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Kieran Macphail's Blog | Understanding spinal pain 01/03/13 16:13
Kieran Macphail's Blog

Understanding spinal pain
Low Back Pain, Modic Changes and Bacterial Infections

Posted on February 23, 2013
Modic changes are edema in the vertebral body, which can only be detected on magnetic resonance imaging
(MRI) and are closely associated with low back pain. There is growing evidence their formation may be related
to bacterial infection. Herniated discs may be susceptible to bacterial infection and these infections may cause
Modic changes. In patients with Modic changes antibiotic treatment appears to reduce symptom severity,
although alternative methods of treatment could be considered.
In alternative medicine fungal infections have been linked with everything from allergies to arthritis (Kauffman
2000). In addition, Kauffman as well as others link chronic pain to fungal infections although there is no clear
mechanism described. Albert et al (2008) published a hypothesis linking Modic changes to either mechanical
causes or bacterial infection.
A mechanical cause: Degeneration of the disc causes loss of soft nuclear material, reduced disc height and
hydrostatic pressure, which increases the shear forces on the endplates and micro fractures may occur. The
observed Modic change could represent oedema secondary to the fracture and subsequent inflammation, or a
result of an inflammatory process from a toxic stimulus from the nucleus pulposus that seeps through the
fractures.
A bacterial cause: Following a tear in the outer fibres of the annulus e.g. disc herniation, new capilarisation and
inflammation develop around the extruded nuclear material. Through this tissue it is possible for anaerobic
bacteria to enter the anaerobic disc and in this environment cause a slowly developing low virulent infection.
The Modic change could be the visible signs of the inflammation and oedema surrounding this infection,
because the anaerobic bacteria cannot thrive in the highly aerobic environment of the Modic change type 1
(Albert et al 2008).
There is empirical evidence to support this view. Sterling et al (2001) found that nucleus pulposus material
removed during surgery from herniated contained the bacteria Proprionibacterium acnes and Cornybacterium
propinquum in 53% of cases. Similarly Corsia et al (2003) found that 71% of the 30 herniated discs they studied
from different subjects had a bacterial infection. In the cervical spine they found 59% of herniated discs were
infected with Staphylococcus being more prominent than proprionibacterium in their study. A follow up study
by Sterling and Jiggins (2002) found the nucleus pulposus was infected in 31% of subjects with lumbar disc
herniation and 0% in subjects with other spinal disorders such as tumor, scoliosis and fracture. This lends
further support to Albert et al’s (2008) hypothesis.
To date no work has shown these bacterial infections cause Modic changes but treatment with antibiotics has
been shown to improve function and decrease pain in patients with Modic changes. Albert et al (2013) found
100 days of Bioclavid, an Amoxicillin based antiobiotic produced improved low back pain, leg pain and function
compared with placebo. Interestingly the results continued to improve after the course of antibiotics at 6-month
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and 1 year follow up. Antibiotics can have an anti-inflammatory effect in their own right. However, Albert et al
used Bioclavid as it has one of the weakest anti-inflammatory effects. Furthermore, anti-inflammatory
medications usually don’t produce a lasting, let a lone improving effect and as such this mechanism of action
seems unlikely.
Tentatively it’s possible to hypothesise this continued improvement may be due to repair of Modic changes. This
however, is highly speculative. Due to the nature of the study we do not know what percentage of patients had
infected discs, if the antibiotics eliminated the bacteria if present, and whether there was any alteration in
Modic changes at 1-year follow up. Nonetheless, this is highly thought provoking work.
So how do we implement these findings? Certainly we need to consider a potential bacterial cause in our
patients with Modic changes. However, assessing a possible infection is difficult and impractical. At this point it
is hard to know if there are any symptoms associated with these bacterial infections that could help with
diagnosis.
Given the results of Albert et al (2013) in stubborn cases of low back pain with Modic changes that do not
respond to mechanical treatment, bacterial based treatment may be considered. In the first instance anti-
bacterial agents such as Uva Ursi or Berberine could be utilised in concert with a diet containing the phenols in
nuts, seeds, vegetables and some herbs, as well as garlic and ginger. In addition, probiotics and prebiotics could
be added to hypothetically promote competition with the potential unwanted bacteria. After a trial period of 3
months if no progress is made antibiotic treatment would be the logical step.
In patients with Modic changes bacterial infection of herniated intervertebral discs should be considered.
Antibiotic treatment has been found to reduce back and leg pain, and improve function in patients with Modic
changes with low back pain. Thus in patients with Modic changes on MRI not responding to a mechanical
approach antibacterial nutritional therapy could be considered.
References
Albert, H.B. Kjaer, P. Jensen, T.S. Sorensen, J.S. Bendix, T. Manniche, C. 2008. Modic changes, possible causes
and relation to low back pain. Med Hypotheses 70, 361–368.
Albert, H.B. Sorensen, J.S. Christensen, B.S. Manniche, C. 2013. Antibiotic treatment in patients with chronic
low back pain and vertebral bone edema (Modic type 1 changes): a double-blind randomized clinical controlled
trial of efficacy. European Spine Journal, Epub ahead of print.
Corsia, M.F. Wack, M. Denys, G. 2003. Low vitulence Bacterial infections of intervertebral discs and the
resultant spinal disease processes. Abstract from Scoliosis Research Society (SRS) annual meeting.
Kauffman, D., 2000. The Fungus Link. MediaTrition: Texas.
Stirling, A. Worthington, T. Rafiq, M. et al 2001. Association between sciatica and Propionebacterium acnes.
Lancet, 357: 2024–2025.
Stirling, A.J. Jiggins, M. 2002. Association between sciatica and skin commensals. International Society for the
Study of the Lumbar Spine, Cleveland.
Posted in Corrective Holistic Exercise Kinesiology, For Diet and Lifestyle Professionals, For Everyone!, For Health Professionals, For Movement Therapists, Low back pain |
Tagged bacteria, low back pain, modic changes, proprionibacterium acnes | Leave a comment
Assess, Treat, Re-assess: Applying The Clinical Audit Process

Intro
The clinical audit process is the process of applying a test or multiple tests with a patient. Then applying an
intervention or combination of interventions and then re-assessing the original test or tests. This process can be
conducted over a period of minutes or months.
It is an incredibly useful methodology giving you feedback on the effect of your treatment. Further, if a patient
centred test is used the patient indicates the success of the intervention himself or herself and thus there is
“buy-in”.
Case Study
A clinical example is shown below. The case history is edited to only the key points for brevity.
The patient attended complaining of an increase in pain to 6/10 on a verbal rating scale over the left sacro-iliac
joint with occasional radiation of pain in to the anterior of the left thigh. The symptoms were aggravated with
walking and getting in and out of a car. She did not report any positions of ease.
The key assessment finding was a difficulty of 4/5 in active straight leg raise (ASLR) on left and 3/5 on right as
described by Mens et al (Get reference). With pressure to approximate the anterior superior iliac spines
difficulty reduced to 4/5 and 3/5 respectively. Pressure to approximate the pelvis at the level of the greater
trochanter had the same effect. However, pressure applied to approximate the posterior superior iliac spines
(PSIS) reduced difficulty to 2/5 and 1/5 respectively. This test was used for the clinical audit process as it was
deemed the most fundamental, prominent and functional (Liebenson 2013).
As pressure to approximate the PSIS’s was most helpfully the multifidus were targeted for neuromuscular
stimulation. To do this the patient was coached through doing the horse stance vertical exercise shown in figure
1.
Figure 1. Horse Stance Vertical
Kneel
down
on all
fours.
Keep
the
knees
under
the
Set up for horse stance vertical Horse stance vertical with dowel rod
hips
and the
wrists
under the shoulders.
Keep the chin tucked and the elbows pointing backwards

and slightly bent.
Keep the dowel rod straight along the spine and if possible
parallel to the ground. (This should touch the base of the
skull, the mid thoracic spine and the sacral base.)
Opposite hand and knee removed to engage multifidus

