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Clinical Reasoning Cyclist Jay Kay

Clinical Reasoning and the development of a 'working hypothesis' in an elite cyclist

by Martin Krause (2010)

Treatment: Left and right ischiococcygeus release; MET right adductor; in prone with one foam role under right hip and another under the left ASIS I used joint mobilistions, STM and dry needling to the right erector spinae group from T12 - L3. Exercises included Prone Spinal Extension (McKenzie), self release of ischiococcygeus, deep abdominal and iliacus stabilisation exercises during knee drop outs in supine, unilateral pelvic rotations/gluteus activation in supine, cross country skiing exercise with blue theratubing

see link to evidence for dry needling

17/03/2010 (4 weeks since accident)

Less painful walking on stairs

MRI findings : non-displaced fractures of the acetabulum

Very little lumbar IVM during lateral flexion, flexion and extension.

Treatment : STM right anteriomedial hip

Joint mobilisations to right T12-L3

Exercise : Sideways stepping (later off a small step), Prone - gluteal activation during initiation of ALE (active leg extension), Swiss Ball - supine bridging for gluteal activation, 'around the world' in side lying using low threshold activation to rotate the ball whilst keeping the pelvis steady; 4 Point Kneeling - abduction and abd/ext rot, lying prone on foam blocks for pelvic alignment (right anterior hip and left anterior pelvis).


No pain on stairs. New seat on bike making him less stable.

Left Concave scoliosis present on forward flexion, poor IVM lumbar spine. Excessive activity in all superficial trunk muscles and hip muscles. More marked left concave scoliosis on the bike. Excessive pelvic rocking to the right in the horizontal plane, whilst dropping the left hip in the saggital plane. Corrected through transverse pressure through the R6-8 rib rings whilst lifting the posterior right R9-12 rib rings.

Treatment : commenced MET's for upper lumbar/low thoracic right rotation; left rib ring lifts R7-8. Right iliopsoas releases.

MET left hamie for correction of left anterior ilial rotation

Exercises : Pilates Reformer - hip abd, ext in standing, superman with lateral and inferior diaphragmatic breathing

Transverse Adbdo - deep Multifidus training using 'guy wire through body suspending the spine' analogy.

Active Leg Extension (ALE) using 'guy wire stabilisation', descending diaphragm and 'Relaxation with Awareness' technique on the low-mid thoracic and upper lumbar spine erector spinae muscles. Stretching thoracic spine with stretches of the hip flexors, hamies and calf muscles

Further treatments on 30/3/10 , 7/4/10 and 14/5/10 as above, however now with even more thoracic emphasis, plus a big emphasis on detraining the superficial muscles, activation of the pelvic floor - diaphragm as well as gaining 'timing' w.r.t lumbopelvic rhythm in the frontal and horizontal planes.

Client becoming rather anxious to get back on the bike. Wife not too happy to have a moody husband 'hanging about the house' Hence gradual recommencement of cycling during this period



Jay returned 2 1/2 months after the last treatment stating that he had been suffering severe knee pain for the past 2 weeks. It had been of an insidious onset. However he had had a bike fit some 6 weeks prior to the onset of knee pain. At the time he had experienced some mild burning pain in the left ribcage after the new set up. He described 3 distinct pains in the leg - one sharp, the other a dull ache, whilst another sensation was that ' of the whole leg feeling dead'. Dull ache at night. Pain in mid popliteal region during push-off phase of walking. Pain in both the posterior knee and posteromedial knee during the upward cycle through Top Dead Centre (TDC) to 1/2 Bottom Dead Centre (BDC).


Extension in lying (modified push up, McKenzie technique) was reduced to 1/4 in the L/S

All hip ROM were once again restricted. The One Leg Standing (OLS) demonstrated an Intrapelvic Torsion (ITP) right, with reduced form closure over the left SIJ.

Importantly, the ITP right was accompanied by horizontal pelvic rotation right (contrary to normal clinical prediction) and the left concave scoliosis is on the side with the longer leg!!

SLR with DF was approx 45 degrees and without DF approx 60 degrees on the left and 60 and 70 degrees on the right resp.

Active SLR +ve : better with left R6-9 ring lifts and/or right anterior rib posterior translation

Hip flexion in sitting : In sitting he was unable to lift either leg beyond 90 degrees hip flexion. Lifting on the left resulted in left pelvic shift, on right resulted in right pelvic rotation, these were accentuated on the bike and were acompanied by a left concave scoliosis in the L/S.

The sacrum was vertical and the low lumbar spine was nearly vertical, with severe wedging into flexion occuring at L2/3 and L3/4 whilst seated on the bike.

Localised tenderness and swelling was present in the popliteus muscle. The semimembranosus, semitendinosis, gracilis and tibial nerve were all tender to palpation.

Active Leg Extension (ALE): severly reversed Glut : Hamie timing. Extremely hamstring dominant with associated excessive tension in the erector spinae of the low thoracic and high lumbar spine.


Typical EMG patterns : note the need for Gluteus Maximus activity during the downward pushing phase of cycling. My thoughts were that lack of early Gluteus Max timing and constant use of Hamstrings were overloading the structures around the knee. Additionally, the semimembranosus and semitendonosis internal rotation vector at the tibia being a counter to the adductor vector of hip internal rotation. Moreover, these were preceded by counter-nutation at the left SIJ. Anterior rotation of the ilia makes it particularly difficult to activate the gluteus maximus. Moreover, anterior rotation of the left ilium would create tension in the ilio-lumbar ligament normally resulting in right rotation of L4, where this was accompanied by a significant counter posture of left concave scoliosis in the upper lumbar spine and low thoracic. The wedging at L2-4 may also have been placing Adverse Neural Dynamics on the obturator nerve.

Link to ALE and ASLR and diaphragm

A program to regain pelvic symmetry and thoracic mobility was instigated using a comibination of joint mobilisations, MET's, dry needling, soft tissue massage, and rib ring lifts. Additionally, Adverse Neural Dynamics signs were treated using techniques to the thoracic spine.

Link to motor control and breathing reference

Scapulo-lumbar stabilisation exercises were also given by using theraband whilst using the bike on the 'home trainer' . Hereby, activation of latissimus dorsi and low fibres of trapezius was instigated which resulted in reduced horizontal rotation of the pelvis during pedaling.

Alexander Technique for Lumbopelvic, Thoracolumbar and Scapulothoracic support through elongation of the Upper Cervical Spine



Connell AT (2008) Concepts for assessment and treatment of anterior knee pain related to altered spinal and pelvic biomechanics: a case report. Manual Therapy, 13, 560-563
This author used 3 sessions of treatment to the T10/11, T11/12, T12/L1 and L5/S1 to improve the ROM and ability to squat in a patient with anterior knee pain.
Grindstaff TL et al (2009) Effects of lumbopelvic joint manipulation on quadriceps activation and strength in healthy individuals. Manual Therapy, 14, 415-420.

These investigators found a significant increase in the ability to produce quadriceps force (+3%) and activation (+5%) immediatley following lumbopelvic joint manipulation

Figure 1: A model of everything : the neuromatrix is used as a model (cognitive process oriented structure) to describe the various input which the therapist can offer to 'enable' the client to engage in their path to recovery. Hereby, an evidence based approach using 'the values and beliefs' of the client is integrated with the scientific evidence base from physiotherapy, the pain sciences and psychology. Importantly, the therapist gains confidence through their success at predictive reasoning, whilst the client gains emotional confidence in their ability to undertake goal-oriented activities without the fear of exacerbation or under-performance.

Heuristics versus Constructivism

Figure 2: A useful instructional model used to describe a 'top-down' clinical approach with a scientific clinical evidence based approach of biomechanics and neurophysiology.

Figure 3: Increasing the validity and reliability of the clinical reasoning by correlating all aspects of the subjective and physical examination into a meaningful clinical picture (pattern recognition) - adapted from Maitland (1986, 1991).

Treatment as a product of a systematic assessment

Although an at 'out of fashion' terminology, the aggravating/easing factors are a disability measure which can be used to assess the neurophysiological and biomechanical state of the pathology. By analyzing the movement and loading characteristics of the aggravating and easing factors the therapist should gain a measurable outcome tool for assessing the efficacy of treatment. Additionally, the information can be used to correlate it with impairment measures of the physical examination. Improving the internal reliability by correlating information across the entire examination process enhances the validity of your treatment and re-examination process. Ideally, the therapist should have at least 3 aggravating/easing factors to assess outcome. Otherwise, a more in depth analysis of the aggravating/easing factors should be undertaken using inductive reasoning. For example, if the client only complains of shoulder pain when lifting a load above their head, then clarify this statement by asking whether it is the movement which is painful, the duration of lifting, the manner of lifting or the size of the load which is being lifted that is significant. Night pain, the frequency of waking and the ability to return to sleep are also useful measurement tools. Psychometric disability measures can also be used if they don't result in resentment or irritation from your client. 
Further aspects of the subjective examination can be used to assess the past history as it relates to the current problem. Is it the same problem re-aggravated or is it a new problem which is influenced by the old injury? Assess the biomechanical aspects of the original mechanisms of injury as well as those of re-exacerbation, as well as the frequency of exacerbation and make a judgement as to whether the problem is getting worse, better or staying the same. If it is getting worse, then why? Are there components of misuse (reduced co-ordination/stability), disuse (atrophy and reduced capacity of loading), abuse (trauma), or overuse (repetitive loading and microtrauma) which are contributing to the 'cause of the cause' of the problem. A long history of problems may identify fear-avoidance behaviour and generalised 'disuse' and/or of more specific 'disuse' of the multifidus and transverse abdominis muscles. Combine this with 'overuse' of the erector spinae muscles leading to excessive compression of the intervertebral disc and consequent neural irritation of the dorsal root ganglia resulting in ectopic impulse generation and increased muscle tone in the deep hip rotators, hip flexors, hamstring and calf muscles which creates 'misuse' of the lower limbs ('the tail that wags the dog phenomena') generating shearing and rotating forces across the pelvis.
Old injuries may not only reduce the biomechanical integrity of the tissue but it may also increase the neurophysiological sensitivity of the neurones whose nerve fibres innervate the territory of injury. Ascertaining the recuperation from previous injury will provide an insight into the clients 'active' and/or 'passive' coping strategies. People who have had frequent passive treatment inputs and have recovered may find it difficult to embrace a more active treatment approach. Those who haven't recovered may be in a state of 'learned helplessness' who will similarly require convincing to embark on a more active form of recuperation. Importantly, the active treatment approach must embrace the impairment and disability measures of the subjective and physical examinations, thereby allowing the client to measure success leading to the ultimate goal of full self management and/or complete recovery. Therefore, this process requires an element of education whereby the therapist's 'hands-on' treatment becomes 'exercise enabling' and/or 'performance enhancing' for the client.

