Monday, March 30, 2009

Fibromyalgia syndrome/Fibromyalgia (FMS)


Is Fibromyalgia a disease?

1. According to Goldenberg DL Fibromyalgia is considered a controversial diagnosis as the disorder is a ‘non-disease’, due in part to a lack of objective laboratory tests or medical imaging studies to confirm the diagnosis.
2. As the criteria accurately diagnosing such an entity (Fibromyalgia) has not yet been thoroughly developed. According to Yunus MB, the recognition that fibromyalgia involves more than just pain has led to the frequent use of the term "fibromyalgia syndrome".

History & meaning:
Historically Fibromyalgia is considered either a musculoskeletal disease or neuropsychiatric condition, evidence from research conducted in the last three decades has revealed abnormalities within the brain CNS regions.
Fibromyalgia (new lat., fibro- fibrous tissue, Gk. myo- muscle, Gk. algos- pain), meaning muscle and connective tissue pain (also referred to as FM or FMS).

S/S: Fibromyalgia is a disorder classified by the presence of chronic widespread pain and a heightened and painful response to gentle touch (tactile allodynia).
Other core features of the disorder include (Not all affected persons experience all the symptoms associated with the greater syndrome.):
1. Debilitating fatigue, sleep disturbance, and joint stiffness.
2. Additional multiple body systems features frequently reported are: difficulty with swallowing, functional bowel and bladder abnormalities, difficulty breathing, diffuse sensations of numbness and tingling (non-dermatomal paresthesia), abnormal motor activity (i.e. nocturnal myoclonus, sleep bruxism), and cognitive dysfunction.
3. An increased prevalence of affective and anxiety-related symptoms is also well known.
Factors worsen fibromyalgia symptoms:

An internet-based survey of 2,596 people with fibromyalgia reported that factors perceived to worsen fibromyalgia symptoms were:

1. Emotional distress (83%),
2. Weather changes (80%),
3. Sleeping problems (79%),
4. Strenuous activity (70%),
5. Mental stress (68%),
6. Worrying (60%),
7. Car travel (57%),
8. Family conflicts (52%),
9. Physical injuries (50%) and
10. Physical inactivity (50%).
11. Other factors included infections, allergies, lack of emotional support, perfectionism, side effects of medications, and chemical exposures.

Differential diagnosis:

According to Reiffenberger DH et al FMS needs to differentiated from 2 other seemingly similar conditions i.e. myofascial pain syndrome (MPS) and chronic fatigue syndrome (CFS).

1. Myofascial Pain Syndrome (or MPS):

Myofascial Pain Syndrome is a term used to describe one of the conditions characterized by chronic pain. It is associated with and caused by "trigger points" (TrPs). The symptoms can range from referred pain through myofascial trigger points to specific pains in other areas of the body.
MPS differs from fibromyalgia by accepted definition, the pain of fibromyalgia is generalized, occurring above and below the waist and on both sides of the body. On the other hand, myofascial pain is more often described as occurring in a more limited area of the body, for example, only around the shoulder and neck, and on only one side of the body.
Neither MPS or FMS (fibromyalgia) is thought to be an inflammatory or degenerative condition, and the best evidence suggests that the problem is one of an altered pain threshold, with more pain reported for a given amount of painful stimuli. This altered pain threshold can be manifest as increased muscle tenderness, especially in the certain areas, e.g., the trapezius muscle. These syndromes tend to occur more often in women than in men, and the pain may be associated with fatigue and sleep disturbances.
The precise cause of MPS is not fully understood and is undergoing research in several medical fields. A fairly new form of therapy called Myofascial Release, using gentle fascia manipulation and massage, is believed by some to be beneficial and pain-relieving.

2. Chronic fatigue syndrome (CFS)

a. Onset: there is ample evidence that majority of CFS cases start suddenly, usually accompanied by a "flu-like illness” which is more likely to occur in winter, while a significant proportion of cases begin within several months of severe adverse stress.
b. Symptoms: The most commonly used diagnostic criteria and definition of CFS is given by

Centers for Disease Control and Prevention (CDC,USA). The CDC definition of CFS requires two criteria be fulfilled:

1. A new onset (not lifelong) of unexplained, persistent fatigue unrelated to exertion and is not substantially relieved by rest, which causes a significant reduction in previous activity levels.
2. Four or more of the following symptoms that last six months or longer:
a. Impaired memory or concentration
b. Post-exertional malaise, where physical or mental exertions bring on "extreme, prolonged exhaustion and sickness"
c. Unrefreshing sleep
d. Muscle pain (myalgia)
e. Pain in multiple joints (arthralgia)
f. Headaches of a new kind or greater severity
g. Sore throat, frequent or recurring
h. Tender lymph nodes (cervical or axillary)
When symptoms are attributable to other conditions, the diagnosis of CFS is excluded. The CDC specifically refers to several illnesses with symptoms resembling those of CFS: "mononucleosis, Lyme disease, lupus, multiple sclerosis, fibromyalgia, primary sleep disorders, severe obesity and major depressive disorders. Medications can also cause side effects that mimic the symptoms of CFS."
3. Activity levels: Patients report critical reductions in levels of physical activity with impairment comparable to other fatiguing medical conditions including multiple sclerosis, late-stage AIDS, lupus, rheumatoid arthritis, heart disease, end-stage renal disease, chronic obstructive pulmonary disease (COPD), and the effects of chemotherapy. The severity of symptoms and disability is the same in both genders with strongly disabling chronic pain, but despite a common diagnosis the functional capacity of individuals with CFS varies greatly. While some lead relatively normal lives, others are totally bed-ridden and unable to care for themselves. Employment rates vary with over half unable to work and nearly two-thirds limited in their work because of their illness.

References:

1. http://en.wikipedia.org/ Fibromyalgia syndrome
2. http://en.wikipedia.org/ myofascial pain syndrome
3. http://en.wikipedia.org/ chronic fatigue syndrome
4. Reiffenberger DH et al; Am Fam Physician. 1996 Apr;53(5):1698-712.



Saturday, March 28, 2009

Neck tongue syndrome (NTS)

Introduction:
Generically, neck-tongue syndrome is an acute presentation brought about by rapid neck movements, and involves a distribution of symptoms only within the face/head, most often reported as numbness in the tongue. This is usually caused by an acute subluxation (partial dislocation) of the top two vertebrae of the neck, which causes abnormal input to cranial nerves and can cause symptoms in the cranium (head).

Definition:
According to McGraw-Hill Concise Dictionary of Modern Medicine; NTS is a condition characterized by sharp pain and tingling of the upper neck and/or occiput on sudden neck rotation, with numbness of the ipsilateral half of the tongue; the NTS is attributed to stretching the C2 ventral ramus, which contains proprioceptive fibers from the lingual nerve to the hypoglossal nerve and 2nd cervical root.
There are 2 categories of NTS: complicated NTS due to the presence of an underlying disease process (inflammatory or degenerative) and uncomplicated NTS (idiopathic or trauma-related) (2).

Patient’s description:

Case 1: A typical description- It's an intense blinding pain at the base of the head and the tongue always goes numb and feels like it swells up and occasionally vision blacks out for a few seconds, and then it all fades away.

Case 2: Strong, sharp pain followed by numbness and tingling of face and tongue, after this episodes plus symptoms on neck, limbs and back are also found in many cases.

Case 3: Neck feels like somethings "popping" and then my face and tongue go numb for a short time.

The summary of descriptions:
1. The pain is usually starts behind ear right where head meets my neck.
2. Seconds later the tongue goes numb.
3. Sometimes the patients also find that dropping his/her head for a short while relaxes the neck enough to stop the throbbing pain.
4. Many patients say that episodes became less violent (only the pain in face/neck are present with numbness of face, tongue and sometimes arms.) with increase in age.

Cause & pathology:
According to N Bogduk (1981); the most likely cause of the simultaneous occurrence of suboccipital pain and ipsilateral numbness of the tongue is an abnormal subluxation of one lateral atlanto-axial joint with impaction of the C2 ventral ramus against the subluxated articular processes. Radiographs revealed a narrowing of the left para-odontoid space. Physical examination revealed a mildly painful restriction in rotation at C1-2 with no apparent muscular hypertonicity (2).
Afferent proprioceptive fibers from the tongue normally travel with the lingual nerve via the hypoglossal nerve to the ventral ramus of the C2 spinal nerve. It is believed that mechanical injury to the C2 ventral ramus can thus cause a referred sensory disturbance of the tongue. In the evaluation of these patients, upper cervical spine, especially atlantoaxial, instability should be considered, along with muscle spasm (1).


The difference between VBI & NTS:

It is important to differentiate between the signs and symptoms of vertebral artery insufficiency, particularly if it is causing dizziness, loss of balance, or drop attacks (fainting). Sustained full rotation of the head can kink/obstruct the artery that goes to your brainstem, as can extending your head backward, and both should never be performed together. Rapid, full range rotation can also cause these. They likely were more severe as a child, because several key stabilizing components of your spine were not yet developed (until about 18 years old).

The hyper-mobility syndrome "double-jointedness":

NTS is so rare condition & so less studied that there are currently no research papers associating NTS to hyper-mobility of cervical joints. How ever it provides a plausible explanation in many cases. Hyper-mobility syndrome is a connective-tissue disorder. Seeing a geneticist for connective tissue disorders can be worth while who can diagnose hyper-mobility syndrome through genetics others can be diagnosed through blood/skin tests, etc.