Engage your inner unit by breathing in diaphagmatically
and then pushing your diaphragm down without allowing
your abdomen to expand.
Then slowly unload one hand / knee just enough to slide a piece of paper underneath – keeping the dowel rod
still.
Hold this position keeping everything else static and then lower and repeat.
Aim to be able to lift one hand and the opposite knee at the same time, without shifting any other part of the
body.
This exercise uses rotational loading of the spine to cause a subconscious contraction of the multifidus as well as
other key spinal stabilisers.
Following four repeitions on each side of 10 second hold with 5 seconds test the ASLR was retested. After just
this set the difficult was reduced to 3/5 on the left and 2/5 on the right.
After two further sets of four repetitions on each side the difficulty reduced to 2/5 on the left and 1/5 on the
right.
As the patient had also had reduced difficulty on initial ASLR with ASIS and greater trochanter approximation
the wall deadbug exercise was used to stimulate the pelvic floor and transversus abdominis as shown in figure 2.
Figure 2. Wall Deadbug
Start with your head 2cm’s from the wall.
Your palms should be flat on the wall, the elbows facing up.
The knees, hips and ankles should be flexed to 90 degrees and the thighs slightly external rotated.
Engage your inner unit by breathing in diaphagmatically and then pushing your
diaphragm down without allowing your abdomen to expand. This will engage the transverse abdominis, pelvic
floor and
diaphragm.
From here
you should
push off the
wall to move
your head a
further 3-
5cm’s away
Set up for the wall the deadbug Lower alternate legs to the ground whilst maintaining a neutral spine from the
wall. This is
to engage
the latissimus dorsi.
Then lower alternate heel to the ground whilst maintaining the angle at your knee and ankle as well as the
pressure against the wall.
Throughout your neck and lumbar spine should be in a neutral position.
Following 6 repetitions of wall deadbug on each leg at a 3-0-3 tempo the ASLR difficulty was reduced to 1/5 on
the left and 0/5 on the right.
A further set each of horse stance and wall deadbug reduced the difficulty to 0.5/5 on the left. Further, at this
point the verbal rating scale was reduced to a 1/10. Most importantly the patient felt much stronger when
walking and was highly motivated to do her exercise programme.
Discussion
Several factors need to be born in mind with this approach.
Firstly it is highly flexible. You could use an orthopaedic medicine assessment, a resisted muscle test for
example. You could use a functional assessment such as an overhead squat. It works equally well with the
movement-based assessments of Sahrmann (2002) and probably with whichever system you use.
Similarly you can use a variety of treatment approaches. For example in this case I could have used reflex
stimulation, GUNN needling to facilitate the local stabilisers of the sacro-iliac joint, joint manipulation or
mobilisation and maybe even energetic or cognitive approaches.
I can also imagine that some therapists might suggest that the response is due to placebo or even credebo as
discussed elsewhere on this site. However, I suspect the majority of the treatment effect can be explained by
cortical reorganisation. (Tsao et al 2008).
Obviously some treatments will not have an instant effect. In some case we may be waiting weeks for a muscle to
hypertrophy in response to a prolonged period of training. In others we may wait over a month for the effects of
nutritional therapy protocol targeted at specific inflammatory pathways to take effect.
Nonetheless for the majority of manual and corrective exercise approaches the clinical audit process
demonstrates the immediate effect these interventions can have.
Conclusion
The clinical audit process allows therapist and patient to get potentially instant feedback on the effect of an
intervention. This can be invaluable in directing treatment and encouraging the patient to do their exercise
programme. The exact mechanism is uncertain but cortical re-organisation appears most likely.
If you have any questions or ideas please comment below or feel free to email me
at kieran@kieranmacphail.com. Skype appointments are available for people interested in consulting with me
but unable to make it the UK to see me in person.
References
Liebenson, C. 2013. Bridging the gap. One day course. Bowskill Clinic: London.
Mens, J.M.A. Vleeming, A. Snijders, C.J. Stam, H.J. Ginai, A.Z. 1999. The active straight leg raise test and
mobility of the pelvic joints. European spine journal, 8 (6), 468-473.
Sahrmann, S.A. 2002. Diagnosis and treatment of movement impairment syndromes. Mosby: St. Louis.
Tsao, H. Galea, M.P. and Hodges, P.W. 2008. Reorganization of the motor cortex is associated with postural
control deficits in recurrent low back pain. Brain, 131, 2161-2171.
Posted in Corrective Holistic Exercise Kinesiology, For Health Professionals, For Movement Therapists, Orthopaedic Medicine, Sacro-iliac joint | Tagged active straight leg
raise, clinical audit process, horse stance, horse stance vertical, Sacro-iliac joint, sij, wall deadbug | Leave a comment
The Complexities of Movement Specific Diagnosis in the Spine

Shirley Sahrmann’s (2002) movement diagnosis approach is undoubtedly one of the most clinically useful I
have studied. She states that the patient’s directional susceptibility to movement or the path of least resistance
is the direction the patient is most likely to get injured in. For example a patient with an increased lumbar curve,
or extension dysfunction is more likely to get inflammation in the lumbar spine facet joints than a patient with
a reduced lumbar curve who is more likely to suffer intervertebral disc related pathology.
In practical application there are more idiosyncrasies to the application of this approach. The “typical” middle-
aged sedentary desk-working male with protrusion and degeneration of the L4/5 intervertebral disc has on the
surface of an initial assessment a flexion dysfunction. He stands with 20˚ of lumbar curve, where 35˚ is normal.
His anterior pelvic tilt is 4˚ bilaterally, where between 4-7˚ is ideal. He has lumbar flexion of 50˚, where 40-60˚
is ideal and only 10˚ in extension, where 20˚ or more is ideal. In the bend pattern he prematurely flexes his
lumbar spine and length tension assessment shows tight hamstrings and gluteals.
On the surface this patient clearly has a flexion dysfunction. However, he gets pain during walking and on the x-
trainer, extension based movements. Furthermore, he gets relief when seated, a flexed position which should
give relief. So what is reason? Why does the assessment not match the patients symptoms?
In this case I believe the patient has an extension dysfunction at the L4/5 motion segment. The chronic flexion
dysfunction leads to a gradual loss of height in the L4/5 intervertebral disc in the asymptomatic stage. Over time
this loss of disc height leads the facets to become approximated, reduces the size of the intervetbral foramen and
reduces the pain free available range in to extension. Meaning physiologic movements are now painful. Further
loss of disc height only exacerbates the problem. Thus the patient has a lumbar spine flexion dysfunction, with a
primary problem of L4/5 extension dysfunction.
Sahrmann’s principles still ring true. This patient has a primary extension dysfunction and they need flexion.
They key is to apply it segmentally. Manually this can be done in side lying. The superior spinous process can be
blocked with one hand and the lower spinous process gapped by gripping with the index finger of lower hand
and taking the patient’s pelvis in to posterior pelvic tilt. This gives us the best chance of isolating the treatment
to the symptomatic level. However, the evidence to date would suggest we are not targeting our treatment as
specifically to the level or depth we think we are.
In this situation Guy Voyer’s, ELDOA or in English LOADS, decompressive exercises at end range can be
especially valuable. These are exercises he developed and checked using x-rays to isolate a gapping movement to
a particular joint. The L4/5 ELDOA is shown below. Voyer reports he has seen the application of these exercises
lead to fibrosing of the intervertebral disc over time. Thus creating a larger discs helping to increase the space
between facets and the size of the intervertebral foramen.
These treatments need to be viewed within the context of the hierarchy of survival reflexes (See article on this
blog). Further it should be utilised in concert with treatment for the inner unit of the lumbar spine, concomitant
dysfunction of the hips and pelvis in particular. Methods directed at the neurological system its self can also be
useful such as GUNN needling, although the exact mechanism for the benefit of such an approach remains to be
ascertained.
Currently fusions are often applied for dysfunctions such as this but such surgeries are known to lead to
increased likelihood of disc pathology in adjacent segments in the following year (Goffin et al 2004). As a result
fusions are last resort procedures. Disc replacements are an exciting development. It may be that as surgical
techniques and disc replacement improve, potentially utilising stem cell technology disc replacements may offer
an excellent back up for those that fail to respond to the approach outlined above.
If you have any questions or ideas please comment below or feel free to email at kieran@kieranmacphail.com.
Skype appointments are available for people interested in consulting with me but unable to make it the UK to
see me in person.
References
Goffin, J. Geusens, E. Vantomme, N. Quintens, E. Waerzeggers, Y. Depreitere, B. and van Loon, J. 2004. Long-
term follow-up after interbody fusion of the cervical spine. Journal of spinal disorders and techniques, 17 (2),
79-85.
Sahrmann, S.A. 2002. Diagnosis and treatment of movement impairment syndromes. Mosby: St. Louis.
Posted in For Health Professionals, For Movement Therapists, Low back pain | Tagged directional susceptibility to movement, disc degeneration, extension dysfunction,
Flexion dysfunction, L4/5, Sahrmann, Sahrmann (2002), Shirley Sahrmann | Leave a comment
Calcium Dumping Syndrome

