wednesday, July 6, 2011

Stiff man syndrome: A neuromotor disorder- Know how for physios

Synonyms: stiff man syndrome (SMS), stiff person syndrome (SPS), stiff leg syndrome (a focal SMS) etc

Introduction & definition:

Moerch and Woltman reported the first 14 cases with this syndrome for more than 50 years since 2010.

Stiff man syndrome (SMS) is an uncommon (rare) neurological disease that manifests with disorder of motor function which is characterized by rigidity of axial musculature and fluctuating painful spasms, which are often induced by startle or emotional stimuli.

Clinical and immunological findings indicate that SMS is a heterogeneous disease, suggesting the need to define its diagnostic criteria. But it has basic 2 forms either it can be generalized or focal. Criteria for the diagnosis of SPS were proposed but there are several variants of this syndrome described. These variants include focal variants of SMS.

Variants include stiff limb syndrome (SLS), jerking SMS and progressive encephalomyelitis with rigidity and myoclonus (PERM). Recognition of the clinical spectrum of SMS is important, particularly the upper-limb, cervical, and cranial nerve involvement that occurs in paraneoplastic variants (Paraneoplastic SMS accounts for approximately 5% of all cases of SMS). However they all share the core clinical features of appendicular and axial rigidity caused by continuous involuntary motor unit activity, and superimposed stimulus-sensitive spasms.

It is associated antineuronal autoimmunity and accompanying autoimmune diseases, most often noted in insulin-dependent diabetes mellitus with following C/F (see below). Several features suggest that SMS is an autoimmune-mediated chronic encephalomyelitis. Neurophysiological studies have demonstrated the presence of continuous motor unit activity in muscle at rest, with abnormally enhanced extereoceptive reflexes.

The disease progresses over the span of months to years rendering many patients wheelchair-bound or bedridden.

Clinical features:

1. Onset: Insidious & progressive
2. Fluctuating stiffness and paroxysmal spasms of the trunk and legs.
3. Symmetrical muscle stiffness and spasms that often lead to skeletal deformity.
4. The spasms characterized by hyperextension of the back (hyper-lordosis) and legs are both spontaneous as well as stimulus-sensitive. Spasms are excruciatingly painful.
5. SMS is frequently accompanied by symptoms of autonomic dysregulation.
6. Sometimes Hyperreflexia may be the only pathological finding on the neurological examination.
7. Mostly there is progressive gait impairment.
8. There may be a variety of additional neurological symptoms and signs such as eye movement disturbances, ataxia, or Babinski signs (progressive encephalomyelitis with rigidity and myoclonus), or be associated with malignant disease (paraneoplastic SMS).
9. Most patients show psychiatric disturbances suggestive of psychogenic movement disorder and this may cause delays in adequate pharmacotherapy.


The electromyographic examination shows continuous motor unit activity of the affected muscles at rest. Spasmodic reflex myoclonus is observed in nearly all SMS patients. It consists of well-reproduced reflex EMG-activity commencing 50-80 ms after medial or tibial nerve stimulation and lasting several seconds thereafter. The activity is first myoclonic then spasmodic in nature, and commonly begins in the muscles most severely affected before spreading bidirectionally along the neuraxis.

Commonest clinical indicators to suspect SMS:

The diagnosis is based on clinical, biochemical and electrophysiological findings.

A characteristic group of symptoms and signs allows a tentative clinical diagnosis. Supportive ancillary findings include (1) the demonstration of continuous muscle activity in trunk and proximal limb muscles despite attempted relaxation, (2) enhanced exteroceptive reflexes, and (3) antibodies to glutamic acid decarboxylase (GAD) in both serum and spinal fluid.


1. There is good evidence for a primary auto-immune aetiology. In addition to that there is clinical evidence of organ-specific autoimmunity predominantly encephalomyelopathic disorder resulting from B-cell-mediated clonal production of autoantibodies against presynaptic inhibitory epitopes on the enzyme glutamic acid decarboxylase (GAD) and the synaptic membrane protein amphiphysin.
However other antibodies such as anti-gephyrin, and anti-gamma-aminobutyric acid A receptor-associated protein (GABARAP) antibodies (14-kD protein localized at the postsynaptic regions of GABAergic synapses) are also detected along with GAD & anti-amphiphysin. In up to 65% of SMS patients, there are circulating anti-GABARAP antibodies that inhibit the GABA(A) receptor expression on GABAergic neurons. Paraneoplastic SMS is associated with anti-amphiphysin, anti-gephyrin, and anti-Ri antibodies. There is strong evidence that in SMS, GABAergic neurotransmission is impaired by these pathogenic autoantibodies; however, the exact antigenic target remains unknown.
Autoantibodies against glutamic acid decarboxylase- GAD in both serum and cerebrospinal fluid help to establish the correct diagnosis. Specifically GAD65 isoform, are present in serum or cerebrospinal fluid of 60-80% of patients with SPS and its variants. A paraneoplastic form of SPS is recognized in about 5%, associated with a different profile of auto-antibodies.
The correlation between antibody levels and severity of disease also offers evidence for a pathogenic role for the anti-GAD and anti-amphiphysin autoantibodies.

