Facet Joint Arthropathy

The facet joints are the most 'pull apartable' structures of the spine, with their freedom controlled by the extraordinarily strong facet capsules (AKA 'capsular ligaments'). Injury to the facet joints causes a primary inflammation of the joint, mainly of the facet capsule and also its sensitive inner lining, the synovial membrane. As with any other synovial joint injury, the joint swells and the muscles swing in to protect it.
Facet joint disorders are some of the most common of all the recurrent, disabling low back and neck problems, and can cause serious symptoms and disability for patients. However, facet joint problems rarely involve the spinal nerves.

causes of Facet Joint arthropathy:

Facet joints, like other synovial joints, are susceptible to wear and tear, degeneration, inflammation and arthritic changes. Inflammation and degenerative changes to the facet joints may result in pain, loss of motion, and if severe encroachment or pinching of the nerve exiting the spinal column. Causes of facet joint arthropathy include:

• Degeneration or general wear and tear of the joint, can cause arthritis.
• Disc degeneration may cause loss of height between vertebra, placing a greater compression force on the posterior facet joints.
• Extension (backward) motions can produce compression on the facet joints which can lead to degenerative and eventual arthritic changes.
• Sudden fall or trauma like a motor vehicle accident can result in a facet joint irritation.
• Genetic factors can contribute to the likelihood of degenerative joint disease.
• Repetitive stress injuries like those from lifting or carrying heavy loads, or performing over the head motions that keep the neck and head in an extended position can cause facet joint irritation.
• Muscle weakness and poor posture.
• Joint stiffness.
• Sedentary lifestyle.

Symptoms of Facet Joint Problems:

A correct diagnosis must await subsidence of the acute problem. Symptoms may include the following:

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

Dry Needling

It is a skilled intervention that uses a thin filiform needle to penetrate the skin and stimulate

underlying myofascial trigger points, muscular, and connective tissues for the management of

neuromusculoskeletal pain and movement impairments. 

Dry needling (DN) is a technique used to treat dysfunctions in skeletal muscle, fascia, and connective tissue, and, diminish persistent peripheral nociceptive input, and reduce or restore impairments of body structure and function leading to improved activity and participation.

DN can be divided into deep and superficial DN. Deep DN has been shown to inactivate TrPs by eliciting local twitch responses (LTR), which are modulated by the central nervous system. A LTR is a spinal cord reflex that is characterized by an involuntary contraction of the contractured taut band, which can be elicited by a snapping palpation or penetration with a needle.

Deep DN of TrPs is associated with reduced local and referred pain, improved range of motion, and decreased TrP irritability both locally and more remotely. Superficial DN is thought to activate mechanoreceptors coupled to slow conducting unmyelinated C fiber afferents, and indirectly, stimulate the anterior cingular cortex. Superficial DN may also be mediated through stimulation of A-δ fibers, or via stretching of fibroblasts in connective tissue. Superficial DN is associated with reduced local and referred pain and improved range of motion.

Indications for Use:

DN may be incorporated into a treatment plan when myofascial TrPs are present, which may lead to impairments in body structure, pain, and functional limitations. TrPs are sources of persistent peripheral nociceptive input and their inactivation is consistent with current pain management insights. DN also is indicated with restrictions in range of motion due to contractured muscle fibers or taut bands, or other soft tissue restrictions, such as fascial adhesions or scar tissue.

Precautions:

There are certain precautions to be considered with the use of DN:

1. Patients with a needle aversion or phobia may object to the physical therapy treatment with DN. With appropriate education, however, these patients may still consider DN.

2. Patients with significant cognitive impairment may have difficulty understanding the treatment parameters and DN intervention.

3. Patients who are unable to communicate directly or via an interpreter may not be appropriate for DN treatments.

4. Patients may not be willing to be treated with DN.

5. Patients need to be able to give consent for the treatment with DN.

6. Local skin lesions must be avoided with DN.

7. Local or systemic infections are generally considered to be contraindicated.

8. Local lymphedema (note: there is no evidence that DN would cause or contribute to increased lymphedema, ie, postmastectomy, and as such is not a contraindication).

9. Severe hyperalgesia or allodynia may interfere with the application of DN, but should not be considered an absolute contraindication.

