Back Clinic Complex Injuries Chiropractic Team. Complex injuries happen when people experience severe or catastrophic injuries, or whose cases are more complex due to multiple trauma, psychological effects, and pre-existing medical histories. Complex injuries can be serial injuries of the upper extremity, severe soft tissue trauma, and concomitant (naturally accompanying or associated), injuries to vessels or nerves. These injuries go beyond the common sprain and strain and require a deeper level of assessment that may not be easily apparent.
El Paso, TX’s Injury specialist, chiropractor, Dr. Alexander Jimenez discusses treatment options, as well as rehabilitation, muscle/strength training, nutrition, and getting back to normal body functions. Our programs are natural and use the body’s ability to achieve specific measured goals, rather than introducing harmful chemicals, controversial hormone replacement, unwanted surgeries, or addictive drugs. We want you to live a functional life that is fulfilled with more energy, a positive attitude, better sleep, and less pain. Our goal is to ultimately empower our patients to maintain the healthiest way of living.
In the first part of the 2-part article on femoro-acetabular impingement (FAI), chiropractor, Dr. Alexander Jimenez discussed FAI and how it can lead to insidious onset abdominal pain and damage the hip joint labrum, leading to early arthritic changes. Given that conservative management generally fails in young athletes and needs operation, part two describes the post-operative rehabilitation period required to take an athlete back to full competition.
The post-operative rehabilitation period is highly dependent on the magnitude of pathology and the subsequent procedure; weight-bearing development is consequently variably reported in the literature.
If the labrum is surgically repaired, then protected weight bearing is encouraged to allow the repair site in order to be protected during the early healing phase. Also, avoiding extremes of flexion (beyond 60�) and also internal/external rotation for the initial 4 to 6 weeks is important to safeguard the repaired labrum. Any positions that possibly create an impingement and boost inflammation ought to be prevented. These include:
Deep squatting
Prolonged sitting
Low couch sitting
Lifting off the ground
Pivoting on a fixed foot
These positions are more safely tolerated following the six week post-operative period. But on account of the selection of hip flexion limitations imposed in the initial six months, usual activities of daily living are rather restricted, making yield to work and daily chores challenging if not impossible from the first few weeks following surgery. Therefore, the post- surgical patient does have to make substantial lifestyle changes and they need assistance in the first six weeks following surgery.
Special precautions in certain types of FAI processes. Reshaping of the femoral head- neck junction can weaken the rectal neck so particular care must be taken in this post- operative period. Fracture of the femoral neck is an unlikely but potentially serious complication after a reshaping process. The athlete may be allowed to bear full weight, but crutches are needed to avoid twisting movements during the initial four weeks after surgery. High impact pursuits and high torsion moves should be prevented in the first 3 months, as bone grafting requires around three weeks to attain full structural integrity.
Furthermore, if microfracture of this femoral head is also done for femoral head cartilage defects, then the athlete ought to be restricted to partial weight- bearing for two weeks so as to optimize the premature maturation of the fibrocartilaginous healing response.
Key points
1. Weight bearing status is dependent on the kind of reshaping procedure, whether the labrum was repaired, and also what the surgeon favors
2. Steer clear of hip flexion beyond 60� in the first 4-6 Weeks
3. Avoid extremes of rotation
Post-Surgical Rehab
Rehabilitation protocols provided in the literature have a tendency to be quite generic in their own advice and at best explain broad transitional phases during the rehab process. They usually describe the transition in weight bearing status, the development of gait through walking into jogging, and give general guidelines as to how to and when to progress activity based on a time dependant strategy.
They then progress describing transitions into twisting and affect actions — usually explained as beginning at 3 weeks following surgery — and generally the guidance is that the speed with which the athlete progresses is variable and might need yet another 1 to 3 months to get full return based on the game. Trainers are usually advised that return to sports after surgical correction of FAI can require 4 to 6 weeks. However it’s critical that progression through rehabilitation phases is driven more by subjective and objective measures during the transition phases. This allows the athlete and therapist to track load (type and quantity) and ascertain whether the joint arrangements are able to withstand changes in load securely.