Figure 4: The application of treatment will vary with the stage, stability, severity and irritability of the condition. The stage describes whether the condition is getting better, worse or staying the same. The stability is considered both mechanically and neurophysiologically. The severity is the impact the injury has on the person's activities of daily living. The irritability defines how easily the symptoms worsen and relates to how quickly they get better. These factors will influence the goals of the client which should direct the aims and objectives of the therapist.

Figure 5: Defining the aspects of the examination heightens the therapists cognitive abilities and hence clinical agility. Reflective skills as treatment is instigated and outcomes are measured enhances the therapist's meta-cognitive skills (thinking about their thinking)

Figure 6: Defining the 'cause of the cause' will get to the root of the problem. By deconstructing the problem clear and precise explanations can be given whereby the aims and objects of treatment commiserate the exercise goals

Cause & effect

Treatment is usually directed at the primary problem for which the client has presented. As the primary problem resolves the cause and affect of the injury must be taken into consideration if an holistic approach is to be considered. Low back pain would address issues of thoracic spine stiffness in rotation, lateral bending and inferior lateral chest expansion as these areas influence the lateral movement of the diaphragm during breathing. In turn this affects the use of the oblique stomach muscles, the transverse abdominus and psoas major. Furthermore, the ganglia of the sympathetic nervous system attach to the anterior aspect of the posterior ribs and their function is influenced by rib movement, which can potentially affect the control of muscle spasms and blood flow to the spine and lower limbs. Finally, deep slow lateral breathing reduces the risk of respiratory alkalosis and hence metabolic acidosis which can affect soft tissue integrity. Looking below the lumbar spine, addressing the pelvis and hips using joint mobilizations, soft tissue massage and muscle energy techniques would affect lumbo-pelvic rhythm. Muscle spasms can be addressed by reducing inflammation and/or relieving mechanical pressure on nerve fibres thereby decreasing ectopic impulse generation. Additionally, dry needling and soft tissue massage of the muscle fibres may also be employed. Exercise regimes to complement the specific impairment outcome measures should be integrated into functional exercises which resemble activities of daily living. Naturally, the clients motivational & emotional state needs to be monitored if a collaborative approach to recovery is to be obtained.


Explanations and References

Manual Therapie in der Behandlung von Schmerzen (Deutsch)

Terapia Manual y dolor (Castellano)

Tratamento do dor e inflamacao com fisioterapia manipulativa (Portuguese)

Manual therapy in the treatment of pain and inflammation (English)

Exercise and the Immune System (English)

Exercise and Sarcopenia (English)

Examples of the assessment process for clinical reasoning

Beispiel von Klinisches Denken

Clinical Reasoning Exercise for low back and lower Limb

Clinical example of treatment for functional instability and radicular LBP

LBP Treatment Progress

Clinical Reasoning Exercise for Neck-Upper Limb

Apresentacao Clinica e Perguntas

Presentation at the conference in Rome in October 2005


  • Neurophysiological Effects of Traction, Rigaku ryohogaku (2000), 27,4, 128 (Japan)
  • Lumbar Spine Traction: Evaluation of effects and recommended application for treatment (2000), Manual Therapy, 5, 2, 72-81
  • Neurophysiological effects of Manual Therapy (1996), Kinesiologia, (Chile)
  • Neurophysiological considerations of SLR and ULTT (1998), Kinesiologia (Chile)

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Adams, M.A., Dolan, P.& Hutton, W.C. (1986). The stages of disc degeneration as revealed by discogram. Journal of Bone and Joint Surgery 68B , 36.

Ahmed, M., Bjurholm, A., Kreicbergs, A.& Schultzberg, M. (1993). Sensory and autonomic innervation of the facet joint in the rat lumbar spine. Spine 18 (14), 2121 to 2126.

 Alkon, D.L.& Rasmussen, H.A. (1988). A spatial-temporal model of cell activation. Science 239 , 998 to 1005.

Attal, N., Filliatreau, G., Perrot, S., Jazat, F., Di Giamberardino, L.& Guilbaud, G. (1994). Behavioural pain-related disorders and contribution of the saphenous nerve in crush and chronic constriction injury of the rat sciatic nerve. Pain 59 , 301 to 312.

Badalemente, M.A., Dee, R., Ghillani, R., Chien, P-F. & Daniels, K. (1987). Mechanical stimulation of dorsal root ganglia induces increased production of substance P : A mechanism for pain following nerve root compromise? Spine 12 , 552 to 555.

Barasi, S.& Lynn, B. (1986). Effects of sympathetic stimulation on mechanoreceptive and nociceptive afferent units from the rabbit pinna. Brain Research 378 , 21 to 27.

Barker, J.N., Mitra, R.S., Griffiths, C.E., Dixit, V.M.& Nicholoff, B.J. (1991). Keratinocytes as initiators of inflammation. Lancet 337 , 211 to 214.

Barrows, H.S., Tamblyn, R.N., (1980). Problem-based learning: an approach o medical education. Springer, New York.

Blottner, D.& Baumgarten, H.G. (1994). Neurotrophy and regeneration in vivo. Acta Anatomica 150 , 235 to 245.

Bogduk, N. (1993). The anatomy and physiology of nociception. In : Crosbie J.& McConnell, J.(Eds.) (1993). Key Issues in Musculoskeletal Physiotherapy (Ch.3). Oxford : Butterworth-Heinemann Ltd.

Butler, D.S., (1991). Mobilisation of the Nervous System . Churchill Livingstone : Melbourne.

Chatani, K., Kawakami, M., Weinstein, J.N., Meller, S.T.& Gebhart, G.F. (1995). Characterization of thermal hyperalgesia, c-fos expression, and alterations in neuropeptides after mechanical irritation of the dorsal root ganglion. Spine 20 (3), 277 to 290.

Coderre, T.J., Basbaum, A.I.& Levine, J.D. (1989). Neural control of vascular permeability : interactions between primary afferents, as cells, and sympathetic efferents. Journal of Neurophysiology 62 , 48 to 58

Coderre, T.J., Chan, A.K., Helms, C.& Levine, J.D. (1991). Increasing sympathetic nerve terminal-dependent plasma extravasation correlates with decreased arthritic joint injury in rats. Neuroscience 40 , 185 to 189.

Coghill, R.C., Mayer, D.J., Price, D.D., (1993). Spinal cord coding of pain : The role of spatial recruitment and discharge frequency in nociception. Pain , 53 , 295 to 309.

Cohen, M.L., (1995). The clinical challenge of secondary hyperalgesia. Moving in on Pain (Abstracts). Adelaide, Australia.

Cohen, M.L., Quintner, J.L., (1993). Fibromyalgia syndrome, a problem of tautology. Lancet , 342 , 906 to 909.

Collingride, G.L.& Singer, W. (1990). Excitatory amino acid receptors and synaptic plasticity. Trends in Pharmacological Science 11 , 290 to 296.

Cornefjord, M., Takahashi, K., Matsui, H., Olmarker, K., Holm, S.& Rydevik, B. (1992). Impairment of nutritional transport at double level cauda equina compression: An experimental study. Neuro Orthopedics 13 , 107 to 112.

Dickenson, A.H.& Sullivan, A.F. (1987). Evidence for a role of the NMDA receptor in the frequency dependent potentiation of deep rat dorsal horn nociceptive neurons following C-fibre stimulation. Neuropharmacology 26 , 1235 to 1238.

Donnerer, J., Amann, R. & Lembeck, F. (1991). Neurogenic and non-neurogenic inflammation in the rat paw following chemical sympathectomy. Neuroscience 45 (3), 761 to 765.

Enwemeka, C.S. & Spielholz, N.I. (1992). Modulation of tendon growth and regeneration by electrical fields and currents. In : Currier, D.P.& Nelson, R.M. (Eds.) (1992). Dynamics of Human Biologic Tissues (ch10). Philadelphia : F.A. Davis Company.

Ferrell, W.R., Wood, L. & Baxendale, R.H. (1988). The effect on acute joint inflammation on flexion reflex excitability in the decerebrate, low-spinal cat. Quarterly Journal Of Experimental Physiology 73 , 95 to 102.

Galea, M.P. & Darien-Smith, I. (1995). Voluntary movement and pain : Focussing on action rather than perception. Moving in on Pain . Adelaide.

Gallin, J.I., Goldstein, I.M. & Snyderman, R. (Eds.) (1992). Inflammation : Basic Principles and Clinical Correlates (2nd ed.). New York : Raven Press.

Gogas, K.R., Presley, R.W., Levine, J.D. & Basbaum, A.,I., (1991). The antinociceptive action of supraspinal opioids results from an increase in descending inhibitory control : Correlation of nociceptive behaviour and C-fos expression. Neuroscience 42 (3), 617 to 628.

Gracely, R.H., Lynch, S.L. & Bennett, G.,J. (1992). Painful neuropathy : Altered central processing, maintained dynamically by peripheral input. Pain 51 , 175 to 194.

Greenbag, P.E., Brown, M.D., Pallares, V.S., Tompkins, J.S. & Mann, N.,H., (1988). Epidural anesthesia for lumbar spine surgery. Journal of Spinal Disorders 1 , 139 to 143.

