Wednesday, July 18, 2012

Entrapment of medial calcaneal nerve (MCN)

Peripheral nerve entrapment is a rare, but important, cause of foot and ankle pain that often is underdiagnosed and mistreated. A peripheral nerve may become entrapped anywhere along its course, but certain anatomic locations are characteristic (2).

The medial calcaneal nerve (MCN)

The Tibial nerve is called the planter nerve in the sole. The tibial nerve passes to the sole of the foot takes a turn on the medial side of the calcaneum is called MCN. The medial calcaneal nerve arises from tibial nerve of the inner side of the ankle, perforates the laciniate ligament, travels downwards passing below the bony projection on the inner side of the ankle, and supplies the skin over the medial aspect of the heel. Hence it is the most important nerve for heel sensations. MCN have 2 branches. The anterior branch dominate the cutaneous sensation of the anterior part of the medial calcaneal and heel weight loading field, while the posterior branch dominate the sensation of the posterior and median part.

How entrapment occurs?

A nerve can become entrapped on its way through the tissue planes. Usually in case of entrapment, the nerve gets compressed between a static and a mobile surface. As the body moves, the nerve is subjected to repeated sliding or friction, leading to compression and trauma. This trauma may damage the outer sheath of the nerve that helps with signal transmission and cause other structural alterations that eventually lead to pain and loss of function.

Causes of MCN entrapment: The medial calcaneal nerve may become entrapped between the tight fascia at the origin of the abductor hallucis muscle and the heel bone (calcaneus). An excessive pronation of the foot may lead to medial calcaneal nerve entrapment. This can occur as a postoperative complication during the release of the lateral plantar nerve branch (4).

S/S of MCN entrapment:
Stages of nerve entrapment (2):Clinically, any nerve entrapment is divided into three stages. 
Stage I: patients feel rest pain and intermittent paresthesias which are worse at night.
Stage II: continued nerve compression leads to paresthesias, numbness, and, occasionally, muscle weakness that does not disappear during the day.
Stage III: patients describe constant pain, muscle atrophy, and permanent sensory loss.

There is pain and parasthesia (burning or tingling) in the areas supplied by the nerve, that is below the inner bony projection of the ankle and under the heel. The pain usually initiates on the inside of the heel and travels towards the center. Any activity may further aggravate the pain.
When the medial calcaneal nerve is trapped the Tinel’s sign is positive. This test is performed by lightly tapping the skin over the nerve, which leads to tingling in the area supplied by the nerve.
Medial calcaneal nerve entrapment should not be confused with other causes of heel pain, such as plantar fasciitis and tarsal tunnel syndrome. Accurate diagnosis is important to achieve the desired results.

Palpation of MCN:
A thorough understanding of the causes of peripheral nerve entrapment, the anatomic course and variation of the peripheral nerves, the diagnostic modalities, and the treatment options can simplify this complex problem (2).
According to Tang et al anatomical position of MCN is relatively constant with 95% accuracy, MCN can be palpated at the following site:

MCNs arises from the tibial nerve at 3.3 cm up the horizontal plane of the tip of medial malleolus. They sent out anterior branches and posterior branches from 0.3 cm below the horizontal plane of the tip of medial malleolus on average.

Physical Testing:

Although diagnostic confusion abounds because of the multiple etiologies of peripheral nerve entrapments and their complex physical and temporal relation David Butler’s neural tension testing is very important to assess the reduced mobility of the nerve within the tissue plane.

Electrophysiological testing:

Electrodiagnosis is a powerful tool for evaluating lower extremity disorders that stem from the peripheral nervous system. Electrodiagnostic testing can help differentiate neurogenic versus non-neurogenic causes of complaints such as pain, weakness, and paresthesias. It can help practitioners pinpoint the anatomic location and reveal the underlying pathology in peripheral nerve lesions.


The first line of treatment includes rest and supportive therapies. Avoid activities that lead to pain; immobilization may also help. Use cold compresses and anti-inflammatory painkillers to reduce the symptoms. Massage or ultrasound therapy is also useful.
If rest and conservative treatment fail to eradicate the symptoms, surgical decompression of the nerve may be required. Surgical treatment usually produces good results.

Author’s comment:

Try Butler’s nerve gliding exercises & Neurodynamic techniques. I have personally tried alternative digital compression-relaxation at the site where the nerve takes a sharp angulation at heel with varied success rates but it is worth trying.  

1. Tang J et al; Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2010 Apr;35(4):386-9. (Anatomic characteristics and clinic significance of the medial calcaneal nerve).
[Article in Chinese]
2. Hirose CB et al; Foot Ankle Clin. 2004 Jun;9(2):255-69. (Peripheral nerve entrapments).
3. Roy PC; Foot Ankle Clin. 2011 Jun;16(2):225-42. (Electrodiagnostic evaluation of lower extremity neurogenic problems).

Thursday, July 5, 2012

Planter heel pain: planter fascitis, Fat pad atrophy, combined PF & FPA.

What the following article is on?Discussion on 3 conditions with mostly similar symptom of planter heel pain.

Synonyms of planter heel pain: Subcalcaneal heal pain, calcaneodynia  etc.
Synonyms of Planter fascitis: Planter fasciosis, Planter fasciopathy etc.

Planter foot pain is seemingly the most innocuous yet significant morbid condition affecting the adults hampering their ADLs & QOL. According to a recent research paper (1) Plantar heel pain can be provoked by PF (Planter fascitis), FPA (Fat pad atrophy), combination of PF + FPA and other causes. Patients with PF or FPA typically show different characteristics in clinical features but overall may look quite similar. Plantar heel pain requires differential diagnosis for appropriate treatment.
DD of planter foot pain includes following:

Planter heel pain can be sub-divided in to neural & non-neural pain. The non-neural pain can again be sub-divided into 2 bony & soft tissue pains.
Bony pathology: Calcaneal stress fracture, apophysitis of the calcaneus (Sever's disease), osteomyelitis, or inflammatory arthropathy.

Soft tissue pathology:  Fat pad atrophy (FPA) or contusion, plantar fascia rupture and plantar fasciitis (PF).

Neural pathology: Entrapment or compression of the first branch of the lateral plantar nerve (Baxter's nerve), medial calcaneal branch of posterior tibial nerve, or nerve to abductor digiti quinti muscle.

Other neural causes include S1 radiculopathy, tarsal tunnel syndrome, and peripheral neuropathy.

Many times planter foot pain is due to combination of different pathologies coexisting together. For example it is reported that Planter fascitis & fat pad atrophy coexist to produce planter foot pain. Similarly Labib et al described the heel pain triad (HPT). HPT is a combination of plantar fasciitis, posterior tibial tendon dysfunction and tarsal tunnel syndrome.

We are going to discuss S/S of 2 different pathologies with similar presentation and they often coexists. 