Scoliosis & NTS:

Scoliosis can cause some issues such as this. As for example A DL spine scoliosis can affect a secondary compensatory curve that can affect upper cervical & cranium positioning severly. Hence it is plausible that if the scoliosis improves through physical therapy or surgery, if it's necessary, the neck-tongue syndrome may too.

Treatment:
Not many treatment options are suggested in the literature when the condition is so rarely encountered & studied.
Borody C treated uncomplicated NTS that responded favorably to spinal manipulative therapy directed at the cervical spine. In the absence of upper cervical instability, spinal manipulative therapy appears to be beneficial and should be considered in all cases of uncomplicated NTS (2).

Reference:
1. Orrell RW, Marsden CD. The neck-tongue syndrome. J Neurol Neurosurg Psychiatry
1994;57:348-352.
2. Borody C. J Manipulative Physiol Ther. 2004 Jun;27(5):e8.




Friday, March 27, 2009

Butterfly vertebra- that mimics a wedge fracture is a uncommon congenital spinal anomaly.



A butterfly vertebra, which is an uncommon congenital spinal anomaly needs to be identified correctly as confused with other pathologic conditions like fractures, infections, and metastases (2). Garcia F et al reported 2 patients, who had injuries to the dorsal spine with diagnosed compression wedge fracture. Similarly a study presented by Patinharayil G et al showed anterior wedging (2). In both a careful study of the anteroposterior radiographs showed that the presumed injury was a butterfly vertebra. This rare congenital anomaly, which is usually without clinical significance, may be mistaken for a wedge fracture unless the anteroposterior view is correctly assessed (1).
Butterfly vertebra: an uncommon congenital spinal anomaly.
Butterfly vertebra presents with:
1. Complaints of low back pain (non-specific)
2. Spinal deformity such as (abnormal bony prominence)
3. Usually routine examination of the motor and sensory system usually is normal.

Investigations of importance:

Radiologic (X-ray, CT scan, MRI) and hematologic investigations. Hematologic evaluation must be done to rule out pathologic causes of anterior wedging of the vertebra like infections and metastases in the spine.

Knowledge of this condition helps in making rational use of extensive noninvasive and invasive diagnostic procedures.

References:

1. Garcia F et al; Int Orthop. 1993;17(1):7-10.

2. Patinharayil G et al; Spine. 2008 Nov 15;33(24):E926-8.

Monday, March 23, 2009

Application of PSBI (Pain Belief Screening Instrument) in musculoskeletal pain disorders


Work of Lethem et al (2):


Lethem et al. introduced a so-called 'fear-avoidance' model to explain how and why some individuals with musculoskeletal pain develop a chronic pain syndrome. The central concept of their model is fear of pain. 'Confrontation' and 'avoidance' are postulated as the two extreme responses to this fear, of which the former leads to the reduction of fear over time. Off late a number of investigations have refined the fear-avoidance model.

Role of pain-related fear, and its immediate and long-term consequences in the initiation and maintenance of chronic pain disability:

1. The possible precursors of pain-related fear include the role negative appraisal of internal and external stimuli, negative affectivity and anxiety sensitivity.
2. A number of fear-related processes including escape and avoidance behaviors resulting in poor behavioral performance, hypervigilance to internal and external illness information, muscular reactivity, and physical disuse lead to de-conditioning and guarded movement.

Role of fear and avoidance in chronicity of musculoskeletal pain in primary health care:

Pain-related fear and avoidance appear to be an essential feature of the development of a chronic problem for a substantial number of patients with musculoskeletal pain (2). New emerging lines of investigation in chronic musclo-skeletal pain are related to information processing and anxiety sensitivity. These factors appear to be closely linked to pain-related avoidance behavior (1). Denison E et al explored the relations between disability, as measured by the Pain Disability Index (PDI) and self-efficacy, fear avoidance variables (kinesiophobia and catastrophizing), and pain intensity (3).

They found (3):
1. Self-efficacy beliefs are more important determinants of disability than fear avoidance beliefs in primary health care patients with musculoskeletal pain.
2. Pain-related beliefs, such as self-efficacy and fear avoidance, in turn, are more important determinants of disability than pain intensity and pain duration in these patients.
3. Gender, age, and pain duration were not related to disability.

Subgroups of Musculoskeletal pain in primary health care (4):

Denison E et al studied subgroup profiles based on self-reported pain intensity, disability, self-efficacy, fear of movement/(re)injury, and catastrophizing in patients with musculoskeletal pain.
While doing a cluster analysis to generate subgroups 3 subgroups were identified & these subgroups of patients with musculoskeletal pain present with different profiles in pain intensity, disability, and psychosocial variables.

The sub groups are:
1. "High self-efficacy-Low fear-avoidance,"
2. "Low self-efficacy-Low fear-avoidance," and
3. "Low self-efficacy-High fear-avoidance"

The subgroups differed significantly in work-status but not in age, gender, or duration of pain. It is further suggested that different management strategies may be relevant in each subgroup. & it is possible to tailor assessment and treatment approaches to each subgroup.

The pain belief screening instrument- PBSI (5):

The Pain Belief Screening Instrument (PBSI) covers pain intensity, disability, self-efficacy, fear avoidance and catastrophizing. Items for the Pain Belief Screening Instrument were derived from principal component analyses of: the Self-efficacy Scale, the Tampa Scale of Kinesiophobia and the Catastrophizing subscale in the Coping Strategies Questionnaire.

Sandborgh M et al worked to develop and test the ability of PBSI to identify subgroups among primary healthcare patients with musculoskeletal pain. PBSI identified 2 groups: high- or low-risk profile for pain-related disability.
Further Sandborgh M et al also found PBSI also can fairly well replicate subgroups. The reliability of items in the screening instrument was acceptable. However they suggested further testing of predictive validity of PBSI for primary healthcare population.

Predictive validity of PSBI for disability status in persistent musculoskeletal pain (6):
Predictive validity of the PBSI for disability was confirmed by Sandborgh M et al’s study (a prospective & correlational study). They also recommend clinical use the PBSI because it could serve as a mean to obtain supplementary and clinically useful information. In Sandborgh M et al’s study High-disability group had increased disability, unchanged pain intensity and decreased work capacity and daily function after 8 months & PSBI correctly classified 72% of the subjects as High-disabled or Low-disabled.

Locate the PSBI:

To know the items in PSBI down load the PDF file from this following link (www.diva-portal.org/diva/getDocument?urn_nbn_se_uu_diva-8665-1__fulltext.pdf -) & then go to table no.3 on page 38 of the downloaded file.

Reference:

1. Asmundson GJ et al; Clin Psychol Rev. 1999 Jan;19(1):97-119.
2. Vlaeyen JW et al; Pain. 2000 Apr;85(3):317-32.
3. Denison E et al; Pain. 2004 Oct;111(3):245-52.
4. Denison E et al; J Pain. 2007 Jan;8(1):67-74. Epub 2006 Sep 1.
5. Sandborgh M et al; J Rehabil Med. 2007 Jul;39(6):461-6.
6. Sandborgh M et al; Disabil Rehabil. 2008;30(15):1123-30.




Sunday, March 22, 2009

HOW CORRECT IS THIS?

Veronica Yu, B.Sc., D.Ac., D.C. ( www.familyhealthoptions.com/uploads/Admin/Sta...) says that all trauma, strains and stresses are stored in your body. Over time this build up can lead to restricted functioning and other health problems.

BODY is comprised of physical, mental, spiritual and emotional components that are integrated together. Which is so true to it's core. Most of us can study the impact of acute & chronic insults on physical aspects. Remember bloggers we are trained to perceive indifferent aspects as different entities & mostly good at studying one aspect only.

I just ponder how necessary for holistic therapies to start functioning globally?



Lower-Crossed Syndrome (LCS)



Change in movement pattern:

The muscles can often serve as “windows” to the function of the CNS. The CNS regulates 2 muscle groups: The tonic muscle group and the phasic muscle group. These muscle groups oppose each other in function. The tonic muscle group functions as a facilitator, the phasic muscle groups inhibition. Pain, pathology or adaptive changes in the system result in compensations or adaptations that lead to systemic and predictable patterns of muscle imbalance. “Altered movement pattern” is a movement pattern in which a change occurs in the coordination of the muscle firing sequences for a specific group of muscles, facilitating a specific joint movement. The primary muscle responsible for specific joint movement may become weak and inhibited, causing a synergistic muscle/muscles to become hyperactive. As a result, a different sequence of muscular contractions occurs. This is a sign of muscle imbalance in the body because of muscular dysfunction.
When any component of the kinetic chain is not working properly (tight or long muscles, reciprocally-inhibited muscles, adhesions, joint dysfunction), neuromuscular control is altered. This results in chronic pain and disability.

