-original author unknown / lost.  found it scribbled on a piece of paper.

TriPlus back pain article page 2

links to page 1 and 2 of a previously published article in Triathlon Plus magazine.

link to article originally published in Triathlon Plus magazine.

See attached link for recent work for Triathlon Plus magazine.

It is commonly thought that the core is comprised of the abdominals and lower back muscles (Rectus abdominus, internal and external obliques, and the transverse abdominus). However, when looking at core training and movement patterns we can not be limited to these three muscle groups. For the lower back/pelvis/hip region there are 29 different muscles that each contribute to providing stability to the core, and this area can not be looked at in isolation from the upper body as issues around the pelvis will effect the shoulders and head stability / positioning, and vice versa.

Any low back pain or discomfort which riders suffer from can be attributed to the vast number of muscles that surround and intersect this region, and which may have been overlooked in any core program. If too much emphasis is placed on certain areas such as the anterior musculature (6 pack!) then muscle imbalances can develop leading to pain and injury. It is therefore necessary to emphasise the importance of a comprehensive core development program to cover the whole lumbar/pelvic/hip region.

Prospective Injuries from poor core stability

Lower back pain (lumbar spine and / or sacroiliac joint)

Abdominal strains

Groin strains

Hip flexor / abductor / adductor strains

Pelvic misalignment

Other musculoskeletal injuries due to compensation

Prospective Performance detriments

Poor balance in your seat causing increased tension in your legs and upper body.

Poor postural alignment

Poor transferability of force from lower to upper extremities and vice versa, eg. Changing body position, communication with the horse.

Inability to withstand and balance external forces from the horse

Core stability exercises can be incorporated into both land based training, and when on the horse. With the warmth and rhythmic movements of the horses movements can help relax tight muscles allowing the core muscles to switch on, and once warmed up the rider can practice simple movements such as pelvic tilts and trunk rotations. Instructors should give coaching cues around ensuring the rider is sat as tall as possible, lengthening through the spine, and activating the abdominals and obliques to support the spine.

Land based exercises can be done on the floor, on gym balls, with exercise bands, pilates trainers or IJoyRide trainer. But the exercise program must be tailored to the individual rider by the instructors and physiotherapist.

An often overlooked aspect of core training though, is endurance. Doing 6-10 reps for 3-4 sets will build the strength in the muscles, but to improve the endurance higher repetitions are needed, typically 25-30 repetitions. Holding contractions (isometric) also builds awareness of the correct positioning as well as strength through the tendons and connective tissues.

So in summary- some of the reasons you should look at incorporating specific core stability sessions into your riding, and off the horse training are:

Improved stability and positioning in the saddle

Greater control and communication with your horse

Lower risk of coming off – able to control/stay in the saddle during a spook/unexpected movement

Greater endurance when trotting/cantering

Reduced risk of injury

Tim Pigott
Physiotherapist - The Performance Clinic
www.theperformanceclinic.co.uk

Research has shown that by following a proactive recovery routine will reduce the stress effects on the body and improve subsequent training sessions and performances. Common practices which have been shown to be effective include:

Contrast bathing (1min cold, 2mins hot, x3-6)

Non-impact active recovery (7-10mins on an exercise bike)

Compression garments 12hrs (until the next morning)

The following is an example of a post match recovery routine:

Within the First 5 minutes – Rehydrate and Refuel

Eat/drink carbohydrates and protein, in a 4:1 ratio, utilizing high Glycemic Index (GI) carbohydrates.
A recovery sports drink is ideal.

5 – 20 minutes—Cool Down
Move lightly for five to eight minutes.
Stretch for eight to ten minutes.

15 – 20 minutes—Neural Recovery
Use a hydrotherapy tool (e.g. contrast showers or cold bath).
Self massage. (Using predominantly shaking techniques to stimulate neural recovery).
Continue to hydrate.

Within the First Hour—Refuel and Psychological Recovery

Continue to rehydrate.
Take in solid food (high and medium GI carbohydrates and protein) to replace carb stores, amino acids and electrolytes.
Carry out a performance review.
Start to unwind, using music for example as appropriate.

In the Evening—Psychological Recovery

Relax as appropriate
Continue to hydrate and refuel as appropriate with a focus on high quality protein to rebuild muscle tissue, maintain glycogen stores, prevent or reduce any inflammation, and optimise body weight.

