Category: disc herniation

 

 

  1. Lumbar spinal stenois (LSS)…defined by any narrowing of the spinal canal and/or nerve root canals…In patients with severe LSS, a space reduction of 67% has been found in the spinal canal.”

 

Spinal stenosis is the narrowing of the holes of the spine. The spine has 3 holes in it in the lumbar region. Each hole carries a nerve. It could either be the nerve of the spinal cord down the middle, and larger, hole. It could be the nerve roots out of the holes on the side of the spine. Each hole needs to be big enough so that it doesn’t irritate the nerve that it allows to pass through the hole. Picture a water pipe. If you put too much stuff in the pipe it will clog up. Sometimes there are tissues that can make their way into the holes of the spine to clog the holes. When the hole is clogged, the nerves don’t have as much room to do their job (transmitting signals to and from the brain). Now take that same pipe and come back and look at it over decades. There will be sludge and stuff built up around the pipe. This is essentially creating a smaller diameter on the inside of the pipe. This smaller diameter due to sludge is also creating a smaller hole. This could happen in the spine with severe arthritis or degenerative disc issues in which the hole gets smaller. A visual is much better so maybe this will help. image for spinal stenosis

 

  1. “…estimated the incidence of LSS in Denmark to 272 per one million inhabitants per year”

 

In other words, it is not very common in Denmark.

 

  1. “…it is important to discriminate between LSS and disc generated pain since these conditions have different prognoses and the range of evidence based treatments are different, as well.”

 

The treatment between the two issues, discogenic back pain and stenotic back pain, is very different. A thorough evaluation can start to correlate symptoms with either discogenic pain or non-discogenic pain. Many patients believe that an MRI will be the answer to why they have pain, but unfortunately this isn’t so.

 

  1. “a valid and reliable clinical assessment protocol for identifying LSS would be valuable in terms of choosing relevant treatment and informing the patient about the prognosis as early as possible.”

 

This article was written in 2009. The medical profession has existed for eons. There is still not a valid way to assess a patient in order to determine spinal stenosis. There are biologically plausible ways, meaning that when I assess you, I can make an educated guess from some of the findings in the history and physical, but it is not a valid (proven) way of coming to a conclusion.

 

  1. “The high sensitivity and specificity of MRI suggests this is a good test for ruling in and out the disease.”

 

The MRI does a great job of telling us what is abnormal, but it doesn’t do a great job of telling us if the abnormal finding is causing symptoms. As seen in the link above, there are abnormal findings in a population without symptoms. We have to take the imaging findings and see if they make sense after performing a physical exam.

 

  1. “…history will provide strong clues to the presence of spinal stenosis…more than 65 years of age…prolonged history of low back pain and intermittent radiating symptoms having developed gradually…limited walking capacity…Movements or positions involving flexion e.g. sitting or stooping, will often abolish symptoms…total loss of lumbar extension range is usually found, while flexion most often is well preserved.”

 

The typical patient with lumbar spinal stenosis will notice that the ability to walk has gradually reduced over time and there is a need to sit due to back or leg pain. Sitting will typically turn down or off the symptoms rapidly. This patient will have limited motion into extension (think of looking over your head to see the stars or bending backwards while standing).

 

  1. “…stenosis from zygapophyseal joint hypertrophy, ligament thickening or other degenerative changes, it cannot be expected that physical exercise or manual treatment will create a lasting change in the degree of space reduction in the spinal canal or intervertebral foramina”

 

In the presence of physical changes to the bones, ligaments or loss of disc height, there is nothing that a PT can do to change these back to the way that they were previously. These have been described as wrinkles on the inside. If we look at your face we can start to see how much age you have based on the wrinkles in the face. This is also done on the inside in that some “degenerative” changes are normal. Wrinkles are normal; they are not symptoms of anything sinister. The same can be said for physical changes on the inside. They don’t have to be pain generators. It takes a physical exam to determine how your symptoms respond and whether or not this matches the images on an MRI or X-ray. Even then, we can’t say that movement won’t help, only that we won’t change the physical “inside wrinkles”.

 

  1. “The main purpose of this pilot study is to evaluate the validity and intertester reliability of an algorithm of physical examination tests, in relation to identifying symptomatic lumbar spinal stenosis.”