What is LCS?
The lower kinetic chain is one of two basic parts of the musculoskeletal system that are controlled and innervated through the CNS.
Lower-crossed syndrome is a postural distortion syndrome affecting the lower kinetic chain (lumbopelvic hip complex, knee, and ankle). Because the structural integrity of the lower kinetic chain is compromised in lower cross syndrome, abnormal distorting forces result on all structures within the kinetic chain. In lower-Crossed syndrome the pattern of muscle imbalances often leads to changes in movement patterns with hip extension, hip abduction and trunk flexion. This alteration may be observed with the patient sitting, standing, or walking. In lower-crossed syndrome the patient usually presents with anterior pelvic tilt, increased lumbar lordosis (swayback), and weak abdominals muscles. These patients usually experience chronic low back pain, piriformis syndrome and anterior knee pain.
The predictable pattern of muscle imbalances most often include the following:
Tight/Faciliated: Iliopsoas, Rectus Femoris, TFL, Adductor Group, Errector Spinae, Gastrocnemius, Soleus
Weak/Inhibited: Rectus Abdominis, Oblique, Gluteus maximus, Gluteus medius, Hamstrings
Because of above said Tight/Faciliated & Weak/Inhibited muscles following things results in: Anterior rotation of pelvis, Increased lumbar lordosis, Hips in flexion, Knees may be hyperextended
Common Injuries that occurs because of changed kinetics: Low back pain, Knee pain, Hamstring strains etc.
Other consequences of this syndrome are seen in anterior tilt of the pelvis and flexion of the hip that exaggerates the lumbar curve. L5-S1 may have soft-tissue and joint stress with pain and discomfort. This progresses to instability of the sacroiliac joints and piriformis, and knee involvement.
What causes LCS?
Lower-cross syndrome may develop from a number of scenarios such as chronic, repetitive actions such as running. Inaction may also have a negative impact on the body’s mechanics, such as immobilization, disuse, or chronic postural stress such as sitting for long periods of time or poor workstation posture. Sports injuries or injuries that never healed properly can lead to pathology. Pain, pathology, or adaptive changes can lead to patterns of muscle imbalance that can lead to a situation of lower-cross syndrome.
Focus points of physical assessment in LCS:

1. Postural assessment
2. Global Assessment
3. Normal Firing Pattern of the Pelvis
4. Thomas Test
5. Forward Bending Test
6. Gluteus Maximus Strength Test
7. Psoas Major Strength Test
8. Erector Spinae
9. Transverse Abdominal Muscle
10. Rectus Femoris
Focus points of treatment in LCS:
A. Stretch

1. Hamstrings
2. Hip Flexors
3. Erector Spinae
4. Gluteus Maximus
B. Strengthen

1. Hamstrings
2. Transverse Abdominals
3. Gluteus Maximus
4. Hip Flexors
5. Erector Spinae


Saturday, March 21, 2009

The Upper Cross Syndrome



Upper Cross Syndrome is a terminology used by V.Janda that refers to a chronic postural error i.e. Upper Cross Syndrome describes a compromise in the musculoskeletal system which tightens or facilitates the anterior compartment of the “upper” torso while at the same time weakening the posterior.

While the majority of muscles involved in Upper Cross Syndrome are anterior to the shoulders there are a few posterior elements to consider as well. The chest muscles & the neck muscles (both posterior and anterior compartments) become tight and shortened (see the diagram). Consequently, you have a weakening or elongating of the scapular muscles.

The tight muscles:

Anteriorly, you have a tightening/shortening of the Pectoralis Major, Pectoralis Minor, Anterior Deltoid fibers, Sternocleidomastoids, and Scalenes. Posteriorly, you have tightening/shortening of the Levator Scapulae, Teres Major, Upper Trapezius, and Suboccipitals.

The weak muscles are:

The weakening of the Scapular muscles includes the Rhomboids, Lower Trapezius, and Serratus Anterior. There is also a weakening of the Longus Coli and Capitus muscles.

Postural effects of tightening & weakening:


The postural effects of these long, weak muscles (as well as the tight muscles) associated with Upper Cross Syndrome manifest themselves as anterior head carriage, rounded shoulders, and internally-rotated upper extremities. As a result, patients with these postural problems will have difficulty performing overhead movements, as well as pushing, pulling, and active stabilization of the cervical spine. Therefore, it is necessary to not only stretch the tight muscles, but also to strengthen the long, weak or reciprocally inhibited groups of muscles.

The altered arthrokinematics:

The altered arthrokinematics are, in large part, a result of synergistic dominance and reciprocal inhibition. Synergistic dominance is compensation in the body for the weak muscle groups that have been reciprocally inhibited.

Where do you typically see Upper Cross Syndrome?


Being that it is predominantly a postural issue, it is seen in individuals who work at a desk or are constantly leaning forward. Through postural adaptation, your body adopts the classical hunching of the upper thoracic spine, internal rotation of the shoulders, and anterior head carriage. Symptoms typically associated with Upper Cross Syndrome include headaches, upper thoracic pain (commonly from trigger points, the Upper Trapezius, and Levator Scapulae), and Thoracic Outlet Syndrome.

The self-test recommended for upper cross syndrome:


"Place two fingers at the top of your right shoulder and feel for a bony notch that protrudes from it. That's your acromion. Now grab a ruler and lie on your back on the floor, your right arm resting alongside your body. With your left hand, measure the distance from your right acromion to the floor, being careful not to raise or lower your right shoulder as you do so. If the distance is more than 1 inch, you have upper-cross syndrome."

Testing for tight & weak muscles:

It is better to carry out muscle testing separately for tonic & phasic muscles as they respond diffeently to dysfunction. Tonic muscles tighten under dysfunction where as phasic muscle weakens under dysfunction.

PHASIC MUSCLES INCLUDE:

Pectoralis Major, Pectoralis Minor, Levator Scapulae, Teres Major, Upper Trapezius, Sternocleidomastoid, Scalenes, Rectus Capitus

POSTURAL MUSCLES INCLUDE:

Rhomboids, Lower Trapezius, Serratus Anterior, Longus Coli and Longus Capitus

Treatment:


1. Stretching of


Pectoralis Major – Clavicular Portion & Sternal Portion, Pectoralis Minor, Levator Scapulae, Teres Major, Upper Trapezius & Lower Trapezius, Sternocleidomastoid, Scalenes, Rhomboids, Serratus Anterior, Cervical Spine (Anterior Muscles)
Cervical Spine (Posterior Muscles)

2. Strengthening of


It is important to strengthen these weak muscle groups so that there is muscular balance throughout the body thus preventing injury upon movement. The strengthening is recommended in 3 phases.

1st Stage of Strengthening
Rhomboids, Lower Trapezius, Serratus Anterior, Longus Coli / Longus Capitus

2nd Stage of Strengthening
Rhomboids, Lower Trapezius, Serratus Anterior, Longus Coli / Longus Capitus

3rd Stage of Strengthening
Rhomboids , Lower Trapezius, Serratus Anterior, Longus Coli / Longus Capitus

Reference:



Finding a trigger point in abdomen!!!


Finding a abdominal trigger point is a hall mark in diagnosing a chronic pelvic pain (CPP). The test that is done to find a abdominal trigger point is called Carnett's sign.

Carnett's sign: (see the picture )
The examiner places his or her finger on the tender area of the patient's abdomen and asks the patient to raise both legs off the table. An increase in the patient's pain during this maneuver is considered a positive test.

Friday, March 20, 2009

Diagram of how posture affects the areas you never thought



See the above link of poor posture to facio-dental abnormalities. this diagram is credited to following site:
www.scielo.br/.../clin/v64n1/a11fig01.gif

Thursday, March 19, 2009

Intra-radicular disc prolapse (review of 11 papers)

History & prevalence:
According to Mut M et al of Turkey Intraradicular disc herniation is a special type of intradural disc herniations (7). The mechanism of the tearing of the dura mater by a herniated disc is not known with certainty (6). Akdemir H et al (1997) presented case in which a fragment of herniated lumbar disc was found within the sheath of the right S1 nerve root (5). How ever before 1997 there have been reports of such cases. According to a paper by Nazzal MM et al in journal of spinal disorder (1995) Intradural disc herniation accounts for < 0.3% of all disc herniations. Intraradicular disc herniation accounts for 4.1% of all such cases.

Clinical signs & symptoms:
The Intraradicular disc herniations may present from no symptoms (!!!) to symptoms presenting with profound neurological deficits (see the case studies below). Lakshmanan P presented 2 case studies one of them presented with no neurological deficit. Hence they have concluded that diagnosis of posterior epidural migration of the sequestrated discs may be difficult even it may be present with subtle clinical features even though the disc transgresses through numerous anatomic restraints including the nerve roots in such cases (10).

Case studies:
Finkel HZ also reported a case of intraradicular, intervertebral disc herniation L5-S1 intervertebral disc into the left S1 nerve root & S1 nerve root was found to be adherent to the underlying disc space. The diagnosis was made at the time of surgery during exploration of the L5-S1 disc space but before surgery this condition was believed to represent a large extradural and extraradicular disc herniation (2).

Nazzal MM et al revealed in 1995 that preoperative diagnosis of Intraradicular disc herniation is difficult, and must be thoroughly examined during surgery for the diagnosis. Back in 1995 when probably myelogram was the examination available at hand showed a block at the involved nerve root in a case presentation discussed by them in journal of spinal disorder (3).

A case study by Süzer T et al is as follows (6):
A 41-year-old man was admitted with a 3-year history of low back pain and sciatica. A neurological examination revealed motor weakness during plantar flexion, positive Lasègue's sign, sensory deficit on the S1 dermatoma, and loss of Achilles reflex. Magnetic resonance imaging revealed disc protrusion at the L5-S1 level.

Report of surgery in this case is as follows:
A standard hemilaminotomy and foraminotomy for a removal of the L5-S1 disc was followed. Interestingly there was no disc protrusion or extruded fragment. The left S1 nerve root was observed to be swollen and immobile. A longitudinal incision was made on the radicular sheet of the S1 root, and a free disc fragment, approximately 2 x 1 x 1 cm, was extirpated in one piece.
The patient was immediately relieved of pain and was discharged on the 7th day after the operation with normal muscle strength. The authors like other group of researchers Ozdemir N et al (8) have presumed that failed back cases are due to such disorders and mostly associated with failed back cases.