Gonzales, R., Goldyne, M.E., Taiwo, Y.O. & Levine, J.D. (1989). Production of hyperalgesic prostaglandins by sympathetic postganglionic neurons. Journal of Neurochemistry 53 , 1595 to 1598.

Gonzales, R., Sherbourne, C.D., Goldyne, M.E. & Levine, J.D., (1991). Noradrenaline-induced prostaglandin production by sympathetic postganglionic neurons is mediated by alpha-2-adrenergic receptors. Journal of Neurochemistry 57 , 1145 to 1150.

Green, P.G., Basbaum, A.I., Helms, C. & Levine, J.D. (1991). Purinergic regulation of bradykinin-induced plasma extravasation and adjuvant-induced arthritis in the rat. Proceedings of the National Academy of Science , U.S.A. 88 , 4162 to 4165.

Green, P.G., Luo, J., Heller, P.H. & Levine, J.D. (1992). Modulation of bradykinin-induced plasma extravasation in the rat knee joint by sympathetic co-transmitters. Neuroscience 52 , 451 to 458.

Groen, G.J., Balget, B. & Drukker, J. (1988). The innervation of the spinal dura mater: anatomy and clinical considerations. Acta Neurochirurgica 92 , 39 to 46.

Groenblad, M., Weinstein, J.N. & Santavirta, S. (1991). Immunohistochemical observation on spinal tissue innervation. Acta Orthopaedic Scandinavia 62 (6), 614 to 622.

Groenblad, M., Virri, J., Tolonen, J., Seitsalo, S., Kaeaepae, E., Kankare, J., Myllynen, P. & Karaharju, E. (1994). A controlled immunohistochemical study of inflammatory cells in disc herniation tissue. Spine 19 (24), 2744 to 2751.

Handwerker, H.O., Forster, C. & Kirchhoff, C., (1991). Discharge patterns of human C-fibres induced by itching and burning stimuli. Journal of Neurophysiology 66 , 307 to 317.

Harvey, G.K., Toyka, K.V. & Hartung, H.-P. (1994). Effects of mast cell degranulation on blood-nerve barrier permeability and nerve conduction in vivo. Journal of the Neurological Sciences 125 , 102 to 109.

Heller, P.H., Green, P.G., Tanner, K.D., Miao, F.J.-P. & Levine, J.D. (1994). Peripheral neural contributions to inflammation. Progress in Pain Management (1st ed.)(pp31-42). Seattle : IASP Press.

Hodges, P., Richardson, C., (1996). Inefficient muscular stabilisation of the lumbar spine associated with low back pain : A motor control evaluation of transverse abdominis. Spine , 21 , 2640 to 2650.

Hodges, P., Richardson, C., Jull, G., (1996). Evaluation of the relationship between laboratory and clinical tests of transverse abdominis function. Physiotherapy Research International , 1 , 30 to 40.

Hu, S. & Zhu, J. (1989). Sympathetic facilitation of sustained discharges of polymodal nociceptors. Pain 38 , 85 to 90.

Hsieh, J-C., Stahle-Backdahl, M., Hagermark, O., Stone-Elander, S., Rosenquist, G., Ingvar, M., (1995). Traumatic nociceptive pain activates the hypothalamus and the periaqueductal gray: a positron emission tomography study. Pain , 64 , 303 to 314.

Issekutz, T.B. (1992). Inhibition of lymphocyte endothelial adhesion and in vivo lymphocyte migration to cutaneous inflammation by TA-3, a new monoclonal antibody to rat LFA-1. Journal of Immunology 149 , 3392 to 3402.

Jaenig, W. (1985). Organization of the lumbar sympathetic outflow to skeletal muscle and skin of the cat hindlimb and tail. Review of Physiology, Biochemistry, Pharmacology 102 , 119 to 213.

Jaenig, W. & Koltzenberg, M. (1991). Receptive properties of pial afferents. Pain 45 , 77 to 85.

Jones, M., (1995). Clinical Reasoning and Pain. Manual Therapy , 1 , 17 to 24.

Jull, G., Zito, G., Trott, P., Potter, H., Shirley, D., Richardson, C., (1997). Inter-examiner reliability to detect painful upper cervical joint dysfunction. Australian Journal of Physiotherapy , 43 , 2, 125 to 129.

Kalso, E.A., Sullivan, A.F., McQuay, H.J., Dickenson, A.H., Roques, B.P., (1993). Cross-tolerance between Mu Opioid and alpha-2 Adrenergic receptors, but not between Mu and Delta receptors in the spinal cord of the rat. The Journal of Pharmacology and Experimental Therapeutics , 265 (2), 551 to 558.

Kambin, P., Abda, S. & Kurpici, F. (1980). Intradiskal pressure and volume recording : Evaluation of normal and abnormal intervertebral disks. Clinical Orthopedics 146 , 140.

Kawakami, M., Weinstein, J.N., Chatani, K.-I., Spratt, K.F., Meller, S.T. & Gebhart, G.F. (1994a). Experimental lumbar radiculopathy : Behavioural and histologic changes in a model of radicular pain after spinal nerve root irritation with chromic gut ligatures in the rat. Spine 19 (16), 1795 to 1802.

Kawakami, M., Weinstein, J.N., Spratt, K.F., Chatani, K-I., Traub, R.J., Meller, S.T. & Gebhart, G.F. (1994b). Experimental lumbar radiculopathy : Immunohistochemical and quantitative demonstrations of pain induced by lumbar nerve root irritation of the rat. Spine 19 (16), 1780 to 1794.

Kobayashi, S., Yoshizawa, H., Hachiya, Y., Ukai, T. & Morita, T. (1993). Vasogenic edema induced by compression injury to the spinal nerve root: Distribution of intravenously injected protein tracers and Gadolinium-Enhanced Magnetic Resonance Imaging. Spine 18 (11), 1410 to 1424.

Koltzenburg, M., Kees, S., Budweiser, S., Ochs, G. & Toyka, K.V. (1994). The properties of unmyelinated nociceptive afferents change in a painful chronic constriction neuropathy. In : Gebhart, G.F., Hammond, D.L. & Jensen, T. S. (Eds.) (1994). Proceedings of the 7th World Congress on Pain : Progress in Pain and Management (2nd ed.) (Ch.35). Seattle : IASP Press.

Korkala, O., Gronblad, M., Liesi, P. & Karaharju, E. (1985). Immunohistochemical demonstration of nociceptors in the ligamentous structures of the lumbar spine. Spine 10 , 156 to 157.

Kuslich, S.D., Ulstrom, C.L. & Michael, C.J. (1991). The tissue origin of low back pain and sciatica: A report of pain response to tissue stimulation during operation on the lumbar spine using local anaesthesia. Orthopedic Clinics North America 22 , 181 to 187.

Laird, J.M.A. & Bennett, G.J. (1993). An electrophysiological study of dorsal horn neurons in the spinal cord of rats with an experimental peripheral neuropathy. Journal of Neurophysiology 69 , 2072 to 2085.

Laird, J.M.A. & Cervero, F. (1990). Tonic descending infuences on receptive-field properties of nociceptive dorsal horn neurons in sacral spinal cord of rat. Journal of Neurophysiology 63 (5), 1022 to 1032.

LaMotte, R.H., Shane, C.N., Simone, D.A. & Tsai, E.F.P. (1991). Neurogenic hyperalgesia : Psychophysical studies of underlying mechanisms. Journal of Neurophysiology , 66 , 190 to 211.

Levine, J.D., Dardick, S.J., Roizen, M.F., Helms, C. & Basbaum, A.I. (1986). The contribution of sensory afferents and sympathetic efferents to joint injury in experimental arthritis. Journal of Neuroscience 6 , 3923 to 3929.

Levine, J.D., Goldstine, J., Mayes, M., Moskowitz, M.A. & Basbaum, A.I. (1986). The neurotoxic effect of gold sodium thiomalate on the peripheral nerves of the rat. Arthritis and Rheumatism 29 , 897 to 901.

Levine, J.D., Taiwo, Y.O., Collins, S.D. & Tam, J.K. (1986a). Noradrenaline hyperalgesia is mediated through interaction with sympathetic postganglionic neurone terminals rather than activation of primary afferent nociceptors. Nature 323 , 158 to 160.

Lotz, M., Vaughn, J.H. & Carson, D. (1988). Effect of neuropeptides on production of inflammatory cytokines by human monocytes. Science 241 , 1218 to 1221.

Lovick, T.A., (1991). Interactions between descending pathways from the dorsal and ventrolateral periaquaductal gray matter in the rat. In ; Depaulis, A., Bandler, R.,(eds). The Midbrain Periaqueductal Gray Matter . Plenium Press, New York, 101 to 120.

Lima, D., Esteves, F. & Coimbra, A., (1994). C- fos activation by noxious input of spinal neurons projecting to the nucleus of the tractus solitarius in the rat. In : Gebhart, G.F., Hammond, D.L. & Jensen, T.S. (Eds.) (1994). Proceedings of the 7th World Congress on Pain : Progress in Pain and Management (2nd ed.) (Ch.30). Seattle : IASP Press.

Liu, J., Roughley, P.J. & Mort, J.S. (1991). Identification of human intervertebral disc stromelysin and its involvement in matrix degeneration. Journal of Orthopedic Research 9 , 568 to 575.

Lundborg, G., (1988). Nerve Injury and Repair . Edinburgh : Churchill Livingstone

MacMillan, J., Schaffer, J.L. & Kambin, P. (1991). Routes and incidence of communication of lumbar discs with surrounding neural structures. Spine 16 , 2, 167 to 171.

Magal, E.L. (1990). Gangliosides prevent ischemia-induced down-regulation of protein kinase C in fetal rat brain. Journal of Neurochemistry 55 , 2126 to 2131.

Maitland, G.D. (Ed.) (1986). Vertebral Manipulation (5th ed.). London : Butterworths.

Maitland, G.,D., (Ed) (1991). Peripheral Manipulation . London : Butterworths.