 

This is good. A pilot study is like a pilot for a t.v. show. This is done to see if additional episodes should be done. This study will conclude if additional studies on this topic should be done.   What it hopes to find is a reliable (consistent) way of determining validity (actually seeing what the test hopes to see) in testing for lumbar spinal stenosis. A test that is both reliable and valid should be able to test for spinal stenosis regardless of who is performing the test and who is measuring the test.

 

  1. “Two patients were classified as “LSS” and five patients “Not LSS”, meaning a 29% prevalence of “LSS” Intertester agreement for overall diagnostic conclusion was 100%”

 

There are so few patients that this study will likely not yield any results that are actionable. The interesting thing is that the examiners agreed 100% of the time. This is not common in the medical field to have 100% agreement on near anything.

 

  1. “…the algorithm in its present form can not be used as a screening test to rule out LSS, although it may be able to diagnose the condition.”

 

There were so few people in the study that it is hard for any clinician to put it to use in the clinic. It may be able to diagnose the condition in that it demonstrated a specificity of 1.0, which is really good.

 

 

Excerpts taken from:

 

Lengsoe L, Lyhne S, Melbye M. An algorithm for clinical identification of spinal stenosis-a pilot study of validity and intertester reliability. International J of MDT. 2009;4(2):21-28.

 

Can’t find the abstract to the study, but it is listed under the author’s CV http://pure.au.dk/portal/en/persons/martin-melbye(ed4ee688-2d9e-4c17-b0b1-44a5b4b59ada)/publications/an-algorithm-for-clinical-identification-of-spinal-stenosis–a-pilot-study-of-validity-and-intertester-reliability(6d714ee0-d910-11de-9e3b-000ea68e967b).html

 

 

 

 

Not all back pain is back pain

“Findings such as disk height loss and disc bulges are common in individuals without low back pain.”
Disc bulges, degenerative joint disease, spinal stenosis, can all be a result of living with gravity. We have gravity acting as a compression force on us almost 16 hours a day. Anytime that there is a problem, we want to blame something or somebody. Low back pain is an enigma at times. We can draw correlations, we can come up with risk factors, we can even tell you how to treat it sometimes, but what we can’t do is tell you is exactly what causes your back pain. 
“Surprisingly, disc protrusions were associated with a lower risk of subsequent back pain. Nerve root contact and central stenosis had the largest hazard ratios on baseline imaging findings, and they were associated with incident back pain in the expected direction but not statistically significant. Self identified depression was the strongest predictor of subsequent back pain, with a greeter hazard ratio than any imaging findings.”
What should be taken from the above statistics is that mental health plays a role in pain. There are a lot of new studies that are associating catastrophizing and external locus of control with increased pain levels. Work by Nadine Foster demonstrates a screen for patients who will have a difficult time improving with therapy alone. New were books, such as the one by Annie O’Connor and Melissa Kolski (two people with whom I’ve studied at our RIC study group), goes into great detail regarding pain science. Big picture, we can not neglect the patient’s emotional well-being when attempting to treat the patient’s physical complaints.
“Our results indicate that depression is a strong predictor of who will subsequently report low back pain than baseline imaging findings.Subjects with self reported depression at baseline were 2.3 times as likely to have back pain compared with those who do not report depression.” 
There is obviously a psychosocial component to low back pain. The question is… Chicken or the egg. Is a person more likely to be depressed because they have back pain that is not improving? Or is that person more likely to have back pain because they are depressed? I don’t think that there are cause and affect articles in the literature at this point, but there is definitely a high correlation between patients who are depressed and patient who continue to report low back pain.
“In our analysis of baseline data, we concluded that central stenosis, nerve root contact, and disc extrusion were the most important imaging findings related to prior low back pain. Our current analysis indicates that central stenosis, disc extrusion, and root contact may also be risk factors for future low back pain.”
In other words, if you have a major deformity you will probably have pain. This doesn’t mean that you will definitely have pain, it just increases your risk of experiencing symptoms.
The moral of the story is that we cannot deny the brain. The brain has the ability to see pain, and some patients are more susceptible to seeing this pain. Don’t get me wrong, a thorough mechanical evaluation should be performed when a patient has pain, but when this patient is not inclined to respond to mechanical therapy, the patient should be referred to someone that can better handle this patient’s pain.Sometimes, that person will be a behavioral therapist, a psychotherapist, or a clinical psychologist. Physical therapists are not always the go to in order to treat a patient’s pain.
Excerpts from:

Jarvik JG, Haegerty PJ, Boyko EJ. Three-Year Incidence of Low Back Pain in an Initially Asymptomatic Cohort. Spine. 2005;30(13):1541-1548.  