2. The scarcity of neuropathological correlates stand in sharp contrast with the severity of the disability in affected individuals and suggests that functional impairment of inhibitory circuits without structural damage is sufficient to develop the full clinical spectrum of SPS.

Treatment options:

There are 2 distinct options:
1. Immunomodulation
2. Symptomatic

The rarity of this condition limits the feasibility of controlled clinical trials in the treatment of SPS, but the available evidence suggest that drugs that increase cortical and spinal inhibition such as benzodiazepines (clonazepam 4 mg/day) and drugs that provide immune modulation such as intravenous immunoglobulin, plasmapheresis, and prednisone are effective treatments.

Rigidity and spasms may be treated symptomatically with benzodiazepines, baclofen, tiagabine and levetiracetam. An alternative of last resort is baclofen administered intrathecally via an implanted pump device.

Treatments for cancer occasionally produce symptomatic improvement in patients with paraneoplastic SPS.


SPS remains a largely underdiagnosed condition.

The syndrome varies from mild to severe, but if untreated it can be progressive and disabling. Generally after an initial progressive phase, patients with SPS generally stabilize over a period of months to years. However, 10% will require prolonged admission to intensive care at some stage during the disease. Sudden death has been reported in as many as 10% of patients because of unexplained metabolic acidosis or autonomic crises.

The prognosis in paraneoplastic SPS, jerking SPS and PERM, in terms of mortality, is generally worse than in primary SPS. It has been reported that reported cases of patients with SPS who were positive for anti-GAD antibodies and subsequently developed cancer. Because SPS often develops before the diagnosis of cancer, patients diagnosed with SPS should be monitored for the development of cancer.

1. Stayer C & Meinck HM; Neurologia. 1998 Feb;13(2):83-8. (Stiff-man syndrome: an overview).
2. Meinck HM; CNS Drugs. 2001;15(7):515-26. (Stiff man syndrome).
3. Fiol M et al; Neurologia. 2001 Feb;16(2):89-91. (Focal stiff-person syndrome).
4. Duddy ME & Baker MR; Front Neurol Neurosci. 2009;26:147-65. Epub 2009 Apr 6. (Stiff person syndrome).
5. Espay AJ & Chen R ; Muscle Nerve. 2006 Dec;34(6):677-90. (Rigidity and spasms from autoimmune encephalomyelopathies: stiff-person syndrome).
6. Ishii A; Brain Nerve. 2010 Apr;62(4):377-85. (Stiff-person syndrome and other myelopathies constitute paraneoplastic neurological syndromes). [Article in Japanese]
7. Dalakas MC; Curr Neurol Neurosci Rep. 2008 Jan;8(1):48-55. (Advances in the pathogenesis and treatment of patients with stiff person syndrome).
8. Meinck HM & Thompson PD; Mov Disord. 2002 Sep;17(5):853-66. (Stiff man syndrome and related conditions).
9. Saiz A et al; Ann Neurol. 1998 Mar;43(3):400-3. (Stiff-leg syndrome: a focal form of stiff-man syndrome).
10. G├╝rol ME et al; Mov Disord. 2001 Nov;16(6):1189-93. (Stiff leg syndrome: case report).

Sunday, June 12, 2011

Soft tissue mobilization by instruments

To spare the treating hands of the clinicians & more to increase the precision of treatment in musculoskeletal therapy, clinicians now days are more and more inclined to use instruments for soft tissue mobilization. None the less these equipments can also be used to diagnose the soft tissue lesions more accurately enhancing the palpation capacity of the clnician.

However, the objectives of this form of treatment are as follows:
• Break down scar within the tissues
• Promote blood flow into the sore area
• Establish healing in damaged tissues
• Release adhesions within the layers of tissue
• Improve lymphatic circulation

David Grastron is the pioneer in developing the new area instruments for soft tissue mobilization. However stylus massage was reported to be used in trigger point deactivation by Russian in Olympic game. Spa professionals use various types of massage equipments during spa sessions.

Three common treatments always come into mind when soft tissue mobilization is assisted by instruments by therapists.
2. SASTM that includes Graston technique (GT)

Let us discuss the 3 mentioned in a greater detail.