Mao, J., Price, D.D., Coghill, R.C., Mayer, D.J. & Hayes, R.L. (1992). Spatial patterns of spinal cord [14C]-2-deoxyglucose metabolic activity in a rat model of painful peripheral mononeuropathy. Pain 50 , 89 to 100.

Markowitz, S., Saito, K., Buzzi, M.G. & Moskowitz, M.A. (1989). The development of neurogenic plasma extravasation in the rat dura mater does not depend upon the degranulation of mast cells. Brain Research 477 , 157 to 165.

Matsui, H., Olmarker, K., Cornefjord, M., Takahashi, K. & Rydevik, B. (1992). Local electrophysiological stimulation in experimental double level cauda equina compression. Spine , 17 (9), 1075 to 1078.

Maixner, W., Gracely, R.H., Zuniga, J.R., Humphrey, C.B & Bloodworth, G.R. (1990). Cardiovascular and sensory responses to forearm ischemia and dynamic hand exercise. American Journal of Physiology 259 , R1156 to R1163.

McKenzie, R.C. & Sauder, D.N. (1990). The role of keratinocyte cytokines in inflammation and immunity. Journal of Investigative Dermatology 95 , S105 to 107.

Morton, C.R., Siegel, J., Xiao, H.-M., Zimmermann, M., (1997). Modulation of cutaneous nociceptor activity by electrical stimulation in the brain stem does not inhibit the nociceptive excitation of dorsal horn neurons. Pain , 71 , 65 to 70.

Morgan, M.M., Sohn, J.-H., Lohof, A.M. Ben-Eliyahu, S. & Liebeskind, J.C. (1989). Characterization of stimulation-produced analgesia from the nucleus tractus solitarius in the rat. Brain Research 486 , 175 to 180.

Nakagawa, I., Omote, K., Kitahata, L.M., Collins, J.G. & Murata, K. (1990). Serotonergic mediation of spinal analgesia and its interaction with noradrenergic systems. Anesthesiology 73 , 474 to 478.

Nishizuka, Y. (1989). The family of protein kinase C for signal transduction. JAMA 262 , 1826 to 1833.

Ochoa, J.L. & Yarnitsky, D. (1993). Mechanical hyperalgesia in neuropathic pain patients : Dynamic and static subtypes. Annals of Neurology 33 , 465 to 472.

Olmarker, K., Rydevik, B., Holm, S. & Bagge, U. (1989). Effects of experimental, graded compression on blood flow in spinal nerve roots. A vital microscope study on the porcine cauda equina. Journal of Orthopedic Research 7 , 817 to 823.

Olmarker, K., Rydevik, B. & Nordborg, C. (1993). Autologous Nucleus Pulposus induces neurophysiological and histological changes in porcine cauda equina nerve roots. Spine 18 (11), 1425 to 1432.

Petersen, N.,P., Vicenzino, B., Wright, A., (1993). The effects of a cervical mobilisation technique on sympathetic outflow to the upper limb in normal subjects. Physiotherapy Theory and Practice , 9 , 149 to 156.

O?Sullivan, P., Twomey, L., Allison, G., Sinclair, J., Miller, K., Knox, J., (1997). Altered patterns of abdominal muscle activation in patients with chronic low back pain. Australian Journal of Physiotherapy , 43 , 91 to 98.

Post, C., Minor, B.G., Davies, M. & Archer, T. (1986). Analgesia induced by 5-hydroxytryptamine-depletion in rats. Brain Research 363 , 18 to 27.

Price, D.D., Long, S. & Huitt, C. (1992). Sensory testing of pathophysiological mechanisms of pain in patients with reflex sympathetic dystrophy. Pain 49 , 163 to 173.

Price, D.D., Mao, J. & Mayer, D.J. (1994). Central neural mechanisms of normal and abnormal pain states. In Fields, H.L. & Liebeskind, J.C. (Eds.)(1994). Progress in Pain Research and Management (1st ed.)(pp61-84). Seattle : IASP Press.

Proudfit, H.K. (1992). The behavioural pharmacology of the noradrenergic descending system. In : Besson, J.M. & Guilbaud, G. (Eds.)(1992). Towards the use of Noradrenergic Agonists for the Treatment of Pain (1st ed.). Amsterdam : Elsevier Science Publishers B.V.

Quintner, J.L., Cohen, M.L., (1994). Referred pain of peripheral nerve origin : an alternative to the 'myofascial pain construct'. Clinical Journal of Pain , 10 , 243 to 251.

Raja, S.N., Meyer, R.A. & Campbell, J.N. (1988). Peripheral mechanisms of somatic pain. Anesthesiology 68 , 571 to 590.

Rees, H., Sluka, K.A., Westlund, K.N. & Willis, W.D. (1994). Do dorsal root reflexes augment peripheral inflammation ? NeuroReport 5 , 821 to 824.

Ren, K., Randich, A. & Gebhart, G.F. (1990). Modulation of spinal nociceptive transmission from nuclei tractus solitarii : A relay for effects of vagal afferent stimulation. Journal of Neurophysiology 63 (5), 971 to 986.

Roberts, W.J. & Elardo, S.M. (1985). Sympathetic activation of unmyelinated mechanoceptors in cat skin. Brain Research 339 , 123 to 125.

Rothwell, N.J. & Hopkins, S.J. (1995). Cytokines and the nervous system II : actions and mechanisms of action. Trends in Neuroscience 18 , 130 to 136.

Rydevik, B.L., Brown, M.D. & Lundborg, G. (1984). Pathoanatomy and pathophysiology of nerve root compression. Spine 9 , 7 to 15.

Rydevik, B.L., Myers, R.R. & Powell, H.C. (1989). Pressure increase in the dorsal root ganglion following mechanical compression: Closed compartment syndrome in nerve roots. Spine 14 (6), 574 to 576.

Sandkuehler, J., Eblien-Zajjur, A., Fu, Q.-G. & Forster, C. (1995). Differential effects of spinilization on discharge patterns and discharge rates of simultaneously recorded nociceptive and non-nociceptive spinal dorsal horn neurons. Pain 60 , 55-65.

Sanjue, H. & Jun, Z. (1989). Sympathetic facilitation of sustained discharges of polymodal nociceptors. Pain 38 , 85-90.

Schmidt, R.F. (1990). Experimental arthritis. Pain (supp) 5 , S215.

Schmidt, R.F., Schaible, H.-G., Messlinger, K., Heppelmann, B., Hanesch, U. & Pawlak, M. (1994). Silent and active nociceptors : Structure, functions, and clinical implications. In : Gebhart, G.F., Hammond, D.L. & Jensen, T. S. (Eds.) (1994). Proceedings of the 7th World Congress on Pain : Progress in Pain and Management (Ch.16) (2nd ed.). Seattle : IASP Press.

Shindo, K., Tsunoda, S-T.& Shiozawa, Z. (1994). Muscle spasm induced sympathetic reflex bursts on microneurography in a case with pontine demyelination. Clinical Autonomic Research 4 , 299 to 302.

Schomburg, E.,D. & Steffens, H. (1992). On the spinal motor function of nociceptive afferents and enkephalins. In : Jami, L., Pierrot-Deseilligny, E. & Zytnicki, D. (Eds.)(1992). Muscle Afferents and Spinal Control of Movement (pp.395 to 400)(1st ed.). Oxford : Pergamon Press.

Suval, W.D., Duran, W.N., Boric, M.P., Hobson, R.W., Berendsen, P.B. & Ritter, A.B. (1987). Microvascular transport and endothelial cell alterations preceding skeletal muscle damage in ischemia and reperfusion injury. The American Journal of Surgery 154 , 211 to 218.

Taiwo, Y.O. & Levine, J.D. (1989). Prostaglandin effects after elimination of indirect hyperalgesic mechanisms in the skin of the rat. Brain Research 492 , 397 to 399.

Takahashi, K., Olmarker, K., Holm, S., Porter, R.W. & Rydevik, B. (1993). Double level cauda equina compression. An experimental study with continuous monitoring of intraneural blood flow in the porcine cauda equina. Journal of Orthopedic Research 11 (1), 104 to 109.

Thompson, S.W.N. & Woolf, C.J. (1991). Primary afferent-evoked prolonged potentials in the spinal cord and their central summation : Role of the NMDA receptor. In : Bond, M.R., Charlton, J.E. & Woolf, C.J. (Eds). Proceedings of the VIth World Congress on Pain (pp291 to 298). Amsterdam : Elsevier

Tillman, L.J. & Cummings, G.S. (1992). Biologic mechanisms of connective tissue mutability. In : Currier, D.P. & Nelson, R.M. (Eds.) (1992). Dynamics of Human Biologic Tissues (pp1-44). Philadelphia : F.A. Davis Company.

Torebjoerk, E. (1994). Nociceptor dynamics in humans. In : Gebhart, G.F., Hammond, D.L. & Jensen, T. S. (Eds.) (1994). Proceedings of the 7th World Congress on Pain : Progress in Pain and Management (Ch.19) (2nd ed.). Seattle : IASP Press.

Troisier, O. & Cypel, D. (1986). Discography: An element of decision. Clinical Orthopedics 206 , 70.

Urban, L. & Randic, M. (1984). Slow excitatory transmission in rat dorsal horn : Possible mediation by peptides. Brain Research 290 , 336 to 341.

Vaccarino, F., Guidotti, A. & Costa, E. (1987). Ganglioside inhibition of glutamate-mediated protein kinase C translocation in primary cultures of cerebellar neurons. Proceedings of the National Academy of Science , U.S.A. 34 , 8707.

Wall, P.D. (1995). Treatment of pain. Moving in on Pain . Adelaide.

Wall, P.D. & Devor, M. (1983). Sensory afferent impulse originate from dorsal root ganglia as well as from the periphery in normal and nerve injured rats. Pain 17 , 321 to 339.

Wall, P.D. & Melzak, R. (1989) (Eds.). Textbook of Pain , (2nd. ed.). Edinburgh : Churchill Livingstone.