Wahoff et al (2014) have provided some standards which may be utilized to guide the transition from one point to the next(1). They describe their rationale and supply a complete description of all of the cited tests in their printed clinical comment. Essentially, the exit criteria they offer in each phase are as follows;
So as to advance through the six clarified stages, the athlete may undergo extensive physiotherapy, focusing on hip range of movement exercises, manual therapy and trigger point releases, active stretching, potentially deloaded activities like hydrotherapy or Alta G walking/ running and strong hip rotator and gluteal strengthening exercises. Much of this will be ‘controlled’ and led by the wishes of the surgeon as they will provide the framework on if and what happens concerning loading.
But more direct physiotherapy Interventions have been devised to direct the physiotherapist through the rehabilitation protocol. The Takla-O�Donnell Protocol (TOP) is a validated physiotherapy intervention program which may be utilized to induce the arthroscopically handled FAI patient (Bennel et al)(2).)�This protocol is shown in box 2.
Hip Muscle Control
The focus of the rest of this article Will be to summarize some common yet powerful hip strengthening exercises which may be used to progress the hip muscle control throughout the rehabilitation phases.
Regaining hip muscle power, particularly in the heavy hip external rotator group, is imperative from the FAI recovering athlete. Good muscle endurance and strength in those muscle groups will ensure adequate hip joint compression happens with motion to reduce any shearing effect between the head of femur and acetabulum(3). The muscle groups needing focus are (see figure 5):
Posterior fibres Gluteus Medius (PGMed)
Gluteus minimus
Superior and Inferior Gemellus
Internal and External Obturator
Quadratus Femoris
Piriformis
There’s plenty of exercises that can be utilized to fortify the hip joint musculature. The chosen ones below are a sample of some effective exercises that can be used throughout the rehabilitation phases. However, the key requirements of the contained exercises include:
1. Performed in neutral stylish places to no more than 60 degrees hip flexion. This range of movement protects the hip joint from any possibly damaging impingement.
2. Minimal rotation of the hip, letting them be used in most stages of the rehabilitation process.
3. Performed isometrically or utilizing little oscillating concentric/eccentric contractions — to contract and hold to maintain the hip joint compacted and stable. This represents how these muscles work in individual function.
Summary
In many ways. hip joint labral tears, capsule sprains, cartilage and muscle accidents and bony architectural issues like FAI can all lead to debilitating hip pain. FAI is a real concern for the athlete as the existence of a bone abnormality may lead to a painful hip impingement, damage to the acetabular labrum and premature onset degeneration. FAI’s don’t respond to conservative management. If the athlete suffers debilitating pain that affects competition then the options are either to cease competition all together or have the FAI surgically corrected. Once corrected by the surgeon, regaining complete motion and muscle strength and ultimate game related functional skills will require some time. Hip rotator muscle strengthening must shape the foundation of all handling post-surgical FAI issues.
References
1. International Journal of Sports Physical Therapy. 9(6); pp 813-826
2. Arthroscopy. 2006;22(12):1304-1311
3. Int J Sports Phys Ther. 2012;7(1):20-30.
In the first part of this 2-part series, chiropractor, Dr. Alexander Jimenez looked at the likely signs and symptoms of disc Herniation, in addition to the selection standards for micro-discectomy surgery in athletes. In this report he discusses the lengthy rehab period following a micro-discectomy procedure, and provides a plethora of strength based exercises.
Surgeries to ease disc herniation, with or without nerve root compromise, comprise traditional open discectomy, micro-discectomy, percutaneous laser discectomy, percutaneous discectomy and micro- endoscopic discectomy (MED). Other surgical conditions are employed in The literature like herniotomy that’s interchangeable with fragmentectomy or sequestrectomy. The saying ‘herniotomy’ is defined as removal of the herniated disc fragment just, and the ‘standard discectomy’ as elimination of the herniated disc along with its degenerative nucleus in the intervertebral disc space.
When surgery is required, minimizing tissue disruption and strict adherence to an aggressive rehabilitation regimen may expedite an athlete’s return to perform(1), that explains why micro discectomy is a favored surgical procedure for athletes. Micro discectomy procedures entails Removing a small part of the vertebral bone over a nerve, or removing the fragmented disc stuff from under the compressed nerve root.
The surgeon can then enter the spine by removing the ligamentum flavum that insures the nerve roots. The nerve roots can be visualized with functioning eyeglasses or with an operating microscope. The surgeon will then move the nerve to your side and to subsequently remove the disc material from beneath the nerve root.