A. Planter fascitis (PF):According to Buchbinder (5) PF is reported to be the most common cause of plantar heel pain. The peak age is between (40-60) years.

Pathology of PF(6):
The pathology is still unknown.
Histopathologic examination of biopsy specimens from patients undergoing excessive extension or microinjuries of the plantar fascia shows secondary degenerative changes in the plantar fascia, with or without fibroblastic proliferation, and without acute inflammation.
However there is aging caused physiological changes are thought leading to PF. There is increased stress on the calcaneus and plantar fascia due to of loss of buffering tissue such as water and collagen of the fat pad.

Risk factors for PF:
1.    running excessively (or suddenly increasing running distance)
2.    occupations that involve long periods of standing
3.    pes planus
4.    limited ankle dorsiflexion
5.    obesity

Basis of clinical diagnosis:1. Pain characteristics: first-step morning pain and relief of pain after walking (most significant finding). Medial calcaneal tuberosity pain must be view is association with morning 1st step pain to diagnose PF. Unilateral pain is more common than bilateral.
2. Association with abnormal foot biomechanics: TA tightness & Limited ankle DF is most commonly associated with PF. Both pes planus & Cavus are associated with PF however Pes palnus is more associated with PF than pes cavus.
Explanation of association of pes planus & TA tightness with PF:
Limited ankle dorsiflexion on the involved side significantly increased the risk of PF. According to Inman et al (7) approximately 10 degrees of ankle dorsiflexion with the knee extended is required during a normal gait. If the Achilles tendon is shortened, limiting ankle dorsiflexion, excessive pronation of the foot may occur to compensate for this limitation. Greater the limitation in ankle dorsiflexion, the more load on the plantar fascia. Excessive pronation of the foot increases tensile loads on the plantar aponeurosis.
Hence repetitive pronatory stress that increases tensile force on the plantar fascia causing the plantar arch to lower is the cause of PF. The pronatory effect increases with age, and is related to limited ankle dorsiflexion caused by decreased elasticity of the tendons, and the reduced range of motion that occurs with age.
Digiovanni et al (8) reported relief or absence of plantar heel pain in 52% of patients participating in exercises to stretch the plantar fascia, and 22% after stretching the Achilles tendon. This provides a good target for treatment.
3. Heel spur: Heel spur is a common incidental finding in PF than FPA.
Diagnosis on the basis of US scanning:
Hypoechoic fusiform-shaped swelling more than 4 mm in thickness at the origin of the plantar fascia.

B. Fat pad atrophy (FPA):There is loss of buffering tissue such as water and collagen of the fat pad under the heel mostly due to age. The fat pad atrophies and shock absorbency diminishes in subjects that were older than 40 years. Yi et al (1) used the following criteria to diagnose FPA. FPA is said to the causing planter heel pain if more than 3 of the following criteria are present:
1.    pain at heel center or margin
2.    worsening pain when barefoot 
3.    worsening pain after a long period of standing
4.    palpable calcaneus
In addition to the above following US scan finding: when the patient had a fat pad that was less than 3 mm in thickness.

1. B/L pain is common than U/L.
2. Pain characteristics:
a. aching pain (commonest) but also tingling, cold (5.4%) and burning sensations. (highest to lowest in that order)
b. pain after a long walk, pain at night and resting pain (highest to lowest in that order).
3. Both pes planus & cavus are associated with FPA.
4. Risk factors of FPA: B/L pain which get more severe with prolonged standing is likely to be caused by FPA.

C. PF+FPA (PFFPA):  PF and FPA may share very similar symptoms and are difficult to distinguish from one another further it has been seen. PF can be co-morbid with FPA. PFFPA shares features common to both PF & FPA. In case of mixed characteristics of PF and FPA, PFFPA should be considered first and ultrasonography should be used as an key diagnostic tool.

Treatment options:
It is imperative to diagnose correctly among seemingly similar S/S in planter foot pain. Many FPA & PFFPA cases are misdiagnosed as having PF and treated with conservative therapy including local steroid injection. In cases treated with steroid to PF there are reports of planter fascia rapture in running, hence it is cautioned to diagnose correctly & treat aptly. 
Though many surgical options are available including minimal invasive techniques, there are myriad non-surgical techniques available. Nevertheless, nonsurgical management of plantar fascitis (a predominate cause of planter heel pain) is successful in approximately 90% of patients (2). The options in physical medicinesfor planter heel pain includes: rest, massage, nonsteroidal anti-inflammatory drugs, night splints, heel cups/pads, custom and off-the-shelf orthoses, injections, casts, and physical therapy measures such as shock wave therapy (2). Stretching exercises of the plantar fascia and Achilles tendon can also relieved pain (1). In many studies standing TA stretching is compared with stretching through a prefabricated night splint. Findings suggest that stretching through a prefabricated night splint is a very good option in managing planter foot pain from PF that also is claimed to speeding up the time to recover (4). Heel cushions, heel cups, or low-dye taping can be applied to relieve the pressure on the calcaneus of FPA patients. In those involved in sports correction of training errors and orthotics are essential components in any treatment program (3).
Surgical treatment should be considered in only a small subset of patients with persistent, severe symptoms refractory to nonsurgical intervention for at least 6 to 12 months (2).

1. Yi TI et al; Ann Rehabil Med. 2011 Aug;35(4):507-13. Epub 2011 Aug 31. Clinical characteristics of the causes of plantar heel pain.
2. Neufeld SK et al; J Am Acad Orthop Surg. 2008 Jun;16(6):338-46. Plantar fasciitis: evaluation and treatment.
3. Ryan J; Am Fam Physician. 1995 Sep 1;52(3):891-8, 901-2. Use of posterior night splints in the treatment of plantar fasciitis.
4. Barry LD et al; J Foot Ankle Surg. 2002 Jul-Aug;41(4):221-7. (A retrospective study of standing gastrocnemius-soleus stretching versus night splinting in the treatment of plantar fasciitis.
5. Buchbinder R. Clinical practice. Plantar fasciitis. N Engl J Med. 2004;350:2159–2166.
6. Lemont H, Ammirati KM, Usen N. Plantar fasciitis: a degenerative process (fasciosis) without inflammation. J Am Podiatr Med Assoc. 2003;93:234–237.
7. Inman VT, Ralston HJ, Todd F. Human walking. 2nd ed. Baltimore: Williams & Wilkins; 1994. pp. 45–72.
8. Digiovanni BF, Nawoczenski DA, Malay DP, Graci PA, Williams TT, Wilding GE, Baumhauer JF. Plantar fascia-specific stretching exercise improves outcomes in patients with chronic plantar fasciitis. A prospective clinical trial with two-year follow-up. J Bone Joint Surg. 2006;88:1775–1781. [PubMed]

Saturday, May 26, 2012

Ulnar wrist pain: TFCC injury & DD of Ulnar sided wrist pain

Many ulnar wrist pains are obscure & according to Bottke both surgical exploration and nonoperative treatment have been less than satisfying. Most of the times specific physical examination and standard radiographs were unrevealing in these cases. Even with specific diagnostics test such as arthroscopy, treatment results could not be correlated with arthrographic findings (1).