10. Some patients may be allergic to certain metals in the needle, such as nickel or chromium. This situation can easily be remedied by using silver or gold plated needles.

11. Patients with an abnormal bleeding tendency, ie, patients on anticoagulant therapy or with thrombocytopenia, must be needled with caution. DN of deep muscles, such as the lateral pterygoid or psoas major muscle, that cannot be approached with direct pressure to create hemostasis may need to be avoided to prevent excessive bleeding.

12. Patients with a compromised immune system may be more susceptible to local or systemic infections from DN, even though there is no documented increased risk of infection with DN.

13. DN during the first trimester of pregnancy, during which miscarriage is fairly common, must be approached with caution, even though there is no evidence that DN has any potential abortifacient effects.

14. DN should not be used in the presence of vascular disease, including varicose veins.

15. Caution is warranted with DN following surgical procedures where the joint capsule has been opened. Although septic arthritis is a concern, DN can still be performed as long as the needle is not directed toward the joint or implant.

Nerve conduction velocity

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Nerve conduction velocity (NCV) is a test to see how fast electrical signals move through a nerve.

How the Test is Performed

Patches called surface electrodes are placed on the skin over nerves at various locations. Each patch gives off a very mild electrical impulse, which stimulates the nerve.

The nerve's resulting electrical activity is recorded by the other electrodes. The distance between electrodes and the time it takes for electrical impulses to travel between electrodes are used to determine the speed of the nerve signals.

Electromyography (recording from needles placed into the muscles) is often done at the same time as this test.

How to Prepare for the Test

You must stay at a normal body temperature. Being too cold slows nerve conduction.

Tell your doctor if you have a cardiac defibrillator or pacemaker. Special steps will need to be taken before the test in you have one of these devices.

How the Test will Feel

The impulse may feel like an electric shock. You may feel some discomfort depending on how strong the impulse is. You should feel no pain once the test is finished.

Often, the nerve conduction test is followed by electromyography (EMG). In this test, needles are placed into a muscle and you are told to contract that muscle. This process can be uncomfortable during the test. You may have muscle soreness after the test at the site of the needles.

Why the Test is Performed

This test is used to diagnose nerve damage or destruction. The test may sometimes be used to evaluate diseases of nerve or muscle, including myopathy, Lambert-Eaton syndrome, or myasthenia gravis.

Normal Results

NCV is related to the diameter of the nerve and the degree of myelination (the presence of a myelin sheath on the axon) of the nerve. Newborn infants have values that are approximately half that of adults. Adult values are normally reached by age 3 or 4.

Note: Normal value ranges may vary slightly among different laboratories. Talk to your doctor about the meaning of your specific test results.

What Abnormal Results Mean

Most often, abnormal results are due to nerve damage or destruction, including:

• Axonopathy (damage to the long portion of the nerve cell)
• Conduction block (the impulse is blocked somewhere along the nerve pathway)
• Demyelination (damage and loss of the fatty insulation surrounding the nerve cell)

The nerve damage or destruction may be due to many different conditions, including:

• Alcoholic neuropathy
• Diabetic neuropathy
• Nerve effects of uremia (from kidney failure)
• Traumatic injury to a nerve
• Guillain-Barré syndrome
• Diphtheria
• Carpal tunnel syndrome
• Brachial plexopathy
• Charcot-Marie-Tooth disease (hereditary)
• Chronic inflammatory polyneuropathy
• Common peroneal nerve dysfunction
• Distal median nerve dysfunction
• Femoral nerve dysfunction
• Friedreich's ataxia
• General paresis
• Mononeuritis multiplex
• Primary amyloidosis
• Radial nerve dysfunction
• Sciatic nerve dysfunction
• Secondary systemic amyloidosis
• Sensorimotor polyneuropathy
• Tibial nerve dysfunction
• Ulnar nerve dysfunction

Any peripheral neuropathy can cause abnormal results. Damage to the spinal cord and disk herniation (herniated nucleus pulposus) with nerve root compression can also cause abnormal results.

Considerations

An NCV test shows the condition of the best surviving nerve fibers, so in some cases the results may be normal even if there is nerve damage.