Calcium dumping syndrome is a traditional naturopathic concept and not recognised medically (Plaskett 2008).
In naturopathy the condition is linked with arthritis, spondylitis, gallstones, renal stones and arterial atheroma.
Naturopaths state that as a result of calcium dumping syndrome the symptoms of calcium deficiency can occur
in the presence of ample dietary calcium. The result is that calcium is excreted from bone and either excreted or
deposited in tissues throughout the body. Dietary calcium deficiency is very rare in the western countries. In
India there is far less osteoporosis despite the average calcium consumption being as low as 400mg/ day
compared with the UK average which some studies put close to 1200mg/ day. Thus clearly others factors are
involved. Naturopathic theories are shown in the table below.
No Factors affecting bone Probable reasons for effect
1 Excessive milk consumption Adverse effect on sodium and

potassium
2 Excessive animal protein consumption Adverse effect on sodium and

potassium
3 Excessive phosphorus diets Stimulates parathyroid secretion
4 Excessive parathyroid hormone Direct stimulus to bone re-absorption

secretion
5 Magnesium deficiency Slowing of cell respiration and

production of ATP: slowing of sodium
pump.
6 Zinc deficiency Slowing of cell respiration and

production of ATP: slowing of sodium
pump
7 Aluminium toxicity Stimulates parathyroid secretion
8 Lack of boron
9 Lack of vitamin D Prevents calcium absorption
10 High alcohol intake Depression of cell respiration and de-

mineralisation effects
11 Lack of exercise
12 Acidification of body fluids from acid Re-dissolves deposited calcium

forming diet (Dependant on genetics and
environmental factors)
13 Chronic heavy metal exposure Depression of cell respiration
14 Coffee, tea, cocoa and red wine Various; stimulant, diuretic, anti-
vitamin and sodium pump inhibition
15 Excessive sodium intake Adverse effect on sodium/ potassium

balance
16 Vitamin C deficiency Slows detoxification and exposes the

cells to free radical attack
17 Liver or kidney under-function Inhibits whole body detoxification
The result is negative calcium balance, the state when the individual looses more calcium each day than they
take in.
References
Plaskett, L. 2008. Calcium. Plaskett Nutritional Medicine College. Folder 2, Section C
Posted in For Diet and Lifestyle Professionals, For Everyone!, For Health Professionals | Tagged calcium dumping syndrome, negative calcium balance | Leave a comment
9 Key Principles I Learned From Guy Voyer

Posted on January 18, 2013
Firstly let me state that Guy is not big on principles. In fact, when I asked him for key principles to help
understand his approach, he asked if I knew who Descartes was and suggested I was too Cartesian. He did not
know how write he was, as I start every review I do by writing down Descartes’ four precepts!
Despite Guy’s abhorrence of principles I will lay down some of the key principles I draw from studying his work
so far.
1. To work a muscle or specific part of the muscle put it under tension.
E.g. to work the pectineus take the hip from abduction in to adduction.
2. To length a muscle strengthen it in outer range. To shorten a muscle, strengthen it in inner range.
E.g. For the rhomboid major, in prone start with the shoulder in flexion and approx 160 degrees abduction.
From here take the shoulder in to full flexion and work the muscle in inner range.
3. Typically mobile joints often require coaptation. Typically stable joints require decoaptation.
E.g. Strengthen a typically unstable shoulder in inner range and a typical osteoarthritic hip in outer range.
4. In scoliosis strengthen both sides at the same intensity to even out the scoliosis over time.
E.g. Do unilateral rhomboid major and quadratus lumborum strengthening equally on both sides to the same
intensity.
5. To work a muscle more distally, fix it proximally. To work a muscle proximally, fix it distally.
E.g. Triceps push down = distal, triceps dips = proximal
6. Alternatively, to work a muscle distally increase the lever arm. To work the muscle proximally decrease the
lever arm.
E.g. for the tricep work with elbow extension from a vertical position of the humerus as opposed to elbow
extension from a horizontal humerus.
7. To work a muscle more superficially put the fascia under tension. To work a muscle deeper relieve the tension
on the fascia.
E.g. Shoulder abduction with wrist flexion = superficial. Wrist extension = deep
8. To increase the stability of a joint by shortening and strengthening muscles start by working on the muscles
closest to the joint.
E.g. Rotator cuff first in the shoulder
9. To increase the stability of a joint by increasing ligament proprioception start on the most superficial
ligaments of the joint.
E.g. Medial and lateral collateral ligaments of the knee before the anterior and posterior cruciate ligaments.
As always if you have any questions around these topics feel free to email me on kieran@kieranmacphail.com
www.kieranmacphail.com
https://www.facebook.com/physiotherapylondonkieranmacphail
Posted in Uncategorized | Tagged Guy Voyer | Leave a comment
Weight Loss and Insomnia Case Study