A case study by Mut M et al is as follows (7):
A 32-year-old male was admitted to hospital having experienced pain in the lower back and right leg for 1 month prior to admission. Neurological examination revealed weakness of the extensor hallucis longus, positive Laségue's sign, decreased ankle reflex in his right lower extremity, and bilateral paravertebral muscle spasm. MRI revealed a disc herniation with a posterolateral extruded fragment on the right at the level of the L5-S1 space.

Report of surgery in this case is as follows: He underwent L5 laminectomy. During the operation, the right S1 root was found to be swollen and immobile. A longitudinal incision was made in the dura of the right S1 root and an intradural free disc fragment was removed, and the S1 root was relieved. The patient was free of pain postoperatively (7).

According to Lakshmanan P at al (UK) Posterior epidural migration is an interesting but rare path taken by a prolapsed intervertebral disc fragment. There are only seven cases reported of a similar migration of the disc fragment in the lumbar spine (10).

Lakshmanan P at al presented 2 case studies.
1. In one patient there was weakness of the ankle dorsiflexors, foot invertors, and toe extensors of the left foot, with sensory loss over the back of the calf and over the lateral three toes. The left ankle jerk was also absent.
2. However, in the other case, there was no objective evidence of neurological deficit distally.

Lakshmanan P at al’s second study biopsy of the specimen taken from surgery confirmed it to be sequestrated disc fragment. Hence they concluded that diagnosis of posterior epidural migration of the sequestrated discs may be difficult even it may be present with subtle clinical features even though the disc transgresses through numerous anatomic restraints including the nerve roots in such cases (10).

An extensive case studies of 9 cases (4).
Schisano G et al doing a retrospective clinical examination on 9 cases found that Intraradicular or intradural disc herniation is a very rare complication of spinal degenerative processes. Lateral perforations of the dural sac are more common than the ventral perforation. 9 cases studied by Schisano G et al ware having intradural disc herniation. Among these, 6 were associated with lateral perforation, the remaining three with intradural herniation and ventral perforation.
According to the data base o these Italian authors
1. Nine cases of intradural herniations comprise 1.51% of the 593 cases of ruptured lumbar disc that underwent surgery from 1980 to 1992.
2. The site most frequently involved is at level L4-L5.
3. 30% of their patients have previously undergone surgery for lumbar disc herniation.
4. Most patients have been complaining of a chronic history of sciatica, complicated later by bilateral neurologic signs. There is no typical neuroradiologic picture of intraradicular herniation, while a total or subtotal block is frequently observed in intradural ventral perforations. Dural perforation is often an unexpected intraoperative finding.

Investigations followed by Schisano G et al to diagnose are by means of myelography and CT; magnetic resonance imaging was performed in one case. Surgery has good to excellent result in these cases. Interlaminar approach (for lateral perforations) or bilateral laminectomy (for ventral perforations) was used.

Association of Intraradicular disc herniation Failed back surgeries:
Ozdemir N et al have presumed that failed back cases are due to such disorders and mostly associated with failed back cases(8). Turgut M et al reported an unusual case of intradural intraradicular lumbar disc herniation, in which an extruded fragment of disc was found within the sheath of the left S1 nerve root after a failed back surgery. This diagnosis of intraradicular extruded disc herniation was only possible at time of surgical exploration of the L5-S1 disc space. Although MRI is a useful diagnostic tool in all patients with lumbar disc herniation, preoperative correct diagnosis is usually difficult in such cases. A careful observation of the root during surgery is indicated to detect such an anatomical abnormality. Bloom B of UK reported the case of a man who underwent urgent surgery to relieve compression of the cauda equina caused by a large L4/5 disc protrusion. A post-operative but not pre-operative MRI scan showed appearances suggestive of intradural migration of a disc fragment, confirmed at re-operation. The authors found that this event happened during the first operation and not before it (11).

What MRI Clue may help diagnosing such cases?
MRI is the “gold standad” in diagnosis of lumbar discogenic pathologies. However it is not efficient in diagnosing Intraradicular extruded disc herniations. Ozer E et al have suggested that the round shape of the sequestrated fragment, as seen on MRI, may help to establish the correct diagnosis (9) of Intraradicular extruded disc herniations.

Reference:
1. Neurol Neurochir Pol. 2008 May-Jun;42(3):251-4; discussion 254.
2. Spine. 1997 May 1;22(9):1028-9.
3. J Spinal Disord. 1995 Feb;8(1):86-8.
4. Surg Neurol. 1995 Dec;44(6):536-43.
5. Neurosurg Rev. 1997;20(1):71-4.
6. Neurosurgery. 1997 Oct;41(4):956-8; discussion 958-9.
7. Spinal Cord. 2001 Oct;39(10):545-8.
8. Br J Neurosurg. 2004 Dec;18(6):637-43.
9. Spine J. 2007 Jan-Feb;7(1):106-10. Epub 2006 Sep 11.
10. Spine J. 2006 Sep-Oct;6(5):583-6.
11. Br J Neurosurg. 2007 Aug;21(4):417-8.





Monday, March 16, 2009

Grades of Evidence & Levels of Recommendations: The Basis of EBP

Grades of Evidence

I: Evidence obtained from at least one properly designed randomized controlled trial.

II-A: Evidence obtained from well-designed controlled trials without randomization.

II-B: Evidence obtained from well-designed cohort or case–control analytic studies, preferably from more than one center or research group.

II-C: Evidence obtained from multiple time series with or without the intervention. Dramatic results in uncontrolled experiments also could be regarded as this type of evidence.

III: Opinions of respected authorities, based on clinical experience, descriptive studies, or reports of expert committees.

Levels of Recommendations

Level A — Recommendations are based on good and consistent scientific evidence.

Level B — Recommendations are based on limited or inconsistent scientific evidence.

Level C — Recommendations are based primarily on consensus and expert opinion.

Sunday, March 15, 2009

Intradural Lumbar Disc Herniations- Synthesis of literature from radio-diagnosis & Neurosurgery (6 Papers discussed)

Intradural disc herniation is a serious complication of intervertebral disc rupture. Intradural disc herniations are thought to be rare events, and there have been relatively few literature reports of intradural disc herniations.

CT finding of epidural gas indicates Intradural disc herniation?

Intradural disc herniation associated with epidural gas (1).

According to Hidalgo-Ovejero AM et al possibility of an intradural herniated disc must always be considered in a patient whose CT scan reveals the presence of epidural gas. They also suggest, in the event where no clear disc herniation is found to justify the clinical symptoms or the previous radiologic findings, an intradural exploration may be indicated.

The study by Hidalgo-Ovejero AM et al:
Hidalgo-Ovejero AM et al in the year1998, presented a case study that cautioned spine surgeons of the possible association of intradural disc herniation and epidural gas, to prevent overlooking intradural disc fragments during surgery. This spine presentation is so rarely studied that only 3 cases were published prior to this study.

In this study, spine surgeons Hidalgo-Ovejero AM et al performed open discectomy. During the open discectomy, after a negative epidural examination, an intradural examination was performed, which revealed a disc herniation, which was removed during the surgery.

Role of MRI in preoperative diagnosis of Intradural lumbar disc herniations (3)

According to the researchers D'Andrea G et al, radiologic diagnosis of intradural herniation is possible in carefully selected patients with MRI with gadolinium. D'Andrea G et al of Italy (2004) discussed the role of MRI in preoperative diagnosis.

D'Andrea G et al analyzed 9 patients of intradural lumbar disc hernia on whom hemilaminectomy was performed. In 6 cases, the diagnosis of intradural herniation was confirmed preoperatively but in 3 remaining, it was confirmed at surgery.

Comparision with CT & Myelography:
1. In 5 cases, CT (with no contrast medium) of the lumbar area revealed disc herniation, but none could it confirm its intradural location.
2. Myelography was performed in 2 cases but also could not prove intradural extrusion.
3. Magnetic resonance imaging study was used in 4 cases.

Is it possible to predict Intradural lumbar disc herniation preoperatively? (4)

To answer this question Choi JY et al of Korea reported study of two cases and they also have tried to explain how a correct preoperative diagnosis helps to aid in good surgical outcome and minimize the nurological deficits. The authors describe two patients with intradural lumbar disc herniations, one with and one without preoperative diagnosis, who had different postoperative outcomes.

The findings in these 2 patients:
Case no.1: (post operative diagnosis)

a. The first patient underwent an extended L3 subtotal laminectomy followed by bilateral medial facetectomy and foraminotomy at L3-L4.
b. A durotomy uncovered large disc fragments comprised of friable disc materials and end plates, after no clear disc herniation was found in the epidural space.

Outcome of surgery: The patient experienced a marked reduction of pain and progressive recovery of sensory disturbance, but neurologic examination showed right foot drop postoperatively. Two years after surgery, she can not walk without a cane because the neurologic deficit of the right ankle has shown no improvement.

Case no.2: (preoperative diagnosis)


The second patient underwent anterior lumbar interbody fusion after a preoperative diagnosis of intradural disc herniation.

Outcome of surgery: Two days after surgery, the second patient was allowed to ambulate with a lumbar orthosis. Neurologic examination showed no motor deficit. Twenty-one months after surgery, the patient reports minimal back pain when sitting on a chair for prolonged periods of time.
This group of researchers concluded:

1. "hawk-beak sign" on axial imaging & abrupt loss of continuity of the posterior longitudinal ligament (PLL) indicates potential presence of an intradural disc herniation. These signs must always be considered preoperatively.
2. This above said association on MRI should be guide; if followed it will result in an adequate surgical approach, thereby reducing the chance of postoperative neurologic deficit.
3. Finally, anterior lumbar interbody fusion can be a reasonable alternative in the treatment of intradural lumbar disc herniations.