Alternative Names

NCV

References

Griggs RC, Jozefowicz RF, Aminoff MJ. Approach to the patient with neurologic disease. In: Goldman L, Schafer AI, eds. Goldman's Cecil Medicine. 24th ed. Philadelphia, PA: Saunders Elsevier; 2011:chap 403.

MERALGIA PARESTHETICA: Lateral Femoral Cutaneous Nerve Neuropathy

Meralgia paresthetica is a rarely encountered sensory problem(mononeuropathy) characterized by paresthesis, pain or sensory impairment along the distribution of the lateral femoral cutaneous nerve caused by entrapment or compression of the nerve as it crosses the anterior superior iliac spine and runs beneth the inguinal ligament. The condition also named as Bernhardt-Rooth syndrome.

In simpler terms Meralgia paresthetica means abnormal sensation or pain in the thigh. Meralgia paresthetica generally occurs unilaterally, in case of bilateral involvement, it rarely have equal effect on both sides.

Symptoms of Meralgia paresthetica:

• Numbness
• Pain
• Burning
• Tingling(prickling)
• Hypersenstivity 
• Aching
• Vague discomfort
• Stinging or "pins & needles".

Causes of Meralgia paresthetica:

Meralgia paresthetica is typically caused by compression or irritation of  lateral femoral cutaneous nerve. Weight gain, weight loss, tight fitting pants, belts, carpenters belt, pregnancy, or lap belt trauma after motor vehicle accident can cause the compression or irritation of this nerve.

there are four predisposing variants which have been implicated in the pathogenesis of  meralgia paresthetica:-

1. Passage of the lateral femoral cutaneous nerve through rather than deep to the inguinal ligament.
2. "Bowing" of the nerve as it crosses the iliacus fascia.
3. Passage of the nerve through the sartorious muscle.
4. Passage of the nerve lateral and posterior to the ASIS.

Any process increasing intra-abdominal or intra-pelvic pressure can cause meralgia paresthetica as well as discrete tumerous enlargement of organs. eg. Ascites, pregnancy.

Systemic disease known to cause neuropathies may occasionally produce an isolated neuropathy of the Lateral femoral cutaneous nerve. Meralgia paresthetica has been reported as the sole complaint in alcoholics, in patients with diabetes mellitus and in led poisoning.  

You may found some other medical conditions associated with meralgia paresthetica such as surgery in the area of the front of the hip/waist, enlarged lymph nodes, braces and hernia support trusses.

Management: 

Management of meralgia paresthetica depends upon what is the cause and how worse your symptoms are. your doctor will work with you to make a most appropriate treatment program as per your need.
Most patients with meralgia paresthetica achieve satisfactory pain relief from conservative treatment such as life style changes, weight loss, reduction or elimination of offending mechanical factors, eg., corset, belt or obesity. If the pain persists, mild analgesics and anti-inflammatory drugs give partial relief in most cases.
You may require single or multiple therapeutic local anesthetic nerve blocks.
In some cases more aggressive interventions may be required, as per the symptoms, such as surgical decompression (neurolysis) or transection of  lateral femoral cutaneous nerve. Unfortunately there is no reliable way of predicting the long term benefit from a surgical decompression.

Physical Therapy Management: 

The modalities and techniques used in physiotherapy may relieve your symptoms without having medications and/or surgical procedures depending upon the progress of your condition.
A gentle electrical stimulation of the skin around  the painful area blocks the pain signals hence relieving the symptoms.
A gentle stretch to the quadriceps and iliopsoas muscle may relieve the compression over lateral femoral cutaneous nerve. another technique named Neurodynamics may help to decrease your symptoms as applied for lateral femoral nerve for few sittings.
       

Ergogenic aids and the athlete

In the complex world of sports, today, many athletes and coaches are in a continuous search “how to gain a competitive advantage to improve athletic performance.” The slightest improvement in athletic performance often means the difference between “the thrill of victory and the agony of defeat.”

Coaches as well as athletes utilize special aids to enhance the athletic performance known as ergogenic aids. An ergogenic aid is any agent, substitute or technique that improves physical performance through its particular effect on human body. The term ergogenic aids also refers to any substance, process or procedure that may enhance the performance through improvement of strength, speed, response time or endurance of the athlete.