It’s also sometimes required to eliminate A small portion of the related facet joint to permit access into the nerve root, and additionally to relieve pressure on the nerve root resulting in the facet joint. This procedure is minimally invasive since the joints, muscles and ligaments are left intact, and the process doesn’t interfere with the mechanical construction of the spinal column.
Endoscopic Lumbar Discectomy
Local Doctor performs lumbar discectomy using minimally invasive techniques.�From the El Paso, TX. Spine Center.
Surgical Outcomes
In general, athletes with lumbar disc Herniation have a favorable prognosis with traditional therapy; more than 90 percent of athletes using a disc herniation improve with non-operative treatment. Many demonstrate a response to conservative treatment with increased pain and sciatica within 6 weeks of the initial onset(2). This implies that the requirement to function immediately could be considered hasty.
However, in case of failed Conservative therapy, or together with the pressure of a significant upcoming competition, surgery might be needed in some instances. Even though it involves surgical therapy, micro-discectomy has been reported to have a high success rate — over 90 percent in some studies(3,4). Patients generally have hardly any pain, are able to return to preinjury activity levels, and therefore are subjectively happy with their results.
The achievement rate of micro-discectomy is The following studies have been summarised to underline the success rate of micro-discectomy procedures:
1. In a survey on 342 professional athletes Diagnosed with lumbar disc herniation in sports like hockey, football, basketball and baseball, it was discovered that powerful return to perform occurred 82% of this time, and 81 percent of surgically treated athletes returned for an additional average of 3.3 years(5).
2. From a limb paresis which might be associated with a disc herniation following surgical treatment. If the preoperative paresis was mild then they could anticipate an 84% likelihood of full recovery. Patients with more severe paresis have less chance of recovery (55%)(6).
3. Wang et al (1999) in a study on 14 athletes demanding discectomy processes found that in single degree disc procedures, the return to game was 90%. However when the procedure involved 2 levels enjoyed considerably less favorable results(7).
4. In a study of 137 National Football League players with lumbar disc herniation, surgical treatment of lumbar disc herniation led to a significantly more career and greater return to play rate than those treated non-operatively(8).
5. Schroeder et al (2013) reported 85% RTP rates in 87 hockey players, with no substantial difference in outcomes or rates between the surgical and nonsurgical cohorts(9).
6. A study by Watkins et al (2003) coping with professional and Olympic athletes revealed the acceptable outcomes of micro-discectomy concerning return to play, since elite athletes in general were highly encouraged to return to perform(10). Also, athletes who had single-level micro- discectomy were more likely to come back to their original heights of sports activities than were people who’d two-level micro- discectomies.
7. A study by Anakwenze et al (2010) investigating open discectomy at National Basketball Association participants demonstrated that 75% of patients returned to perform again compared with 88 percent in control subjects who did not undergo the operation(11).
8. A recent review found that conservative therapy, or micro-discectomy, in athletes using lumbar disc herniation seemed to be satisfactory concerning returning the injured athletes into their initial levels of sports activities(12).
These studies conclude that though a Analysis of lumbar disc herniation has career-ending potential, most gamers have the ability to return to play and generate excellent performance-based outcomes, even if surgery is required.
What is also apparent from research Studies is the level of this disc herniation can also determine prognosis after surgery. Athletes shower a greater difference in progress between surgical and non-operative treatment for upper amount herniations (L2-L3 and L3-L4) compared to herniations at the L4-L5 and L5-S1 levels. Patients using the upper level herniations needed less progress with non-operative treatment and marginally better operative outcomes than those with lower degree herniations(13).
There are several possible explanations A range of studies have revealed that low spinal canal cross-sectional area is associated with an increased likelihood of symptomatic disc herniation, and increased intensity of herniation symptoms. The spinal cross-sectional region is the smallest (thus contains a larger possibility of nerve compromise) at the most upper posterior section and the cross-sectional region increases further down to the lower lumbar spine(14).
The location of the disc herniation�(foraminal, posterolateral or central) may also contribute to differences.�In this study, upper lumbar herniations were more likely to happen in the much lateral and foraminal positions than were people in the lower two intervertebral degrees(13).
Post-Surgical Rehab
After micro-discectomy surgery, the Small incision and restricted soft tissue injury makes it possible for the patient to be ambulatory reasonably fast, and they’re usually encouraged to start rehabilitation sooner or later during the 2-6 weeks after surgery.