Weinstein, J.N., Claverie, W. & Gibson, S. (1988). The pain of discography. Spine 13 (12), 1344 to 1348.

Williams, T.J. & Hellewell, P.G. (1992). Endothelial cell biology. Adhesions molecules involved in the microvascular inflammatory response. American Review of Respiratory Disease 146 , S45 to 50.

Wiltse, L.L., Fonseca, A.S., Amster, J., Dimartino, P. & Ravessoud, F.A. (1993). Relationship of the dura, Hofmann's ligaments, Batson's plexus, and a fibrovascular membrane lying on the posterior surface of the vertebral bodies and attaching to the deep layer of the posterior longitudinal ligament: An anatomical, radiological, and clinical study. Spine 18 (8), 1030 to 1043.

Woolf, C.J. (1983). Evidence for a central component of post-injury pain hypersensitivity. Nature 306 , 686 to 688.

Woolf, C.J. (1984). Long-term alterations in the excitability of the flexion reflex produced by peripheral tissue injury in the chronic decerebrate rat. Pain 18 , 325 to 343.

Woolf, C.J. & McMahon, S.B. (1985). Injury-induced plasticity of the fexor reflex in chronic decerebrate rats. Neuroscience 16 , 395 to 404.

Woolf, C.J., Shortland, P. & Sivilotti, L.G. (1994). Sensitization of high mechanothreshold superficial dorsal horn and flexor motor neurones following chemosensitive primary afferent activation. Pain 58 , 141 to 155.

Woolf, C.J. & Swett, J.E. (1984). The cutaneous contribution to the hamstring flexor reflex in the rat : an electrophysiological and anatomical study. Brain Research 303 , 299 to 312.

Woolf, C.J. & Wall, P.D. (1986). Relative effectivenss of C primary afferent fibres in evoking a prolonged facilitation of the flexor reflex in the rat. The Journal of Neuroscience 6 , 1433 to 1442.

Wright, A., Vicenzino, B., (1995). Cervical mobilisation techniques, sympathetic nervous system effects and their relationship to analgesia. In : Schacklock, M.,O., (ed.). (1995). Moving in on Pain , Butterworth-Heineman, 164 to 173.

Xavier, A.V., Farrell, C.E., McDanal, J. & Kissin, I. (1990). Does antidromic activation of nociceptors play a role in sciatic radicular pain? Pain 40 , 77 to79.

Zochodne, D.W. (1993). Epineural peptides : A role in neuropathic pain? Canadian Journal of Neurological Sciences 20 (1), 69 to 72.


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  • Sat 18 Nov 2017

    Beetroot Juice Increases Human Muscle Force

    Beetroot juice increases human muscle force Beetroot juice has been shown to improve low frequency muscle force independent of Calcium-handling-proteins or REDOX reaction (Whitefield et al 2017, Med Sc Sp Ex, 49, 10, 2016-2024). Further benefits of beetroot juice are thought to include reduction of blood pressure protection from pre-mature aging aiding cancer survival lowering serveral inflammatory markers including interleukin-6, C-reactive protein and tumor necrosis factor alpha stabilising blood suger improving sexual performance anti-arthritic effects blood purification and enhanced red blood cells removing 'bad' estrogens from our blood stream Uploaded : 18 November 2017 F Read More
  • Wed 01 Nov 2017

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  • Sun 15 Oct 2017

    Neuroplasticity in Tendon Dysfunction

    Neuroplasticity in Tendinopathy by Martin Krause A multitude of contributing factors to altered motor control must be addressed when treating tendon dysfunction. What we have failed to consider in the past when dealing with chronic or recurrent tendon issues are motor control problems encompassing corticospinal control of excitation and inhibition as well as belief systems about pain and contextual factors related to imaging.  Research by Ebonie Rio et al (2015) (BJSM Sept 25, 10.1136/bjsports-2015-095215) suggest that the pain state sets up an adaptive pathway whereby the ipsilateral kinetic chain is directly inhibited by reflexogenic pathways, as well as being inhibited by contralateral hemispheric activity. Simultaneously excitation is enhanced in the opposite limb as well as in least in the case of enhanced excitation of the hamstrings in quadricep tendinopathy. If this is true, then so much for training the contralateral limb for 'cross training' purposes! This may also explain why a lot of people seem to have "all their injuries on the same side" (of the body). Furthermore, they recommend enhancing corticospinal drive through the use of 30-60 second isometric holds at 70-80% MVC to load the muscle whilst using isokinetics to load the tendon. Moreover, they recommend the use of a metronome at 60bpm (stages 1 and 2) with a count of 3 up, 2 down for quads, and 2 up, 3 down for calf isokinetics to optimally engage corticospinal drive through the visual and auditory stimuli (also shown by Kohei et al 2012 for motor imagery and M1 stimulation) more Cortical mapping of infraspinatus muscle in chronic shoulder pain demonstrating higher motor thresholds (aMT= activation MT) and hence reduced excitability on the affected side (39 vs 35) (Ngomo et al 2015 Clinical Neurophysiol, 126, 2, 365-371) Cortical mapping of pain and fear. Lots of overlap suggesting that taking away the fear from the pain with clear clinical explanations and a focused goal directed program using specific functional outcomes is important.  Individuals with patellofemoral pain (PFP) had reduced map volumes and an anterior shift in the M1 representations, greater overlap of the M1 representation and a reduction in cortical peaks across all three quadriceps (RF, VL, VMO) muscles compared with controls.(Te et al 2017 Pain Medicine, pnx036,  Uploaded : 18 October 2017 Read More
  • Mon 09 Oct 2017


    Do I need a scan? "a picture tells a thousand words" - not really! by Martin Krause A scan, in it's self, will not improve anyone's condition. The purpose of a scan is to gain more information about the pathology. Sometimes this information may be irrelevant to the management of a patient's condition. For example, if you knocked your elbow on a door frame and suffered a bruise, which was already beginning to resolve, an ultrasound scan may show some minor soft tissue damage, but that was already obvious by the fact of the bruise, and the information gained from the scan has not helped nor changed the management of the bruise. Therefore, the main reason for getting a scan would be because there is concern that the presence of certain pathologies may lead to a change in the medical management. For example, sometimes a rolled ankle can be more than sprained ligaments, and may require surgey or immobilisation in a boot. If the therapists suspects this might be the case, then they will recommend or refer for a scan (probably an X-Ray) to check the integrity of the bones (especially the fibular and talar dome), because if there is no bony damage then the patient can be managed conservatively with taping, exercises, ultrasound, massage, joint mobilisations etc. However, if there is boney damage, for example, then it might be necessary for the ankle to be immobilised in a boot for three - six weeks, for example. This dramatically different medical management depends on the results of a scan, and it is therefore worth doing. However, scans have no predictive value to the presence or severity of pain. Thirty-three articles reporting imaging findings, in the low back, for 3110 asymptomatic individuals were investigated for pathology. The prevalence of disk degeneration in asymptomatic individuals increased from 37% of 20-year-old individuals to 96% of 80-year-old individuals. Disk bulge prevalence increased from 30% of those 20 years of age to 84% of those 80 years of age. Disk protrusion prevalence increased from 29% of those 20 years of age to 43% of those 80 years of age. The prevalence of annular fissure increased from 19% of those 20 years of age to 29% of those 80 years of age. (Brinjikji, W et al Spine Published November 27, 2014 as 10.3174/ajnr.A4173). Hence, the results of imaging need to be assessed within the context of the entire clinical picture. Frequently too much emphasis is placed on the imaging not only by the clinician but also by the patient. Some people react to pathology seen on scanning as an affirmation of their problem and can either use it to gain clarity and become better or conversely become worse. Moreover, some people find imaging with inconclusive results as a 'panic moment' - "no one knows what is wrong". Similarly, ultrasound imaging of the tendond has good predictive diagnostic and aids in clinical reasoning when it comes to full tears. However, with partial tears it is a totally different 'ball game'. Ultrasound is highly user dependent, with specifically trained musculoskeletal radiologists able to produce high-quality images that may provide more clinically relevant information than those produced by clinicians with less experience in imaging. Sean Docking, a leading tendon researcher at Monash University, cited 7 authors who found pathological tendon chnages in 59% of asymptomatic individuals, whereas he found that 52% of asymptomatic elite AFL sportsmen had tendon pathology on imaging! Furthermore, symptomatic individuals who improved clinically to the point of resuming play, weren't shown to have improvements on imaging. Again, the clinical context and the clinical reasoning can in many instances prove to be the 'gold standard' not the imaging itself, when considering management options. Shoulder supraspintatus tendon pathology, in the abscence of trauma, is known, in many instances, to be a disorder of immune-metabolic compromise of the tendon and bursa. Imaging may show some changes in signal intensity but, unless it's a complete tear, it can reveal neither the intensity nor the severity of pain when taken outside of the clinical context. A thorough physical and subjective examination integrating all the clinical dimensions of the problem will have far greater value than any one single imaging modality. Yet, imaging still should be used in instances of progressive rapid deterioration and suspected serious pathology which may require surgery and/or immediate medical intervention. In summary, sometimes it is worthwhile getting a scan, because the information gained from that scan will determined the type of medical management that is employed. However, at other times, the scan may be unneccessary, because the information may be irrelevant or lead to an incorrect change in medical management, due to over-reporting of 'false positives'. You will be able to make this decision on the advice of your health care professional. On occasions it can actually be detrimental to have a scan, because some patients can become overly obsessed with the medical terms used to describe their scan results, which then can become the major focus for the clinician and the patient, rather than the more prefereable focus on their symptoms and functional abilities. For example, many people have lumbar buldging discs yet have no symptoms, yet sometimes when these patients have an MRI or CT scan, they can develop symptoms because they think they should have pain if the scan says so! Conversely, for some people the results of imaging can have a positive and reassuring affect. Therefore, it is very important to assess a clients attitude to scans before prescibing them so that the patient's expectations are managed appropriately, and not burdened by the additional, sometimes confusing, information supplied by a scan. Uploaded : 10 October 2017 Read More
  • Thu 14 Sep 2017

