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I am just a concerned father of a 13 year old girl who has been playing competitive soccer for four years now.At what age do girls become more at risk to acl injuries and can anyone suggest what exercises she can do to minimize the chances of this happening.

Conflict of Interest:

None declared

Dear Editors,

The dorsal horns are not merely passive transmission stations but sites at which dynamic activities (inhibition, excitation and modulation) occur. [18]

Via a series of filters and amplifiers, the nociceptive message is integrated and analysed in the cerebral cortex, with interconnections with various areas. [1]

The processing of pain takes place in an integrated matrix throughout the neuroaxis and occurs on at least three levels, at peripheral, spinal, and supraspinal sites. [9]

Knowledge of the modalities of pain control is essential to correctly adapt treatment strategies (drugs, neurostimulation, psycho-behavioural therapy, etc.).

Dysfunction of pain control systems causes neuropathic pain. [1]

Spinal Cord Stimulation modalities evolved from the gate-control theory postulating a spinal modulation of noxious inflow. [16] [2] [7] [11] [12] [15] [17] [20] [22] [23] [24] [25] [26]

It has been demonstrated in multiple studies that dorsal horn neuronal activity caused by peripheral noxious stimuli could be inhibited by concomitant stimulation of the dorsal columns. [8]

Pain relief was more prominent at pain ascending through C fibers than pain ascending through Adelta fibers. [21]

Many theories on the mechanism of action of Spinal Cord Stimulation have been suggested, including activation of gate control mechanisms, conductance blockade of the spinothalamic tracts, activation of supraspinal mechanisms, blockade of supraspinal sympathetic mechanisms, and activation or release of putative neuromodulators. [14]

At present, Spinal Cord Stimulation is a well established form of treatment for failed back surgery syndrome, complex regional pain syndromes (CRPS), low back pain with radiculopathy and refractory pain due to ischemia. [4] [3] [8] [13]

Stimulation produced analgesia can provide a level of analgesia and efficacy that is unattainable by other treatment modalities. [19]

Spinal Cord Stimulation for the treatment of chronic pain is cost- effective when used in the context of a pain treatment continuum. [14]

Precise subcutaneous field stimulation is targeted to specific areas of neuropathic pain. [6]

We aim at attenuation or blockade of pain through intervention at the periphery, by activation of inhibitory processes that gate pain at the spinal cord and brain. [9]

Segmental noxious stimulation produces a stronger analgesic effect than segmental innocuous stimulation. [10]

That is exactly what intradermal sterile water injections do!

This therapeutic approach should not be limited only to elite athletes.

It can work for every patient with back pain.

References

[1] Prog Urol. 2010 Nov;20(12):843-52. Epub 2010 Oct 20. Anatomy and physiology of chronic pelvic and perineal pain. Labat JJ, Robert R, Delavierre D, Sibert L, Rigaud J. Centre federatif de pelviperineologie, clinique urologique, CHU Hotel- Dieu, 1, place Alexis-Ricordeau, 44093 Nantes, France.

http://www.ncbi.nlm.nih.gov/pubmed/21056357

[2] Int J Rehabil Res. 2010 Sep;33(3):211-7. Effect of transcutaneous electrical nerve stimulation on sensation thresholds in patients with painful diabetic neuropathy: an observational study. Moharic M, Burger H. Department of Physical and Rehabilitation Medicine, Linhartova 51, SI-1000 Ljubljana, Slovenia.

http://www.ncbi.nlm.nih.gov/pubmed/20042866

[3] Conf Proc IEEE Eng Med Biol Soc. 2009;2009:2033-6. Spinal cord stimulation for complex regional pain syndrome. Shrivastav M, Musley S. Medtronic Neuromodulation, 7000 Central Ave NE, Minneapolis, Minnesota, 55432 USA.

http://www.ncbi.nlm.nih.gov/pubmed/19964771

[4] J Clin Monit Comput. 2009 Oct;23(5):333-9. Spinal cord stimulation: principles of past, present and future practice: a review. Kunnumpurath S, Srinivasagopalan R, Vadivelu N. St George's School of Anaesthesia, Tooting, London, UK.

http://www.ncbi.nlm.nih.gov/pubmed/19728120

[5] Brain Res Rev. 2009 Apr;60(1):149-70. Epub 2008 Dec 31. Chloride regulation in the pain pathway. Price TJ, Cervero F, Gold MS, Hammond DL, Prescott SA. University of Arizona, Department of Pharmacology, USA.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2903433/?tool=pubmed