Ulnar wrist pain,Distal RUJ & TFCC:
The distal radioulnar joint (DRUJ) acts in concert with the proximal radioulnar joint to control forearm rotation. The DRUJ is stabilized by the triangular fibrocartilage complex (TFCC). This complex of fibrocartilage and ligaments support the joint through its arc of rotation, as well as provide a smooth surface for the ulnar side of the carpus. TFCC and DRUJ injuries are part of the common pattern of injuries we see with distal radius fractures. While much attention has been paid to the treatment of the distal radius fractures, many of the poor outcomes are due to untreated or unrecognized injuries to the DRUJ and its components (2).
Triangular fibrocartilage complex (TFCC) tears are a common source of ulnar sided wrist pain. Originally described by Palmer, in 1981, as a complex of several structures, our understanding of the anatomy and the function of the TFCC has been refined by histologic studies. The TFCC plays an important role in load bearing across the wrist as well as in distal radioulnar joint (DRUJ) stabilization. A thorough knowledge of the anatomy as well as the Palmer classification system helps to guide treatment options (3).

Palmer’s Classifications of TFCC Lesions (4)
Class 1: Traumatic
A. Central perforation

B. Ulnar avulsion

- With styloid fracture
- Without styloid fracture

C. Distal Avulsion (from carpus)

D. Radial avulsion

- With sigmoid notch fracture
- Without sigmoid notch fracture

Class 2: Degenerative (Ulnar Impaction Syndrome)
A. TFCC wear

B. TFCC wear

+ lunate and/or ulnar head chondromalacia

C. TFCC perforation

+ lunate and/or ulnar head chondromalacia

D. TFCC perforation

+ lunate and/or ulnar head chondromalacia
+ lunotriquetral ligament perforation

E. TFCC perforation

+ lunate and/or ulnar head chondromalacia
+ lunotriquetral ligament perforation
+ Ulnocarpal arthritis

For further reading on TFCC readers are directed to: (5)

Differential diagnosis of Ulnar sided wrist pain (6):
1. TFCC injury:
S/S:  1. Ulnar wrist pain 2. Snapping or clicking
Physical Tests:  1. TFCC compression test  2. Piano key sign 3. Supination lift test 4. Palpation

2. Lunotriquetral Interosseous Ligament (LTIL) Injury:
S/S:  1. Joint tenderness 2. Decreased ROM 3. Decreased grip strength 4. Painful clunk with radial & ulnar deviation
Physical Tests:  1. Ballottement test 2. Shuck test 3. Shear test 4. Ulnar snuffbox test

3. Arthritis (DRUJ /Pisotriquetral):
S/S:  1. Pain & crepitus with loading 2. Decreased ROM 3. Decreased grip strength 4. Localized pain
Physical Tests:  1. Grind tests 2. Palpation of joint lines 3. Ballottement tests 4. ROM

4. DRUJ Instability:
S/S:  1. Pain with forearm rotation
Physical Tests:  1. Grind tests 2. Palpation

5. ECU Pathology:
S/S:  1. Pain specific to ECU tendon 2. ECU subluxation
Physical Tests: 1. Palpation of ECU tendon over ulnar head 2. Resisted wrist extension & ulnar deviation 3. Active forearm supination & ulnar deviation

6. Fracture (Ulnar styloid, Triquetrum, Hamate):
S/S:  1. Tenderness & edema 2. Decreased ROM 3. Decreased wrist strength 4. Pain with motion

Physical Tests: 1. Palpation of bony landmarks 2. DRUJ stability (ulnar styloid) 3. Resisted 5th digit flexion (hamate)

7. Midcarpal Instability:

S/S:  1. Midcarpal clunk with ulnar deviation & pronation 2. Volar sag at ulnar wrist 3. Often bilateral

Physical Tests: 1. Mid carpal shift test

8. Kienbock's Disease:

S/S:  1. Chronic wrist pain without trauma 2. Tender dorsal lunate 3. Decrease ROM 4. Decreased grip strength 5. Arthritis (late stage)

Physical Tests: 1. Palpation of Lunate

9. Ulnar Nerve Entrapment:

S/S:  1. Paresthesia to 4th & 5th digits 2. Hand intrinsic weakness

Physical Tests: 1. Tinel's to Guyon's Canal 2. History/pattern of symptoms

10. Ulnar Artery Thrombosis:

S/S:  1. Night pain 2. Pain with repetitive activity 3. Cold intolerance 4. Exquisite tenderness at site of pathology 5. Dependent rubor or ulceration or 4th or 5th fingertips 6. Sympathetic fiber excitation of ulnar proper digital nerves

Physical Tests: 1. Allen test.

11. Dorsal Ulnar Cutaneous Nerve Neuritis

S/S:  1.  Sensory changes to 4th & 5th digits 2. Pain or sensory changes at elbow and/or hand weakness, indicative of more proximal ulnar nerve pathology .                                                           
Physical Tests: 1. Sensory exam 2. Palpation 3. Wartenburg sign (motor pathology) 4. Froment sign (motor pathology)

Comments on DD of TFCC:
N.B. Acute trauma to the triangular fibrocartilage complex includes tears of the fibrocartilage articular disk substance and meniscal homolog as well as radioulnar ligament avulsions, with or without an associated fracture (7).
The critical distinction is in differentiating injuries that produce instability of the distal radioulnar joint from those that do not. Also important is the recognition of acute injuries in the context of an ongoing degenerative pattern (ie, Palmer class 2 lesions) (7). Subluxation of the ulnar head relative to the sigmoid notch of the radius, as assessed by MRI with the wrist in pronation, is a predictor of tears of the foveal attachment of the TFCC (8). Horizontal tear and fibrillation of TFCC disk without TFCC tear at the radiocarpal joint present with ulnar-sided wrist pain due to isolated triangular fibrocartilage complex. Arthroscopic debridement only relieves pain after surgery and helps in achieving good functional recovery (9).

Patient evaluation includes clinical examination, imaging studies, and wrist arthroscopy (diagnostic). The Palmer classification is typically used to define injuries to the triangular fibrocartilage complex (10).

TFCC management outline:
Both surgical & Non-surgical therapies have claimed success. Nonsurgical management includes temporary splint immobilization of the wrist and forearm, oral nonsteroidal anti-inflammatory medication, corticosteroid joint injection, and physical therapy. Surgical strategies include d├ębridement, acute repair, and subacute repair. Most surgical procedures can be performed arthroscopically. However, open ligament repair may be needed in the setting of distal radioulnar joint instability.