Prior to Bed—Sleep Optimization

Use relaxation skills to switch off.
Follow your sleep guidelines.

For detailed nutritional advice Claire Harrison (www.theperformanceclinic.co.uk) is available for consultation.

Further reading

Gill, Beaven and Cook (2006) Effectiveness of post match recovery strategies in rugby players. Br J. Sports Med. 40:260-263

Spondylosis is part of the normal aging process of the spine. Dixon (1980) refers to the sequence of changes affecting one of more levels of disc degeneration, disc narrowing, osteophyte formation and osteoarthritis of the facet joints. Degeneration is characterized by slow, destructive changes which are not balanced by the regeneration that occurs in younger tissues (Grieve, 1981).

Roland and Van Tulder (1998) found that roughly 40% of patients with advanced disc degeneration on radiography do not have backpain, indicating that symptoms and radiographic changes may be unrelated.

In old age, the range of lumbar movement decreases. Originally this was thought to be due to the thinning of the intervertebral discs, however, it is now thought that only 30% of discs become thinner and in old age most discs increase in volume, become thicker centrally and more convex. Loss of vertebral column height is caused by loss of vertebral body height. The reason for loss of movement is thought to be due to disc stiffness or reduction of the elasticity of the disc (Twomey and Tayler 1983). The histological and biochemical changes include an increase in the total number of collagen fibres, a decreased in water content and a change in the prosteoglycagen ratios. There is also an increase in the “failure fatigue” of collagen in the older cartilage. These changes lead to a decrease in compliance of the disc fibrocartilage therefore making it less capable as acting as an efficient shock absorber. If the disc becomes vascularised, which can occur when the end plates are damaged, disc degeneration is accelerated. Nerve fibres then accompany the blood vessels into the disc and may serve a nocioceptive function.

Aging is accompanied by loss of both trabecular and cortical bone which results in a decrease in bone strength. The rate at which bone loss occurs is influenced by such factors as the menopause, declining calcium absorption, smoking and reduced physical exercise. The height of the vertebral bodies declines in old age, principally due to the reduction of transverse trabeculae which acts as “cross-braces” to the vertical trabeculae. As the trabeculae weaken, the vertebral body becomes less resistant to deformation and injury.

Osteophytes are outgrowths of healthy bone from the vertebrae. Their development is an important defensive mechanism against compressive forces which exceed the capacity fo the bone to resist them. They are composed of more compact, stronger bone, than the rest of the vertebral body. A young person with normal vertebrae may develop osteophytes when the pressure on the vertebral body is excessive, as in heavy manual work. Disc degeneration and the subsequent impaired shock-absorbing capacity of the vertebral column can also lead to their formation, as can pathological processes such as osteoporosis. Quite marked osteophytosis may be present without giving rise to symptoms.

Progressive resorption and thinning of the articular cartilage in the end plates occurs, with replacement by bone, so that over the age of 60 there is often only a thin layer of calcified cartilage separating the disc from the vertebral body. With increasing age, it is likely that there is a decrease in the diffusion of substances though the end plates. Since the cells in the disc are dependent on this route for the supply of nutrients and the removal of waste products, closure of the end plate route leads to nutritional deficiencies and a build up of metabolic products.

The epidemiology of spondylosis increases markedly with age and is uncommon below 45years of age. The normal aging process can be accelerated by increased exposure to mechanical stresses, which then give rise to degenerative changes. Which part of a motion segment is initially affected depends on the particular mechanical stresses or postures to which the spine is subjected and the integrity of the tissues themselves.

With age, there is a progressive decrease in the water-biding capacity of the nucleus of the disc.

Degenerative changes of intervertebral discs were classified in 1966 by Rolander based on their appearance on mid-dagital sections.

Grade 0 – Macroscopically normal / juvenile discs

Grade 1 – Normal adult discs, white in colour, the nucleus bulges.

Grade 2 – Age changes, less distinct boundary between nucleus and annulus, yellowish colour.

Grade 3 – Frank disc dessication, multiple fissures in nucleus and annulus, disc thinning.