The use of doping substances in many sports and on all continents has become a major public health issue. The problem of drug abuse in sports first was tackled by the international sports authorities, in the form of the International Olympic Committee (IOC), during the 1960s. An official definition of doping first was given by the IOC in 1964 and the first programs of antidoping tests were activated by the IOC and its newborn Medical Commission in 1967. The global and universal characteristics of doping led to the formation in 1999 of the World Anti-Doping Agency (WADA), a unique collaboration between sports and governments. WADA is founded on equal partnership between public authorities and Olympic sport. Since then, as mandated by the World Anti Doping Code, the WADA has been responsible for the upgrade and publication of the list of “Prohibited substances and practices”. The 2014 list of Prohibited substances is now available at http://www.wada-ama.org/en/Science-Medicine/Prohibited-List 

Classification of performance-enhancing aids:

• Acceptable practices or substances. 
• Questionable or potentially harmful practices and substances. 
• Illegal practices and substances.

Acceptable practices or substances:

• amino acids, protiens
• sports drinks
• vitamin E
• relaxation techniques
• carbohydrate approaches (loading,feeding, replenishment)
• water (prehydration, hydration, rehydration)
• minerals and liquid food suppliments
• psychological approaches.

Questionable or potentially harmful practices and substances:

• caffeine
• alcohol
• nicotine- tobacco, Heroin
• oxygen utilization (before, during and after performance)
• marijuana, bee pollen, bicarbonate ingestion

Illegal practices and substances:

• anabolic-androgenic steroids
• diuretics, 
• amphetamines, cocaine
• blood doping (RBC reinfusion)
• beta blockers
• human growth hormone

Rationale for use of performance-enhancing aids: Use or Abuse?

• greater success and potential in sports.
• accessibility of and exposure to ergogenic aids.
• peer pressure and peer acceptance.
• pressure by coach, trainer, or physician.
• legality of substance or technique.
• shortcut to goal attainment.
• ease of administration.
• lack of fear of potential adverse health effect.
• performance stress relief.

references:

• Zachazewski , J.E.: Athletic Injuries and Rehabilitation. W.B. Saunders Company
• Drug Abuse in Sports, Utox Update 2002, volume 4, number 1.
• Catlin D. H. Medicine and science in the fight against doping in sport. J Intern Med 2008; 264: 99–114.

continued........................

           a POWER POINT PRESENTATION ON

   Periarthritis shoulder

Introduction

ÒPA is a condition characterized by pain & progressive limitation of GH movements.

ÒIt is the initial manifestation of ongoing pathology which usually culminates in frozen shoulder.

ÒDuplay in 1872 referred the condition as humerocapsular Periarthritis.

ÒCodman in 1934 coined the term ‘Frozen shoulder’ – painful loss of motion with normal radiographic studies.

ÒIn 1946, Naviaser ,named the condition ‘adhesive capsulitis’ based on his work & radiographic appearance.

ÒIn 1949, Simmonds, proposed that rotator cuff inflammation preceds PA shoulder.

ÒIn 1973, Macnab illustrated that degenerative changes in supraspinatus, leads to an autoimmune reaction, produces diffuse capsulitis.    

ÒPA shoulder/ frozen shoulder –

ÉPrimary adhesive capsulitis

ÉSecondary adhesive capsulitis / acquired shoulder stiffness.

ÒUncommon in athletes, may occur due to prolonged immobilization.

 

Etiology
ÒExact cause is unknown.
ÒCertain factors considered to contribute to development of PA are:

ÉPain

ÉDisuse / immobilization

É& periarthritic personality.

Pathoanatomy
ÒThickening & contracture of joint capsule with obliteration of inferior recess.
Òcollagen band bridging across recesses, random collagen production.
ÒAcquired cases reflects the underlying causes :

ÉSurgery

ÉTrauma

ÉOther pathological conditions like insulin dependent diabetes, reflex sympathetic dystrophy, etc.

Clinical presentation:

PRIMARY ADHESIVE CAPSULITIS

ÒInsidious and idiopathic

ÒUsually older than 40 yr. of age.

