Saturday, May 30, 2009
Professional Practice
Tuesday, May 19, 2009
Pathology: Condition 1
Condition 1: Osteoporosis
Final due: 5th June, Peer assessment: 19th June 2009.
Description:
Osteoporosis is defined as a systemic skeletal condition in which the bone tissue deteriorates faster than it is being formed, leading to thinning and weakness of bones. It is not possible to cure osteoporosis (Laroche, 2008), which is an irreversable, degenerative disease of the bone. According to Nevitt (1994), prevention is the best form of cure, as the loss of bone strength that occurs as a result of the loss of bone tissue is permanent. The risk is greatly increased in the elderly due to the slowed production of bone and the heightened possibility of falling and therefore fracturing bones. The best prevention is to build up stronger bones during childhood/adolescence when metabolism is at its peak, in order to reduce the likelihood of osteoporosis occurring later in life.
Etiology:
Osteoporosis is a standard part of the ageing process, and can occur as a secondary condition alongside other systemic diseases and endocrine disorders such as hyperthyroidism and diabetes (Sweet, Sweet, Jeremiah & Galazka, 2009).
It is characterised by loss of bone density and greater fragility of bone tissue, which is exacerbated by various etiological factors, such as a family history of osteoporosis, regular smoking and alcohol consumption and insufficient sun exposure, resulting in low vitamin D levels (Morgan & Kitchin, 2008). A diet low in calcium, certain medications (e.g. glucocorticoids) and low oestrogen levels also increase the likelihood of this disease (Sweet et al, 2009).
In women, the onset of osteoporosis appears most commonly after menopause, in anorexics, and otherwise hormonally or nutritionally deficient individuals (Morgan & Kitchin, 2008).
According to Premkumar (1999) bone pain and stress fractures may be present in the initial stages but as the progression is so subtle, the condition may go unnoticed until the event of a fracture, by which time the disease is in its advanced stage and acute damage has occurred. As osteoporosis is a subtle condition that gradually appears during the later stages of the client's life, there is no way of identifying the exact date of initial bone deterioration, and due to its irreversable nature it may require the remainder of the client's life to reach the peak of its expression. Loss of height and bone deformities such as kyphosis of the spine can indicate that the acute stages of the disease are present in the spinal bones (Holt, 2008).
Morphology:
A deficiency in the minerals that form bone tissue, particularly calcium and phosphate, can force the body to extract these from the bones in an effort to achieve homeostasis. This leads to accelerated osteoclastic resorption (Laroche, 2008) which results in the bone tissue presenting as demineralised, brittle and fragile, breaking easily with little stress (Premkumar, 1999).
Incidence:
1.3 million bone fractures per annum in the overall population have been caused by osteoporosis in the United States (Cooper, 1999). Within this population, 1 in 8 men will suffer from an osteoporotic fracture in their lifetime as will 1 in 2 white women (Sweet et al, 2009).
Indications for MT:Exercise, gentle massage particularly excercising caution over bones and bone structures, light to medium massage pressure over stiff neighbouring muscles using the fingertips in a circular motion or alternatively, the palm of the hand (Salvo, 2008).
Contraindications for MT:
Deeper massage over bones and greater stroke pressure. Deep tissue massage techniques near the site of osteoporotic bone are also contraindicated as these may aggravate the progression of bone fractures and so must only be used with necessary caution by a qualified practitioner (Leidig-Bruckner et al, 1997).
References:
Boschert, S. (2002) Risk Factors Don't Always Predict Osteoporosis. San Francisco: Internal Medicine News. Retrieved on the 16th May, 2009 from: http://www.internalmedicinenews.com//article/PIIS109786900271086X/fulltext
Cooper, C. (1999) Epidemiology of Osteoporosis. Southampton: Osteoporosis International. Retrieved on the 16th May, 2009 from: http://www.springerlink.com/content/865w7gj0t4496n1p/fulltext.pdf?page=1
Holt, E. (2008) Osteoporosis. Retrieved on the 16th May, 2009 from: http://www.nlm.nih.gov/medlineplus/ency/article/000360.htm
Laroche, M. (2008) Treatment of Osteoporosis: All the Questions We Still Cannot Answer. The American Journal of Medicine, 121 (9), p. 746.
Leidig-Bruckner, G., Minne, H., Schlaich, C., Wagner, G., Scheidt-Nave, C., Bruckner, T., Gebest, H. et al. (1997) Clinical Grading of Spinal Osteoporosis: Quality of Life Components and Spinal Deformity in Women with Chronic Lower Back Pain and Women with Vertebral Osteoporosis. Journal of Bone and Mineral Research, 12 (4), pp. 663 - 675.
Morgan, S. & Kitchin, B. (2008) Osteoporosis: Handy Tools for Detection, Helpful Tips for Treatment. The Journal of Family Practice, 57 (5), p. 313.
Nevitt, M. (1994) Epidemiology of Osteoporosis. San Francisco: University of California. Retrieved on the 16th May, 2009 from: http://www.ncbi.nlm.nih.gov/pubmed/7984777
Premkumar, K. (1999) Pathology A - Z: A Handbook for Massage Therapists. Calgary: Lippincott Williams & Wilkins.
Salvo, S. (2008) Mosby's Pathology for Massage Therapists. New York: Elsevier Health Sciences, p. 112.
Sweet, M., Sweet, J., Jeremiah, M. & Galazka, S. (2009) Diagnosis and Treatment of Osteoporosis. American Family Physician, 79 (3), p.193 - 200, Table 2.
Wednesday, April 8, 2009
Assessment task 1 - Blog 4 - Evaluation of Research Findings, Tessa Grinlinton.