Posted on December 8, 2012
Patient X
Female
Age 59
Height 1.60 m
Weight 78 kg
Married with 2 sons aged 28 & 26. Another son died suddenly of complications due to cystic fibrosis 2 years ago,
aged 21. The 26 year old son has cystic fibrosis and lives at home.
Job: psychotherapist for victims of abuse
Main goals: to reduce weight and insomnia
Weight: problems since teens, has yoyo dieted throughout life. Family has weight problems. Stocky strong build,
with quite good muscle tone on arms and legs. Carries excess weight around middle.
Lost a lot of weight after death of son 2 years ago, but then gradually gained weight and is still gaining despite
trying to control intake.
Very active, gardening, decorating, housework, also does step exercises on stairs at home.
Insomnia: has never needed much sleep and does not fret when awake at night, uses the time to study, catch up
with paper work etc. Is always on the go. The problem became worse while caring for her sons with cystic
fibrosis. Resistant to sleeping tablets/herbal remedies.
Current Symptoms
Digestion: Generally regular bowel movements x 1 per day, a.m., good consistency and colour, but may become
constipated if away from home and out of normal eating pattern. Mild bloating & belching and sometimes
suffers from moderate heartburn. Has been diagnosed with Hiatus hernia.
Energy and Emotions: Fluctuates between fatigue and hyperactivity. Feels very tired midafternoon and has
recently suffered from bouts of extreme fatigue.
Recently noticed problems with concentration, and bouts of mild dizziness.
Often feels restless, anxious, stressed and sometimes depressed.
Sleeps for just 3-4 hours per night. Often goes to bed after midnight, has problems falling asleep and wakes a
few hours later.
Joints/ muscles: Has mild arthritis in one knee and has been recently diagnosed with Carpal Tunnel Syndrome
Skin: Suffers from dry, itchy skin, itchy ears
Other symptoms include a blocked nose and frequent clearing of throat
Appearance: tense, fidgety; eyebrows thin with outer third missing. Dry skin, pallor
Medical history
Usual childhood illnesses
Suffered from fibroids throughout adult life and is now post menopause.
Problems with sinuses throughout life; several operations on sinuses. This has improved, but not cured sinus
problems.
Diet
Eats fairly regularly, but has a long gap (6 hours) from lunch till dinner, when she is seeing patients. Sips cold
black coffee (3 large mugs perday) throughout the day to keep going, particularly during afternoon.
Several portions of fruit and vegetables per day. Likes salad and raw broccoli
Tries to avoid sweet foods, but admits to eating some when depressed due to comfort eating. Likes icecream and
chocolate.
Eats moderate portions of carbohydrates with each meal, but these tend to be refined e.g. white rice, white
bread, special K breakfast cereal.
Eats fish including oily fish x 1-2 per week. Red meat x 1 per week. Diet regularly includes processed meats, hard
cheeses and moderate amounts of dairy foods.
Calorie intake is not excessive, considering height , weight and activity levels
Drinks a reasonable amount of water (x 3-4 glasses per day). Drinks occasional wine socially with food.
Has good knowledge of calories and some knowledge about nutrition. Does not take any nutritional or other
supplements/ remedies.
Personality & background
Polish Jew, family are holocaust survivors. A very intelligent, stoical, compassionate person. Puts others needs
before her own. Very driven, always gaining more qualifications in her area, and does everything at home for
family as well as working nearly full time.
Current stress levels rated at 8/10 due to concern about son’s health and work stress. Does not relax easily or
carry out any activities to relax at present.
Current Medical Diagnosis and Medication
Mild hiatus hernia, takes antacids (Rennies) x 3-4 a month if symptoms are severe.
Arthritis in right knee
Carpal tunnel syndrome, is booked in for an operation.
Takes occasional paracetamol/ibuprofen for pain in knee and hand, but generally avoids medication.
Family Medical History
Cardio-vascular disease and cancer
The case history highlights symptoms across multiple systems. The inter-relationship between the client’s diet
and lifestyle, physiological imbalances, symptoms and potential future conditions related to her current status is
illustrated in the mind map in appendix 1. These symptoms need to be interpreted and linked to possible
imbalances driving them and the potential causes for these imbalances. Once the imbalances analysed priorities
for treatment can be drawn up and then a management plan.
In clients struggling to loose weight thyroid dysfunction is frequent concern. In the case history there are
symptoms and potential causes of thyroid dysfunction. The client’s fatigue, increased weight, dry skin and
depression are all symptoms of hypothyroidism (Ladenson et al 2010). Further the itchy skin and ears, thinning
of the eyebrows and carpal tunnel syndrome are all possible symptoms of myxedema, resulting from untreated
hypothyroidism (Mansourian 2010). Additionally the insomnia may be related to myxedema (Mansourian
2010). However, typically myxedema causes a lack of desire for sleep and the importance of desire for sleep in
the client’s insomnia remains to be ascertained. The inability to clear the throat can be a symptom of
compression as a result of benign and malignant thyroid disease (Banks et al 2012). Typically other symptoms
would coexist but the possibility of compression needs to be considered. The client will likely have had elevated
cortisol levels from their diet (Hutchinson 2002, Corti et al 2002) and her work and life stressors (Sapolsky et al
1986) which are known to inhibit thyroid function (Duick and Wahner 1979). Interestingly the case history
mentions the unusual habbit of consuming raw broccoli. Broccoli is a known goitrogen (Latte et al 2011) and
will be more potent when consumed raw.
The case history shows multiple symptoms of adrenal dysfunction, which may be driven by stress of different
types. Of the patient’s symptoms fluctuating between fatigue and hyperactivity (Wilson 2006), fatigue,
decreased concentration, needing stimulants in the afternoon, depression, anxiousness (Anderson 2008),
visceral fat (Whitworth 2005) and insomnia (Head and Kelly 2009) have all been linked with adrenal
dysfunction. Indeed the symptoms of hypothyroidism may be caused by an inadequate stress response caused
by adrenal insufficiency (Chrosous and Gold 1992). This may result from an elevated cortisol level directly
inhibiting thyroid function in the alarm phase (Duick and Wahner 1979). It is the stress response that appears
to be a key driver of the patient’s possible adrenal dysfunction symptoms. Stress is summated in the body
(Sapolsky et al 1986). In this case the patients mental emotional stress and dietary habits may both have caused
chronic stimulation of the hypothalamic-pituitary adrenal axis. The blood sugar imbalances from regular coffee
consumption and yoyo dieting (Hutchinson 2002) will have elevated cortisol levels (Corti et al 2002). Further
her work stress, life stresses and lifestyle driven by her personality type will have elevated her cortisol levels.
Over time the chronic elevation of cortisol levels causes desensitisation and damage to hippocampus receptors,
which leads to feed forward over-production of cortisol (Sapolsky et al 1986). It is unknown if this damage is
permanent. The symptom profile suggests the patient has passed through the alarm reaction and resistance
phase and is entering the exhaustion phase (Selye 1978).
Insulin resistance can be at least partly caused by elevated cortisol (Walker 2006, Wang 2005). The clearest
indications of insulin resistance in this client are fluctuating from hyperactivity to fatigue, increased visceral
body fat (Whitworth et al 2005), decreased concentration, the need for coffee in the afternoon and her increased
body fat (Kelly 2000). The clients coffee consumption (Hutchinson 2011), yo-yo dieting (Corti et al 2002), high
carbohydrate diet and consumption of high glycaemic foods (Kelly 2000) could have contributed towards
insulin resistance. Similarly, the psychogenic stress from her work and life stressors may have caused further
short-term blood sugar spikes (Kelly 2000). Interestingly blood insulin resistance has been linked with
hypercortisolism (Fossati and Fontaine 1993) and leptin resistance (Kelly 2000). Thus further illustrating the
interlinking of her symptoms.
There are also multiple signs of other biochemical imbalances. The history of yo-yo dieting may be linked with
low serotonin levels (Jimerson et al 1992). Additionally depression is well known to be associated with low
serotonin levels (Karg et al 2011). Her stress levels may have caused this as cortisol has an inverse relationship
with serotonin levels (Field et al 2005). Elevated cortisol may also have caused the gastrointestinal symptoms
(Stengel and Taché 2010) and food intolerance symptoms (Zopf et al 2009). However, the association between
stress and gastrointestinal symptoms is complex as gastric symptoms are related to the formation of a proximal
acid pocket in the postprandial period (Rohof et al 2012). The reduced gastric activity due to hypothalamic-
pituitary adrenal axis stimulation may facilitate this process but there is a paucity of work discussing the
minutia. Struggling to clear the throat and sinus problems are linked with excessive mucus formation possibly
as a result of food intolerances (Hodge et al 2009). These symptoms may be more completely viewed as part of
the adrenal dysfunction picture. The prolonged stress results in an increased immune response in the resistance
stage (Selye 1978), which has been linked with the onset of food intolerances (Gabby 1998). The metabolic
effects of stress are associated with oestrogen dominance (McKern 2009), which may be at the root of her
previous fibroids (Davis 2009). In addition the clients age and the fact they are post menopause increase the
likelihood oestrogen dominance.
The case history shows symptoms linking back to thyroid dysfunction, adrenal dysfunction and insulin
resistance most prominently. In addition there are weaker signs of low serotonin levels, food intolerance and a
low stomach pH. There appears to be a common cause to all the patient’s imbalances of prolonged exposure to
both psychogenic and dietary stress. Using Selye’s general adaptation syndrome the client looks to have
progressed to the exhaustion phase.
References
Andreson, D.C. (2008) Assessment and nutraceutical management of stress-induced adrenal dysfunction.
Integrative medicine, 7 (5), p.18-25.
Banks, C.A. Ayers, C.M. Hornig, J.D. Lentsch, E.J. Day, T.A. Nguyen, S.A. and Gillespie, M.B. (2012) Thyroid
disease and compressive symptoms. The Laryngoscope, 22 (1), p.13-16.
Chrosous, G.P. and Gold, P.W. (1992) The concepts of stress and stress system disorders: Overview of physical
and behavioral homeostasis. Journal of the American Medical Association, 257 (9), p.1244-1252.
Corti, R. Binggeli, C. Sudano, I. Spieker, L. Hänseler, E. Ruschitzka, F. Chaplin, W.F, Lüscher, T.F. and Noll, G.
(2002) Coffee acutely increases sympathetic nerve activity and blood pressure independently of caffeine.
Circulation, 106, p.2935-2940.
Davis, C.J. (2009) The surgical management of polycystic ovarian syndrome. Diagnosis and management of
polycystic ovary syndrome, 4, p.259-263.
Duick, D.S. and Wahner, H.W. (1979) Thyroid axis in patients with Cushing’s syndrome. Archives of internal
medicine, 139 (7), p.767-772.
Field, T. Hernandez-Reif, M. Diego, M. Schanberg, S. and Kuhn, C. (2005) Cortisol decreases and serotonin and
dopamine increase following massage therapy. International journal of neuroscience, 115 (10), p.1397-413.
Fossati, P. and Fontaine, P. (1993) Endocrine and metabolic consequences of massive obesity. Revue du
praticien, 43, p.1935-1939.
Gaby, A.R. (1998) The role of hidden food allergy/intolerance in chronic disease.
Alternative medicine review, 3 (2), p.90-100.
Head, K.A. and Kelly, G.S. (2009) Nutrients and botanicals for treatment of stress: Adrenal fatigue,
neurotransmitter imbalance, anxiety, and restless sleep. Alternative medicine review, 14 (2), p.114-140.
Hutchinson, E. (2011) Systems neuroscience: The stress of dieting. Nature Reviews Neuroscience, 12, p.65.
Jimerson, D.C. Lesem, M.D. Kaye, W.H. and Brewerton, T.D. (1992) Low serotonin and dopamine metabolite
concentrations in cerebrospinal fluid from bulimic patients with frequent binge episodes. Archives of general
psychiatry, 49 (2), p.132-8.
Karg, K. Burmeister, M. Shedden, K. and Sen, S. (2011) The serotonin transporter promoter variant (5-
HTTLPR), stress, and depression meta-analysis revisited evidence of genetic moderation. Archive of general
psychiatry, 68 (5), 444-454.
Kelly, G.S. (2000) Insulin resistance: Lifestyle and nutritional interventions. Alternative medicine review, 5 (2),
p.109-32.
Ladenson, P.W. Singer, P.A. Ain, K.B. Bagchi, N. Bigos, S.T. Levy, E.G. Smith, S.A. Daniels, G.H. and Cohen,
H.D. (2000) American Thyroid Association guidelines for detection of thyroid dysfunction. Archives of internal
medicine, 12, 160 (11), p.1573-5.
Latté, K.P. Appel, K.E. and Lampen, A. (2011) Health benefits and possible risks of broccoli – An overview. Food
and chemical toxicology, 49 (12), p.3287-3309.
Mansourian, A.R. (2010) A review on post puberty hypothyroidism: A glance at myxedema. Pakistan journal of
biological sciences, 13 (8), p.866-878.
McKern, J. (2009) Hormone balancing.Journal of complementary medicine, 8 (1), p.12-18.
Rohof, W.O. Bennink, R.J. de Ruigh, A.A. Hirsch, D.P. Zwinderman, A.H. and Boeckxstaens, GE. (2012) Effect
of azithromycin on acid reflux, hiatus hernia and proximal acid pocket in the postprandial period. Gut. [Epub
ahead of print]. Available from; [Accessed 11th May 2012].
Sapolsky, R.M. Kry, L.C. and McEwen, B.S. (1986) The neuroendocrinology of stress and aging: The
glucocorticoid cascade hypothesis. Endocrine review, 7 (3), p.284-301.
Selye H. (1978) The stress of life. 2nd ed. New York, NY: McGraw-Hill.
Stengel, A. and Taché, Y. (2010) Corticotropin-releasing factor signaling and visceral response to stress.
Experimental biology and medicine, 235 (10), p.1168-1178.
Walker, B.R. (2006) Cortisol – cause and cure for metabolic syndrome? Diabetic medicine, 23 (12), p.1281-
1288.
Wang, M. (2005) The role of glucocorticoid action in the pathophysiology of the metabolic syndrome. Nutrition
and metabolism, 2, 3.
Whitworth, J.A. Williamson, P.M. Mangos, G. and Kelly, J.J. (2005) Cardiovascular consequences of cortisol
excess. Vascular health and risk management, 1 (4), p.291-299.
Wilson, J.L. (2006) Adrenal fatigue: The 21st century stress syndrome. Petaluma, CA: Smart.
Zopf, Y. Hahn, E.G. Raithel, M. Baenkler, H.W. and Silbermann, A., 2009. The Differential Diagnosis of Food
Intolerance. Deutsches ärzteblatt international, 106 (21), p.359–370.
It is critical initially to clear the patient for potential red flags and any need for medical referral. This client
doesn’t report any of the Nutritional Therapy Council’s (NTC) red flag symptoms (NTC 2007). However, the
case history does show fatigue, increased weight, skin abnormalities, thinning of the eyebrows and carpal tunnel
syndrome all possible symptoms of myxedema, resulting from untreated hypothyroidism (Mansourian 2010).
Additionally the patient mentions feelings of depression. Kendrick and Peveler (2010) highlight the importance
of screening for depression. In particular their recommendations of a 2-week follow up for those patients with
active symptoms illustrate the urgency of the referral. The client also mentions symptoms of inability to clear
the throat, which can be a symptom of compression as a result of benign and malignant thyroid disease (Banks
et al 2012). Consequently, this client should be referred back to their GP, with the client’s consent, with a
referral letter highlighting the key symptoms they’ve reported, the therapist’s concerns and politely asking for
the GP’s input and guidance as shown in appendix 2. This paves the way for the clinician to follow up with the
client explaining that they would like them to return to their GP but there are some elements of the initial
assessment, which require clarification.
Further subjective information would inform the choice of potential functional assessments and aid the
formation of a management programme. Establishing the types of cancer her family members have experienced
may point the clinician towards potential bowel pathology or more oestrogen dominant cancers. Similarly, it
would be prudent to establish if the client received hormone replacement therapy during her menopause, which
could point towards oestrogen dominance. It would be interesting to know if the client was interested in
learning a relaxation technique due to the role psychogenic stress appears to play in their symptoms (Lee et al
2010) and the case history suggests she may not be competent in relaxing. Lastly further questioning on how
long she has had the insomnia and how it has progressed over time would be helpful. In particular asking when
she started to loose the desire for sleep and how this correlated with her symptoms. This would provide an
indication as to the involvement of myxedema contributing towards her symptom profile. Answers to these
questions would help narrow the focus of the management programme.
The late Broda Barnes (1942) was an advocate of using axillary basal body temperature as a diagnostic tool for
hypothyroidism. Unfortunately there is a dearth of peer-reviewed papers discussing the validity and application
of this approach. There is support from understanding the physiology of the thyroid gland and the association of
low triiodothyronine (T3) with low body temperature (Nogues et al 1995). Although it should be noted that
Nogues et al’s work had several flaws in its analysis and methodology highlighted by Mosse (1995). Nonetheless
the link between T3 and temperature was accurately assessed.
A difference of opinion exists on what tests are necessary to assess thyroid function. Volpe (1997) state that for
initial screening or clients where thyroid dysfunction is unlikely serum thyroid stimulating hormone (TSH)
assay is all that is required. TSH remains the most reliable indicator of thyroid dysfunction (Landerson et al
2010). However, it has been demonstrated that using TSH alone leads to under reporting hypopituitarism
(Wardle et al 2001). As the suspicion in this case is that the patient may have an underactive thyroid, serum
TSH and T4 should assessed (Schiefer and Fatourechi 2008). It seems logical to think there may be more
benefit from assessing free T4 levels as free hormones are presumed to be the only hormones that are
physiologically active (Midgley 1993). However, it’s known that free T4 (fT4) rises during the second and third
trimester of pregnancy without any known physiologic effect (Midgely 1993). This doesn’t mean there is no
effect but this is the currently accepted belief amongst endocrinologists. Despite this it’s necessary to measure
serum free thyroxine (T4) to assess for cases of secondary hypothyroidism (Ladenson et al 2010). After
receiving the referral it is likely based on the client’s symptoms profile their GP would assess the clients, TSH,
fT4 and fT3 levels (NHS 2012).
Deeper functional testing for potential subclinical hypothyroidism is also indicated. Subclinical hypothyroidism
is defined as an elevated serum TSH concentration in the presence of serum thyroid-hormone concentrations
within the population-based reference range (Feldt-Rasmussen 2009). Gaby (2004) highlighted that elevated
TSH levels may not be necessarily be essential for Hypothyroidism to be present. For example the level may be
elevated relative the individual norm. Reverse T3 needs to be assessed to check for peripheral conversion of T4
to active T3. Thyroid antibodies should also be screened to clear for potential autoimmune disease and to
potentially detect metabolic irregularities. Further clinical significance can be gleaned from testing by
comparing either 8 am TSH or 4 pm TSH with time-of-day normal range (Rose 2010). This can identify TSH
elevation. Low am/pm TSH ratio (FT4 in lowest one-third of normal) confirms central hypothyroidism.
Although this research was conducted in children and there’s a paucity of evidence investigating this
phenomenon in adults the similarity of the physiology is valid. However, this is not yet readily commercially
available. Consequently the comprehensive thyroid assessment offered by Genova diagnostics will provide
further insight for a justifiable cost to benefit.
The case history illustrates signs of hypothyroidism and possibly myxedema, which suggest a referral to her GP
is important despite the absence of red flags. The questions outlined will help provide further clues to her
imbalances further clarifying the appropriate way to proceed. On the information currently available the key
imbalance driving her symptoms may be coming from under-functioning of her thyroid. The basal body
temperature readings, GP testing and comprehensive thyroid assessment will then clarify how to proceed with
the patient’s programme.
References
Banks, C.A. Ayers, C.M. Hornig, J.D. Lentsch, E.J. Day, T.A. Nguyen, S.A. and Gillespie, M.B. (2012) Thyroid
disease and compressive symptoms. The laryngoscope, 22 (1), p.13-16.
Barnes, B. (1942) Basal temperature versus basal metabolism. Journal of the American medical association, 119
(14), p.1072-1074.
Feldt-Rasmussen, U. (2009) Is the treatment of subclinical hypothyroidism beneficial? Nature reviews