IASTM stands for Instrument Assisted Soft Tissue Mobilization. The original form of IASTM has its roots in Traditional Chinese Medicine (TCM). Gua Sha, as it is called, involves use of the edge of an object such as a coin, a spoon, or piece of horn or jade to “scrape” along the skin.

IASTM involves use of a precision tool to stroke along the involved area. The repeated action of gliding the tool along the sore area helps to improve lymphatic drainage, improve mobility in the soft tissues, and improve blood flow. IASTM treatment may be somewhat uncomfortable at first, it is highly effective in releasing tissue adhesions and scar tissue that contribute to tendonitis, chronic pain, and sport- or work-related injuries.


Soft tissue mobilization has been used to treat a number of diagnoses for some time. SASTM is another form of this process, but it utilizes instruments designed for treatment of soft tissue disorders. SASTM stands for Sound Assisted Soft Tissue Mobilization. SASTS is regarded as the next generation development of Graston technique. SASTM is also developed by David Graston of USA. Like earlier Graston equipments SASTM is a set of handheld instruments that effectively break down fascial restrictions and scar tissue.

How SASTM works?

It is theorized that S.A.S.T.M. is effective because of the following:

Instruments effectively break down fascial restrictions and scar tissue. The ergonomic design of these instruments provides the clinician with the ability to locate restrictions through sound waves. This allows the clinician to treat the affected area with the appropriate amount of pressure, due to square surface concept.

The introduction of controlled microtrauma to affected soft tissue initiates reabsorption of excessive scar tissue and facilitates a cascade of healing activities resulting in remodeling of affected soft tissue structures. Adhesions and scar tissue within the soft tissue that may have developed as a result of surgery, immobilization, repeated strain, or other mechanisms, are broken down allowing full functional restoration to occur.

Graston Technique (GT):

Graston Technique (GT) is a therapeutic method for diagnosing and treating disorders of the skeletal muscles and related connective tissue. The method employs a collection of six stainless steel tools of particular shape and size, which are used by practitioners to palpate patients' bodies in order to detect and resolve adhesions in the muscles and tendons.

The Graston Technique is proprietary—the name of the treatment is trademarked and the instruments are subject to patents held by a licensing corporation, TherapyCare Resources Inc. Practitioners must be licensed by the parent corporation in order to use the Graston Technique trademark or the patented instruments. The Graston Technique was developed by David Graston who now operates SASTM (Sound Assisted Soft-Tissue Mobilization).

The Graston Technique has not been rigorously scientifically tested and its evidence basis and assumptions are considered questionable by physician Harriet Hall. However according to Eric Schoenberg (MSPT, CSCS) Graston technique concept is grounded in the works of English orthopedist James Cyriax and the concept of cross fiber treatment. The treatment edge of the Graston instruments allows for improved precision in the treatment of fascial restriction and fibrotic/scar tissue.

He (Eric Schoenberg) also enlists the following clinical observations working with Graston equipments
1. The specificity of the treatment edge and the ability to provide uniform pressure is what sets the technique apart from other manual approaches.
2. The instruments truly enhance the clinician’s ability to detect and treat fascial restrictions and adhesions (particularly effective in positions of provocation).
3. Incorporating stretching and strengthening (tendon-loading) exercises with the instrument assisted soft tissue mobilization is the key to promoting re-alignment of the fibers and helping to fully remodel the injured tissue.
4. Coupling Graston in the clinical setting with self myofascial release (SMR) products, such as foam rollers and other similar equipment at home or in an athletic setting (pre/post activity) is an ideal way to achieve maximum success.

Finally Eric enumerate that most exciting part of using Graston Technique in the clinical setting is feeling better suited to treat the more difficult diagnoses (plantar fasciitis, chronic tendonosis, etc) with the expectation of good clinical outcomes.


ASTYM is augmented soft tissue mobilization (ASTM). ASTYM allows the clinician to stimulate the body's own capacity for healing in patients with soft tissue degeneration or fibrosis and chronic inflammation. This leading edge, non-invasive treatment is performed with ergonomically designed instruments that initiate the healing process necessary for tissue remodeling.

How does ASTYM work?

The ASTYM System's effectiveness is theorized to be due to the following:

• Adhesions and inappropriate fibrosis within soft tissue can result from trauma, surgery, immobilization or repetitive strain. The ASTYM System stimulates the breakdown of this dysfunctional tissue and allows functional restoration to occur.
• Soft tissue adhesions and resulting restrictions are identified and broken down.
• Controlled microtrauma initiates a local inflammatory response that leads to the resorption of inappropriate fibrosis or excessive scar tissue.
• In chronic tendonopathies, doses of controlled microtrauma stimulate regeneration of the affected tendons.
• Existing collagen is remodeled and new collagen is influenced by a program of specific functional activities and stretching.