In a review on the efficacy of busy Rehabilitation in patients following lumbar spine discectomy, it may be reasoned that individuals can safely take part in high or low-intensity supervised or home-based exercises initiated at 4 to 6 weeks following first-time lumbar discectomy(15).
Herbert et al (2010) discovered that with Effective post-surgical rehabilitation plans, there was a key accent on lumbar stabilisation exercises(16). Second, positive trials tended to initiate rehabilitation earlier in the postoperative interval compared to negative trials (about 4 vs 7 weeks).
Outcome Measures
The most widely used result Measure following back injury and/or disc surgery is the Oswestry Disability Questionnaire(17). This questionnaire is reported to have good levels of test-retest reliability, responsiveness, and also a minimum clinically important difference estimated as 6 percent(18) Furthermore, treatment success has been defined as a 50 percent decrease in the Modified Oswestry Disability Questionnaire score(19).
Concerning physical performance measures following back disc or pain operation, a commonly used clinical examination is that the Beiring-Sorensen Back Extension examination (see Figure 1)(20). This test is performed in a prone/horizontal body position with the spine and lower extremity joints at neutral position, arms crossed at the chest, lower extremities and pelvis supported with the top back unsupported against gravity.
Rehabilitation Program
Presented below is a five-stage rehabilitation program. The stages involved in rehabilitation are:
1. Optimize tissue healing — protection and regeneration
2. Early loading and foundation
3. Progressive loading
4. Load buildup
5. Maximum load
This program has been designed to get a field hockey player with had a L5/S1 lumbar spine discectomy. Even though the progressions from one point to the next are driven by the exit standards related to that stage, it might be anticipated that the athlete could progress in post-surgery to ‘fit to compete’ in about 12-13 weeks.
In this phase it’s anticipated that the athlete will remain relatively quiet for 2-3 weeks post surgery. This allows for full tissue recovery to happen, including scar tissue maturation. The athlete is allowed to completely mobilize in full weight-bearing; however care needs to be taken using any flexion and rotation motions and no lifting will be allowed.
The athlete can begin with the physiotherapist with the objective to manage any gluteal and lumbar muscle trigger points and start�nerve mobilization techniques that show how to engage the TrA and LM muscles (see Figures 2a and 2b).�If the physiotherapist has access to your muscle stimulator (Compex), then this can be utilized in atrophy manner on the lumbar spine multifidus and erector spinae. The key criteria to exit this early phase are curable walking as well as also an Oswestry Disability Score of 41-60%.
Early Loading & Foundation
The primary feature of this phase is that the athlete can start early and low-load strength exercises focusing on muscle activation in a neutral spine position, along with a progressive selection of motion program to improve lumbar spine flexion, extension and rotation. In this stage that the physiotherapist will guide the athlete through safe and gentle stretches to your hip quadrant muscles like the hip flexors, gluteals, hamstrings and adductors. The athlete also lasts gentle neuro-mobilization exercises to advance the freedom of the sciatic nerve — an issue in this condition as neurological tethering is a chance as a result of scar tissue formation caused by the surgical procedure.
The athlete can also be encouraged to start hydrotherapy in the form of walking in water (waist high) along with swimming fitnesscenter. In addition, he/she must start a string of low degree muscle activation drills in this stage (see Figure 3) that can be performed every day. This exercise teaches the athlete to hip flex (fashionable hinge) whilst maintaining a neutral spine. The neutral spine is maintained by using a light broomstick aligned with the back with the touch points being the occiput, the 6th thoracic vertebrae (T6) and the posterior sacrum.
Progressive Loading
In this phase the athlete continues with a variety of movement progression along with the physiotherapist progresses manual therapy to the pelvis and lumbar spine. Neuro-mobilization techniques can also be progressed. The significant change in this phase is that the progression of load on many of the strength and muscle control exercises.�Two exercises here are the �standing twisties� and the �crook lying pelvic rotation� exercise (Figures 4 and 5).�These movements are the introductory spinning based movements. The primary progression about fitness drills is the athlete can begin pool running drills.
Load Accumulation
This is the stage where the athlete begins to advance the load in strength-based exercises. Resistance is used in the form of barbell load and band resistance. Three exceptional exercises performed here are the ‘kneeling hip thruster’, ‘deadbug antirotation press’ and also the ‘quadruped walkout’ (Figures 6-8 — explained in detail in the online database of exercises).