Outline to back pain presentation

žCentralization

žCentralization, although first described by McKenzie14, has been replicated in multiple research studies15,16,17.

žCentralization is the movement of symptoms from an area distal to the spine to a more proximal segment14,18.

žPeripherilization is the movement of symptoms, originating from the spine, from a more proximal and central location to a more distal location14.

žThe centralization phenomenon, when produced in patients, correlates with good outcome9,10,18,19.

žPatients presenting as non-centralizers are six times more likely to require surgical intervention19.

žCentralization is shown to highly correlate with a discogenic lesion20.

žOTHER CONSIDERATIONS

  • Spinal Stenosis= reduction of the surface area of the spinal canal or foramen

–No clinical feature or diagnostic test can confirm that stenosis is the cause of symptoms

–A literature review determined that “all studies favored decompressive surgery for improvement of pain, function and quality of life, as well as in terms of patient satisfaction” compared to conservative care24

  • The advantage of surgery was noted within 3-6 months and remained constant for up to 4 years.
  • Surgery is more cost-effective for this group of patients
  • Appropriate for patients that have not improved with 12 weeks of conservative care.

žEPIDURAL STEROID INJECTIONS

žThere are multiple systematic reviews demonstrating that ESI’s can be effective in the short term and long term for managing back pain for both discogenic pain and stenotic pain21,22

žFollowing an ESI, about 45% of patients then demonstrate centralization and report 90% satisfaction of results after 1 year23

žAny questions?

žreference

1.Garzillo MJD, Garzillo TAF. Review of the Literature: Does Obesity Cause Low Back Pain? JMPT 1994;17(9):601-604.

2.Hill JC, Whitehurst DGT, Lewis M, et al. Comparison of stratified primary care management for low back pain with the current best practice (STarT Back): a randomised controlled trial. Lancet. 2011;378:1560-1571.

3.Walker BF, Williamson OD. Mechanical or inflammatory low back pain. What are the potential signs and symptoms? Manual Therapy 2009;14:314-320.

4.Fritz JM, Cleland JA, Speckman M, et al. Physical Therapy for Acute Low Back Pain: Associations with Subsequent Healthcare Costs. Spine 2008;33(16):1800-1805.

5.Shin G, Mirka G. An in vivo assessment of the low back response to prolonged flexion: Interplay between active and passive tissues. Clin Biomech 2007;22:965-971.

6.Kelsey JL, Githens PB, White AA, et al. An Epidemiologic Study of Lifting and Twisting on the Job and Risk for Acute Prolapsed Lumbar Intervertebral disc. J Orthop Research 1984;2:61-66.

7.Pople IK, Griffith HB. Prediction of an Extruded Fragment in Lumbar Disc Patients from Clinical Presentations. Spine 1994;19(2):156-158.

8.Natural history of lumbar disc hernia with radicular leg pain: Spontaneous MRI changes of the herniated mass and correlation with clinical outcome. J orthopedic surg 2001;9(1):1-7.

9.Long A, Donelson R, Fung T. Does it Matter Which Exercise? A Randomized Control Trial of Exercise for Low Back Pain. Spine 2004. 29(23):2593-2602.

10.Long A, May S, Fung T. Specific Directional Exercises for Patients with Low Back Pain: A Case Series. Physiotherapy Canada 2008;60:307-317.

ž

  1. Kovacs FM, Urrutia G, Alarcon JD. Surgery Versus Conservative Treatment for Symptomatic Lumbar Spinal Stenosis: A Systematic Review of Randomized Controlled Trials. Spine 2011;36(20):1334-1351.
  2. Urquhart DM, Bell R, Cicuttini FM, et al. Low back pain and disability in community-based women: prevalence and associated factors. Menopause 2009;16(1):24-29.
  3. Konstantinou K, Dunn K. Sciatica: Review of Epidemiological Studies and Prevalence Estimates. Spine 2008;33(22):2464-2472.
  4. McKenzie R, May S. The Lumbar Spine: Mechanical Diagnosis and Therapy. 2nd ed. Waikanae, New Zealand: Spinal Publication Ltd;2003.