Comments of the author: Manual therapy: Many cases of mild-moderate ulnar sided wrist pain can be helped by MWM technique of Mulligan i.e. Medial glide to intercalar segment with wrist F/E.  

1. Bottke CA et al; Orthopedics. 1989 Aug;12(8):1075-9. Diagnosis and treatment of obscure ulnar-sided wrist pain.

2. Tsai PC et al; Bull NYU Hosp Jt Dis. 2009;67(1):90-6. The distal radioulnar joint.

3. Ahn AK et al;Bull NYU Hosp Jt Dis. 2006;64(3-4):114-8. Triangular fibrocartilage complex tears: a review.

4. Green’s operative hand surgery, fifth edition, Distal radioulnar joint instability, blz: 613-616



7. Henry MH; J Am Acad Orthop Surg. 2008 Jun;16(6):320-9. Management of acute triangular fibrocartilage complex injury of the wrist.

8. Ehman EC et al; J Hand Surg Am. 2011 Nov;36(11):1780-4. Subluxation of the distal radioulnar joint as a predictor of foveal triangular fibrocartilage complex tears.

9. Abe Y et al; Hand Surg. 2011;16(2):177-80. Ulnar-sided wrist pain due to isolated disk tear of triangular fibrocartilage complex within the distal radioulnar joint: two case reports.

10. Henry MH; J Am Acad Orthop Surg. 2008 Jun;16(6):320-9. Management of acute triangular fibrocartilage complex injury of the wrist.

Thursday, May 10, 2012

Differential diagnosis of Anatomic (Radial) snuffbox pain: It is not always DeQuervain’s tenosynovitis.

Tendon, Bone & Ligament causes:
1. DeQuervain’s tenosynovitis:
Swelling of tendon of APL (Abductor pollicis longus) & extensor pollicis brevis at lateral wrist near anatomic snuff box.  The primary complaint is radial sided wrist pain that radiates up the forearm with grasping or extension of the thumb. The pain has been described as a “constant aching, burning, pulling sensation." Pain is often aggravated by repetitive lifting, gripping, or twisting motions of the hand. Swelling in the anatomical snuff box, tenderness at the radial styloid process, decreased CMC abduction ROM of the 1st digit, palpable thickening of the extensor sheaths of the 1st dorsal compartment and crepitus of the tendons moving from the extensor sheath may be found upon examination. Other possible findings include weakness and paresthesia in the hand. Finkelstein’s diagnostic test will present positive provoking the patient’s symptoms.

If left untreated, the inflammation and progressive narrowing (stenosis) can cause scarring that further limits thumb motion.

 2. Carpal Instabilities:
Altered biomechanics of the wrist may produce pain. Scapholunate disassociation, scapho-trapezio-trapezoidal joint degeneratioin, and lunatotriquetral dissociation could all present with radial sided wrist pain.

3. Scaphoid Fracture
A scaphoid fracture commonly present with radial sided wrist pain, tenderness and possible swelling in the anatomical snuff box, and limited ROM with pain especially at end ranges.

4. Osteoarthritis of the 1st CMC
Osteoarthritis of the 1st CMC typically occurs in individuals greater than 50 years old, and will most frequently present with morning stiffness of the 1st CMC joint, a general decrease in ROM of the joint, tenderness along the joint line, and a positive grind test.

Neural Causes:

1. Cheiralgia paresthetica:
Cheiralgia paresthetica is commonly referred to as handcuff neuropathy. It is a neuropathy of the hand generally caused by compression or trauma to the superficial branch of the radial nerve.

The area affected is typically on the back or side of the hand at the base of the thumb, near the anatomical snuffbox, but may extend up the back of the thumb and index finger and across the back of the hand. /S includesnumbness, tingling, burning or pain. Since the nerve branch is sensory there is no motor impairment.

Differentiating point: It may be distinguished from de Quervain syndrome because it is not dependent on motion of the hand or fingers.

2. C6 Cervical Radiculopahy:
Compression on a spinal nerve root can cause sensory disturbances, myotomal weakness, and diminished reflexes throughout the root's distribution. The dermatomal key point for the C6 nerve root is the radial aspect of the 2nd metacarpal and index finger which is close to the area of pain experienced with De Quervain’s. Since a radiculopathy can present much like De Quervain’s a thorough screen of the cervical spine is necessary.

Saturday, April 28, 2012

Carpal instability: Types, Place of VISI & DISI

 Key word: Carpal instability, Data base: Pubmed

Wrist anatomy- extrinsic & and intrinsic ligaments

The extrinsic (radiocarpal) and intrinsic (intercarpal) ligaments maintain carpal stability. The major extrinsic ligaments are the radioscaphocapitate, radiolunotriquetral, short radiolunate, and dorsal radiocarpal ligaments. The scapholunate and lunotriquetral ligaments are the most important intrinsic ligaments and the primary wrist stabilizers. The most common causes of carpal instability are unstable fracture of the scaphoid, scapholunate dissociation, and lunotriquetral dissociation (7).
Let us discuss the causes of carpal instability. Classification of carpal instability is presented below is based on anatomic and kinematic characteristics of the wrist. A classification of the subtle patterns of carpal instability is presented below.  

Navarro's concept of the carpus (1921):

Carpals of wrist are arranged in 3 vertical longitudinal columns: lateral (scaphoid); central (lunate and distal carpal row); medial (triquetrum).

Carpal dislocation occurs between:
1.    lateral and central columns- called lateral instability
2.    within the central column- called central instability
3.    central column and the triquetrum- called medial instability and
4.    between the entire carpus and the distal radioulnar articular surface- is called proximal instability

Classification of lateral instability: Lateral carpal instabilities are further subdivided according to the different components of the central column that articulate with the scaphoid. Therefore, 3 main lateral patterns may be identified:

1.    scaphoid-trapezium-trapezoid subluxation
2.    scaphoid-capitate diastasis
3.    scaphoid-lunate dissociation (rotatory subluxation of the scaphoid)

Classification of medial instability: Medical carpal instability may take place between the triquetrum and the lunate, or the triquetrum and the hamate. Dissociation between lunate and triquetrum results in static forms of instability, while disruption of triquetrohamate support leads to dynamic forms of instability.

VISI (volar-flexed intercalated segment instability): It is example of medial instability. In lunate-triquetrum instability, is believed responsible for VISI in which the lunate collapses into a volar-flexed position and there is longitudinal "crumpling" of the radiocarpal link.

Proximal instability:
Proximal carpal instability may lead to disruption at the level of the radiocarpal joint or at the level of the midcarpal joint. Proximal carpal or radiocarpal instability may occur in an ulnar (ulnar translocation), dorsal (dorsal subluxation), or volar direction (volar subluxation). It is usually associated with loss of the anatomic alignment of the distal radius.