The athlete also begins running drills at this phase and it might be expected that as well as building running Amount, the athlete should progress over four weeks to close to full sprint speeds. This is also the stage whereby they would initiate mild to moderate sports special skills drills. Another characteristic of this stage is that the athlete starts the ‘Sorensen test’ exercise (Figure 9) and it will be expected that they can maintain the position for no less than 90 seconds before advancing to the next phase.
Maximum Load
In this final stage, the athlete spreads all core and strength exercises to maximum loads, and they work with the fitness trainer on coming to squat and functional fitness center lift movements. Skill progression can also be advanced alongside sprint and agility drills. The last exit standards prior to advancing to endless strength and training work is they have to keep the ‘Sorensen test’ for 180 seconds and their self documented Oswestry scale ought to be someplace between 0-20%.
Chiropractor, Dr. Alex Jimenez looks at lumbar spine disc herniation. What are the Likely signs and symptoms associated with disc herniation, and what would be the selection criteria for micro-discectomy operation in athletes? Complaint in the young college age athlete and professional athlete, and it’s been estimated that over 30% of athletes complain of back pain at least once in the profession(1).
Lumbar spinal disc herniation is one kind Of lumbar injury that can’t just cause painful low back pain, but can also compress nerve roots and create radicular referral of pain into the lower leg with related sensation changes and muscle contraction. This injury will not only influence the short-term opponent ability of the athlete, but might also reoccur and eventually become persistent possibly causing a career ending injury.
Managing disc herniation from the athlete Usually begins with conservative therapy and if this fails, surgical solutions are considered. But often elite athletes will request a quicker resolution to their symptoms to minimize time away from competitors. Therefore, providing the criteria for lumbar spine surgery are suggested, the conservative period will often be compressed, and surgery will be sought earlier. The favored surgical process for the athlete with a disc herniation is that the lumbar disc micro-discectomy.
Anatomy & Biomechanics
A significant biomechanical role in the spine, allowing for motion between the spinal segments while spreading compressive, shear, and torsional forces(2). These discs include a thick outer ring of fibrous cartilage termed the annulus fibrosis (akin to the onion rings enclosing the center of the onion), which encompasses a more gelatinous core called the nucleus pulposus, which is included within the cartilage end plates inferiorly and superiorly.
The intervertebral disc consists of Cells and substances such as collagen, proteoglycans, and thin fibrochondrocytic tissues, which enable transmission and absorption of forces arising from body weight and muscle activity. To do so, the disc depends mainly on the structural condition of the nucleus pulposus, annulus fibrosis and the vertebra lend plate. If the disc is normal and is functioning optimally, then forces are spread across the disc evenly(3).
But disc degeneration (mobile Degradation, lack of hydration( disc failure) may decrease the capacity of the disc to withstand extrinsic forces, as forces are no longer distributed and spread evenly. Tears and fissures from the annulus can lead, and with adequate external forces, the disc material may herniate. Alternatively, a sizable biomechanical force set on a healthy, ordinary disc may cause extrusion of disc material as a result of crushing failure of this annular fibers — illustrations include a hefty compression type mechanism because of a fall on the tailbone, or strong muscle contraction such as heavy weight lifting(4).
Herniations represent protrusions of Disc material beyond the confines of this annular lining and in the spinal canal (see Figure 1)(5). If the protrusion does not invade the canal or undermine nerve roots then back pain may be the only symptom.
Endoscopic Discectomy 3D Simulation
The pain associated with lumbar Radiculopathy happens due to a mix of nerve root ischemia (due to compression) and inflammation (because of neurochemical inflammatory mediators released from the disc). Throughout a herniation, the nucleus pulposus puts pressure on weakened regions of the annulus, and proceeds through the diminished websites in the annulus in which it ultimately forms a herniation(6 ft). It follows from this that some kind of disc degeneration may exist prior to the disc may really herniated(7).
In contrast to other respiratory Tissues, discs have a inclination to degenerate earlier in life, with some studies demonstrating adolescents presenting signs of degeneration between the ages of 11 to 16(8). With increasing age, there’s further degeneration of the intervertebral discs.