However despite of above study describing the ease of diagnosing the disorder from "hawk-beak sign" & integrity of PPL; according to Oztürk A et al of Turkey preoperative diagnosis of intradural disc herniation is still difficult despite new neuroradiologic investigation possibilities including CT and MRI and it is usually diagnosed by during surgery (6).

Intradural herniation of intervertebral disc at the level of Lumbar 1-Lumbar 2 (6).

Oztürk A et al of Turkey presented an case study of intradural disc herniation at the level of L1-L2 with significant myelopathic neurologic deficits.
The case is as follows:
1. A 50-year-old female patient was admitted to the hospital in Turkey with pain and weakness in both legs.
2. Her neurological examination revealed paraparesis.
3. Magnetic resonance imaging showed an extruded disc hernia of central localization at the L1-L2 level.
Surgery:

This patient underwent total laminectomy at the level of L1-L2 and her intradural disc fragment was extirpated by microsurgical methods. Hence the surgery was a combination of ablative surgery & microsurgical methods.

Cervical intradural disc herniation (5).

Cervical intradural disc herniation is an extremely rare condition. The pathogenesis remains obscure. Iwamura Yet al of Japan presented a cervical intradural disc herniation. Including this case study only 17 cases of cervical intradural disc herniation have been reported.

The case study:

1. A 45-year-old man who had Brown-Sequard syndrome diagnosed on neurologic examination.
2. A cervical intradural disc herniation at C6-C7, with localized hypertrophy and segmentally ossified posterior longitudinal ligament, is reported in Neuroradiologic, operative, and histologic findings.
Upon en bloc resected posterior vertebral portion of C6 and C7, to evaluation for discussion of the pathogenesis.

Following are found:

1. Adhesion of dura mater and hypertrophic posterior longitudinal ligament was observed around a perforated portion of the herniated disc.
2. Histologic study showed irregularity in fiber alignment accompanied by scattered inflammatory cell infiltration and hypertrophy in the posterior longitudinal ligament.

Hence the salient points to be considered are the adhesion and fragility of dura mater and posterior longitudinal ligament. This was caused by hypertrophy, with chronic inflammation and ossification of the posterior longitudinal ligament sustaining chronic mechanical irritation to the dura mater, leading to perforation of the herniated disc by an accidental force.

Surgery:
The cervical intradural disc herniation was removed successfully and followed by C5-Th1 anterior interbody fusion with fibular strut graft.
Neurologic recovery was complete except for minor residual sensory disturbance in the leg 7 years after the surgery.

Report of 3 cases of intradural lumbar disc herniations from Germanany (2).
According to neurosurgeons Prestar FJ et al (1995) of Germany; Intradural lumbar disc herniation is a rare pathological entity. According to database of these researchers 3 new cases among a series of 5000 lumbar spine operations are added to the about 60 previous case reports in the literature.

Report of 3 cases:

1. In one patient the location of the free disc fragment was medial within the dural sac
2. In other two patients the free disc fragment had penetrated the dural sac from the axilla of the nerve root.

Prestar FJ et al suggested the pathogenesis as:

1. Congenital adhesions of the dura mater to the posterior longitudinal ligament at the lower lumbar spine.
2. Weakness of the dura mater ventrally and at the axilla of the nerve root.

Prestar FJ et al further suggested to include a multiplanar MRI to correctly investigate the free disc hernia within the dural sac preoperatively.

Reference:
1. Hidalgo-Ovejero AM et al, Intradural disc herniation associated with epidural gas; Spine. 1998 Jan 15;23(2):281-3.
2. Prestar FJ et al, Intradural lumbar disc herniations: report of three cases; Minim Invasive Neurosurg. 1995 Sep;38(3):125-8.
3. D'Andrea G et al, Intradural lumbar disc herniations: the role of MRI in preoperative diagnosis and review of the literature; Neurosurg Rev. 2004 Apr;27(2):75-80; discussion 81-2. Epub 2003 Oct 15.
4. Choi JY et al, Intradural lumbar disc herniation--is it predictable preoperatively? A report of two cases; Spine J. 2007 Jan-Feb;7(1):111-7. Epub 2006 Nov 20.
5. Iwamura Y et al, Cervical intradural disc herniation; Spine. 2001 Mar 15;26(6):698-702.
6. Oztürk A et al, Intradural herniation of intervertebral disc at the level of Lumbar 1-Lumbar 2; Turk Neurosurg. 2007 Apr;17(2):134-7.








Saturday, March 14, 2009

Chronic pelvic pain syndromes:

The purpose of this article is to introduce the reader to pudendal neuropathy & physical therapy treatment options.
Chronic pelvic pain can present in various pain syndromes (1). PPOD (pelvic pain and organic dysfunction) is not an uncommon finding in the low back pain patient. Women appear to be more frequently involved than men (2).
3 types of pelvic pain syndromes (1):
1. Pudendal neuralgia,
2. Piriformis syndrome, and
3. "Border nerve" syndrome (ilioinguinal, iliohypogastric, and genitofemoral nerve neuropathy).

Piriformis syndrome is an uncommon cause of buttock and leg pain. Chronic neuropathic pain arise from the lesion or dysfunction of the ilioinguinal nerve, iliohypograstric nerve, and genitofemoral nerve (1).

Pudendal neuralgia commonly presents as chronic debilitating pain in the penis, scrotum, labia, perineum, or anorectal region. The pudendal nerve is located between the sacrospinous and sacrotuberous ligaments at the level of ischial spine (1). The results of recent electrophysiologic investigations indicate that many patients with urological, bowel or anorectal dysfunction demonstrate evidence of denervation neuropathy in muscles innervated by the branches of the pudendal nerve (2).

Diagnostic criteria for pudendal neuralgia by pudendal nerve entrapment (Nantes criteria) (4):

The 5 diagnostic criteria are:
(1) Pain in the anatomical territory of the pudendal nerve.
(2) Worsened by sitting.
(3) The patient is not woken at night by the pain.
(4) No objective sensory loss on clinical examination.
(5) Positive anesthetic pudendal nerve block.

Other clinical criteria can provide additional arguments in favor of the diagnosis of pudendal neuralgia. Exclusion criteria are also proposed: purely coccygeal, gluteal, or hypogastric pain, exclusively paroxysmal pain, exclusive pruritus, presence of imaging abnormalities able to explain the symptoms.

Role of ENMG in pudendal neuropathy (3):

Electroneuromyographic (ENMG) investigation is often performed in this context, based on needle electromyography and the study of sacral reflex and pudendal nerve motor latencies.
ENMG do not assess directly the pathophysiological mechanisms of pain but rather correlate to structural alterations of the pudendal nerve (demyelination or axonal loss). In addition, only direct or reflex motor innervation is investigated, whereas sensory nerve conduction studies should be more sensitive to detect nerve compression. Finally, ENMG cannot differentiate entrapment from other causes of pudendal nerve lesion (stretch induced by surgical procedures, obstetrical damage, chronic constipation…). Thus, perineal ENMG has a limited sensitivity and specificity in the diagnosis of pudendal nerve entrapment syndrome and does not give direct information about pain mechanisms. Pudendal neuralgia related to nerve entrapment is mainly suspected on specific clinical features and perineal ENMG examination provides additional, but no definitive clues, for the diagnosis or the localization of the site of compression. In fact, the main value of ENMG is to assess objectively pudendal motor innervation when a surgical decompression is considered.

Goals of Physical therapy management of pelvi/perineal and perianal pain syndromes (5).
A major feature of pelvi/perineal and perianal pain syndromes commonly encountered by multidisciplinary clinicians is pelvic floor imbalance and incoordination.

Pelvic floor physical therapy is considered to be effective in the management of functional urogenital and anorectal disorders.

A functioning pelvic floor is integral to
1. increases in intra-abdominal pressure,
2. provides rectal support during defecation,
3. has an inhibitory effect on bladder activity,
4. helps support pelvic organs, and
5. assists in lumbopelvic stability.

Coordinated release of the sphincters within a supporting extensible levator ani allows complete and effortless emptying. Precise pelvic floor and abdominal muscle coactivity, based on research, is used clinically. Motor and cognitive learning which can alter peripheral and central pain mechanisms and produce physical changes in the CNS, viscera, smooth and musculoskeletal tissues is the basis of physical therapy in pelvic floor and pelvic organ pain management.

Reference:
1. Peng PW; Pain Physician. 2008 Mar-Apr;11(2):215-24.
2. Browning JE; J Manipulative Physiol Ther. 1989 Aug;12(4):265-74.
3. Neurophysiologie Clinique/Clinical Neurophysiology; Volume 37, Issue 4, August-September 2007, Pages 223-228
4. Jean-Jacques Labat et al; Diagnostic criteria for pudendal neuralgia by pudendal nerve entrapment (Nantes criteria); Neurourology and Urodynamics; Volume 27 Issue 4, Pages 306 – 310; Published Online: 7 Sep 2007
5. Markwell SJ; World J Urol. 2001 Jun;19(3):194-9.


Friday, March 13, 2009

Understanding Cycling factors & Physiological factors for efficient cycling

Historically, the bicycle has evolved through the stages of a machine for efficient human transportation, a toy for children, a finely-tuned racing machine, and a tool for physical fitness development, maintenance and testing (2).
The underlying principle of positioning a cyclist on a bicycle is to remember that the bicycle is adjustable, and the cyclist is adaptable (1).