Exclusive discussions on VISI & DISI:

Navarro’s carpus concept can be called column concept. But "The row concept best explains the behaviour of the carpal bones. 8 carpals comprising of 2 row of 4 carpals each. The proximal row acts as an intercalated segment- there is no direct control of this row. It is controlled by the bones surrounding it via the short interosseous ligaments. It has a natural tendency if isolated to 'pop out' and tilt dorsally."
Intercalated segment: The intercalated segment is the proximal carpal row identified by the lunate. The term 'intercalated segment' refers to it being the part in between the proximal segment of the wrist consisting of the radius and the ulna and the distal segment, represented by the distal carpal row and the metacarpals.

DISI: DISI, or dorsiflexion instability, the lunate is angulated dorsally. It is the most frequent mid carpal instability. It occurs due to complete tear of scapho-lunate ligament.

DISI pattern:
1.    when the scapholunate joint is dissociated, the scaphoid is palmar flexed and the lunate is dorsiflexed
2.    Scapho-lunate angle usually 30- 60degrees (average 46 degrees) and with DISI it is greater than 70degrees

What you look in lateral wrist X-ray if you suspect DISI: If you think the lunate is tilted, measure the scapholunate angle ( 30-60°is normal, 60-80°is questionably abnormal, >80° is abnormal) and the capitolunate angle (<30° is normal).

What you look in AP wrist X-ray if you suspect DISI: Guilula’ arc.

VISI: It is a palmar flexion instability where the lunate is tilted palmarly too much. While most DISI is abnormal, in many cases VISI is a normal variant, especially if the wrist is very lax. It occurs due to complete tear of lunotriquetral ligament. There is posterior subluxation of both lunate & scaphoid due to lack of union with triquetrum. Scaphoid & Lunate remain interdependent hence the scapho-lunate angle is normal.

VISI pattern:
1.    lunate palmar flexed
2.    if the lunate and triquetrum can be seen, the normal lunotriquetral angle of approximately -16 degrees becomes neutral or positive

Note: in conventional radiography: According to Toms et al (8) Conventional radiographic abnormalities are usually limited to volar intercalated segment instability (VISI) patterns of carpal alignment and are not specific.

Mid carpal instability:
Midcarpal instability (MCI) is the result of complex abnormal carpal motion at the midcarpal joint of the wrist.
Palmar, dorsal, ulnar midcarpal instability, and capitolunate or chronic capitolunate instability are all descriptions of types of MCI with often overlapping features.
It is a form of non-dissociative carpal instability (CIND) (see below for dissociative & non- dissociative carpal instability) and can be caused by various combinations of extrinsic ligament injuries that then result in one of several subtypes of MCI.
Palmar midcarpal instability (PMCI) is the most commonly reported type of MCI. It has been described as resulting from deficiencies in the ulna limb of the palmar arcuate ligament (triquetrohamate-capitate) or the dorsal radiotriquetral ligaments, or both.

Another broad classification of carpal instability:Dissociative & non- dissociative carpal instability.

The causes of carpal instability are dissociation of the intercarpal ligaments on either side of the lunate, are so-called scapholunate dissociation or a luno-triquetral dissociation. Carpal instability non-dissociative is generally due to a laxity or attenuation of the intrinsic ligaments of the carpus and are associated with deformity of the distal radius (6).
Ulnar translation of the carpus on the distal radioulnar articular surfaces occurs with shear stretching of the origins of the radiocarpal ligaments. The radial styloid attenuation of the ligaments may result in abnormal motions of the carpal bones going from ulnar to radial deviation at which time a catch-up click may occur (6).

Radiography choices in carpal instability (8):

1.    Stress view radiographs (To demonstrate carpal instability)
2.    Videofluoroscopy (To demonstrate abnormal carpal kinematics)
3.    Dynamic US can be also used to demonstrate midcarpal dyskinesia including the characteristic triquetral "catch-up" clunk.
4.    Tears of the extrinsic ligaments can be demonstrated with MR arthrography, and probably with CT arthrography.

Treatment approach:
Plan of management for carpal dislocations are based upon the following basic criteria: whether the dislocation is perilunate or lunate dislocation. In most cases they are managed identically (5).
Step 1: In all cases anatomic restoration of the 3 key elements (scaphoid, lunate, and capitate) is essential.
Step 2: Following initial closed reduction, rotary subluxation of the scaphoid and intercalary segment instability must be specifically looked for and corrected in the patient with perilunate or lunate dislocation without fracture of the scaphoid.
Failure to obtain or maintain anatomic position by closed methods is an indication for open reduction and internal fixation.

Operative methods & choices:
1.    Unstable carpal articulations can be treated with limited carpal arthrodesis.
2.    Ligamentous defects can be treated with capsulorrhaphy or ligament reconstruction.

Complications:As with all ligamentous injuries, early diagnosis and treatment are essential. Missing the concomitant injuries include median nerve damage, osteochondral fractures of the carpal bones, and fracture of the radial styloid. Pain & Post-op stiffness are a usual complications.

1.    Taleisnik J; Clin Orthop Relat Res. 1980 Jun;(149):73-82. (Post-traumatic carpal instability).
3.    LK Ruby; The Journal of Hand Surgery. Volume 13, Issue 1, January 1988, Pages 1–10 (Relative motion of selected carpal bones: A kinematic analysis of the normal wrist)
4.    Taleisnik J; Bull Hosp Jt Dis Orthop Inst. 1984 Fall;44(2):511-31.
5.    Green DP; Clin Orthop Relat Res. 1980 Jun;(149):55-72. (Classification and management of carpal dislocations).
6.    Linscheid RL et al;Orthopade. 1993 Feb;22(1):72-8. (Carpal instability).
7.    Timins ME et al; Radiographics. 1995 May;15(3):575-87. (MR imaging of the major carpal stabilizing ligaments: normal anatomy and clinical examples).
8.    Toms AP; Skeletal Radiol. 2011 May;40(5):533-41. Epub 2010 May 14. (Midcarpal instability: a radiological perspective).

Sunday, March 11, 2012

LASER therapy in physiotherapy

•    Therapeutic Laser
•    Low Level Laser Therapy
•    Low Power Laser Therapy
•    Low Level Laser
•    Low Power Laser
•    Low-energy Laser
•    Soft Laser
•    Low-reactive-level Laser
•    Low-intensity-level Laser
•    Photobiostimulation Laser
•    Photobiomodulation Laser
•    Mid-Laser
•    Medical Laser
•    Biostimulating Laser
•    Bioregulating Laser

4 categories of lasers
–    Crystal & Glass (solid - rod)
•    Synthetic ruby & others (synthetic ensures purity)

–    Gas (chamber) – 1961
•    HeNe, argon, CO2, & others

–    Semiconductor (diode - channel) - 1962
•    Gallium Arsenide (GaAs under investigation)

–    Liquid (Dye) - Organic dyes as lasing medium

–    Chemical – extremely high powered, frequently used for military purposes

Types of laser:

Lasers are of 3 different type soft laser, mid laser, power laser. Soft lasers are used for dermatological purposes where depth of penetration is only superficial, Physiotherapy lasers are mid lasers where depth of penetration is from .5-2cm for class III lasers up to 10 cm in type IV lasers. Power lasers are destructive lasers used in different medical & dental surgery.
There are 4 different classes of laser i.e. Class I-IV. All 4 class are used in physiotherapy. However class I-III lasers are commonly used. Class IV physiotherapy & surgical lasers are not to be confused with each other.