What can the patient expect?

The ASTYM System program begins with a thorough evaluation. The clinician then administers a 10 to 15 minute treatment addressing the entire kinetic chain. A regimen of specific strengthening and stretching exercises is prescribed, customized to the patient's work, athletic or recreational activities. Patients experience a decrease in pain and rapid improvement in function which results in high patient compliance and satisfaction.

What benefits does ASTYM provide?

Multiple studies demonstrate the effectiveness of the System in restoring mobility and hastening recovery in patients with cumulative trauma disorders and other soft tissue dysfunctions. In a vast majority of cases it offers these distinct advantages:

• Restoration to pre-injury level of activity
• Enjoyment of maximal results with a minimal number of treatments through an emphasis on re-establishing function
• Maintenance of normal activity in conjunction with the treatment
• Decreased need for splints, braces or job site modifications
• Decreased need for surgical intervention

Indications for all soft tissue mobilization by instruments:

Here is a list of disorders that instrument-assisted soft tissue mobilization has most effectively been used for in the restoration of function and pain reduction.

Upper Extremity

• Bicep Tendinitis
• Carpal Tunnel Syndrome
• DeQuervain's Syndrome
• Frozen Shoulder
• Joint Contractures
• Medial/Lateral Epicondylitis
• Rotator Cuff Tendinitis
• Scars (Surgical/Traumatic)
• Trigger Finger

Lower Extremity

• Achilles Tendinitis(Heel Pain)
• Ankle Strains/Sprains
• Groin Pulls
• Hammer Toe
• Hamstring Injuries
• Hip Replacements
• Joint Contractures
• Knee Replacements
• Knee Sprains
• Morton's Neuroma
• Patellar Tendinitis
• Quadricep Injuries
• Scars (Surgical/Traumatic)
• Shin Splints
• Tarsal Tunnel Syndrome
• Tibialis Posterior Tendinitis
• Turf Toe
• Musculoskeletal Imbalances

Neck and Spine

• Cervical (Neck Pain)
• Lumbar/Sacral (Low Back Pain)
• SI Pain
• Thoracic (Mid Back Pain)
• Trigger Points (Muscle Knots)

Wednesday, May 25, 2011

GIRD- Glenohumeral internal rotation deficit

Definition of GIRD:
GIRD is a 20° or greater loss of internal rotation of the dominant shoulder compared with the non-dominant shoulder.

Glenohumeral internal rotation deficit, often diagnosed in players of overhead sports, has been associated with the development of secondary shoulder lesions. Conditions such as labral and rotator cuff injuries have been linked with decreases in glenohumeral internal-rotation and increases in external-rotation motion. This group also shows a loss of horizontal or cross-body adduction in the throwing shoulder when compared with the non-throwing shoulder. GIRD is also strongly associated with scapular dyskinesis.

Tennis players, swimmers & athletes in throwing sports are commonly affected by GIRD. Deficit in dominant shoulder of tennis players is about twice the deficit found in swimmers. Data suggest that GIRD and scapular position change worsens as the level of competition increases in overhead sports. Pathologic conditions in the shoulder of a throwing athlete frequently represent a breakdown of multiple elements of the shoulder restraint system, both static and dynamic, and also a breakdown in the kinetic chain.

GIRD a structural adaptation for good or bad
Altered shoulder mobility reported in overhead athletes and is thought to develop secondary to adaptive structural changes resulting from the extreme physiological demands of overhead activity. Debate continues as to whether these altered mobility patterns arise from soft-tissue or osseous adaptations within and around the shoulder.

People who support the onset through osseous adaptations argue humeral retroversion are thought to develop over time in young pre-adolescent throwers when the proximal humeral epiphysis is not yet completely fused. Retroversion is thought to account for changes in the rotational ROM in overhead athletes. This may lead to superimposition of soft tissue adaptations i.e. capsulo-ligamentous adaptations such as anterior-inferior stretching (accountable for increased ER) or posterior-inferior contracture (accountable for increased IR) upon the osseous changes. This may ultimately lead to pathological manifestations such as secondary impingement, type II superior labrum from anterior to posterior (SLAP) lesions and/or internal (glenoid) impingement.

Internal impingement & GIRD
GIRD and posterior shoulder tightness (capsule, rotator cuff) have been linked to internal impingement. Increased posterior shoulder tightness and glenohumeral internal rotation deficit that exceeds the accompanying external rotation gain, are suggested contributors to throwing-related shoulder injuries such as pathologic internal impingement. On the contrary Mayers et al found throwing athletes with internal impingement demonstrated significantly greater glenohumeral internal rotation deficit and posterior shoulder tightness in the absence of significant differences in external rotation gain.