While the disc might be in danger of harm in All fundamental planes of motion, it’s particularly susceptible during repetitive flexion, or hyper-flexion, combined with lateral bending or rotation(10). Traumatic events such as excessive axial compression may also damage the inner structure of the disc. This can occur as a result of a fall or powerful muscular forces developed during tasks such as heavy lifting.
Athletes are generally exposed to high loading conditions. Examples of this include:
1. World-class power lifters, in which the calculated compressive loads on the backbone are involving 18800 Newtons (N) and also 36400N acting in the L3-4 motion segment(11).
2. Elite level football linesmen who have Been proven to present time-related hypertrophy of this disc and changes in vertebrae endplate in response to this repetitive high loading and axial pressure(12).
3. Long distance runners have been Shown to undergo significant strain into the intervertebral disc, indicated by a reduction in disc height(13).
Herniations could be classified depending on Ultimately, herniations are also identified based on level, with most herniations happening at the L4/5 and L5/S1 intervertebral disc level; these can then in turn affect the L5 and S1 nerve roots resulting in clinical sciatica(15). Upper level herniations are less common, and when they do occur with radiculopathy, they will affect the femoral nerve. Finally, the prevalence of disc injury rises increasingly caudally, with the best numbers at the L5/S1 degrees(16).
Herniation In Athletes
The offending movements implicated in The 20-35 age group are the most common group to herniate a disc, most likely because of the fluid nature of the nucleus pulposis and due to behavior(18). This age group are more likely to participate in sports which need high lots of flexion and spinning or are reckless with their positions and positions during loading.
The sports most at risk of disc herniation are:
Hockey
Wrestling
Soccer
Swimming
Basketball
Golf
Tennis
Weightlifting
Rowing
Throwing events
These are the sports that involve either significant Furthermore, those who take part in more and more severe training regimes seem to be at higher risk of spinal pathologies, as do people involved in sports.
Signs & Symptoms Indicating Discectomy
The efficacy of management programs for lumbar spine disc herniation — in terms of the decision to operate or treat conservatively — will be discussed in greater depth in part 2 of this series. However, the decision to operate within an athlete is generally driven by the motivation and approaching goals the athlete has put themselves. They may in fact favor a comparatively simple micro-discectomy instead of waiting for symptoms to abate through an extended period of rehabilitation.
This conservative period of Management may involve medicine therapy, epidural injections, relative back and back muscle recovery, acupuncture, osteo/chiropractic interventions. On the other hand, the normal presenting symptoms and signs that suggest a substantial disc herniation that will require surgical intervention in the athlete comprise:
Low back pain with pain radiating down one or both legs
Positive straight leg raise test
Radicular pain and neurological signs consistent with the nerve root level affected
Mild weakness of distal muscles such as extensor hallucis longus, peroneals, tibialis anterior and soleus. These would fit with the myotome relevant for the disc level
MRI confirming a disc herniation
Possible bladder and bowel symptoms
Failed conservative rehabilitation
Time span in which to enable conservative rehabilitation to be effective. In the overall population, medical practitioners will most likely prescribe a minimal 6-week traditional period of treatment with an overview at 6 weeks as to whether to expand the rehabilitation a further 6 weeks or to seek a specialist opinion. The expert may then attempt more medically orientated interventions such as epidural injections.
The athlete nevertheless will have these They might be more inclined to experience an epidural very early in the conservative period to assess the effectiveness of this procedure. If no signs of progress are evident in a couple of weeks then they may choose to get an immediate lumbar spine micro- discectomy.
Endoscopic Lumbar Discectomy
Local Doctor performs lumbar discectomy using minimally invasive techniques. From the El Paso, TX. Spine Center.
Imaging
MRI remains the favored system of Identifying lumbar spine disc herniation, since it’s also very sensitive to detecting nerve root impingements(23). However, abnormal MRI scans can occur in otherwise asymptomatic patients(25); hence, clinical correlation is always essential before any surgical thought. What’s more, patients can present with clinical signs and symptoms which suggest the diagnosis of acute herniated disc, and yet lack evidence of sufficient pathology on MRI to warrant operation.
Therefore it has been proposed that a Volumetric analysis of a herniated disc on MRI may be potentially beneficial in checking the suitability for operation. Several writers have previously mentioned the possible value of volumetric evaluation of herniated disc on MRI as part of their selection criteria for lumbar surgery(26).