    Cervical Spine implications in concussion

    Neck aetiology, autonomic and immune implications, exercise and diet in the musculoskeletal physiotherapy management of Post Concussion Syndrome (PCS) by Martin Krause, MAPA, Titled member Musculoskeletal Physiotherapy Association of Australia  A 14 year old boy presented to A&E, in August 2016, after receiving an impact to the head during AFL (Australian Rules Football). Although his SCAT3 scores were relatively mild, he went on to suffer severe lethergy, resulting in a lengthy abscence from school, culminating in a return to school for exams in the first week of December 2016. Even by December, even a 30 minute walk was extremely fatiguing. To place this into perspective, he had been playing elite academy grade AFL for several seasons and was an extremely fit outdoor adventurer. Confounding Variables : end of season injury and hence no follow up from the academy suffers from Hypermobile Joint Syndrome (HJS) and possibly Ehlers Danlos Syndrome (EDS), however Beighton score 4/9. suffers from food intolerances, particularly to Glutin and diary, but also some other foods. Potential IBS and autoimmune issues. had just gone through a growth spurt (190cm) Imaging : Brain MRI normal Medical Examination : Balance remained impaired to tandem walking and single leg stance. The vestibular occular motor scale showed significant accomodation deficit of 15cm and there was a mild exacerbation of symptoms. ImPACT testing revealed adequate scores and reaction time of 0.65 which is within acceptable range. History : School holidays December - January. Return to school and was placed in the lower classes. Prior to his concussion he was a top 10 student at an academically selective high school. Took up basketball and rowing as summer sports. Academic results tanked. Several Basketball injuries (Feb - April 17') as a result of what apppeared to be muscular imbalances from the relatively recent growth spurt, as well as taking on a new sport. Showed little interest in returning to AFL as no-one had followed him up during the previous year.  Current History : September 2017 showed a continued decline in academic levels. School teachers noted an inability to concentrate. Academic results still well below pre-concussion levels. Fatigue continuing to be problematic.  Literature Review : Post Concussion Syndrom (PCS) is defined as "cognitive deficits in attention or memory and at least three or more of the following symptoms: fatigue, sleep disturbances, headache, dizziness, irritability, affective disturbance, apathy, or personality change"  Further complications of PCS also appear to be an increased risk of musculoskeletal injury Nordstrom et al (2014, BMJ Sports Med, 48, 19, Predictors of PCS are uncertain. However, the following clinical variables are considered factors at increasing risk. These include prior history of concussion, sex (females more prominant), younger age, history of cognitive dysfunction, and affective disorders such as anxiety and depression (Leddy et al 2012, Sports Health, 4, 2, 147-154). Unlike the 'good old days' which recommended a dark room and rest for several weeks post concussion, the consensus appears to be a graded return to exercise in order to restore metabolic homeostasis. Incredibly, highly trained young individuals can find even exercises in bed extremely demanding. Kozlowski et al (2013, J Ath Train, 48, 5, 627-635) used 34 people 226 days post injury to conclude significant physiological annomalies in response to exercise which may be the result of 'diffuse cerebral swelling'. Researchers have noted lower systolic and higher diastolic blood pressure in PCS (Leddy et al 2010, Clin J Sports Med, 20, 1, 21-27). Due to autonomic dysfunction manifested in altered cardiovascular and pulmonary responses (Mossberg et 2007, Arch Phys Med Rehab, 88, 3, 15-320) some clinicians have recommended the use of the exercise program for POTS (Postural Orthostatic Tachycardia Syndrome). This is a 5 month program which recommends mainly exercise in the horizontal and sitting positions for 1-4 months, including recumbent bike, rowing ergometer and swimming laps or kicking laps with a kick board. Month 4 upright bike and Month 5 upright training such as a elliptical trainer or treadmill. Other progressive exercise therapies have also included 20 minutes per day, 6 days per week, for 12 weeks of either treadmill or home gym exercises at 80% of the heart rate at which their concussion symtoms are exacerbated. Their programs were individually modified as the heart rate provoking symptoms increased. When compared to the 'control group', this intervention was shown to improve cerebral perfusion on fMRI, increase exercise tolerance at a higher heart rate, less fatigue and were showing activation patterns in areas of the brain on performing math processing test which were now normalised (Leddy et al 2010, Clin J Sports Med, 20, 1, 21-27). Graded exercises could also have included 'motor imagery' as espouse by the NOI group and the work of Lorrimer Moseley (University South Australia) when dealing with chronic pain. Ongoing Symptoms : The literature review by Leddy et al (2012) found that ongoing symptoms are either a prolonged version of concussion pathophysiology or a manifestation of other processes, such as cervical injury, migraine headaches, depression, chronic pain, vestibular dysfunction, visual disturbance, or some combination of conditions. Physiotherapy Assessment : One year PCS, fatigue continued to persist. Cognitive deficits with school work were reported to becoming more apparent. Assessment using various one leg standing tests employing oscillatory movement aroud the hips and knees for kinetic limb stability and lumbopelvic stability, which had been employed 6 months previously for his Basketball injuries were exhibiting deficits, despite these being 'somewhat good' previously. Physical Examination : cervical and thoracic spine Due to the Joint Hypermobility Syndrome (JHS) it was difficult to ascertain neck dysfunction based on range of movement testing. ROM were unremarkable except for lateral flexion which demonstrated altered intervertebral motion in both directions. Palpation using Australian and New Zealand manual therapy techniques such as passive accessory glides (upslopes and downslopes and traction) exhibited muscles spasms in the upper right cervical spine. In particular, the right C1/2 regions demonstrated most marked restrictions in movement. Eye - Neck proprioceptive assessment using blind folds and laser pointer also  revealed marked variance from the normal. Repositioning error using the laser pointer with rotation demonstrated marked inability to reposition accurately from the left, tending to be short and at times completely missing the bullseye. Gaze stability with body rotation was NAD. Gaze stability whilst walking displayed some difficulty. Laser pointer tracing of the alphabet was wildly inaccurate. Thoracic ring relocation testing also revealed several annomalies, which may have also accounted for some autonomic dysfunction.  Occulomotor assessment and training Upper Cervical Spine : The upper cervical spine (atlas and axis) represents approximately 50% of the available rotation. An investigation into the environmental and physiological factors affecting football head impct biomechanics found that rotational acceleration was one of the few factors approaching significance and concluded that more research should be undertaken to evaluate this (Mihalik et al 2017 Med Sc Sp Ex, 49, 10, 2093-2101). Headache : Commonly referred to as cervicogenic headaches, one in five headaches in the general population are thought to be due to the cervical spine. The Upper Cervical Spine is particularly vulnerable to trauma because it is the most mobile part of the vertebral column, with a complex proprioceptive system connecting the vestibular apparatus and visual systems. It also coincides with the lower region of the brainstem and fourth ventricle. The brainstem houses many neurones associated with autonomic responses to pain and balance. Imaging of the fourth ventricle for swelling of the 'tonsils' and Arnold Chiari malformations are recommended when symptoms persist. In particular, children and adolescents are more vulnerable to neck contusions due to the proportionately larger head and less developed musculature. Cervical vertigo and dizziness after whiplash can mimic symptoms of PCS.. Mechanoreceptor dysfunction and vertebrobasilar artery insufficiency should be part of the differential diagnosis. Mechanical instability of the Upper Cervical Spine should also not be missed. Cervicogenic Headaches Further Interventions : Neurocognitive rehabilitation of attention processes. Psychological intervention using cognitive behavioural therapy (CBT). Neuro-opthalmologist to assess and treat smooth pursuit eye tracking. Naturopath for food intolerances and dietician for the optimisation of diet. Diet :  In cases with chronic fatiguing factors, nutrition can be become a vital aspect into the reparative process. This may include energy and mineral rich foods such as bananas, green leafy vegetables for iron and magnesium (200-300mg), oranges for vitamin C (anit-oxidant and helps with the absorption of iron), anti-oxidant rich foods such as EPA/DHA (1000mg) fish oil, curcumin (tumeric), Cats Claw, Devils Claw, Chia seeds, fruits of the forest (berries), and CoQ10 with Vitamin B. Folate and Ferritin levels should also be checked. Calorific energy intake should balance with energy exependiture. However, as we are often dealing with young individuals, as in this case, some form of comfort food may be appropriate such as, nuts, legumes, homus and sushi. Protein intake prior to carbohydrate intake may help ameliorate any blood suger fluctuations due to Glycemic Index factors, however simple carbohydrates (high GI) should be avoided wherever practical. Even oats need to be soaked overnight and cooked briefly, otherwise they become a high GI food and may even affect the absorption of iron. The type of rice used can also influence GI, hence the addition of protein such as fish. Protein supplementations are generally over-used. Daily protein intake should not exceed 1.2g per kg of body weight per day. Dosage for children is less than that for adults. See Nutritional Section of this Site Conclusion  Investigations, into people with persisting PCS, demonstrated that they applied more force over time to control balance. Helmich et al (2016, Med Sc Ex Sp, 48,  12, 2362-2368) proposed that in regard to cognitive processes, the increase of cerebral activation indicates an increase of attention demanding processes during postural control in altered environments. This is relevant in so far as individuals with post concussive symptomatology have a variety of symptoms including headache, dizziness, and cognitive difficulties that usually resolve over a few days to weeks. However, a subgroup of patients can have persistent symptoms which last months and even years. Complications in differential diagnosis, can arise clinically, when neck dysfunction and altered motor control occur concurrently due to both neck and cerebral pathology. For example, Whiplash and other traumatic head and neck injuries can result in pathology to both regions, whereas, more discreet altered cognitive processing from concussion can result in altered neck motor control. Musculoskelatal Physiotherapy can play a vital part in the treatment of neck dysfunction including the re-establishment of occulomotor proprioception and managing localized strength and cardiovascular exercise regimes. A total body, multi-disciplinary approach which is well co-ordinated amongst practitioners is vital to an optimal outcome.    Uploaded : 17 November 2017 Read More
  • Thu 24 Aug 2017