Proper bicycle fit requires (1)
1. Careful review of bicycle selection,
2. Saddle height for proper leg extension,
3. Fore-and-aft positioning of the knee over the pedal,
4. Saddle tilt,
5. Handlebar position, and
6. Positioning of the upper body for optimum comfort and performance.
7. Maintaining an aerodynamic position for extended periods of time (Recently, major strides have been made in the aerodynamic design of the bicycle. These innovations have resulted in new land speed records for human powered machines. N.B. fatigue patterns in lower and upper body musculature play an important role in maintaining aerodynamic position on the cycle).

Performance in cycling is affected by a variety of factors (2)
1. Aerobic and anaerobic capacity,
2. Muscular strength and endurance, and
3. Body composition.

Short and long interval training, blended with long distance tempo cycling, will exploit both the anaerobic and aerobic systems. Strength training, to be effective, must be performed with the specific muscle groups used in cycling, and at specific angles of involvement.

Physiological Testing (2):
Bicycle races range from a 200m sprint to approximately 5000km. This vast range of competitive racing requires special attention to the principle of specificity of training.
The physiological demands of cycling have been examined through the use of (2)
Bicycle ergometers, rollers, cycling trainers, treadmill cycling, high speed photography, computer graphics, strain gauges, electromyography, wind tunnels, muscle biopsy, and body composition analysis.

Nutrition in cycling (2):
Prolonged cycling requires special nutritional considerations. Ingestion of carbohydrates, in solid form and carefully timed, influences performance. Caffeine appears to enhance lipid metabolism.

Few other important factors in leisure time & competitive cycling (2):
1. Injuries, particularly knee problems which are prevalent among cyclists, may be avoided through the use of proper gearing and orthotics.
2. Air pollution has been shown to impair physical performance. When pollution levels are high, training should be altered or curtailed .

Reference
1. Burke ER; Clin Sports Med. 1994 Jan;13(1):1-14.
2. Faria IE; Sports Med. 1984 May-Jun;1(3):187-204.


Patient’s description of symphalgia:

The description of pain or altered sensation in the involvement of autonomic nesvous system especially sympathetic nervous system are as follows:

1. feeling of foreign body
2. feeling of a stake
3. feeling of a lump within
4. feeling of heaviness of the part
5. feeling of a tennis ball within
6. feeling of a gnawing
7. a crawling feeling

*Pain in CRPS i.e. RSOD (reflex sympathetic osteodystrophy) must also be compared to above said description.

Thursday, March 12, 2009

Epidural gas presenting as Spinal Space occupying lesion- A review of 8 paper since 1994


Introduction:
Among unusual abnormalities of the lumbar spine reported since the introduction of Computed Tomography (CT), the presence of gas lucency in the spinal canal, known as vacuum phenomenon, is often demonstrated (7). The finding of gas within the vertebral disc space (vacuum phenomenon) is relatively common. This disorder often presents major diagnostic and therapeutic challenges, especially in the presence of multiple degenerative changes and chronic back pain in elderly patients. Kloc W (8) describes pathophysiology and diagnostics of gaseous degeneration associated with the herniated disc. Degenerative spine disease, gaseous degeneration of the intervertebral disc and epidural gas can be disclosed by imaging studies. The presence of epidural gas is attributed to gaseous disc degeneration. This pathology may cause radicular pain similar to sciatic pain produced by disc herniation. Surgery might be indicated in these cases.
The initial reports on epidural gas (6):
The authors Cheng TM et al (1994) described two patients with presentations and findings that have not been previously described in the literature. Both patients had histories of upper lumbar back and leg pain. Degenerative spine disease, gaseous degeneration of the intervertebral discs, and epidural gas in the lateral recesses were noted on imaging studies. However, because both patients had undergone prior epidural diagnostic and therapeutic procedures, the epidural gas in the lateral recesses could be attributed either to gaseous disc degeneration or to the previous intraspinal procedures. One patient was found to have a large, far lateral extruded disc fragment that contained air. The nerve root in the second patient was impaled by an unusual combination of a small extruded disc fragment as well as an air-filled sac that was surrounded by the walled-off fragment's capsule and which freely communicated with the gaseous degenerated disc space. Cheng TM et al discussed the suspected mechanism of root compression. The possibility of disc herniation should be seriously considered in cases of nerve root compression in which epidural gas is present, especially those associated with gaseous degenerated discs.
Epidural gas pseudocyst (4,7):
Epidural gas pseudocyst compressing a nerve root in patients with a lateral disc herniation has rarely been reported. Salpietro FM et al reported a case of a 44-year-old man who experienced violent low back pain and monolateral sciatica, exacerbated by orthostatic position, one week before admission. A lumbosacral spine CT showed the presence of vacuum phenomenon associated with a degenerated disc material and a capsulated epidural gas collection with evidence of root compression.
A microsurgical interlaminar approach was carried out and, before the posterior longitudinal ligament was entered, a spherical "bubble" compressing the nerve roots was observed. The capsulated pseudocyst was dissected out, peeled off and excised en bloc. A large part of the posterior longitudinal ligament and the lateral disc herniation were removed. Postoperatively the patient was completely free of symptoms.
Salpietro FM et al have associated the mechanism of exacerbation of pain was probably due to the increased radicular compression in the upright posture and, besides the presence of a lateral disc herniation, could be related to a pneumatic squeezing of gas from the intervertebral space into the well capsulated sac by the solicitated L4-L5 motion segment. Histological study of the wall of the pseudocyst showed the presence of fibrous tissue identical to the ligament. They concluded that, in case of a lumbar disc herniation, it is recommended to perform a complete microdiscectomy and an accurate removal of the involved portion of posterior longitudinal ligament in order to prevent pseudocystic formations.
CT in detecting intra-spinal gas (5):
Tsitouridis I et al of Radiology Department, Papageorgiou General Hospital, Greece reported Disc-like herniation in association with gas collection in the spinal canal.
Gas production as a part of disk degeneration can occur but rarely causes nerve compression syndromes. Few cases have been reported in which lumbar intraspinal epidural gas cause nerve root compression symptoms. We present 12 cases of gas collection in the spinal canal that were presented to the orthopaedic out-patient department with symptoms of low back pain and sciatica. CT showed the presence of free epidural gas collections adjacent to or over the affected nerve roots. Relief of symptoms was noted with the change of positions, lying down or sleeping. In this study, we conclude that the presence of lumbar intraspinal epidural gas that causes radicular compressing phenomena, can be easily detected with the use of CT.
Recurrent radiculopathy caused by epidural gas after spinal surgery (3):
Vacuum phenomenon (gas accumulation in an intervertebral disc) is relatively common. Gas can also spontaneously enter and collect in the epidural space, but symptomatic epidural gas after spinal surgery is very rare.
Sasani M et reported primary disorders in the 4 new cases were disc extrusion at L2-L3 (Case 1), disc degeneration and herniation at L4-L5 (Case 2), stenosis of the lumbar spinal canal (Case 3), and disc herniation at L5-S1 with spinal canal stenosis (Case 4). The corresponding surgeries performed were L2-L3 microdiscectomy, L4-L5 microdiscectomy with instrumentation, right unilateral hemilaminotomy with complete instrumentation, and L5-S1 microdiscectomy.
All 4 patients developed unexpected postoperative complaints of low back and radicular pain. Each was investigated with computed tomography and magnetic resonance imaging. The images revealed epidural gas collections compressing the thecal sac and/or nerve roots.
Epidural gas after lumbar surgery is very rare but can cause unexpected postoperative back or radicular pain. Combined computed tomography and magnetic resonance imaging should be used to identify the problem and rule out other disorders. This is a iatrogenic complication that raise concern among the spinal surgeons. However Sasani M et reported combined computed tomography and magnetic resonance imaging should be used to identify the problem and rule out other disorders. Conservative treatment should be the first-line approach but surgery is often necessary if this does not resolve the problem.
Association of Intradural disc herniation and epidural gas: more than a informal association? (1,2)
Hidalgo-Ovejero AM et al alerted spine surgeons to this potential association between Intradural disc herniation and epidural gas. According to Hidalgo-Ovejero AM et al this association is found in 2% of the patients with intraspinal gas.
Hidalgo-Ovejero AM et al concluded potential presence of an intradural disc herniation must always be considered when performing an open discectomy on a patient whose CT scan study shows the presence of epidural gas. This association is particularly striking given the relative rarity of intradural herniations and intraspinal gas. In the event that no clear disc herniation was found, an intradural examination may be indicated to justify clinical signs and symptoms or previous radiologic studies.

References:
1. Spine. 1998 Jan 15;23(2):281-3.
2. Spine. 2004 Oct 15;29(20):E463-7
3. Spine. 2007 May 1;32(10):E320-5.
4. J Neurosurg Sci. 2002 Jun;46(2):93-5; discussion 95.
5. Eur J Radiol. 2005 Oct;56(1):1-4
6. J Neurosurg. 1994 Sep;81(3):453-8.
7. J Neurosurg Sci. 2002 Jun;46(2):93-5; discussion 95.
8. Chir Narzadow Ruchu Ortop Pol. 1998;63(2):117-22; discussion 123-4.








A rare cause of LBA & associated radiculopathy


Epidural engorged veins due to inferior vena cava obstruction or occlusion cause sciatica and low back pain.