ÒHigher incidence in females.

ÒHistory of progressive shoulder stiffness associated with diffuse pain

Òadhesive capsulitis is classically characterized by three stages:

ÉInitial/ freezing phase

ÉSecond / frozen phase

ÉFinal/ thawing phase

( Reeves B:The natural history of the frozen shoulder syndrome. Scand J Rheumatol 4;193,1975) 

ÒInitial/ freezing phase

ÉOnset of diffuse, aching pain in the shoulder.

ÉPhase can last for 2 to 9 months.

ÉPatient position the arm in abduction & internal rotation.

ÉAssociated with acute inflammatory synovitis.

ÒSecond / frozen phase

ÉPain at rest usually diminishes .

ÉADLs becomes severely restricted according to capsular pattern.

ÉSevere pain occurs attempted motion.

ÉThis stiffening phase can last for 4 to 12 months.

ÉGH motion lost under anesthesia.

ÉHypervascular proliferative synovitis & Capsular fibrosis

ÒFinal/ thawing phase

ÉOccurs with slow recovery of motion.

ÉGradual resumption of ADLs

ÉThis phase can last for 6 months to 2 years.

ÉThe capsule is now very scarred, thick, fibrotic, & hypovascular.

SECONDARY OR ACQUIRED SHOULDER STIFFNESS

ÒThis condition is associated with a known predisposing condition of the shoulder

ÒPatient with acquired stiff shoulder have much clearer & concise history.

ÒLoss of external rotation, abduction & flexion.

ÒRadiographs are helpful in acquired cases.

Differential diagnosis

ÒPartial rupture of supraspinatus tendon.

ÒSupraspinatus tendinitis.

ÒBrachial neuritis.

ÒOA of the AC joint.

ÒTuberculous arthritis of shoulder

Treatment : 

PHYSIOTHERAPY  Treatment

ÒPhase 1: weeks 0-8

ÉRelieve pain

ÉRestore motion

ÐExercises

×AROM

×AAROM

×PROM

ÉHome exercise program should be instituted from beginning.

ÒPhase 2: Weeks 8-16

ÉContinue the treatment program of phase 1 &

ÉExercises for strengthening of rotator cuff & scapular stabilizers.

ÐClosed chain isometric strengthening

ÐOpen chain strengthening

ÐLight isotonic dumbbell exercise

ÒPhase 3: Months 4 & beyond

ÉThere should be resolution of pain & significant functional recovery of shoulder motion.

ÉHome exercise program should be continued.

ÒMaximum improvement may be achieved 6-9 months after treatment initiation.

Surgical treatment

ÒSurgical intervention may be indicated, if no improvement is seen after 3 months of management:

ÉClosed manipulation under anesthesia

ÉArthroscopic capsular release.

ÉOpen release.

Postop. management

ÒShould begin on the day of surgery.
ÒTherapy should begun with ROM exercises.
ÒTherapy should consist a stretching program in all planes.
ÒOnce pain free arc is regained, a strengthening
program may be added.

references:

ÒHunter James M: Rehabilitation of the hand & upper extremity. 5th Ed.

ÒBrotzman S Brent: Clinical orthopedic rehabilitation.2nd Ed.

ÒDonatelli Robert A: Physical Therapy of Shoulder.2nd Ed.

ÒCyriax J: text book of orthopedic medicine volume 1. 8th Ed.

ÒSolomon L: Apley’s system of orthopedics & fractures. 8th Ed

ÒReid David C: Sports injury Assessment & rehabilition

ÒMaitland GD: Peripheral Manipulation. 2nd Ed.

ÒSimonds FA: SHOULDER PAIN With Particular Reference to the “ Frozen” Shoulder . The Journal Of Bone And Joint Surgery 31B:426,1949

ÒNEVIASER JS: ADHESIVE CAPSULITIS OF THE SHOULDER: A Study Pathological Findings in Periarthritis of the Shoulder. J Bone Joint Surg Am. 1945;27:211-222.

ÒManske Robert C: Diagnosis and management of adhesive capsulitis. Curr Rev Musculoskelet Med (2008) 1:180–189

ÒCharnley J: Periarthritis of shoulder