    Pain in the Brain - neural plasticity

    Pain in the Brain and Neural Plasticity by Martin Krause There are several mechanisms that can create a sensation of pain, which has been described as 'an unpleasent sensory and emotional experience in response to perceived or potential tissue damage'. Pain can be the result of peripheral sensitisation from peripheral inflammation, vascular compromise, necrosis, swelling, etc. Importantly, higher centres of the central nervous system not only perceive such sensitization of the peripheral nerve receptors, they can also modulate and control the intensity and tolerability of the perceived sensation through descending modulation at the peripheral receptor and in the spinal cord and through transcortical mechanisms depending on the 'meaning' and 'context given to the pain. Moreoever, the higher centres can create a 'state' of perceived 'threat' to the body through emotions such as fear and anxiety. Rather than the brain acting as a filter of unwanted sensation, in the higher centre induced pain state, rumination and magnification of sensations occur to create a pathological state.  Paradoxically, representation of body parts such as limbs and individual muscles can reduce in perceived size. In such instances the pain doesn't represent the sensation of pathology but rather pain has become the pathology. Hence, the brain generates pain in the brain, where the pain is perceived to be some sort of non-existant inflammatory or pathological sensation in the periphery. Evidence for this neural plasticity comes from imaging studies, where brain white matter structural properties have been shown to predict transition to chronic pain (Mansour et al 2013, Pain, 154, 10, 2160-2168). Specifically, differential structural connectivity to medial vs lateral prefrontal cortex and connectivity between medial prefrontal cortex and nucleus accumbens has been shown in people with persistent low back pain. In this case the back pain becomes the inciting event and given the persons' structural propensity, establishes specific functional coonectivity strength.  further reading Peripheral input is a powerful driver to neuroplasticity. Information gathered by touch, movement and vision, in the context of pain can lead to mal-adaptive plasticity, including the reorganisation of the somatosensory, and motor cortices, altered cortical excitability and central sensitisation. Examples of somatosensory reorganisation come from the work of Abrahao Baptista when investigating chronic anterior knee pain, who not only demonstrated reduced volume of Vastus Medialis but also is cortical translocation to another part of the cortex. ndividuals with patellofemoral pain (PFP) had reduced map volumes and an anterior shift in the M1 representations, greater overlap of the M1 representation and a reduction in cortical peaks across all three quadriceps (RF, VL, VMO) muscles compared with controls.(Te et al 2017 Pain Medicine, pnx036,   AKP = anterior knee pain The same researcher (Abrahao Baptista) has shown that maximal tolerable electrical stimulation (eg TENS) of muscles can induce normalisation of the cortical changes through a process called 'smudging'. Transcortical stumilation has also been applied as a cortical 'primer' prior to the application of more traditional therapy such as motor re-training, exercise, and manipulation. Body illusions are another novel way to promote the normalisation of cortical function through adaptive neuroplasticity. Examples come from people with hand athritis, whose perception of their hand size is underestimated (Gilpin et al 2015 Rheumatology, 54, 4, 678-682). Using a curved mirror, similar to that in theme parks, the visual input can be increased to perceive the body part as larger (Preston et al 2011 DOI: 10.1093/rheumatology/ker104 · Source:PubMed ) . Irrespective of size, watching a reflection of the hand while performing synchronised movements enhances the embodiment of the reflection of the hand (Whitkopf et al 2017, Exp Brain res, 23, 5, 1933-1944). These visual inputs are thought to affect the altered functional connectivity between areas of the brain thereby affecting the 'pain matrix'. Another, novel way of looking at movement and pain perception is the concept of the motor engram. This has been defined as motor skill acquisition through the modification and organisation of muscle synergies into effective movement sequences. The learning process is thought to be acquired as a child through experientially based play activity. The specific neural mechanisms involved are unknown, however they are thought to include motor map topography reflecting the capacity for skilled movement reorganisation of motor maps in a manner that reflects the kinematics of aquired skilled movement map plasticity is supported by a reorganisation of cortical microcircuitry involving changes in synaptic efficacy motor map integrity and topography are influenced by various neurochemical signals that coordinate changes in cortical circuitry to encode motor experience (Monfils 2005 Neuroscientist, 11, 5, 471-483). Interestingly, it is an intriguing notion that accessing motor engrams from patterns aquired prior to the pain experience might lead a normalisation of brain activity. My personal experience of severe sciatica with leg pain, sleepness nights and a SLR of less than 30 degrees, happened to coincide with training my 9 year old sons soccer training. I was noticing that the nights after i trained the children, I slept much better and my range of movement improved. I commenced a daily program of soccer ball tricks which i had been showing the kids, including 'juggling', 'rainbows' and 'around the worlds'. Eventually, I even took up playing soccer again after a 30 year abscence from the sport. Other than new activity related pain issues (DOMS), four years on, the sciatica hasn't returned. I can only conclude that this activity activated dormant childhood motor engram, worked on global balance, mobilised my nerve, encouraged cross cortical activity and turned my focus into finctional improvement. Further explainations for my expereience comes from evidence suggesting that a peripheral adaptive pain state is initiated, whereby transcortical inhibiton occurs by the contralaleral hemisphere to the one which controls the affected limb. Additionally, excitation cortical (M1) drive of the muscles of the contralateral limb to the one which is in pain also occurs. In such cases re-establishement of motor drive to the affected side is important. In terms of tendon rehabilitation, external audtory and visual cues using a metronome have been employed and are showing promising results (Ebonie Rio et al 2017 Personal communication). In terms of my experience with the soccer ball tricks, the external visual cues and the cross talk from using left and right feet, head, shoulders, and chest during ball juggling manouvers, whilst calling the rhythm to the kids may have been the crucial factor to overcome the dysfunctional brain induced pain - muscle inco-ordination cycle, which I was in. Additionally, I was cycling which allowed me to focus on motor drive into the affected.limb. However, work by Lorrimer Moseley on CRPS has established that 'brain laterality' must be established before commencing trans-cortical rehabilitation techniques. Lorrimer's clinical interventions use 'mirror imaging' techniques which are only effective once the patient is able to discriminate the left and right sides of the affected body parts, presented visually, in various twists and angles.   Alternatively, the altered pain state can result in a hostage like situation, whereby the pain takes control. Similar to the 'Stockholm Syndrome' where the hostage begins to sympathise with their captors, so do some peoples brain states, where it begin to sympathise with the pain, creating an intractable bondage and dysfunctional state. One screening question which may reflect commitment to the process of rehabilitatation is to question whether they were able to resist the cookie jar when they were a child? Or were they committed to any sporting endeavours as a child? This may give some indication for the presence of motor engrams which can be used to overcome dysfunctional pain induced muscle synergies (neurotags), but also indicate an ability to be self disciplined, as well as being able to reconcile and identify goal oriented objectives, in spite of the cognitive pain processes? Remember that neurons that fire together, wire together. Uploaded : 18 October 2017 Read More
  • Thu 03 Aug 2017

    Sickle Cell Trait and Acute Low Back Pain

    Researchers believe that lumbar paraspinal myonecrosis (LPSMN) may contribute to the uncommon paraspinal compartment syndrome and that sickle cell trait (SCT) may play a role. Sustained, intense exertion of these lumbar paraspinal muscles can acutely increase muscle size and compartment pressure and so decrease arterial perfusion pressure. This same exertion can evoke diverse metabolic forces that in concert can lead to sickling in SCT that can compromise perfusion in the microvasculature of working muscles. In this manner, they believe that SCT may represent an additional risk factor for LPSMN. Accordingly, they presented six cases of LPSMN in elite African American football players with SCT. See link below Read More
  • Thu 03 Aug 2017

    Ibuprofen, Resistance Training, Bone Density

    Taking Ibuprofen immediately after resistance training has a deleterious effect on bone mineral content at the distal radius, whereas taking Ibuprofen or undertaking resistance training individually prevented bone mineral loss. Read More
  • Tue 11 Jul 2017

    Mitochondrial Health and Sarcopenia

    The aging process (AKA 30 years of age onwards), in the presence of high ROS (reactive oxygen species) and/or damaged mitochondrial DNA, can induce widespred mitochondrial dysfunction. In the healthy cell, mitophagy results in the removal of dysfunctional mitochondria and related material. In the abscence of functional removal of unwanted mitochondrial material, a retrograde and anterograde signalling process is potentially instigated, which results in both motor neuronal and muscle fibre apoptosis (death) (Alway, Mohamed, Myers 2017, Ex Sp Sc Rev, 45, 2, 58-69). This process is irreversible. Investigations in healthy populations, have shown that regular exercise improves the ability to cope with regular oxidative stress by the buffering and 'mopping up' of ROS agents which are induced as a result of exercise. It is plausible and highly probable that regular exercise throughout life can mitigate against muscle fibre death (Sarcopenia). Importantly, this process of muscle fibre death can commence in the 4th decade of life. and be as much as 1% per year. Reduction of muscle mass can result in immune and metabolic compromise, including subclinical inflammation, type II diabetes as well as the obvious reduction in functional capacity for activities of daily living. Published 11 July 2017 Read More
  • Thu 22 Dec 2016