Class of lasers:

Class I: Low power lasers
Class II: Power out put up to 1mW (400-700 nm wavelength).
Class IIIa: Power out put up to 5mW.
Class IIIb: Power out put up to 5-500mW.
Class IV: Power out put up to 500-7500mW.

* All lasers can cause eye damage except Class I laser. As the power increases the potential of causing eye damage is more.

* Class III lasers are also known as LLLT i.e. low level laser therapy.

* Class IV lasers are also known as high power laser therapy.

* High-power lasers (class IV) have power output of up to 7,500 mW; and supposedly offer more power, deeper penetration (can penetrate up to 10 cm instead of 0.5 to 2.0 cm for class III lasers) and a larger surface treatment area (cover up to 77 cm2 instead of 0.3 to 5.0 cm2 for class III lasers) 

Modes of Laser:

Either it is continuous or Pulsed. In pulsed laser frequency is a key area for therapeutic efficiency.

Why red or IR lasers are used?
•    Red light affects all cell types
–    Absorbed by the mitochondrial present in all cells
–    Cytochromes (respiratory chain enzymes) within the mitochondria have been identified as the primary biostimulation chromophores (primary light-absorbing molecules).
–    Since enzymes are catalysts with the capability of processing thousands of substrate molecules, they provide amplification of initiation of a biological response with light.

•    Infrared light is more selective absorbed by specific proteins in the cell membrane & affects permeability directly

Tissue response:

•    Magnitude of tissue’s reaction are based on physical characteristics of:
–    Output wavelength/frequency
–    Density of power
–    Duration of treatment
–    Vascularity of target tissues

•    Direct effect - occurs from absorption of photons
•    Indirect effect – produced by chemical events caused by interaction of photons emitted from laser & the tissues

Patient & Laser parameters:

•    Patient parameters
–    Need medical history & proper diagnosis
•    Diabetes – may alter clinical efficacy
–    Medications
•    Photosensitivity (antibiotics)
–    Pigmentation
•    Dark skin absorbs light energy better

 Laser Parameters

–    Wavelength
–    Output power
–    Average power
–    Intensity
–    Dosage

Laser Wavelength:
This is measured in Nanometers (nm). Longer wavelength (lower frequency) imparts greater penetration. Wavelength is affected by power.

Laser output:
It is measured in Watts or milliwatts (W or mW). It is important in categorizing laser for safety. It is not adjustable.

Power Density or Laser intensity:
Beam diameter determines power density. Units of measurement is W or mW/cm2.It takes into consideration actual beam diameter. If light spread over lager area then there is there is lower power density.

Average Power:
It is dependant on the mode of laser beam delivery i.e. Continuous or pulse-train (burst) frequency mode. Knowing average power is important in determining dosage with pulsed laser. If laser is continuous laser then avg. power = peak output power. If laser is pulsed (burst) then avg. power is = to peak output power multiplied by duty cycle (frequency).

DOSAGE: Laser dosage is amount of energy applied per unit area. It is measured in Joules/square cm (J/cm2). Joule is unit of energy &1 Joule = 1 W/sec. Dosage is dependent on:
–    Output of laser in mW
–    Time of exposure in seconds
–    Beam surface area of laser in cm2
Various dosage ranges per site (1-9 J/cm2).

Recommended Dosage Range
–    Therapeutic response = 0.001-10 J/cm2
–    Minimal window threshold to elicit response
–    Too much – suppressive effect
–    Open wounds – 0.5-1.0 J/cm2
–    Intact skin – 2.0-4.0 J/cm2
–    Average treatment – 6 J /cm2

Different common lasers in physiotherapy:

1. Helium-Neon Lasers

•    Uses a gas mixture in a pressurized tube
•    Now available in semiconductor laser
•    Emits red light
•    Wavelength:  632.8 nm
•    Power output: 1.0-25.0 mW
•    Energy depth: 6-10 mm
•    The higher the output of the lasers (even though they are still low power) lower the delivery time

2. Indium-Gallium-Aluminum-Phosphide Lasers

•    InGaAip
•    Replacing HeNe lasers
•    Semiconductor
•    Wavelength:    630-700 nm
•    Power output:  same as HeNe
•    Energy depth: superficial wound care

3. Gallium ArsenideLasers

•    Semiconductor - produces an infrared (invisible) laser
•    Wavelength:  904–910 nm
•    Power output: may produce up to 100 mW
•    Energy depth: 30-50 mm
•    Short pulse-train (burst) duration (100-200 ns)

4. Gallium Aluminum ArsenideLasers

•    GaAIAs
•    Semiconductor
•    Wavelength: 780-890 nm
•    Power Output: 30-100 mW (up to 1000 mW)
•    Energy Depth: Very high more than the above said laser

Laser Application techniques:

•    Gridding Technique
•    Divide treatment areas into grids of square centimeters
•    Scanning Technique
•    No contact between laser tip in skin; tip is held 5-10 mm from wound
•    Wanding Technique
•    A grid area is bathed with the laser in an oscillating fashion; distance should be no farther than 1 cm from skin
•    Point Application (On acupuncture point)

Treatment techniques for contact treatment:

Dosage is the most important variable in laser therapy & may be difficult to determine. However it may be simplified i.e. for general application, only treatment time & pulse rate vary. Usually there is a handheld applicator & tip should be in light contact with skin while laser is engaged for pre-calculated time. Maintain laser perpendicular to treatment surface. Put firm contact unless open wound. Clean area prior to treatment.

Always begin with minimal treatment and gradually increase (Better to underexpose than to overexpose). Check for pre/post-treatment changes. Ask the patient how they are doing prior to next treatment because you may have to adjust dosage.

Avoid direct exposure into eyes (If lasing for extended periods of time, safety glasses are recommended). May experience a syncope episode during treatment during chronic pain, but it is very rarely reported.

Application of heat & cold with LASER:
If icing – use BEFORE phototherapy because it enhances light penetration. If using heat therapy – use AFTER phototherapy because it decreases light penetration.

Use of Laser therapy in different field of medicine

1. Vascular condition: Venous ulcer (Ref: M.E. Sugrue et al; Annals of Vascular Surgery, Volume 4, Issue 2 , Pages 179-181, March 1990). Results of this pilot study are encouraging. Raynaud's phenomenon is also treated by Laser therapy (Hirschl et al, 2004). Popularly pressure ulcers are treated by laser therapy in neurorehab words.