The incidence of disc degeneration does increase in old age and the lower two lumbar levels are most affected as these levels are subject to greatest physical stress. Fissuring of the annulus is seen with increasing frequency in old age. The etiology of degerative disc disease includes both genetic and environmental factors. The incidence of disc degeneration in the spine as a whole is highest at the lowest two lumbar levels, particularly in the lumbosacral disc. This is because there is a large amount of movement at this level and the shear forces acting on the disc with the lordotic posture in the standing posture also increase the forces on the disc. Degenerative changes may predominantly affect the disc in some individuals, while in others they affect the facet joints, at least in the initial stages of degeneration.

Secondary chondrosis interverbralis (osteochondrosis intervertebralis) describes parthological changes outside the intervertebral disc and is characterized by changes in the cartilage end plates and sclerosis of the adjacent spongiosa of the vertebral bodies resulting in erosive chondrosis. Bony osteophytes develop in the region of the vertebral bodies (Spondylosis deformans).

As a result of the changes in the intervertebral discs and subsequent decrease in height, there are degenerative changes in the zygopophyseal joints (spondyloarthrosis). The decrease in height of the vertebral column causes a caudal dislocation of the inferior articular process and stresses the capsule of the joints.

Clinical Presentation

Age onset

• Usually middle aged and older
• Often heavy manual work
• Gradual onset

Pain

• Can be confined to lumbar region but may experience symptoms referred to the lower limbs

Diurnal Pattern

• worse first thing am./ stiffness, eases off fairly quickly
• activity dependent.

Subjective

Pain

• Variable, vague, ache, dull
• Low back pain, unilateral or bilateral lower limbs
• Often aggravated with walking, standing (extension activities)
• Often eased by flexion
• Eased by movement / resting in neutral

Objective

Posture - Flattened lumbar lordosis

Rom - Stiff lumbar segments, usually in an articular restriction

• Extension and side flexions usually worse than flexion

Neuro - Depends on whether nerve roots are involved.

Treatment

Postural correction / Back care advice / use of heat/ice.

Isometric exercises to strengthen the abdominal and spinal muscles.

Advise re: medication (analgesia, NSAIDS, glucosamine sulphate, amitriptyline)

Address muscle imbalance / stability as appropriate

Address joint restriction as appropriate, spinal mobilization techniques, often starting in the direction opposite to that of pain aggravation. Most effective in the first 6 weeks.

General activity programme / pacing advice.

Weight reduction if appropriate.

Erganomic adjustments if appropriate.

Prognosis

Dependent upon the level and degree of degeneration. Most cases of acute pain begin to settle within 6 weeks.

References

Adams, M., Bogduk, N., Burton, K., Dolan, P. The biomechanics of backpain. Churchill livingstone.

Andersson, G. (1997) The epidemiology of spinal disorders. The adult spine: principles and practice. Lippincott-Raven. Philadelphia 93-141

Dixon, A. (1980) Diagnosis of low back pain. The lumbar Spine and Backpain. 2^nd Ed. Pitman Medical. P135

Fujiwara, A., Lim, T.H., An, H.S., Tanaka, N., Jean, C.H., Adesson, G., Houghton, V.M. (2000) The effect of disc degeneration and facet joint OA on the segmental flexibility of the lumbar spine. Spine. 25(3) 3036-3044

Grieve, G.P. (1988) Clinical features. In: Grieve, G.P., ed. Common Vertebral joint problems, 2^nd ed. New York, Churchill Livingston 299-353.

Prescher, A. (1998) Anatomy of the aging spine. European Journal of Radiology. 181-195

Roland, M., Van Tulder. (1998) Should radiologists change the way they report plain radiographs of the spine. Lancet. 352, 229-230

Rolander, S.,D. (1996) Motion of the lumbar spine with special reference to the stability effect of posterior fusion. Orthopaedic Scandinavia.

Twomey, L.T., Taylor, J.R. (1993) Sagital movements of the human intervertebral lumbar column: a quantitative study of the role of the posterior vertebral elements. Archives of physical medicine and rehabilitation. 64, 322-325

With that in mind, it’s time to change the S+C program to further develop strength and skill sets in the gym.