    Ehlers Danlos Syndrome

    Is your child suffering Ehlers Danlos Syndrome? Hypermobile joints, frequent bruising, recurrent sprains and pains? Although a difficult manifestation to treat, physiotherapy can help. Joint Hypermobility Syndrome (JHS) by Martin Krause When joint hypermobility coexists with arthralgias in >4 joints or other signs of connective tissue disorder (CTD), it is termed Joint Hypermobility Syndrome (JHS). This includes conditions such as Marfan's Syndrome and Ehlers-Danlos Syndrome and Osteogenesis imperfecta. These people are thought to have a higher proportion of type III to type I collagen, where type I collagen exhibits highly organised fibres resulting in high tensile strength, whereas type III collagen fibres are much more extensible, disorganised and occurring primarily in organs such as the gut, skin and blood vessels. The predominant presenting complaint is widespread pain lasting from a day to decades. Additional symptoms associated with joints, such as stiffness, 'feeling like a 90 year old', clicking, clunking, popping, subluxations, dislocations, instability, feeling that the joints are vulnerable, as well as symptoms affecting other tissue such as paraesthesia, tiredness, faintness, feeling unwell and suffering flu-like symptoms. Autonomic nervous system dysfunction in the form of 'dysautonomia' frequently occur. Broad paper like scars appear in the skin where wounds have healed. Other extra-articular manifestations include ocular ptosis, varicose veins, Raynauds phenomenon, neuropathies, tarsal and carpal tunnel syndrome, alterations in neuromuscular reflex action, development motor co-ordination delay (DCD), fibromyalgia, low bone density, anxiety and panic states and depression. Age, sex and gender play a role in presentaton as it appears more common in African and Asian females with a prevalence rate of between 5% and 25% . Despite this relatively high prevalence, JHS continues to be under-recognised, poorly understood and inadequately managed (Simmonds & Kerr, Manual Therapy, 2007, 12, 298-309). In my clinical experience, these people tend to move fast, rely on inertia for stability, have long muscles creating large degrees of freedom and potential kinetic energy, resembling ballistic 'floppies', and are either highly co-ordinated or clumsy. Stabilisation strategies consist of fast movements using large muscle groups. They tend to activities such as swimming, yoga, gymnastics, sprinting, strikers at soccer. Treatment has consisted of soft tissue techniques similar to those used in fibromyalgia, including but not limited to, dry needling, myofascial release and trigger point massage, kinesiotape, strapping for stability in sporting endeavours, pressure garment use such as SKINS, BSc, 2XU, venous stockings. Effectiveness of massage has been shown to be usefull in people suffering from chronic fatigue syndrome (Njjs et al 2006, Man Ther, 11, 187-91), a condition displaying several clinical similarities to people suffering from EDS-HT. Specific exercise regimes more attuned to co-ordination and stability (proprioception) than to excessive non-stabilising stretching. A multi-modal approach including muscle energy techniques, dry needling, mobilisations with movement (Mulligans), thoracic ring relocations (especially good with autonomic symptoms), hydrotherapy, herbal supplementaion such as Devils Claw, Cats Claw, Curcumin and Green Tee can all be useful in the management of this condition. Additionally, Arnica cream can also be used for bruising. Encouragment of non-weight bearing endurance activities such as swimming, and cycling to stimulate the endurance red muscle fibres over the ballistic white muscles fibres, since the latter are preferably used in this movement population. End of range movements are either avoided or done with care where stability is emphasized over mobility. People frequently complain of subluxation and dislocating knee caps and shoulders whilst undertaking a spectrum of activities from sleeping to sporting endeavours. A good friend of mine, Brazilian Physiotherapist and Researcher, Dr Abrahao Baptista, has used muscle electrical stimulation on knees and shoulders to retrain the brain to enhance muscular cortical representation which reduce the incidence of subluxations and dislocations. Abrahao wrote : "my daughter has a mild EDS III and used to dislocate her shoulder many times during sleeping.  I tried many alternatives with her, including strenghtening exercises and education to prevent bad postures before sleeping (e.g. positioning her arm over her head).  What we found to really help her was electrostimulation of the supraspinatus and posterior deltoid.  I followed the ideas of some works from Michael Ridding and others (Clinical Neurophysiology, 112, 1461-1469, 2001; Exp Brain Research, 143, 342-349 ,2002), which show that 30Hz electrostim, provoking mild muscle contractions for 45' leads to increased excitability of the muscle representation in the brain (at the primary motor cortex).  Stimulation of the supraspinatus and deltoid is an old technique to hemiplegic painful shoulder, but used with a little different parameters.  Previous studies showed that this type of stimulation increases brain excitability for 3 days, and so we used two times a week, for two weeks.  After that, her discolcations improved a lot.  It is important to note that, during stimulation, you have to clearly see the humerus head going up to the glenoid fossa" Surgery : The effect of surgical intervention has been shown to be favourable in only a limited percentage of patients (33.9% Rombaut et al 2011, Arch Phys Med Rehab, 92, 1106-1112). Three basic problems arise. First, tissues are less robust; Second, blood vessel fragility can cause technical problems in wound closure; Third, healing is often delayed and may remain incomplete.  Voluntary Posterior Shoulder Subluxation : Clinical Presentation A 27 year old male presented with a history of posterior shoulder weakness, characterised by severe fatigue and heaviness when 'working out' at the gym. His usual routine was one which involved sets of 15 repetitions, hence endurance oriented rather than power oriented. He described major problems when trying to execute bench presses and Japanese style push ups. In a comprehensive review of 300 articles on shoulder instability, Heller et al. (Heller, K. D., J. Forst, R. Forst, and B. Cohen. Posterior dislocation of the shoulder: recommendations for a classification. Arch. Orthop. Trauma Surg. 113:228-231, 1994) concluded that posterior dislocation constitutes only 2.1% of all shoulder dislocations. The differential diagnosis in patients with posterior instability of the shoulder includes traumatic posterior instability, atraumatic posterior instability, voluntary posterior instability, and posterior instability associated with multidirectional instability. Laxity testing was performed with a posterior draw sign. The laxity was graded with a modified Hawkins scale : grade I, humeral head displacement that locks out beyond the glenoid rim; grade II, humeral displacement that is over the glenoid rim but is easily reducable; and grade III, humeral head displacement that locks out beyond the glenoid rim. This client had grade III laxity in both shoulders. A sulcus sign test was performed on both shoulders and graded to commonly accepted grading scales: grade I, a depression <1cm: grade 2, between 1.5 and 2cm; and grade 3, a depression > 2cm. The client had a grade 3 sulcus sign bilaterally regardless if the arm was in neutral or external rotation. The client met the criteria of Carter and Wilkinson for generalized liagmentous laxity by exhibiting hyperextension of both elbows > 10o, genu recurvatum of both knees > 19o, and the ability to touch his thumbto his forearm Headaches Jacome (1999, Cephalagia, 19, 791-796) reported that migraine headaches occured in 11/18 patients with EDS. Hakim et al (2004, Rheumatology, 43, 1194-1195) found 40% of 170 patients with EDS-HT/JHS had previously been diagnosed with migraine compared with 20% of the control population. in addition, the frequency of migraine attacks was 1.7 times increased and the headache related disability was 3.0 times greater in migraineurs with EDS-HT/JHS as compared to controls with migraine (Bendick et al 2011, Cephalgia, 31, 603-613). People suffering from soft tissue hypermobility, connective tissue disorder, Marfans Syndrome, and Ehler Danlos syndrome may be predisposed to upper cervical spine instability. Dural laxity, vascular irregularities and ligamentous laxity with or without Arnold Chiari Malformations may be accompanied by symptoms of intracranial hypotension, POTS (postural orthostatic tachycardia syndrome), dysautonomia, suboccipital "Coat Hanger" headaches (Martin & Neilson 2014 Headaches, September, 1403-1411). Scoliosis and spondylolisthesis occurs in 63% and 6-15% of patients with Marfans syndrome repsectively (Sponseller et al 1995, JBJS Am, 77, 867-876). These manifestations need to be borne in mind as not all upper cervical spine instabilities are the result of trauma. Clinically, serious neurological complications can arise in the presence of upper cervical spine instability, including a stroke or even death. Additionally, vertebral artery and even carotid artery dissections have been reported during and after chiropractic manipulation. Added caution may be needed after Whiplash type injuries. The clinician needs to be aware of this possibility in the presence of these symptoms, assess upper cervical joint hypermobility with manual therapy techniques and treat appropriately, including exercises to improve the control of musculature around the cervical and thoracic spine. Atlantoaxial instability can be diagnosed by flexion/extension X-rays or MRI's, but is best evaluated by using rotational 3D CT scanning. Surgical intervention is sometimes necessary. An interesting case of EDS and it's affect on post concussion syndrome can be read elsewhere on this site. Temperomandibular Joint (TMJ) Disorders The prevelence of TMJ disorders have been reported to be as high as 80% in people with JHD (Kavucu et al 2006, Rheum Int., 26, 257-260). Joint clicking of the TMJ was 1.7 times more likely in JHD than in controls (Hirsch et al 2008, Eur J Oral Sci, 116, 525-539). Headaches associated with TMJ disorders tend to be in the temporal/masseter (side of head) region. TMJ issues increase in prevelence in the presence of both migraine and chronic daily headache (Goncalves et al 2011, Clin J Pain, 27, 611-615). I've treated a colleague who spontaneously dislocated her jaw whilst yawning at work one morning. stressful for me and her! Generally, people with JHD have increased jaw opening (>40mm from upper to lower incisors). Updated 17 October 2017  Read More
  • Fri 09 Dec 2016

    Physiotherapy with Sharna Hinchliff

    Physiotherapy with Sharna Hinchliff    Martin is pleased to welcome the very experienced physiotherapist Sharna Hinchliff to Back in Business Physiotherapy for one on one physiotherapy sessions with clients in 2017.  Sharna is a passionate triathelete and mother and has had several years experience working locally and internationally (New York and London) in the field of physiotherapy. Originally from Western Australia, Sharna graduated from the world renowned Masters of Manipulative Physiotherapy at Curtin University. read more Read More

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Updated : 10 May 2014

No responsibility is assumed by Back in Business Physiotherapy for any injury and/or damage to persons or property as a matter of product liability, negligence, or from any use of any methods, products, instruction, or ideas contained in the material in this and it's related websites. Because of rapid advances in the medical sciences, the author recommends that there should be independent verification of diagnoses and exercise prescription. The information provided on Back in Business Physiotherapy is designed to support, not replace, the relationship that exists between a patient/site visitor and their treating health professional.

Copyright Martin Krause 1999 - material is presented as a free educational resource however all intellectual property rights should be acknowledged and respected