15.Delitto A, Cibulka MT, Erhard RE, et al. Evidence for an extension-mobilization category in acute low back syndrome: A prescriptive validation pilot study. Phys Ther 1993;73:216-228.

16.Donelson R, Silva G, Murphy K. The centralizaiotn phenomenon: Its usefulness in evaluationg and treating referred pain. Spine 1990;15:211-215.

17.Donelson R, Grant W, Kamps C, Medcalf R. Pain response to sagittal end-range spinal motion: A multi-centered, prospective randomized trial. Spine 1991;16:S206-212.

  1. Werneke MW, Hart DL, Cutrone G, et al. Association Between Directional Preference and Centralization in Patients with Low Back Pain. JOSPT 2011;41(1): 22-31.
  2. Skytte L, May S, Peterson P. Centralization: its prognostic value in patients with referred symptoms and sciatica. Spine 2005;30(11):293-299
  3. Laslett M, Oberg B, Aprill C, McDonald B. Centralization as a predictor of provocation discography results in chronic low back pain, and the influence of disability and distress on diagnostic power. Spine Journal 2005;5:370-380.

ž

  1. Manchikanti L, Kaye AD, Manchikanti K, et al. Efficacy of epidural injections in the treatment of lumbar central spinal stenosis: a systematic review. Anesth Pain Med. 2015;5(1):e23139.
  2. ManchikantiL, Buenaventura RM, Manchikanti K, et al. Effectiveness of therapeutic lumbar transforaminal epidural steroid injections in managing lumbar spinal pain. Pain Physician. 2012;15(3):E199-245.
  3. van Helvoirt H, Apeldoorn AT, Ostelo RW, et al. Transforaminal Epidural Steroid Injections followed by mechanical diagnosis and therapy to prevent surgery for lumbar disc herniation. Pain Med. 2014;15(7):1100-1108.

ž

Directional preference compared to “evidenced based practice”

The Audrey Long article is commonly cited as one of the landmark articles for those of us that treat spines utilizing directional preference and centralization.  As well it should be! The results are unbelievable.  This researcher…I take that back…clinician performing research in the clinic published an article that, up until this time, was only speculation.  How could patients not get better using evidence based practice?  For a long time, the evidence was based on expert opinion and not really research.  I enjoy reading the publications on spine and it is interesting to read the changes in the Clinical Practice Guidelines for Low Back, published in JOSPT over the years.  Prior to the most recent publication, flexion based exercises were the rage and directional preference was only moderately supported.  Thanks to clinicians such as Audrey Long, this type of treatment has gained more support in the practice guidelines.  When I was in PT school (I sound like an old man, and year to year this is true, but not yet) this was a very small talking point in our curriculum.  Students now come out of school with a better awareness, though not a true understanding, of the concept of directional preference.

 

A Critical Appraisal of Directional Preference Exercises Compared to Two Other Exercise Paradigms

 

P: For patients with low back pain, with or without leg pain, demonstrating a directional preference

I: is treatment with a directional preference

C: as compared to treatment in the opposite direction of the directional preference or an evidence based approach

O: more beneficial when compared with subjective outcome measures

 

Reviewer:

Vincent Gutierrez, PT, MPT, cert. MDT

 

Search:

Pedro.org with the keyword terms “directional preference and low back pain”. Nine results were found and the article with the highest score was chosen.

 

Date of Search: February 15,2014

 

Citation:

Long A, Donelson R, Fung T. Does it Matter Which Exercise? A Randomized Control Trial of Exercise for Low Back Pain. Spine 2004;29(23):2593-2602.

 

Summary:

 

Eleven clinics, from five separate countries, participated in the study. Consecutive patients presenting for treatment of LBP, with or without leg pain, were asked to participate in the study. The inclusion criteria is as follows: consecutive patients with low back pain, with or without one neurological sign, age 18-65 years and demonstrating a directional preference. The exclusion criteria is as follows: cauda equina, two or more neurological signs, spinal fractures, post surgical, off work for one year or more due to low back pain, medical causes, uncontrolled medical conditions, pregnancy, inability to read English (except for those from Germany), patients with prior knowledge of, or specific physician referral for, the Mckenzie method, or no directional preference (DP) elicited.