endocrinology, 5, p.86-87.
Kendrick, T. and Peveler, R. (2010) Guidelines for the management of depression: NICE work? The British
journal of psychiatry, 197, p.345-347.
Ladenson, P.W. Singer, P.A. Ain, K.B. Bagchi, N. Bigos, S.T. Levy, E.G. Smith, S.A. Daniels, G.H. and Cohen,
H.D. (2000) American Thyroid Association guidelines for detection of thyroid dysfunction. Archives of internal
medicine, 12, 160 (11), p.1573-5.
Lee, R.T. Lovell, B. and Brotheridge, C.M. (2010) Tenderness and steadiness: relating job and interpersonal
demands and resources with burnout and physical symptoms of stress in Canadian physicians. Journal of
applied social psychology, 40 (9), p.2319-2342 (24).
Mansourian, A.R. (2010) A review on post puberty hypothyroidism: A glance at myxedema. Pakistan journal of
biological sciences, 13 (8), p.866-878.
Massé J. (1995) Nutrition, thyroid hormones, body temperature, and mortality of elderly patients with acute
illnesses. American journal of clinical nutrition, 62 (3), p.647-9.
Midgley JE. (1993) The free thyroid hormone hypothesis and measurement of free hormones. Clinical
chemistry, 39 (6), p.1342-4.
NHS, (2012) Hypothyroidisim. [Online]. Available from;