[6] Curr Pain Headache Rep. 2008 Jan;12(1):28-31. Peripheral nerve stimulation for chronic pain. Henderson JM. Stereotactic and Functional Neurosurgery, Stanford University School of Medicine, 300 Pasteur Drive, Edwards Building/R-227, Stanford, CA 94305, USA.

http://www.ncbi.nlm.nih.gov/pubmed/18417020

[7] Schmerz. 2007 Aug;21(4):307-10, 312-7. From Descartes to fMRI. Pain theories and pain concepts. Handwerker HO. Institut fur Physiologie und Pathophysiologie, Universitat Erlangen/Nurnberg, Deutschland.

http://www.ncbi.nlm.nih.gov/pubmed/17674057

[8] Pain Physician. 2002 Apr;5(2):156-66. Spinal cord stimulation. Stojanovic MP, Abdi S. Interventional Pain Program, MGH Pain Center, Department of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School, Cambridge, MA 02135, USA.

http://www.ncbi.nlm.nih.gov/pubmed/16902666

[9] J Bone Joint Surg Am. 2006 Apr;88 Suppl 2:58-62. Basic science of pain. DeLeo JA. Dartmouth-Hitchcock Medical Center, Dartmouth Medical School, Neuroscience Center at Dartmouth, Department of Anesthesiology, Lebanon, NH 03756, USA.

http://www.ncbi.nlm.nih.gov/pubmed/16595445

[10] Pain. 2005 May;115(1-2):152-60. Segmental noxious versus innocuous electrical stimulation for chronic pain relief and the effect of fading sensation during treatment. Defrin R, Ariel E, Peretz C. Department of Physical Therapy, School of Allied Health Professions, Sackler Faculty of Medicine, Tel-Aviv University, 69978 Ramat Aviv, Israel.

http://www.ncbi.nlm.nih.gov/pubmed/15836978

[11] Annu Rev Neurosci. 2003;26:1-30. Epub 2003 Mar 6. Pain mechanisms: labeled lines versus convergence in central processing. Craig AD. Atkinson Pain Research Laboratory, Barrow Neurological Institute, 350 W.Thomas Road, Phoenix, AZ 85013, USA.

http://www.ncbi.nlm.nih.gov/pubmed/12651967

[12] Sports Med. 2002;32(4):251-67. Return-to-work interventions for low back pain: a descriptive review of contents and concepts of working mechanisms. Staal JB, Hlobil H, van Tulder MW, K?ke AJ, Smid T, van Mechelen W. Department of Social Medicine and Research Centre on Work, Physical Activity and Health, VU University Medical Center, Van der Boechorststraat 7, Amsterdam, The Netherlands.

http://www.ncbi.nlm.nih.gov/pubmed/11929354

[13] Curr Pain Headache Rep. 2001 Apr;5(2):130-7. Stimulation methods for neuropathic pain control. Stojanovic MP. MGH Pain Center, Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, MA 02114, USA.

http://www.ncbi.nlm.nih.gov/pubmed/11252147

[14] Curr Rev Pain. 1999;3(6):419-426. Spinal Cord Stimulation: Indications, Mechanism of Action, and Efficacy. Krames E. Pacific Pain Treatment Centers, 2000 Van Ness Avenue, Suite 402, San Francisco, CA 94109, USA.

http://www.ncbi.nlm.nih.gov/pubmed/10998699

[15] Ann Pharm Fr. 2000 Mar;58(2):77-83. Pain and its main transmitters. Costentin J. Unite de Neuropsychopharmacologie Experimentale, ESA 6036 CNRS, Institut Federatif de Recherches Multidisciplinaires sur les Peptides=IFR 23, Faculte de Medecine et Pharmacie, 22, bd Gambetta, F 76000 Rouen.

http://www.ncbi.nlm.nih.gov/pubmed/10790600

[16] Neurol Res. 2000 Apr;22(3):285-92. Mechanisms of spinal cord stimulation in neuropathic pain. Meyerson BA, Linderoth B. Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.

http://www.ncbi.nlm.nih.gov/pubmed/10769822

[17] Pain. 1999 Aug;Suppl 6:S149-52. Regulation of spinal nociceptive processing: where we went when we wandered onto the path marked by the gate. Yaksh TL. Department of Anesthesiology, University of California, San Diego, USA.