In a survey conducted in Michigan State University, it was found that the size and positioning of the herniated disc determined that the likelihood for operation with what researchers called ‘types 2-B’ and ‘types 2-AB’ being the most likely candidates for surgery(27).
The MRI protocol to your lumbar spine consists of (see Figure 2)
1.Sagittal plane echo T1- weighted sequence
2. Sagittal fast spin echo proton density sequence
3. Sagittal fast spin echo inversion recovery sequence
4.Axial spin echo T1- weighted sequence
Summary
Disc herniations are not a common Complaint in athletes, but they do happen in sports which involve high loads or repetitive flexion and rotation movements. Sufferers of a disc herniation will normally feel focused low-back pain, maybe with referral in the lower limb with associated neurological symptoms if the nerve root was compressed.
Managing a disc herniation within an General population as frequently the risk of a Protracted failed rehabilitation period is Bypassed for the protected and low risk Micro-discectomy procedure. In the Discuss the exact surgical alternatives involved Observing a lumbar spine micro-discectomy.
References
1. Sports Med. 1996;21(4):313�20
2. Radiology. Oct 2007;245(1):62-77
3. Arthritis Research & Therapy. 2003;5(3):120-30
4. The Journal of Bone and Joint Surgery. American volume. Feb 2004;86-A(2):382 � 96
5. Radiology. Oct 2007;245(1):43-61
6. Spine. Sep 15 1996;21(18):2149-55
7. Spine. May-Jun 1982;7(3):184-91
8. Spine. Dec 1 2002;27(23):2631-44
9. Lancet 1986;2:1366�7
10. Disease-A-Month:DM. Dec 2004;50(12):636-69
11. Spine. Mar 1987;12(2):146-9
12. The American Journal of Sports Medicine. Sep 2004;32(6):1434-9
13. The Journal of International Medical Research. 2011;39(2):569-79
14. Spine. 2001;26:E93-113
15. Spine. 1990;15:679-82
16. British Journal of Sports Medicine. Jun 2003;37(3):263-6
17. Prim Care. 2005;32(1):201�29
18. McGill, S.M. Low back disorders: Evidence based prevention and rehabilitation, Human Kinetics Publishers, Champaign, IL, U.S.A., 2002. Second Edition, 2007
19. Spine. Apr 1991;16(4):437-43
20. Skeletal radiology. Jul 2006;35(7):503-9
21. British Journal of Sports Medicine. Nov 2007;41(11):836-41
22. The American Journal of Sports Medicine. Jun 2009;37(6):1208-13
23. Spine. Mar 15 1995;20(6):699-709
24. Phys Sportsmed. 2005;33(4):21�7
25. J Bone Joint Surg Am 1990 . 2:403�408
26. J Orthop Surg (Hong Kong) 2001. 9:1�7
27. Eur Spine J (2010) 19:1087�1093
Chiropractor, Dr. Alexander Jimenez examines the role of biomechanics in medial tibial stress syndrome…
Medial tibial stress syndrome (MTSS � commonly known as shin splints) is not medically serious, yet can suddenly side- line an otherwise healthy athlete. Roughly five percent of all athletic injuries are diagnosed as MTSS(1).
The incidence increases in specific populations, accounting for 13-20% of injuries in runners and up to 35% in military recruits(1,2). MTSS is defined as pain along the posterior-medial border of the lower half of the tibia, which is present during exercise and (usually) diminishes during rest. Athletes identify the lower front half of the leg or shin as the location of discomfort. Palpation along the medial tibia usually reproduces the pain.
Causes Of MTSS
There are two main hypothesized causes for MTSS. The first is that contracting leg�muscles place a repeated strain upon the medial portion of the tibia, inducing periostitis � inflammation of the periosteal outer layer of bone. While the pain of a shin splint is felt along the anterior leg, the muscles that arise from this area are the posterior calf muscles (see figure 1). The tibialis posterior, flexor digitorum longus, and the soleus all arise from the posterior- medial aspect of the proximal half of the tibia. Therefore, the traction force from these muscles on the tibia is unlikely to be the cause of the pain typically felt on the distal portion of the leg.