Pathology:
Abnormalities or pathological changes of epidural venous network may give rise to symptoms similar to or mimicking lumbar disc herniation or spinal stenosis. Multiple lumbar epidural varices can cause nerve root and thecal sac compression. Lumbar epidural varices have been infrequently described in the literature. To date, the cause of anterior epidural venous enlargement has been poorly understood, and both congenital and acquired causes have been proposed. This report describes enlarged epidural veins in patients with inferior vena caval thrombosis or obstruction presenting with radicular syndromes.

About the study:
Paksoy Y have examined 9640 patients experiencing back pain or sciatica, using MRI. There were 13 (0.13%) patients who had radicular symptoms that clinically mimicked lumbar disc herniation or spinal stenosis. All of these patients had inferior vena caval obstruction or occlusion that caused engorgement in the epidural and paravertebral venous system, causing nerve root compression.

Out of 13 patients with radicular symptoms all of the patients had inferior vena caval obstruction or occlusion that caused engorgement in the epidural veins, causing nerve root compression. The ages of these patients ranged from 20 to 53 (mean, 30) years.

All of the patients were examined with color Doppler ultrasonography and magnetic resonance scanner. The Results are as follows:
1. Ten of 13 patients had inferior vena cava thrombosis located just under the renal vein orifices.
2. In two patients, there was compression to inferior vena cava due to parity.
3. In the remaining patient, a huge intra-abdominal mass was observed, and this mass was causing inferior vena cava obstruction and invasion.
4. Enlargements of epidural venous plexus were demonstrated in all of these cases.
5. All of the patients presented with the acute onset of low back pain followed shortly thereafter by acute radicular symptoms.

So from Paksoy Yet al’s study it is apparent that epidural venous engorgement should be considered when the symptoms of patients with deep venous and inferior vena cava thrombosis are accompanied by radicular and/or back pain, because pathologic processes compressing a nerve root can cause pain.

Reference:
Paksoy Yet al ;Spine. 2004 Nov 1;29(21):2419-24.


Tuesday, March 10, 2009

Revisiting Foot Drop:

Foot drop is a common and distressing problem that can lead to falls and injury.

Causes:
1. Most frequent cause is a (common) peroneal neuropathy at the neck of the fibula,
2. Anterior horn cell disease,
3. Lumbar plexopathies,
4. L5 radiculopathy and
5. Partial sciatic neuropathy.
6. Habitual leg crossing may well be the most frequent cause and most patients improve when they stop this habit.

Even when the nerve lesion is clearly at the fibular neck there are a variety of causes that may not be immediately obvious. A meticulous neurological evaluation goes a long way to ascertain the site of the lesion.

Basic investigations:
1. Nerve conduction and electromyographic studies are useful adjuncts in localising the site of injury, establishing the degree of damage and predicting the degree of recovery.
2. Imaging is important in establishing the cause of foot drop if it is at the level of the spine, along the course of the sciatic nerve or in the popliteal fossa;
Imaging tools are: ultrasonography, CT and MR imaging.

Foot drop of any cause must be immediately prescribed with an ankle foot orthosis is a helpful device that enables them to walk better and more safely (helps not to lose the muscle stretch reflex).

Reference:

Stewart JD; Pract Neurol. 2008 Jun;8(3):158-69.

Monday, March 9, 2009

Forward versus backward pedaling in cycling: implications for rehabilitation strategies.


Pedaling has been shown to be an effective rehabilitation exercise for a variety of knee disorders. Recently, backward gait has been shown to produce greater knee extensor moments and reduced patellofemoral joint loads compared to forward gait. No study has examined the efficacy of backward pedaling as a safe alternative to forward pedaling in rehabilitation programs. Neptune RR et al compared the knee joint loads while knee is performing during forward and backward pedaling. The aim was to determine whether backward pedaling offers theoretical advantages over forward pedaling to rehabilitate common knee disorders.

The study:
1. This study primarily quantified Tibiofemoral and Patellofemoral joint reaction forces.
2. Lower tibiofemoral compressive loads, but higher patellofemoral compressive loads, were observed in backward pedaling.
3. Lower protective anterior-posterior shear force was observed in backward pedaling near peak extension.

Clinical notes for implementation:
1. Backward pedaling offers reduced tibiofemoral compressive loads for those patients with knee disorders such as menisci damage and osteoarthritis, but higher patellofemoral compressive loads.
2. Therefore due to above said reasons, backward pedaling is not recommended for patients experiencing patellofemoral pain.
3. Further, backward pedaling should not be recommended after anterior cruciate ligament injury or reconstruction.

Caution to clinicians:
The results of this study indicate that the design of rehabilitation programs including pedaling exercises should be injury specific with particular attention paid to the mechanics of the task.

Reference:
Neptune RR et al; Clin Biomech (Bristol, Avon). 2000 Aug;15(7):528-35.



CPM use after TKR- just or unjust?

The usefulness of continuous passive motion after total knee arthroplasty remains controversial.

The reported benefits include:

1. Decreased rates of knee manipulation,
2. Decreased rates of deep vein thrombosis,
3. Decreased rates of postoperative use of analgesics,
4. Greater range of motion.

The reported disadvantages include:

Many studies have reported
1. Increased wound complications, bleeding, and pain.

Confusion & debate on use of CPM:
Lack of consensus on the use of continuous passive motion exists because reported studies include many confusing variables.

Advocating for use of CPM:

1. Several studies have shown that continuous passive motion in the hospital decreased the rate of knee manipulation from as high as 21% to as low as 0%. However, many studies show that range of motion may improve more rapidly with continuous passive motion but the ultimate range of motion at follow-up is unchanged.

2. Continuous passive motion is used three times per day (1 hour sessions), beginning on the first postoperative day, within a 4 to 5 day inpatient hospital pathway. Lachiewicz PF in his center found of 132 knees that had a primary posterior-stabilized total knee arthroplasty, 7 (5%) had a manipulation for failure to obtain greater than 70 degrees flexion. No patients had major wound complications that required re-operation. There is no specific charge to the patient for the continuous passive motion because it is included in the hospital per diem charge.

3. According to Lachiewicz PF there is literature support of the use of continuous passive motion to decrease the rate of manipulation (and its costs) for poor range of motion after total knee arthroplasty.

4. If patients follow fixed inpatient hospital pathways, the length (and possibly cost) of hospital stay is not changed by use of continuous passive motion.

5. The data on the effect of continuous passive motion on overall analgesic use and prevalence of deep vein thrombosis are not clear.

Reference:
Lachiewicz PF; Clin Orthop Relat Res. 2000 Nov;(380):144-50.

Causes of stiffness after TKR



Postoperative stiffness is a debilitating complication of total knee arthroplasty. Preoperative risk factors include limited range of motion, underlying diagnosis, and history of prior surgery.
Intra-operative factors:

1. Improper flexion-extension gap balancing
2. Oversizing or malpositioning of components
3. Inadequate femoral or tibial resection
4. Excessive joint line elevation
5. Creation of an anterior tibial slope and
6. Inadequate resection of posterior osteophytes.
Postoperative factors:

1. poor patient motivation
2. arthrofibrosis
3. infection
4. complex regional pain syndrome (CRPS) and
5. heterotopic ossification.

The first steps in treating stiffness are mobilizing the patient and instituting physical therapy. If these interventions fail, options include manipulation, lysis of adhesions, and revision arthroplasty. Closed manipulation is most successful within the first 3 months after total knee arthroplasty.

Arthroscopic or modified open lysis of adhesions can be considered after 3 months. Revision arthroplasty is preferred for stiffness from malpositioned or oversized components.

Patients who initially achieve adequate range of motion (>90 degrees of flexion) but subsequently develop stiffness more than 3 months after surgery should be assessed for intrinsic as well as extrinsic causes.

Reference: Bong MR et al; J Am Acad Orthop Surg. 2004 May-Jun;12(3):164-71.

Patellar problem is the major cause of stiffness after total knee arthroplasty!!!

Yercan HS et al investigated the prevalence of stiffness after total knee arthroplasty, and the results of the treatment options. Yercan HS et al performed 1188 posterior-stabilized total knee arthroplasties between 1987 and 2003.

They found:
1. The prevalence of stiffness was 5.3%, at a mean follow-up 31 months postoperatively. The average age was 71 years (range, 54-88).
2. The patients with painful stiffness were treated by two modalities: manipulation and secondary surgery.
3. In the manipulation group (n:46), the mean range of motion improved from 67 degrees before manipulation to 117 degrees afterward. This improvement was maintained at final follow-up as 114 degrees.
4. There was no significant difference between the motion, immediately after manipulation and at final follow-up. However, motion at final follow-up was better for those manipulated early to those done later (p=0.021).
5. In the secondary surgery group (n:10), the mean gain in motion was 49 degrees at final follow-up and average pain score was found 43.
6. Patellar problems--component loosening and clunk syndromes--were found in 4 patients (40%).

Conclusion:
1. Early manipulation gives better gain of motion than done later and our patients had not lost flexion during follow-up.
2. The patella should always be evaluated in every stiff arthroplasty.
3. The researching surgeons opined, patellar problems are a good prognostic factor for the success of revision surgery.
4. The researching surgeons also opined that open arthrolysis does not correct a limited flexion arc, but it does relieve pain.
5. Arthroscopic release is not reliable for severely stiff knees and we prefer to perform it in less painful and moderately stiff knees within 3 to 6 months after operation.

References:
Yercan HS et al; Knee. 2006 Mar;13(2):111-7. Epub 2006 Feb 20.


Recovery characteristics in first-time acute hamstring strains incurred during stretching.

Hamstring strains can be of 2 types with different injury mechanisms, 1 occurring during high-speed running and the other during stretching exercises.