2. Neurological condition: Stroke (Ref: Int J Stroke. 2012 Feb 2. doi: 10.1111/j.1747-4949.2011.00754.x.). This study named transcranial laser therapy for acute ischemic stroke: a pooled analysis of NEST-1 and NEST-2, support the likelihood that transcranial laser therapy is effective for the treatment of acute ischemic stroke when initiated within 24 h of stroke onset. If ultimately confirmed, transcranial laser therapy will change management and improve outcomes of far more patients with acute ischemic stroke.

Similarly laser therapy is also reported to be beneficial in number of other neurological conditions both in animal & human subjects. Examples are closed-head traumatic brain injury (mice)( In mice it is reported that there is less neurological deficits in post-traumatic brain injury treated with laser for traumatic brain injury.), neurodegenerative diseases (humans) example Alzheimer’s disease. 

3. ENT conditions: Tonsillitis (Vestn Otorinolaringol. 2006;(3):19-22. Russian.), Tinnitus (FrankW et al; GMS Health Technol Assess. 2006 Aug 30;2:Doc17).

4. Surgical conditions: Chronic wound healing, Kaviani and colleagues (2006) examined the effects of low level laser therapy (LLLT) in the treatment of post-mastectomy lymphedema & concluded that LLLT has encouraging results on this condition. LLLT can be used as a conservative therapy for arm lymphoedema secondary to breast cancer treatment (BC Cancer Agency; 2007). Mastodynia is also treated successfully. Lymphangitis is also reported to be treated successfully

5. Dental conditions: post-operative pain after endodontic surgery (Kreisler et al; 2004). Markovic and Todorovic (2007) found after lower third molar surgery laser therapy can be recommended to minimize swelling & oedema. TMJ conditions also show encouraging results.

6. Musculoskeletal conditions: Bursitis, Tendinitis, Ligament injuries, CTS, Neck pain, LBA, myofascial pain syndrome (MPS), Post exercise pain (to treat plyometric induced pain), planter heel pain(Crawford and Thomson, 2003; Landorf and Menz, 2007).

7. Rheumatological conditions: RA (most studied) other rheumatologic pain

8. Other conditions: After effects of tuberculosis, Smoking cessation, Dysmenorrhea etc. 


Wednesday, February 29, 2012

Classification of spondyloarthritides (SpA) & USpA

Classification of spondyloarthritides (SpA) & USpA
Definition: The spondyloarthritides (SpA) are an interrelated group of rheumatic diseases that are characterized by common clinical symptoms and genetic similarities.

For clinical purposes, 5 subgroups are differentiated:
1.    AS (ankylosing spondylitis)
2.    Psoriatic SpA (PsSpA)
3.    Reactive SpA (ReSpA)
4.    SpA associated with inflammatory bowel disease (SpAIBD) and
5.    Undifferentiated SpA (uSpA)

Features of SpA:

Important clinical features of the SpA are
1.    inflammatory back pain (IBP)
2.    asymmetric peripheral oligoarthritis predominantly of the lower limbs
3.    enthesitis
4.    specific organ involvement such as anterior uveitis (eye) , psoriasis (skin) and chronic inflammatory bowel disease

The most important subtype of SpA is ankylosing spondylitis (AS), which is now considered part of axial spondyloarthritis.
ASAS Classification: ASAS stands for Assessment of SpondyloArthritis International Society. 
ASAS group has recently developed criteria to classify patients with axial SpA with or without radiographic sacroiliitis, and criteria to classify patients with peripheral SpA.

Axial SpA:
1. LBA (>3 months almost every day)
2. Radiographs and magnetic resonance imaging (MRI can detect active inflammation and structural damage associated with SpA.)
3. HLA-B27 (Leucocyte antigen): SpA are genetically linked (90% of cases), the strongest contributing factor being HLA B27.
According to the ASAS axial SpA criteria, patients with chronic back pain aged less than 45 years at onset can be classified as having axial SpA if sacroiliitis on imaging (radiographs or MRI) plus 1 further SpA feature are present, or if HLA-B27 plus 2 further SpA features are present.

Peripheral SpA:
1. Patients with peripheral arthritis (usually asymmetric arthritis predominantly involving the lower limbs) enthesitis, or dactylitis.
2. Patients can be classified as having peripheral SpA if 1 of the following features is present: uveitis, HLA-B27, preceding genitourinary or gastrointestinal infection, psoriasis, inflammatory bowel disease, sacroiliitis on imaging (radiographs or MRI) in addition to point no 1.
3. Or if 2 of the following features besides the entry feature are present: arthritis, enthesitis, dactylitis, inflammatory back pain, or a positive family history of SpA.


Clinical features of USpA:
Vast majority of USpA have IBP (Inflammatory back pain) & asymmetrical peripheral arthritis predominately of lower limbs.

HLA B27 is more helpful uSpA diagnosis: Liao et al analysed the clinical features of Chinese undifferentiated spondyloarthritis (USpA) patients with predominantly axial involvement. They found in Chinese population Both HLA-B27 status and SIJ MRI findings influence the classification of Chinese axial USpA patients, but HLA-B27 seems of more value.

1. Braun J & Sieper J; Z Rheumatol. 2010 Jul;69(5):425-32; quiz 433-4. Spondyloarthritides.
2. van den Berg R & van der Heijde DM; Pol Arch Med Wewn. 2010 Nov;120(11):452-7. How should we diagnose spondyloarthritis according to the ASAS classification criteria: a guide for practicing physicians.
3. Liao Z et al; Scand J Rheumatol. 2011 Nov;40(6):439-43. Epub 2011 Jul 4. Clinical features of axial undifferentiated spondyloarthritis (USpA) in China: HLA-B27 is more useful for classification than MRI of the sacroiliac joint.

Thursday, February 16, 2012

Eosinophilic Fascitis: 300 cases in 35 years

All people dealing with soft tissue pain & dysfunction "Eosinophilic Fascitis" is rearrest of the rare condition to encounter.

Take a note of it. It is a matter of debate for all fascia researchers & people involved in "Fascia research congress"

Pubmed link to "Eosinophilic Fascitis":

Thursday, February 2, 2012

Lumbar Retrolisthesis: Introduction, types, physiotherapy treatment

A retrolisthesis is a posterior displacement of one vertebral body with respect to the adjacent vertebrae to a degree less than a luxation (dislocation). Retrolisthesis is relatively rare but when present has been associated with increased back pain and impaired back function. Clinically speaking, retrolisthesis is the opposite of spondylolisthesis (anterior displacement of one vertebral body on the subjacent vertebral body). Retrolistheses are most easily diagnosed on lateral x-ray views of the spine. Views, where care has been taken to expose for a true lateral view without any rotation, offer the best diagnostic quality.