The author contradicts themself in the ambiguous description of "sometoemotional release... again here we only deal with physical unwinding". By simply reading the term sometoemotional release we assume that a large portion of this will involve emotional and somatic releases, therefore we are not purely dealing with physical unwinding (which cannot be seperated from emotional or somatic phenomena, as they are all interconnected in the field of myofascial unwinding) but an infusion of all three. This would suggest that again the writer of this article has only investigated the topic from a limited set of viewpoints and has yet to see the whole picture. If they are however attempting to insinuate that pure physical unwinding has purely somatic and emotional effects they are still not linking the three bodies which are essentially part of this holistic field, and the ambiguous nature of the statement leaves the reader confused.
In the article 'Unravelling the Mysteries of Fascial Unwinding' the researchers have compiled a very relevant list of specialised articles related to myofascial release and the ideomotor effect (in which the subject makes movements unconsciously facilitating said release). Neuromuscular therapy, craniosacral therapy and bodywork journals boost the quality of reference sources, an article in the new scientist appears from the heading to be representing a skeptics point of view regarding the phenomenon of fascial unwinding: 'Greatest Myth of All'. However on close inspection of the article in question, we discover that it relates in fact to the unconscious processes of the brain related to perception and action. Again, the ambiguity of the reference heading may reflect an ambiguity in the article itself, reflecting an ongoing theme of ambiguity projected by the author.
The 'Healing ancient wounds: the renegades system' article is one of the main articles seeming to suggest that fascial unwinding and indeed tense fascia may have a psychological, subconscious and even spiritual connection, transcending original science based theory and simultaneously linking with it. There are also extensive references to neurobiology, the medical side of fascial unwinding and ideomotor reflexes, lending a scientifically proven base to these findings.
Overall, the writer seems to have attempted to isolate and detach the phenomenon of fascial unwinding as a seperate event in order to portray it in a conventionally scientific format, unfortunately this has not worked in his favour due to the inherently holistic nature of fascial unwinding. He has utilised many quality reference sources, namely peer reviewed journals, but his downfall lies in his communication of these findings in what should have been an academically rigorous manner.
References:
Halligan, P. & Oakley, D. (2000) Greatest Myth of All. New Scientist 168 (2265), 35 - 39.
My own thoughts.
Terra Rosa Bodywork E-News. (2008) Unravelling the Mysteries of Fascial Unwinding. Retrieved on the 26th April 2009, from: http://74.125.95.132/custom?q=cache:5ptBtbTPEsoJ:www.terrarosa.com.au/articles/Terra_News2a.pdf+unraveling+the+mysteries+of+unwinding&cd=1&hl=en&ct=clnk
Thursday, April 2, 2009
My Search Process: Memo
Pathology of Tennis Elbow (lateral epicondylitis)
Etiology:
Tennis elbow is a repetitive strain injury caused by recurrent twisting and jarring movements through the lateral forearm and elbow. Unlike its name suggests, it is not necessarily caused by playing tennis (O'Young, Young & Stiens, 2002). These initial movements cause minute tears in the muscular tissue and tendon fibres which have a cumulative effect resulting in pain from chronic overuse. Tendinitis is the initial inflammation of the forearm extensors and lateral epicondyle, which then develops into lateral epicondylitis (Shultz, Houglum & Perrin, 2005) as described below in Pathogenesis. Risk factors for the development of tennis elbow/lateral epicondylitis include middle age groups (30 - 50 year olds), professional athletes who use a racquet, bodybuilders and occupations such as construction and carpentry (Kraft, 2009).
Pathogenesis:
Once the tears have occurred, the continued repetition of jerky movements aggravates this tissue damage, resulting in inflammation through the radial portion of the forearm, restricting movement and causing pain (Cyriax, J., 1936). The radial tendon continues to rub against the inflamed periosteum of the lateral epicondyle, and according to Davies (2006) causes further swelling, pain when resting, restriction of movement and weakness through the affected forearm in the long term.
Morphology:
Once lateral epicondylitis has been triggered off by the initial tendinitis, morphological and histological changes occur. The fibroblasts and collagen fibres produced as part of the body's healing mechanism in response to injury, lay down a new extracellular matrix to knit together the tendinous tissues (Shultz et al, 2005). The collagen fibres then strengthen and harden into a tougher matrix of granulation tissue containing more fibroblasts, blood vessels, collagen and fibrinogen leading to 'scar' tissue (Wikipedia, 2009) at the site of the lesion.
Epidemiology:
Incidence - Tennis elbow/lateral epicondylitis affects 4-7 individuals per 1,000 patients as seen by a GP annually (Selby, 2004).
Prevalence - As indicated by research conducted by Allander (1974, cited in Pecina, 2004), tennis elbow/lateral epicondylitis was found to exist in 1 - 5% of a population of 15,268 individuals within an age range of 31 - 74 years.
References:
Cyriax, J. (1936) The Pathology and Treatment of Tennis Elbow (Electronic Version). The Journal of Bone and Joint Surgery, Inc., 18, pp. 921 - 940.
Davies, C. (2006) Self-Treatment of Tennis Elbow, Golfer's Elbow, Lateral Epicondylitis, Medial Epicondylitis, Elbow Tendinitis, Elbow Bursitis: The Trigger Point Therapy Workbook. Retrieved the 30th March, 2009 from: http://www.triggerpointbook.com/tennisel.htm
O'Young, B., Young, M. & Stiens, S. (2002) Physical Medicine and Rehabilitation Secrets. Philadelphia: Elsevier Health Sciences, pg. 267.
Shultz, S., Houglum, P. & Perrin, D. (2005) Examination of Musculoskeletal Injuries. Illinois: Human Kinetics, p. 280.
Wikipedia. (2009) Wound Healing. Retrieved the 30th March, 2009 from: http://en.wikipedia.org/wiki/Wound_healing