However it is very clear now that repetitive forces in overhead sports cause adaptive soft tissue and bone changes that initially improve performance but ultimately may lead to shoulder pathologies.

The cardinal lesions of internal impingement, articular-sided rotator cuff tears and posterosuperior labral lesions, have been shown to occur in association with a number of other findings, most importantly GIRD and SICK scapula syndrome, but also with posterior humeral head lesions, posterior glenoid bony injury and, rarely, with Bankart and inferior glenohumeral ligament lesions.

GIRD is difficult to treat by physiotherapy
Physical therapy and rehabilitation should be, with only a few exceptions, the primary treatment for throwing athletes before operative treatment is considered. According to Myers JB shoulder internal impingement management should include stretching to restore flexibility to the posterior shoulder. However Tyler TF et al reported resolution of symptoms after physical therapy treatment for internal impingement is due to correction of posterior shoulder tightness but not correction of GIRD. But Braun S et al reported throwing athletes who have a glenohumeral internal rotation deficit have a good response, in most cases, to stretching of the posteroinferior aspect of the capsule.

Wilk KE reported compared with pitchers without GIRD, pitchers with GIRD appear to be at a higher risk for injury and shoulder surgery.

1. Wilk KE et al; Am J Sports Med. 2011 Feb;39(2):329-35. Epub 2010 Dec 4.
2. Torres RR et al; Am J Sports Med. 2009 May;37(5):1017-23. Epub 2009 Mar 4.
3. Thomas SJ et al; J Athl Train. 2010 Jan-Feb;45(1):44-50.
4. Tyler TF et al; Am J Sports Med. 2010 Jan;38(1):114-9. Epub 2009 Dec 4.
5. Myers JB et al; Am J Sports Med. 2006 Mar;34(3):385-91. Epub 2005 Nov 22.
6. Braun S et al; J Bone Joint Surg Am. 2009 Apr;91(4):966-78.
7. Kirchhoff C et al; Int Orthop. 2010 Oct;34(7):1049-58. Epub 2010 May 19.
8. Borsa PA et al; Sports Med. 2008;38(1):17-36.

Monday, May 9, 2011

Radiological interpretation of joint space narrowing & Kellgren-Lawrence (K-L) scale

Grade 0 = Normal

Grade 1 = Doubtful narrowing of the joint space & possible osteophytic lipping

Grade 2 = Definite Osteophytes & definite narrowing of joint space

Grade 3 = Moderate multiple Osteophytes, definite narrowing of joint space, some sclerosis & possible deformity of bone contour

Grade 4 = Large Osteophytes, marked narrowing of joint space, severe sclerosis & definite deformity of bone contour

Saturday, May 7, 2011

Internal impingement of shoulder: A simple overview

The impingement in shoulder can clearly be classified into internal & external varieties.

Internal impingement:

The internal impingement syndromes result from the impingement of the soft tissues of the rotator cuff and/or joint capsule on the glenoid or between the glenoid and the humerus.

External impingement:

The external impingement syndromes result from the impingement of the soft tissues of rotator cuff and bursa on the structures of the coracoacromial arch.

External shoulder impingement and rotator cuff disease has been corroborative despite of research arguments. Attempts have been made to identify objective imaging criteria that confirm the diagnosis of impingement, but at present external impingement remains primarily a clinical diagnosis.

Mainly shoulder impingement is caused by compression of the supraspinatus tendon underneath the coracoacromial arch, mostly in forward flexion of the arm.

Stages of external impingement:
Different stages of impingement syndrome are described.
Stage I: There is edema and hemorrhage of the supraspinatus tendon.
Stage II: There is characterized by bursal inflammation and fibrosis, as well as tendinopathy.
Stage III: there is a tear of the rotator cuff.

It is important to remember that clinical signs may overlap in these described stages.

The internal impingement syndrome:

Internal impingement was first described by Walch in 1992 and defined as contact between the supraspinatus tendon and posterior-superior glenoid rim with the shoulder in the cocked, throwing position of 90 degrees of abduction and maximum external rotation.

It is debatable whether internal impingement syndromes truly the result of impingement. Internal impingement seems to be a normal physiological occurrence with the shoulder in certain positions. Imaging findings in internal impingements reveals that these conditions there are 3 different pathologies: undersurface partial-thickness cuff tears, superior labral pathology, and bone changes. According to Paley et al’s study (N=41) in overhead throwing athletes suffering from internal impingement; undersurface cuff fraying was found in 93%, posterosuperior labral fraying was found in 88%, and anterior labral fraying was found in 36% of the subjects.