http://www.patient.co.uk/doctor/Hypothyroidism.htm [Accessed 11 May 2012].
Nogues, R. Sitges-Serra, A. Sancho, J.J. Sanz, F. Monne, J. Girvent, M. Gubern, J.M. (1995) Influence of
nutrition, thyroid hormones, and rectal temperature on in-hospital mortality of elderly patients with acute
illness. American journal of clinical nutrition, 61 (3), p.597-602.
Nutritional Therapy Council, (2007) Core curriculum for training in nutritional therapy. [Online]. Available
from; http://www.nutritionaltherapycouncil.org.uk/trainers-1_3_3171181096.pdf [Accessed 11 May 2012].
Rose, S.R. (2010) Improved diagnosis of mild hypothyroidism using time-of-day normal ranges for thyrotropin.
Journal of pediatrics, 157 (4), p.662-7; 667.e1.
Schiefer, R. and Fatourechi, V. (2008) Laboratory Diagnosis of Thyroid Disease. Thyroid disorders with
cutaneous manifestations, p.23-36. Available from; http://www.springerlink.com/content/u757351472044227/
[Accessed 10 May 2012].
Volpé, R. (1997) Rational use of thyroid function tests. Critical reviews of clinical laboratory science, 4 (5),
p.405-38.
Wardle, C.A. Fraser, W.D. and Squire, C.R. (2001) Pitfalls in the use of thyrotropin concentration as a first-line
thyroid-function test. Lancet, 357 (9261), p.1013-4.
Posted in Uncategorized | Tagged Weight loss and Insomnia, Weight loss and Insomnia Case Study | Leave a comment
L4/5 Disc Protrusion Case Study