Day 1
Semi supinated chins 2020 x8
Incline rotating chest press 2020 x15
Bulgarian split squat 2020 x15
X3-4 90sec rest 

Glute bridge 4141 x10
Deadlift 30x0 x15
Step downs 30x0 x15
X3-4 90sec rest 

Reverse fly 8-10 control
Reverse lunge with overhead DB 2020 x15
Bent over barbell row supinated 2020 x10
Incline bench reverse curl 3020 x20
X3-4 90sec rest 

Day 2
Push press bb 30x0  8-10
Back squat with DB heels raised 20x0 x15
Single arm row 8-10 3010
Gym ball hamstring curl 3010 x15
X3 with 120 rest

Single arm clean and press DB 10 each arm 1010
Power shrug with triple extension x8
X3 120 rest

Dips x8  4020
Seated DB rotator cuff 3010 x12
Ab crunch feet on bench toes inverted x15 3010
X3  90 sec rest

“A benign, painful, non-suppurative localised swelling of the costosternal, sternoclavicular or costochondral joints, most often involving the area of the 2^nd and 3^rd ribs.”

n Tietze’s syndrome, the cartilage of the costochondral joint becomes inflamed and swollen, causing pain and tenderness.

Tietze’s syndrome is very similar to another condition called costochondritis, which also causes pain in the costochondral joint. Sometimes, Tietze’s syndrome and costochondritis are thought to be the same, although only Tietze’s syndrome results in both pain and inflammation.

Aetiology

The cause is unknown but may occur following upper respiratory infections and excessive coughing.

The cause of Tietze’s syndrome is not fully understood, although it may be linked to upper respiratory tract infections, such as sinusitis and laryngitis. In some people with Tietze’s syndrome, it is thought that severe coughing may be a cause.

Anyone can develop Tietze’s syndrome, although it is most common among people who are between 20-40 years of age. The condition affects twice as many men as women.

Tietze’s syndrome could be more a part of seronegative disease than has been previously recognized (Aeschlimann A, Kahn MF 1990)

Pathological Process

Relatively unkown, nutritional and vitamin dificiencies have been suggested as well as traumatic pathogenesis including recurrent microtrauma, severe coughing and alterations of the ligamentus structures. There has also been an association reported with respiratory tract infections. Histological descriptions vary from unchanged costal cartilages to increased vascularity and degenerative changes with calcification or loss of ground substance resulting in a fibrillar appearace.

Clinical Presentation

Subjective

sharp pain at the sternum

Can be gradual or sudden onset

Can also affect the 2^nd and 3^rd ribs

Aggravated by physical activity, movement, coughing, sneezing, deep breath

Objective

Localised tenderness

Localised swelling, normally at the 2^nd and 3^rd ribs.

Pain may radiate to the arm.

Differential Diagnosis

MI

Pneumonia

Malignancy

Rheumatoid disorders

Infection

Non-Traumatic conditions affecting the SCJ

Fracture

Gout

Trigger points

Investigations

USS may aid diagnosis

Chest X-ray to rule out other pathologies

ECG to exclude cardiovascular conditions

CT scan

MRI

Blood testing (sedimentation rate or C-reactive protein test) can show signs of inflammation in patients with Tietze syndrome, whereas patients with costochondritis alone typically have normal tests for inflammation.

a combination of X-ray, CT, MRI and nuclear medicine is the best way to diagnose the disease and rule out other disorders. (Guglielmi G et. al. 2009)

Treatment

Reassurrance

NSAIDs

Local corticosteroid injection

Intercostal nerve blocks

Resection of the involved cartilage

Ice packs applied to local swelling can sometimes help to reduce pain and inflammation

Local lidocaine analgesic patch (Lidoderm) application can reduce pain.

Prognosis

Pain usually subsides within a few weeks, with some residual swelling persisting.

The course of the condition varies from spontaneous recovery to persistent symptoms over years.

References

Guglielmi G, Cascavilla A, Scalzo G, Salaffi F, Grassi W. Imaging of sternocostoclavicular joint in spondyloarthropaties and other rheumatic conditions. Clin Exp Rheumatol. 2009 May-Jun;27(3):402-8.

http://www.nhs.uk/Conditions/Tietzes-syndrome/Pages/Symptoms.aspx

Aeschlimann A, Kahn MF Tietze’s syndrome: a critical review. Clin Exp Rheumatol. 1990 Jul-Aug;8(4):407-12.