Theory explaining the internal impingement in overhead athletes:

In athletes where position of extreme abduction and external rotation (ABER position) are repeatedly taken this type of internal impingement occurs. However in simple ABER position also showed physical contact between the undersurface of the rotator cuff and the posterior superior glenoid. In athletes repeated contact between the undersurface of the rotator cuff and the posterosuperior glenoid rim leads to articular-sided partial-thickness rotator cuff tears and superior labral lesions. Hence the "kissing lesions" of undersurface rotator cuff tears and posterosuperior labral damage may be explained by mechanisms other than "internal impingement."

Interestingly Kim et al (2004) have demonstrated flexion as a cause of internal impingement as it affects the labrum. Labral pathologies lead to internal impingement. This study showed that internal impingement in flexion may contribute to the development of Type II SLAP lesions and rotator cuff disease.

Shoulder laxity & instability also has been incriminated as a source of internal impingement but McFarland et al have reported otherwise.

However even the non athletes also suffer from internal impingement. According to McFarland et al contact of the rotator cuff to the posterosuperior glenoid with the arm in abduction and external rotation can occur in a wide spectrum of shoulder disease and is not limited to the throwing athlete.

According to Halbrecht et al internal impingement is also seen in asymptomatic population.


1. Grainger AJ; Semin Musculoskelet Radiol. 2008 Jun;12(2):127-35.
2. Campbell RS et al; Semin Musculoskelet Radiol. 2008 Jun;12(2):107-26.
3. Hodler J; Radiologe. 1996 Dec;36(12):944-50.
4. Budoff JE et al;Arthroscopy. 2003 Oct;19(8):810-4.
5. Kaplan LD et al; Arthroscopy. 2004 Sep;20(7):701-4.
6. Kim TK et al; Clin Orthop Relat Res. 2004 Apr;(421):112-9.
7. McFarland EG et al; J Shoulder Elbow Surg. 1999 Sep-Oct;8(5):458-60.
8. Paley KJ et al; Arthroscopy. 2000 Jan-Feb;16(1):35-40.
9. Halbrecht JL et al; Arthroscopy. 1999 Apr;15(3):253-8.

Wednesday, April 20, 2011

Claw toe deformity

A claw toe is a toe that is contracted at the PIP and DIP joints and can lead to severe pressure and pain. Ligaments and tendons that have tightened cause the toe's joints to curl downwards. Claw toes may occur in any toe, except the big toe. There is often discomfort at the top part of the toe that is rubbing against the shoe and at the end of the toe that is pressed against the bottom of the shoe.


Claw toe deformity results from altered anatomy and/or neurologic deficit, resulting in an imbalance between the intrinsic and extrinsic musculature to the toes.

1. Claw toe deformity can develop as a complication of fracture of the tibia. The deformity develops following a tibia fracture is basically due to adhesions of the flexor hallucis longus (FHL) and flexor digitorum longus (FDL) muscles to the surrounding structures under or just proximal to the flexor retinaculum.

According to Fitoussi et al it may be related to a subclinical compartment syndrome localized in the distal part of the deep posterior compartment. Soft-tissue release without tendon lengthening allowed recovery in all patients.

2. Involvement of distal tibial nerve in claw toe. Generally clawing in the foot is related to the lateral plantar nerve involvement but surgeons Dellon & colleagues’ demonstrated improvement in toe clawing may result from neurolysis of the tibial nerve as well as the lateral plantar nerve.

3. Claw toe may develop secondary to diabetic neuropathy affecting foot. Clawing of the toes in the diabetic neuropathic foot is believed to be caused by muscle imbalance resulting from intrinsic muscle atrophy.

According to Bus et al neither intrinsic muscle atrophy nor muscle imbalance causes claw toe deformity in diabetic neuropathy. They also suggested that the role of these muscle factors in claw toe development may not be primary. Their research also suggested a complex nature of development, potentially involving anatomical and physiological predisposing factors.
Claw toe of relatively rapid progression is possibly due to neural involvement. Consult a neurologist as soon as possible.


1. Fitoussi F et al; J Child Orthop. 2009 Oct;3(5):339-43. Epub 2009 Aug 22.
2. Dellon AL et al; Microsurgery. 2008;28(5):303-5.
3. Bus SA et al; Diabetes Care. 2009 Jun;32(6):1063-7. Epub 2009 Mar 11.

Monday, April 11, 2011

See how physical therapy specilists are certified in USA

Asian physios please see the following web site to appreciate the job APTA is doing uplifting the physical therapy profession.