Posted on November 30, 2012
Introduction
This case report will outline the relevant subjective history and discuss the relevance of the objective
examination. Then the analysis behind the rationale for the clinical diagnosis is reviewed. This is followed by an
outline of the treatment plan and the discussion and evaluation that led to its formation. Why the objective
markers were chosen is discussed, followed by how the treatment progressed and an explanation of why
modifications were made. Lastly a reflection on the effectiveness of the treatment is given including the impact
of the orthopaedic medicine course on the treatment approach and improvements for the future are presented.
History (Subjective Examination)
The patient was a twenty seven year old female academic. She had a five-month history of back pain, which had
developed insidiously. Initially it was attributed to a reduced lumbar curve and she was treated with an epidural
steroid injection to L4/5. This resolved the pain. One week ago the pain returned at much more severe level at
10/10 on numerical rating scale (NRS). She underwent lumbar spine magnetic resonance imaging that showed a
disc protrusion at the L4/5 level. As a result she received another epidural corticosteroid injection at L4/5 level,
which helped to reduce the pain to a 6/10 on NRS. The pain also radiated laterally to the mid point of iliotibial
band. Prolonged sitting aggravates and lying down or walking help reduce the symptoms. Her symptoms were
worse as the day progressed. 400mg three times a day of Ibuprofen was controlling her pain. Her pain
disability questionnaire (PDQ) score was 42/100.
She spends the majority of the day seated in a fully flexed position usually but at initial assessment she stated
she could only sit pain free for five minutes before the pain came on. She goes to the gym three times a week
doing mainly cardiovascular exercise on the x-trainer and plays tennis once a week.
Examination (Objective Examination)
On observation there were no changes in facial expression or gait. She had a visually obvious layered syndrome
posture with a flat lumbar spine, increased thoracic kyphosis, and a forward head posture.
On inspection, postural assessment showed a lumbar lordosis of 17˚, where 30-35˚ is considered normal. There
were no obvious deviations in the coronal or transverse planes, colour changes, wasting or obvious swelling. At
rest she had 6/10 pain on NRS. She pointed to the region of L4/5.
On examination by selective tension in standing she had 35 degrees of active extension and no pain. On right
side flexion her pain was reproduced at 7/10, left side flexion was pain free. Side flexion range was full
bilaterally. However, active flexion was limited by pain of 8/10 at 40°. She described this as her pain. All
neurological tests were negative.
Posterior sacroiliac shear testing produced a minor pain on all three positions bilaterally. She did not feel this
was her pain, but she had experienced this before when sitting crosslegged and bent over from extended
periods. She scored the active straight leg raise (ASLR) test as a 2/5 on the right and 1/5 on the left. This was not
affected by compression at the anterior superior iliac spine level or level of the greater trochanter. However,
difficulty in lifting the leg was reduced to 0/5 with a supero-medial compression to the ilia at the level of the
posterior superior iliac spine. This suggested multifidus weakness.
On palpation her supraspinous ligaments at L4/5 and L5/S1 were tender as were her long dorsal sacroiliac
ligaments bilaterally. The iliolumbar, sacrospinous, sacrotuberous and Champenois’ band were negative. In
addition there was a lack of muscle bulk in the multifidus from the L4 level down. Multifidus activation was
decreased on the right compared to the left.
Analysis of her seated posture showed that she was sitting in an excessively flexed position, with a decreased
lumbar lordosis and an excessive thoracic kyphosis coupled with a significant forward head posture.
Clinical Diagnosis
There are no red flags and this appears an acute episode back pain. The assessment and history suggest
mechanical low back pain brought on through sitting for extended periods leading to creep in passive structures
(Panjabi 2006) and cumulative trauma to the passive structures of the spine (Tozzi 2012). The assessment
findings suggest her presentation fits with clinical model 1 as there was a gradual onset, pain is not below the
knee, the pain appeared to be precipitated by prolonged flexion, there were no neurological signs, there was
pain on side flexion to the painful side and a non capsular pattern (Kesson and Atkins 2005).
The pain on posterior sacroiliac sheer and on palpation of the long dorsal sacroiliac ligament suggest strain to
the long dorsal sacroiliac ligaments. Similarly, the pain at the L4/5 level on flexion fits with the MRI finding of
L4/5 level disc protrusion. These tissue lesions are most likely chronic. Hashemirad et al (2010) found that as
little as 7 minutes was sufficient to delay the flexor-relaxation phenomenon, which Panjabi (2006) discuss can
lead to a chronic response over time. The optimal response is a switch from active system support to passive
system support at 90% of full flexion or 45˚ of trunk flexion. Passive support involves contraction of abdominal
inner unit, transversus abdominis and internal oblique among others to place tension through the
thoracolumbar fascia. The thoracolumbar fascia applies an extension moment on the lumbar spine and the
whole posterior ligamentous system through its direct connections (Willard et al 2012). Once this response is
delayed greater erector spinae contraction remains for longer, the lumbar spine goes in to increased flexion and
there is greater load on the posterior of the annulus fibrosis of the intervertebral disc and posterior ligamentous
system may be under an increased load (Wallden 2010).
The weakness on ASLR that was alleviated with supero-medial compression of the ilia at the level of the PSIS
suggests weakness of the multifidus. From manual assessment and palpation, the right side appeared to swell
less than the left side, suggesting the right side was either atrophied or receiving less neural stimulation.
Treatment Plan
The aim of treatment for the patient to be able sit for up to six hours pain free within six weeks and reduce the
likelihood of future episodes. To achieve this the goals were to eliminate pain on flexion. The longer-term goal
was to increase the patient’s lumbar lordosis to 30-35 degrees, for the patient to have pain free ligament
provocation tests and 0/5 both sides for the ASLR.
To achieve this orthopaedic medicine treatment (Kesson and Atkins 2005) was used in the context of the
integrated model of joint function (Lee 2004). The integrated model of joint function builds on the seminal
hypothesis of Panjabi (1992). The model outlines the importance of four elements in joint stability, active,
passive, neural and cognitive. In this patient the aim was to optimise the passive structures through grade C
manipulation firstly. This was done with the hypothesis that successful manipulation does not alter joint
position but does reset mechanoreceptors. Optimising mechanoreceptor feedback may help normalise the
flexor-relaxation mechanism.
The technique used was the distraction technique described by Kesson and Atkins (2005). The couch was
lowered to near the bottom of its range to suit the 192cm tall therapist. The patient was positioned in left side
lying with the painful right side, facing up. The upper hip and knee were flexed with the knee resting just off the
bed and the lower leg extended. The underneath shoulder was then gently pulled forward so that the uppermost
shoulder was positioned backwards and the pelvis was positioned forwards. One hand was placed on the greater
trochanter, skin exposed to ensure grip, with the fingers facing down the femur. The cranial hand was placed on
the ipsilateral shoulder with the fingers facing away from the lower hand, From this position the weight was
applied evenly between both hands until all the slack was taken up and then a high velocity low amplitude thrust
was applied with therapist using the trigger of nodding his head. An audible cavitation was heard and the
treatment was considered successful.
On re-examination the NRS was reduced to 2/10. In addition right side flexion was no longer painful and flexion
only produced a 4/10 pain. There were no changes in her ligament provocation tests or ASLR.
Following this the neural system was targeted with work in prone to facilitate the contraction of the multifidus
muscles. This approach was based on the work of improving motor cortex reorganisation as described by Tsao
et al (2010b). The intervention used was similar to that described by Tsao et al (2010a) in improving multifidus
recruitment in their skilled exercise group. After five minutes of intermittent work on consciously contracting
these muscles the patient had an improved ability to swell the multifidus and ASLR difficulty was 0/5
bilaterally. The patient was then shown extension in prone with patient overpressure as described in McKenzie
and May (2003). This can be viewed as a specific form of grade B mobilisation. After repeating two sets of 10
repetitions she had no pain. She was asked to return the following day to be taken through her exercise
programme.
I then wrote to the patient’s general practitioner (GP) and the referring pain management specialist and
discussed the strategy with the senior physiotherapist at my clinic. He agreed with my plan to use further
manipulation as appropriate and a corrective stretching and exercise programme. He suggested that if she
returned with no pain at rest then there is probably no indication for manual treatment at that time. If her pain
had returned to a two or more on a NRS then he recommended the potential use of posterior-anterior
mobilisation to the lumbar spine starting at the L4 level. I agreed this was an option, but that as the patient had
responded favourably to manipulation on the initial visit at least one further treatment with manipulation
would be indicated if symptoms returned.
The following day the patient returned to be taken through their corrective stretching and exercise programme
which combined grade A and B mobilisations. This took the form of a structured rehabilitation programme
shown in Appendix A. The patient was instructed in how to do each stretch and exercise, and repeated them
herself for a full set each with prompting on correct technique where appropriate. Facilitation of the right
multifidus was repeated and incorporated in to the alternating superman exercise. The patient was asked to
complete the programme on alternate days for 1 week and then return for reassessment.
Information, therapeutic patient education and functional restoration were provided as suggested by Rozenberg
et al (2012). In addition, the pathophysiology of intervertebral discs injuries was explained so as to confer that it
was a minor injury that can heal over time and is often asymptomatic. This was done to avoid the patient
catastrophising their condition. The patient was also given therapeutic education on sitting posture, standing
posture, turning, sit to stand and using stairs. Functional restoration was encouraged through the guidance on
pacing and a graded return to more demanding daily activities.
Reassessment
The patient emailed the therapist one week after she was due to return for follow up. She reported she had not
returned as she had been too busy but she was still pain free at rest and could now sit for two hours without
pain. She felt her pain was coming on because was slouching at that point and after doing the McKenzie prone
extension exercise she could return to sitting pain free.
She returned for assessment two later, four weeks after initial assessment. On assessment her lumbar lordosis
was 25˚. This of course is no guarantee that the resting lordosis in standing had increased this much. The
patient may well have been very aware of what was being measured and consciously or subconsciously increased
her lordosis. ASLR difficulty was 0/5 bilaterally and ligament provocation tests were negative.
The patient was taught the multi-directional lunge exercise as preparatory exercise for returning to tennis and
advised to continue with the rehabilitation programme.
The patient confirmed via email that at six weeks she was able to sit for six hours as long she got up and walked
around throughout the day. She has returned to tennis and considers herself fully rehabilitated with a PDQ of
0/150.
Discussion and Evaluation
The programme overall produced a positive result. The patient’s aim of being able to sit for six hour periods was
achieved. In addition she has retuned to tennis. Further the patient made good progress in reaching the
postural objectives set and although not assessed the indication from the early progress was that she was
progressing towards having a normal lumbar lordosis. Whilst the programme produced the desired result in the
short term it is possible the result could have been achieved faster.
The European guidelines (van Tulder et al 2009) for treatment of acute non-specific low back pain advise
adequate information and reassuring the patient, not to prescribe bed rest as a treatment, advise patients to stay
active and continue normal daily activities including work if possible, prescribe medication if necessary for pain
relief. All of these were implemented with this patient. They further state that spinal manipulation should be
considered for patients who are failing to return to normal activities. In contrast, Edzard Ernst has conducted
systematic review of systematic reviews on spinal manipulation (Ernst and Canter 2006). Ernst is a vocal anti-
alternative writer and it is not surprising he concludes that there is no support for manipulative treatment.
However, there is some bias in his analysis and other groups producing guidelines have disagreed with his
findings as discussed above. This patient was struggling to return to normal activities, thus the application
followed the European guidelines.
The evidence for exercise based approaches remains controversial. Hayden et al (2005) found that in acute low
back pain exercise therapy was no more effective than no exercise or other conservative treatments. In contrast,
Machado et al (2006) found some support for the use of the McKenzie approach in acute low back in their meta-
analysis. Therefore whilst a general exercise approach may not be indicated, an approach based on a directional
preference may have value.
In this instance I only communicated with the patient’s GP and the senior physiotherapist at my clinic. I was
right to inform the patient’s GP and should ensure I continue to do this in future. Potentially I could have gained
more insight by consulting with additional professionals at the clinic I work in.
Completing the orthopaedic medicine module B has greatly improved my theoretical knowledge. Coming from a
corrective exercise background prior to studying physiotherapy I have always worked mainly from a functional
holistic model of rehabilitation. Now I integrate the two approaches and I have found frequently I can conduct
shorter assessments and treatments and achieve more immediate results in acute patients. I am also able to gain
patient confidence with treatments and assessments that are highly specific. Furthermore in chronic patients I
am more able to identify the specific structure that is giving rise to symptoms. I still view this specific tissue
within a functional holistic model but with a more specific diagnosis I can target the functional approach more
directly. For example, a specific postural rehabilitation protocol based on specific measurement may be
prescribed for conditions known to be associated with poor posture such as low back pain. Although this
concept remains controversial, despite being widely accepted (Lederman 2011).
Conclusion
This case history describes a patient referred for acute low back pain, and MRI findings consistent with a
posterior disc protrusion at the L4/5 level following prolonged periods of flexed sitting. On assessment there
was a 6/10 pain on NRS at rest, reduction in lumbar lordosis and pain at 8/10 on NRS produced on lumbar
flexion. The patient’s presentation fitted with clinical model ….. After treatment with grade C spinal
manipulation there was an immediate reduction the NRS to 2/10. This was further reduced with repeated prone
extension and successfully managed using a corrective stretching and exercise programme. The patient’s care
was discussed with the senior physiotherapist at the clinic and the referring consultant and the patient’s GP
were informed. The patient failed to return for follow up when advised but did respond favourably. On
reviewing the evidence the treatment provided fits with current guidelines although elements of the philosophy
on which the treatment was based remain controversial. My work with this patient and many others has been
improved for studying the orthopaedic medicine programme. The programme has added specificity to my
existing functional rehabilitation paradigm.
References
Ernst, E. and Canter, P.H., 2006. A systematic review of systematic reviews of spinal manipulation. J R Soc
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Posted in Acute Low Back Pain, Corrective Holistic Exercise Kinesiology, For Health Professionals, For Movement Therapists, Low back pain, Orthopaedic Medicine | Tagged
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Kieran Macphail's Blog