In a study involving Case series (prognosis); Askling CM et al found Stretching exercises can give rise to a specific type of strain injury to the posterior thigh. A precise history and careful palpation provide the clinician enough information to predict a prolonged time until return to pre-injury level. One factor underlying prolonged recovery time could be the involvement of the free tendon of the semimembranosus muscle.

About the study:
1. 15 professional dancers with acute first-time hamstring strains were prospectively included in the study.
2. All subjects were examined, clinically and with magnetic resonance imaging, on 4 occasions after injury: at day 2 to 4, 10, 21, and 42.
3. The clinical follow-up period was 2 years.

How & where injury occurred:
1. All dancers were injured during slow hip-flexion movements with extended knee and experienced relatively mild acute symptoms.
2. All injuries were located proximally in the posterior thigh close to the ischial tuberosity.
3. The injury involved the semimembranosus (87%), quadratus femoris (87%), and adductor magnus (33%).
4. All injuries to the semimembranosus involved its proximal free tendon.

Another important point that was found:
There were no significant correlations between clinical or MRI parameters and the time to return to preinjury level.

Reference:
Askling CM et al; Am J Sports Med. 2007 Oct;35(10):1716-24. Epub 2007 Jun 13

Saturday, March 7, 2009

Hip joint muscle strength In PFPS

Proximal joint stability leads to controlled execution of distal joint motions & functions. Hence decreased hip strength may be associated with poor control of lower extremity motion during weight-bearing activities, leading to abnormal Patellofemoral motions and pain.

Studies exploring the presence of hip strength impairments in subjects with PFPS have reported conflicting results.

In a cross-sectional (female only study) Robinson RL et al investigated whether females seeking physical therapy treatment for unilateral patellofemoral pain syndrome (PFPS) exhibit deficiencies in hip strength compared to a control group.

Sample & method:

1. 20 aged 12 to 35 years, participated in the study. Ten subjects with unilateral PFPS were compared to 10 control subjects with no known knee pathologies.
2. Hip abduction, extension, and external rotation strength were tested using a handheld dynamometer.
3. A limb symmetry index (LSI) was used to quantify physical performance for all tests.

Result & conclusion:
1. The symptomatic limbs of subjects with PFPS exhibited impairments in hip strength for all variables tested.
2. LSI values in subjects with PFPS (range, 71%-79%) were significantly lower than those in control subjects (range, 93%-101%) (P< or =".007)." p =" .007)," p=" .004)" style="font-weight: bold;">Females aged 12 to 35 presenting with unilateral PFPS demonstrate significant impairments in hip strength compared to control subjects.

My suggestion for Clinicians:

Folks in case of a PFJ dysfunction (I am generalizing, please check)

1. Check the Lumbar spine (manipulate for a asymmetric movement assuring for a symmetrical Lumbo-pelvic mechanism)- see the Blogs down in this context
2. Strength training of hip musculature.

Reference:

J Orthop Sports Phys Ther. 2007 May;37(5):232-8.

Develping a CPR (clinical prediction rule) for PFPS depending on Lumbopelvic manipulation.

Quadriceps muscle function in patients with PFPS was recently shown to improve following treatment with lumbopelvic manipulation. No previous study has determined if individuals with PFPS experience symptomatic relief of activity-related pain immediately following this manipulation technique.

Iverson CA et al tried to determine the predictive validity of selected clinical exam items and to develop a clinical prediction rule (CPR) to determine which patients with patellofemoral pain syndrome (PFPS) have a positive immediate response to lumbopelvic manipulation.

Sample & method:
1. 50 subjects (26 male, 24 female; age range, 18-45 years) with PFPS underwent a standardized history and physical examination.
2. After the evaluation, each subject performed 3 typically pain-producing functional activities (squatting, stepping up a 20-cm step, and stepping down a 20-cm step).
3. The pain level perceived during each activity was rated on a numerical pain scale (0 representing no pain and 10 the worst possible pain).
4. Following the assessment, all subjects were treated with a lumbopelvic manipulation, which was immediately followed by retesting the 3 functional activities to determine if there was any change in pain ratings.
5. An immediate overall 50% or greater reduction in pain, or moderate or greater improvement on a global rating of change questionnaire, was considered a treatment success.
6. Likelihood ratios (LRs) were calculated to determine which examination items were most predictive of treatment outcome.

Result & conclusion:
1. Out of 49 subjects who were included in the data analysis, 22 (45%) had a successful outcome.
2. Five predictor variables were identified. The most powerful predictor of treatment success was a side-to-side difference in hip internal rotation range of motion greater than 14 masculine (+LR, 4.9).
3. If this variable was present, the chance of experiencing a successful outcome improved from 45% to 80%.

Reference:
Iverson CA et al J Orthop Sports Phys Ther. 2008 Jun;38(6):297-309; discussion 309-12. Epub 2008 Jan 22.

Analysis of 2 papers on tests of PFPS

Data regarding validity of clinical and radiographic findings in diagnosing patellofemoral pain syndrome are inconclusive.

1. 5 clinical tests in patellofemoral pain syndrome are:

1. Vastus medialis coordination test
2. Patellar apprehension test
3. Waldron's test
4. Clarke's test
5. Eccentric step test.

Nijs J et al examinied the validity of five clinical patellofemoral tests used in the diagnosis of patellofemoral pain syndrome (PFPS). Nijs J et al examinied above said 5 clinical tests in Likelihood ratio. (See below for interpretation of likelihood ratio)

Sample size:
45 knee patients were divided into either the PFPS or the non-PFPS group, based on the fulfilment of the diagnostic criteria for PFPS.

Focus points:
1. The positive likelihood ratio was 2.26 for both the vastus medialis coordination test and the patellar apprehension test.
2. For the eccentric step test, the positive likelihood ratio was 2.34.
Hence a positive outcome on either the vastus medialis coordination test, the patellar apprehension test, or the eccentric step test increases the probability of PFPS to a small, but sometimes important, degree.
3. For the remaining tests, the positive likelihood ratios were below the threshold value of 2, indicating that given a positive test result, the probability that the patient has PFPS is altered to a small, and rarely important degree.

However according to Nijs J et al negative likelihood ratios for all tests exceeded the threshold value of 0.5, suggestive of clinically irrelevant information. These data question the validity of clinical tests for the diagnosis of PFPS.

Information on likelihood ratios:
When we decide to order a diagnostic test, we want to know which test (or tests) will best help us rule-in or rule-out disease in our patient. In the language of clinical epidemiology, we take our initial assessment of the likelihood of disease (“pre-test probability”), do a test to help us shift our suspicion one way or the other, and then determine a final assessment of the likelihood of disease (“post-test probability”).
The “positive likelihood ratio” (LR+) tells us how much to increase the probability of disease if the test is positive, while the “negative likelihood ratio” (LR-) tells us how much to decrease it if the test is negative.

Likelihood ratio have unique properties that make them particularly relevant to clinicians:
• The LR+ corresponds to the clinical concept of "ruling-in disease"
• The LR- corresponds to the clinical concept of "ruling-out disease"
• The LR+ and LR- don't change as the underlying probability of disease changes (predictive values do change, as you just learned)
• LR's using multiple "levels" of positive (i.e. not just a simple yes/no or positive/negative result) provide much richer, more useful information to you as a clinician.
Interpreting likelihood ratios: general guidelines

The first thing to realize about LR’s is that an LR > 1 indicates an increased probability that the target disorder is present, and an LR < 1 indicates a decreased probability that the target disorder is present. The following are general guidelines, which must be correlated with the clinical scenario:
1. LR > 10: Large and often conclusive increase in the likelihood of disease
2. 5 – 10: Moderate increase in the likelihood of disease
3. 2 – 5: Small increase in the likelihood of disease
4. 1 - 2 : Minimal increase in the likelihood of disease
5. 1: No change in the likelihood of disease
6. 0.5 - 1.0 : Minimal decrease in the likelihood of disease
7. 0.2 - 0.5: Small decrease in the likelihood of disease
8. 0.1 - 0.2: Moderate decrease in the likelihood of disease
9. LR< 0.1: Large and often conclusive decrease in the likelihood of disease

2. Validity of clinical and radiological features

Haim A et al assessed how sensitive and specific key patellofemoral physical examination tests are, and evaluated the prevalence of physical examination and radiographic findings.
Sample size:
61 infantry soldiers with patellofemoral pain syndrome and 25 control subjects were evaluated.

Focus points:
1. The sensitivity of the patellar tilt, active instability, patella alta, and apprehension tests was low (less than 50%); specificity ranged between 72% and 100%.
2. Although the prevalence of positive patellar tilt and active instability tests was significantly greater in subjects with patellofemoral pain syndrome, there were no significant differences between the groups in the results of the other two tests.
3. Soldiers with patellofemoral pain syndrome presented with increased quadriceps angle, lateral and medial retinacular tenderness, patellofemoral crepitation, squinting patella, and reduced mobility of the patella.
4. There were no differences between the groups in the prevalence of lower limb and foot posture alignment and knee effusion.
5. Plain radiography showed increased patellar subluxation in soldiers with patellofemoral pain syndrome. Other radiographic measures (sulcus angle, Laurin angle, Merchant angle, and Insall-Salvati index) were similar in both groups.
6. Haim et al have also found that physical examinations were more useful than plain radiography.

Reference:
1. Nijs J et al, Man Ther. 2006 Feb;11(1):69-77. Epub 2005 Jun 13.
2. Haim A et al, Clin Orthop Relat Res. 2006 Oct;451:223-8
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