American board of physical therapy specialists (APTA certifying the physical therapy specialists)


Wednesday, February 23, 2011

Analysis of sitting posture

Introduction: Occupations & occupational demands have changed in the recent era. Modernization & Industrialization has changed the face of occupational activities & need of work related physical performances. We have slowly crawled in to mostly a sedentary era. On the other side passive leisure time pursuits are taking over active leisure time pursuits. The situation is such that the average office going adult hardly moves his or her axial & apendicular joints in it’s full range of motion.
Mean temporal classification of ADL (activity of daily living) closely equates 7-8 hours of sleeping; 8-10 hours of working and rest of hours are spent in house hold activities like washing, watching TV, purchasing grocery, rarely gardening or a sports etc. Office hour activities span more than one third of the day. Except in blue collar jobs (manual labor class) office hours consists of at least 2-4 hours sitting to full office hour invested in sitting like in banking, IT sector jobs, and similar office going professionals etc. Invention of computers has lead to increased sitting hours in the office. However occupational sitting differs in western & eastern populations. Urban & rural occupations are different and thus different occupational sitting postures are seen in the people dwelling in these areas. Mostly in Asian rural areas cross legged sitting or it’s variant is used in occupation.
With change in demands on sitting posture at working & home environment there is parallel increase in low back pain in the working population (both office bound & non-office bound) & population in general to epidemic proportions. However, till the last medical review published in 2010, causal relationship of LBA (low back ache) to that of occupational sitting has not been established.

Hence we have chosen to highlight the impact of sitting of lumbar spine ergonomics, possible ways to explain pain production in sitting form dynamic Mckenzie disc model. In the due course we would try to explain the Lumbar spine flexion relaxation phenomenon & stress transfer from contractile to inert structure, spine asymmetry & asymmetric sitting, acquiring awkward posture, ideal spine- neutral zone weight transfer & ideal sitting posture, simple ergonomic correction advices (postural correction, lumbar roll, orthopedic back rest).

Implication of occupational LBA form epidemiological studies:

Low back pain is a major cause of morbidity in high-, middle- and low-income countries, yet to date it has been relatively under-prioritised and under-funded (Hoy D).
LBA in world population: According to a review article by Schochat T et al on epidemiological studies of LBA in the general population two different set of information are available. First comes from the general health surveys and the other from surveys with specific reference to back pain. Data from general health surveys depict point prevalences of LBA between 0.8% and 41% and 1-year prevalences between 15% and 56%. LBA data specially designed to evaluate the prevalence of back pain shows prevalence ranges between 14% and 42% and the lifetime period prevalence between 51% and 84% with highest prevalence is found at age 50 to 64. Either there is no difference between men and women or only a slightly higher prevalence in women.
LBA prevalence rates in high & low income countries & it’s implication: A literature review by Volinn E on LBA epidemiology in high & low income countries is interesting in our context of discussion. According to this study high-income countries comprise less than 15% of the world's population. There is an intra population variation in both high & low income countries depending on where they live. Urban dwelling population in each case had more prevalence rates then their rural counter parts. A 2-4 time higher prevalence is noted among the general populations of high-income countries. This type of consistent behavior indicates a certain factor common in urban population in both high & low income countries noted among workers in particular worksites, referred to as "enclosed workshops." Higher rates among workers in enclosed workshops of low-income countries suggest a disturbing trend: low back pain prevalence may be on the rise among vast numbers of workers as urbanization and rapid industrialization proceed. Considerably lower rates among populations of low-income farmers compared with rates of the affluent populations is contrary to the hypothesis that hard physical labor itself is not necessarily related to low back pain.

Different varieties sitting postures:

A. Common sitting postures:

1. Chair sitting
2. Crossed sitting
3. Crossed sitting with arms wrapped around both knees & locked in front
4. Half crossed sitting
5. Crook sitting
6. Inclined sitting (to back)
7. Inclined sitting (to sides)
8. Inclined long sitting
9. Side sitting
10. Stoop sitting
11. Fall out sitting
12. Ride sitting
13. Kneel sitting
14. Crouch sitting

B. Activities in sitting:

1. Twisting in sitting
2. Bending & reaching in sitting (sidewise- office works & in front- driving)
3. Hitching & Hiking (to relieve pressure on buttocks in prolonged sitting)

C. Co-existing unavoidable stress factors in sitting:

1. Whole body vibration (driving)
2. Noise stress
3. Visual stress
4. Psychological stress

Analysis of muscle work in ideal quiet sitting posture:

Ideal sitting posture: The following discussion is in the context of a quiet ideal chair sitting posture without any upper limb activity. The position is taken on a flat base chair or stool, the height & width of the sitting area allow the thighs to supported & hips and knees is flexed to 900 . In ideal sitting femora are parallel to each other & feet rest on the floor with ankle at 900 where as hells are vertically below the knees.