Low Back Pain, Modic Changes and Bacterial Infections

Kauffman, D., 2000. The Fungus Link. MediaTrition: Texas.

Assess, Treat, Re-assess: Applying The Clinical Audit Process

Figure 1. Horse Stance Vertical

Keep the chin tucked and the elbows pointing backwards

Opposite hand and knee removed to engage multifidus

Figure 2. Wall Deadbug

Start with your head 2cm’s from the wall.

Throughout your neck and lumbar spine should be in a neutral position.

Several factors need to be born in mind with this approach.

The Complexities of Movement Specific Diagnosis in the Spine

Calcium Dumping Syndrome

No Factors affecting bone Probable reasons for effect

1 Excessive milk consumption Adverse effect on sodium and

2 Excessive animal protein consumption Adverse effect on sodium and

3 Excessive phosphorus diets Stimulates parathyroid secretion

4 Excessive parathyroid hormone Direct stimulus to bone re-absorption

5 Magnesium deficiency Slowing of cell respiration and

6 Zinc deficiency Slowing of cell respiration and

7 Aluminium toxicity Stimulates parathyroid secretion

9 Lack of vitamin D Prevents calcium absorption

10 High alcohol intake Depression of cell respiration and de-

12 Acidification of body fluids from acid Re-dissolves deposited calcium

13 Chronic heavy metal exposure Depression of cell respiration

15 Excessive sodium intake Adverse effect on sodium/ potassium

16 Vitamin C deficiency Slows detoxification and exposes the

17 Liver or kidney under-function Inhibits whole body detoxification

Plaskett, L. 2008. Calcium. Plaskett Nutritional Medicine College. Folder 2, Section C

9 Key Principles I Learned From Guy Voyer

1. To work a muscle or specific part of the muscle put it under tension.

E.g. Triceps push down = distal, triceps dips = proximal

E.g. Rotator cuff first in the shoulder

Posted in Uncategorized | Tagged Guy Voyer | Leave a comment

Weight Loss and Insomnia Case Study

Job: psychotherapist for victims of abuse

Main goals: to reduce weight and insomnia

Recently noticed problems with concentration, and bouts of mild dizziness.

Often feels restless, anxious, stressed and sometimes depressed.

Skin: Suffers from dry, itchy skin, itchy ears

Other symptoms include a blocked nose and frequent clearing of throat

Usual childhood illnesses

Personality & background

Current Medical Diagnosis and Medication

Arthritis in right knee

Carpal tunnel syndrome, is booked in for an operation.

Family Medical History

Cardio-vascular disease and cancer

Alternative medicine review, 3 (2), p.90-100.

McKern, J. (2009) Hormone balancing.Journal of complementary medicine, 8 (1), p.12-18.

glucocorticoid cascade hypothesis. Endocrine review, 7 (3), p.284-301.

questions would help narrow the focus of the management programme.

Feldt-Rasmussen, U. (2009) Is the treatment of subclinical hypothyroidism beneficial? Nature reviews

NHS, (2012) Hypothyroidisim. [Online]. Available from;

L4/5 Disc Protrusion Case Study

History (Subjective Examination)

Discussion and Evaluation

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