http://www.ncbi.nlm.nih.gov/pubmed/10491984

[18] Pain. 1999 Aug;Suppl 6:S121-6. From the gate to the neuromatrix. Melzack R. Department of Psychology, McGill University, Montreal, Quebec, Canada.

http://www.ncbi.nlm.nih.gov/pubmed/10491980

[19] J Clin Neurophysiol. 1997 Jan;14(1):46-62. Stimulation of the central and peripheral nervous system for the control of pain. Stanton-Hicks M, Salamon J. Anaesthesia Pain Management Center, Cleveland Clinic Foundation, OH 44195, USA.

http://www.ncbi.nlm.nih.gov/pubmed/9013359

[20] Percept Psychophys. 1996 Jul;58(5):693-703. An investigation of the gate control theory of pain using the experimental pain stimulus of potassium iontophoresis. Humphries SA, Johnson MH, Long NR. Department of Psychology, Massey University, Palmerston North, New Zealand.

http://www.ncbi.nlm.nih.gov/pubmed/8710448

[21] J Peripher Nerv Syst. 1996;1(3):189-98. Pain relief by various kinds of interference stimulation applied to the peripheral skin in humans: pain-related brain potentials following CO2 laser stimulation. Kakigi R, Watanabe S. Department of Integrative Physiology, National Institute for Physiological Sciences, Okazaki, Japan.

http://www.ncbi.nlm.nih.gov/pubmed/10970109

[22] Nurs Stand. 1993 Jul 28-Aug 3;7(45):25-7. Pain: opening up the gate control theory. Davis P.

http://www.ncbi.nlm.nih.gov/pubmed/8398721

[23] Bull Acad Natl Med. 1989 Oct;173(7):855-60; discussion 860-1. Gate control of the nociceptive message: applications to the treatment of pain. Cambier J.

http://www.ncbi.nlm.nih.gov/pubmed/2620243

[24] Brain Res. 1983 Dec 5;280(2):217-31. Thalamic nucleus ventro-postero-lateralis inhibits nucleus parafascicularis response to noxious stimuli through a non-opioid pathway. Benabid AL, Henriksen SJ, McGinty JF, Bloom FE.

http://www.ncbi.nlm.nih.gov/pubmed/6652483

[25] Psychosom Med. 1979 Mar;41(2):101-8. A signal detection analysis of the effects of transcutaneous stimulation on pain. Malow RM, Dougher MJ.

http://www.ncbi.nlm.nih.gov/pubmed/441227

[26] GATE CONTROL OF ION FLUX IN AXONS. GOLDMAN DE. J Gen Physiol. 1965 May;48:SUPPL:75-7.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2213778/pdf/75.pdf

Conflict of Interest:

None declared

Subjective measure of monitoring exercise performance: Borg scale VIKRAM MOHAN 1 SRIJIT DAS 2

1.Department of Physiotherapy, Faculty of Health Sciences, Universiti Teknologi MARA, 42300, Puncak Alam,Malaysia 2.Department of Anatomy, Faculty of Medicine, Universiti Kebangsaan Malaysia, Jalan Raja Muda Abd Aziz, 50300 Kuala Lumpur,Malaysia

Subjective measure of monitoring exercise performance: Borg scale

We read with much interest the published article 'Manipulation effects of prior exercise intensity feedback by the Borg scale during open -loop cycling' by Pires and Hammond (1). We wish to share few scientific facts related to the article. Employment of rate of perceived exertion scale for prescribing exercise intensity in deception and on informed conditions was well portrayed in this article carried out by the authors. Functional exercise tolerance test such as six minute walk test and shuttle walk test were used to predict the functional limitation of the patients. These tests can be terminated by using the rate of perceived exertion (RPE) scale or Borg's scale when the subjects reach exhaustion. Prediction of functional limitation and termination of exercise was purely based on patient's subjective interpretation of ranges of scale. We would like to add some thoughts and suggestions on the methodology employed in this study such as on training protocol and later on, the Borg's scale. In the training protocol, it was mentioned that they underwent regular recreational physical conditioning programs for a period of six months. Even though it was mentioned as recreational physical conditioning programs, we are eager under which intensity, duration and frequency, these physical conditioning programs were carried out. Next, on the Borg's scale, we would like to query about the educational standards being considered for including the subjects for the study. This is because it needs a certain level of understanding to comprehend the range of scale. The authors suggest that their Borg's scale strategy failed to deceive subjects. Even though it failed to deceive subjects in the present study in which healthy subjects were recruited, our thoughts are aimed to carry out a study in chronic obstructive pulmonary disease subjects, in which the patients may have a tendency to develop exertion even when they walk for few meters or to perform basic activities of daily living. Moreover, healthy subjects may not be much aware of the exertion like pulmonary subjects whose condition may progress day by day. Hence, we suggest that centrally regulated effort model and psychological model which was explained in the present study, could be better explained in the deceived subjects when it was applied to patient population. Apart from that, we support the author's views that future studies are needed with more of objective measures such as functional magnetic resonance imaging (MRI) and physiological variables on the rate of perceived exertion. Rate pressure product (RPP) is one such physiological variable which can be used easily in the clinical set up to know the measure of energy consumption of the heart (2). Hence, in order to further explore this area of research, it can be added that RPP can also be utilized as one such an objective measures in future for prescribing exercise along with RPE scale. We applaud the meticulous work by the authors and appreciate the editor for publishing such an important work.