Therapists credentialed or diplomaed in the McKenzie method performed the assessments. The directional preference was noted as either extension, flexion or lateral, but the subjects were shielded from the significance of directional preference. The subjects were then randomized to one of three groups: matched directional preference exercises, opposite directional preference (ODP) exercises, or evidence-based care (EBC). There were no baseline differences among the groups regarding demographics

The subjects attended at least three and no more than six sessions over the course of two weeks. Those in the DP group received exercises that matched the DP and were instructed to avoid all activities that increase intensity or radiation of symptoms. Those in the ODP group received exercises that were opposite to the DP, and the EBC group performed mid-range exerices and stretches for the hips and thighs. The final two groups also were instructed to return to remain active.

 

The outcome measures utilized in the study are as follows: back and leg pain intensity ratings using an 11 point visual analogue scale, the Roland Morris Disability Questionnaire (RMDQ), and medication use.

 

Five hundred three subjects were assessed and 230 demonstrated a DP as follows: 83% extension, 7% flexion and 10% lateral. Twenty-nine dropped out of the study at two weeks, and the remaining 201 were eligible for analysis. There were 36 withdrawals, which indicated that the subjects worsened or had no change in symptoms and were transitioned to alternative care. None of the DP group withdrew, but 16 in the ODP and 20 in the EBC withdrew. All outcome measures improved in the three groups over the course of two weeks, with the DP group demonstrating significant improvement compared to the ODP and EBC.

 

Appraisal:

The authors satisfied eight of the ten questions regarding the Quality Appraisal Checklist. The subjects’ group design was not blinded to those enrolling the subjects and this was a comparison study of varying interventions, which indicates that a true control group was absent.

 

This study will have a direct impact for clinical therapists. Because this study compared three different interventions, opposed to identifying the efficacy of a single intervention compared to a control group, it mimicked clinical practice. The authors compared evidence based care with a directional preference treatment paradigm, which would be similar to a question asked in clinical practice.

 

Conclusion:

Directional preference exercises are superior to performing exercises opposite to the directional preference or “evidence based care”. Patients that demonstrate a directional preference and are treated accordingly perform significantly better in outcomes measured in this study. There appears to be no harm in treating a patient with directional preference exercises, but the same does not hold true for performing exercises opposite of the directional preference or “evidence based care”.

The following is breakdown of the systems involved in “assessing” research articles.

 

  1. Were the subjects randomly assigned into groups?

Yes. The subjects were randomly assigned to one of three groups.

 

  1. Was each subject’s group assignment concealed from the people enrolling individuals in the study?

No. Because the study is a multi-centered study in outpatient practice, it was not acceptable to the authors to have patients drop out of the study due to changing therapists.

 

  1. Did groups have similar characteristics at the start of the study?

Yes. The authors note that there were “no differences among the three treatment groups in any baseline demographic characteristics or outcome measures.”

 

  1. Were subjects masked or blinded to their group assignment?

Yes. Although subjects couldn’t be blinded to the treatment, they were unaware of the specific grouping (i.e. matched vs unmatched vs EBP)

 

  1. Were clinicians and/or outcome assessors blinded to the subjects group assignment?

No and yes. Although the clinicians were not blinded, which is common in practice, the assessors of the outcome measures were blinded. The outcome measures were subjective measurements in order to minimize therapist bias.

 

  1. Did the investigators manage all of the groups in the same way except for the experimental investigation?

No. Because this is an intervention study in patient’s seeking treatment, it was impossible to withhold treatment to establish a true control group. The types of treatment for the opposite direction and EBP groups were vaguely described.

 

  1. Did the investigators apply the study protocol and collect follow-up data on all subjects over a time frame long enough for the outcomes of interest to occur?

No. There was a 12% dropout rate, which was anticipated by the authors when determining the number of patients needed to maintain a power of .90. Thirty-eight patients withdrew from the study, as opposed to dropped out, due to no improvement or worsening of symptoms in the EBP and unmatched group. Two weeks was long enough in order to assess change.

 

  1. Did subject attrition occur over the course of the study?

Yes. Twenty-nine subjects dropped out of the study, with 12 of the 29 dropping out due to no change or worsening of symptoms. Although these participants did not “drop out”, indicating that follow-up information was unattainable, 36 subjects withdrew early due to no change or worsening of symptoms. No subjects from the matched group withdrew. Those that withdrew completed the outcome measures prior to 2 weeks in order to seek alternative care.