Muscle work in ideal sitting posture:

a. Joints of lower extremity have no muscle work except at hip. Flexors of hip work in reverse origin insertion fashion to prevent slumping of the lumbar spine.
b. Joints of spine:
i. Global extensor muscles of the spine (Ex-Multifidus): these postural muscles keep the trunk upright. Action of these muscles may be counterproductive at lumbar & cervical spine where it’s action produces a bow string effect & increases the lordotic curvature leading to reduction in the over all height of the spine at these places. Therefore at the lumbar & cervical spine this action must be counteracted by the local flexors (lumbar & cervical spine flexors) to ensure local spine lengthening and maintain the correct & ideal local spine posture.
ii. Flexors of the lumbar spine (Abdominals): In sitting they must work to prevent the bow string effect produced by the global extensor muscle. Scientific literature indicates they contract in an in to out fashion. Hence transverse abdominis is of prime importance in maintaining the core stability & correct spinal alignment. Where as the straight abdominals (rectus abdominis) maintain the correct pelvic tilt matching the spine alignment so that correct contact points are maintained at the chair base- body interface.
iii. Flexors of the cervical spine (pre-vertebral neck muscles) act to prevent the bow string effect produced by the global extensor muscle.
iv. Posture of the head on the cervical spine is finely controlled at the CVJ & at atlanto-axial joint by own set of flexors-extensors to maintain this sagittal posture.

c. Other joints in sitting:
i. TMJ: elevators of the mandible close the mouth against the pull of the gravity.
ii. Thoraco-scapular junction: Thoraco scapular muscle (rhomboids) retracts the scapula so that the glenoid cavity faces laterally. Cervico scapular muscles (levator scapulae) work to elevate a depress scapula due to the pull of the gravity.

d. Joints of upper extremity: No muscle work is required for quite sitting but sitting with occupational arm demands may leads to more activation of the external rotators of the arm, abductors, elbow flexors, forearm pronators, wrist extensors & finger flexors.

Search words:
Low back pain, Occupational low back pain, occupational low back pain in sitting, Low back pain epidemiology, Ergonomics, Work ergonomics, dynamic spine model, Mechanical diagnosis & therapy, Mckenzie therapy etc

Can occupational sitting cause LBA?


Sociocultural, economic, and manufacturing factors are 3 different major factors that influence sitting. "Correct" seated posture is associated with spine health was known to people possibly from Hippocratic era. But the debate has not dampened yet whether the sitting is directly a cause of LBA or it predisposes or precipitates LBA. From 1980s much of research has been put into ergonomically correct sitting & providing a work environment for correct sitting posture. However there is a question; is there any medically correct sitting posture? The correct sitting posture refers to maintenance of a correct lumbar spine lordosis actively (muscle contraction) or passively (chair or sitting back support) (described below elaborately in neutral spine position). Passive maintenance is sought because it is noticed that within minutes of sitting lordosis is reversed or lost. According to Ernst even the correct sitting is not out of danger because of the repetitive nature of compressive loads on vital spine tissues having multiple avenues of pain production. But certainly correct sitting posture & correct work ergonomics may lead to minimize injury.

Importance of Lordosis in seating ergonomics:

Sagittal balanced spinal posture is a goal for spinal surgery and conservative ergonomics. The configuration of the spine, postural position, and weight transfer is different in the 3 types of sitting: anterior, middle, and posterior. Among these 3 different; flat, long lordosis, short lordosis seating postures, flat posture show the least muscle activity similar to the slump posture.

Ergonomic advices for jobs with sitting: Lumbar lordosis is affected by trunk-thigh angle (THA) and the knee angle (KA). THA 110 to 130 degrees with arm rest, back rest & concomitant lumbar support (or a pneumatic support) has the lowest disc pressures and lowest muscle activity from spinal muscles. A seat-bottom posterior inclination of 5 degrees and armrests can further reduce lumbar disc pressures and muscle activity while seated. To reduce forward translated head postures, a seat-back inclination of 110 degrees is preferable over higher inclinations.

Ergonomic advices for jobs with sitting & whole body vibration: Adjustable seat back incline of 110 degrees from horizontal, a changeable depth of seat back to front edge of seat bottom, adjustable height, an adjustable seat bottom incline, firm (dense) foam in the seat bottom cushion, horizontally and vertically adjustable lumbar support, adjustable bilateral arm rests, adjustable head restraint with lordosis pad, seat shock absorbers to dampen frequencies in the 1 to 20 Hz range, and linear front-back travel of the seat enabling drivers of all sizes to reach the pedals. The lumbar support should be pulsating in depth to reduce static load. The seat back should be damped to reduce rebounding of the torso in rear-end impacts.

This is a part of one of my international seminar on “Occupational health & hygiene” held at bhubaneswar, Orissa, India 23-25 feb 2011. I was invited as a speaker on the first day of the congress. My topic was “Can sitting cause occupational LBA?”

* With due apology we want to mention that the references here are not published.