REFERENCES 1.Pires FO, Hammond J. Manipulation effects of prior exercise intensity feedback by the Borg scale during open-loop cycling. Br J Sports Med 2012; 46:18-22. 2.White WB. Heart rate and the rate-pressure product as determinants of cardiovascular risk in patients with hypertension. Am J Hypertens 1999; 12:50S-55S.

Conflict of Interest:

None declared

Exercise Induced lower leg pain is a common condition with a number of differential diagnoses which commonly overlap, one of which is chronic exertional compartment syndrome (CECS). Traditionally, CECS is thought to be caused by elevated pressures in a muscular compartment and is commonly diagnosed by measuring elevated intramuscular pressures.

However, as discussed by Hislop and Batt (2011), there continues to remain uncertainties with regards to methodological issues, risks involved and the necessity of resting and bilateral pressure measurements and debate on the types of compartments measured. Roberts & Franklyn- Millar (published online, 2011) found in their systematic review that the pressures used to diagnose CECS overlap with normal healthy subjects without symptoms.

Surely the question we need to ask is that, are we diagnosing, investigating and treating these patients effectively? As clinicians, we need to be sure that the intervention administered is necessary and beneficial. Given uncertainties, it would be prudent to understand the pathophysiology of the condition and the presenting symptoms.

Poor biomechanics can predispose to overload of muscular or tendon structures resulting in overuse and pain. Correcting the biomechanical element that is causing these symptoms can be a method to treat patients who present with symptoms akin to CECS.

A study done in patients with patello-femoral syndrome found that gait retraining resulted in significant improvement in hip mechanics that was associated with a reduction in pain and improvements in function (Noehran et.al, 2011). It is thought that the reduction in vertical load rates may be protective for the knee and reduce the risk for other running related injuries. It may be that this rationale can be extrapolated in exercise induced lower leg pain and is a way forward to treating these patients prior to subjecting them to invasive tests.

References

Hislop & Batt (2011) Chronic Exertional Compartment Syndrome. Br J Sports Med; Vol 45 (12): 954-955

Noehren, Scholz & Davis (2011) The effect of real-time gait retraining on hip kinematics, pain and function in subjects with patellofemoral pain syndrome. Br J Sports Med; Vol 45 (9): 691-696

Roberts & Franklyn-Millar (2011) The Validity of the diagnostic criteria used in Chronic Exertional Compartment Syndrome: A systematic review. Scand J Med Sci Sports. First published online: 13 Sep 2011

Conflict of Interest:

None declared

This study provides a useful additional information with regard to the merits of injection therapy in the management of resistant elbow tendinopathy. It would have been helpful if the authors had commented on the relative costs (time/money) of the treatments given the current pressures on minimising health care costs. There are variety of systems available for producing platelet rich plasma injections which can result in a significant cost burden to the health care provider or patient. Studies such of this will be picked up by manufacturers of these systems and used in their marketing.However if there is no significant difference in clinical outcome by using simple autologous blood injections then the authors should conclude that there is no enhanced benefit from using PRP and its associated costs are not justified. The volume of blood injected was not described in the section on "technique" and this should be corrected to make the methodology clear and reproducible. It is assumed that the 1.5 mL 'siphoned from the buffy coat layer' was used for the PRP injectionbut this needs to be clarified. Finally,whether it is the injection procedure and physical disruption of the tissue or the contents of the syringe that are important in stimulating a response remains unclear.

Conflict of Interest:

None declared