Retrolisthesis may occur more commonly than initially believed. However retrolisthesis (backwards slippage of one vertebral body on another) has historically been regarded as an incidental finding, one which doesn’t cause any symptoms, and is considered to be of little or no clinical significance. But there is a possible association between retrolisthesis and increased back pain and impaired back function.

Retrolisthesis may be present in up to 30% of extension radiographs of patients complaining of chronic low back pain. Retrolisthesis has been found to be associated with disc degeneration, decrease in lumbar lordosis, and decrease in vertebral endplate angle.

According to Shen et al (Shen M et al; Spine J. 2007; 7(4): 406–413) it is possible that the contribution of pain or dysfunction related to retrolisthesis was far overshadowed by the presence of symptoms due to the concomitant disc herniation.

Crucial questions in musculoskeletal medicine in retrolysthesis:

1. Do individuals with lumbar disc herniations have increased levels of back pain, back dysfunction, and decreased quality of life pre-operatively if they have concomitant retrolisthesis at the involved herniated disc level?

2. Does the presence of degenerative changes (disc degeneration, degenerative endplate changes, posterior element degenerative changes) along with retrolisthesis worsen the symptoms and / or possibly the prognosis in these operative cases?

Grading & Classification:

Classification system:
Complete Retrolisthesis - The body of one vertebra is posterior to both the vertebral body of the segment of the spine above as well as below.
Stairstepped Retrolisthesis - The body of one vertebra is posterior to the body of the spinal segment above, but is anterior to the one below.
Partial Retrolisthesis - The body of one vertebra is posterior to the body of the spinal segment either above or below.

Since the vertebral body in a retrolisthesis moves in a posterior direction, the grading used for spondylolistheses is of little use. Clinicians & researchers use the following grading systems after following X ray reading:

There are always 2 vertebrae involved in measuring the magnitude of a retrolisthesis for translation (slippage). The lower segment is considered the position of stability. The upper segment rests on it. The upper segment is considered the segment of mobility and is the one being determined for retrolisthesis.

1) A line is drawn along the top of the vertebral body of the lower spinal segment.
2) Then at the top-back most portion of the lower vertebral body, draw line at 90 degrees to line, till it projects well into the body of the vertebra above.
3) Then draw another line parallel to the line just drawn this time at the posterior most lower portion of the upper vertebral body.
4) The distance between the upright lines and is measured. Any distance of 3mm or greater is a retrolisthesis. This measurement represents the degree of translation (slippage) of the upper of the two segments.

1. Few clinicians follow the following criteria:

Percent subluxation can be calculated for any individual with greater than or equal to 3 mm of posterior displacement. A cut-off point of 3 mm has been used previously both in orthopaedic research and clinical practice. This 3mm cut-off corresponds to a slip of 8% which is used as the lower limit to define retrolisthesis.

2. Other few follow the following criteria:

In this grading system anterior to posterior dimension of the intervertebral foramina (IVF) is divided into four equal units. A posterior displacement of up to ¼ of the IVF is graded as Grade 1, ¼ to ½ as Grade 2, ½ to ¾ as Grade 3, ¾ to total occlusion of the IVF as Grade 4.

Joint stability & retrolisthesis: 

Joint stability is easily evaluated by the use of flexion and extension lateral x-ray views of the spine. If vertebral translation present on standing (stressed by gravity) lateral view x-rays then it indicates that the spinal joints at those levels are already in a "significantly stressed" state. It further means that if this is the condition then there may be degree of soft tissue looseness at best and soft tissue tearing at worst otherwise a positional translation of this magnitude could not be present.

Implications of joint instability are derived from DRE (Diagnosis related estimates) tables. If translation of 4.5mm & angular change of 15 degree or more at L1, L2 or L 3, 20 degree or more at L4 and 25 degree or more at L5 is found then Category IV instability is present. This would mean that 20% to 23% “whole person impairment” is present at each level where this if found.
Pathology & structures involved:

Retrolysthesis is caused in lumbar by flexion injury or by prolonged & continual use of lumber spine flexion over a period of time.

Spine instability causes damage to of the connecting soft tissues especially juxtaposed ligaments, discs, muscles, tendons and fascia. Muscle spasm may also be present. Nerve compression may be present at intervertebral foramen (IVF). The compression of the IVF’s contents include spinal (sensory and motor) nerves, arteries, veins and lymphatic vessels which cater to the nutritional and waste removal needs of the spinal cord.

Degenerative spinal changes are often seen at the levels where a retrolisthesis is found. These changes are more pronounced as time progresses evidenced by end plate osteophytosis, disc damage, disc narrowing, tearing failure and eventually results in disc bulging.
“A retrolisthesis hyper loads at least one disc and puts shearing forces on the anterior longitudinal ligament, the annular rings, nucleus pulposis, cartilage end plates and capsular ligaments. The bulging, twisting and straining tissues attached to the endplates pull, push and stretch it. It is worsened with time, gradually
becoming irreversible. This is the aetiology of degenerative joint disease in retrolysthesis.

X-ray & radiological findings:

•    Vacuum phenomenon (in the nucleus pulposis of the intervertebral disc below the retrolisthesis),
•    Reduction of disc height with corresponding loss of the disc space,
•    Marginal sclerosis (more dense due to stress) of the adjacent vertebral bodies,
•    Osteophyte (spur) formation and
•    Apophyseal (guiding) joint instability.
•    With a retrolisthesis there is always a less than ideal positioning of spinal segments. (subluxation)
•    There is also always a reduced anterior to posterior dimension of the spinal canal compared to the way it is supposed to be. This leads to nerve signal alteration.
•    The greater the posterior displacement, the more significant it is for producing nerve root impingement and irritation, a dysfunctional spinal cord even to the point of a cauda equina compression syndrome if present in the lower lumbar spine.

Patient clinical presentation:

Patients present with varied S/S with retrolysthesis from little pain to severe disabling pain. Patient may also present with sciatica with or without neurological deficits. In patients with neural claudication lumbar canal stenosis due to lysthesis is also seen.


Both IV joints & facet joints may produce pain & radiation.

Maitland transverse glides/ lateral PA glides on to the side of pain can be administered in cases associated mostly with facet restrictions. Central PA is also administered in appropriate cases with mutifidus & other spinal exercises. LS belt in majority cases may aid relief from pain.

McKenzie’s exercises to stretch the anterior spinal structures both with mobilization & manipulation in McKenzie style along with home exercises in McKenzie is highly advisable.

Spine muscle atrophy is seen in many cases of long standing retrolythesis. Spine stabilization exercises are sought in most cases and appropriate home exercises must be advised with follow ups with the physiotherapist.

Electrotherapy is directed to reduce pain. Few clinicians also believe that modalities like SWD or MWD can reduce the rate of degeneration hence also used in degenerative retrolysthesis.

Friday, January 13, 2012

Sitting ergonomics: Different sitting postures & analysis of chair sitting muscle work

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 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.