A variation of this tension theory is that the deep crural fascia (DCF) � the though- connective tissue that surrounds the deep posterior compartment muscles of the leg � pulls excessively on the tibia, again causing trauma to the bone. Researchers at�the University of Honolulu examined a single leg from five male and 11 female adult cadavers. They confirmed that in these specimens, the muscles of the posterior compartment originated above the portion of the leg that is typically painful in MTSS, and the DCF indeed attached along the entire length of the medial tibia(3).
Doctors at the Swedish Medical Centre in Seattle, Washington wondered if, given the anatomy, could the tension from the posterior calf muscles produce a related strain on the tibia at the insertion of the DCF, and thus be the mechanism of injury(4)?
In a descriptive laboratory pilot study of three fresh cadaver specimens, they found that strain at the insertion site of the DCF along the medial tibia progressed linearly as tension increased in the posterior leg muscles. This confirmed that a mechanism for a tension-induced injury at the medial tibia is plausible. However, studies of bone periosteum in MTSS patients have yet to find inflammatory markers consistently enough to confirm the periostitis theory(5).
Tibial Bowing
The second causation theory for MTSS is that repetitive or excessive loading causes a bone-stress reaction in the tibia. The tibia, unable to adequately bear the load, bends during weight bearing. The overload results in micro damage within the bone, and not just along the outer layer. When the repetitive loading outpaces the bone�s ability to repair, localized osteopenia can result. Thus, some consider a tibial stress fracture to be the result of a continuum of bone stress reactions that include MTSS(1).
Magnetic resonance imaging (MRI) of the symptomatic leg often shows bone�marrow edema, periosteal lifting, and areas of increased bony resorption in patients with MTSS(1,5). This supports the bone- stress reaction theory. Magnetic resonance imaging of an athlete with a clinical presentation of MTSS can also help rule out other causes of lower leg pain such as tibial stress fracture, deep posterior compartment syndrome, and popliteal artery entrapment syndrome.
Risk Factors For MTSS
While the aetiology of MTSS is still theoretical, the risk factors for athletes developing it are well determined. A large navicular drop, as determined by the navicular drop test (NDT), significantly correlates with a diagnosis of MTSS(2,5). The NDT measures the difference in height position of the navicular bone, from a neutral subtalar joint position in supported non-weight bearing, to full weight bearing (see figures 2 and 3). The NDT is an indication of the degree of arch collapse during weight bearing. An excursion of more than 10 mm is considered excessive and a significant risk factor for the development of MTSS(5).
Research suggests that athletes with MTSS are found more likely to be female, have a higher BMI, less running experience, and a previous history of MTSS(2,5). Running kinematics for females can differ from males and fit a pattern that is known to leave them vulnerable to anterior cruciate ligament tears and patellofemoral pain syndrome(5). This same biomechanical pattern may also predispose females to MTSS. Hormonal considerations and low bone density are possibly contributing factors in increasing the risk of MTSS in the female athlete as well.
A higher BMI in an athlete likely indicates they have more muscle mass rather than they are overweight. The end result, however, is the same in that the legs bear a significantly heavy load. It is thought that in these instances, the bone growth�stimulated by the tibial bowing may not progress rapidly enough, and injury to the bone occurs. Therefore, those with a higher BMI may need to progress their training programs more slowly, to allow for adaptation.
Those with less running experience are more likely to make training errors (often identified by the athlete) as the catalyst for MTSS. These include increasing distance�too rapidly, changing terrain, overtraining, poor equipment (shoes), etc. Inexperience may also lead the athlete to return to activity too soon, thus accounting for the higher prevalence of MTSS in those who had suffered MTSS previously. Full recovery from MTSS can take anywhere from six to ten months, and if the cause of injury was not rectified or the athlete returns to training too soon, the chances are good the pain will return(5).
Biomechanical Considerations
The NDT is used as a measurable indication of foot pronation. Pronation is a tri-planar movement comprised of eversion at the hind foot, abduction of the forefoot, and dorsiflexion of the ankle. Pronation is a normal movement, and essential in walking and running. When the foot strikes the ground at the initial contact phase of running, the foot begins to pronate and the joints of the foot assume a loose-packed position. This flexibility helps the foot absorb ground reaction forces (see figure 4).
During the loading response phase, the foot further pronates, reaching peak pronation by around 40% of stance phase(6). In mid stance, the foot moves out of pronation and back to a neutral position. During terminal stance, the foot supinates, moving the joints into a closed packed position and creating a rigid lever arm from which to generate the forces for toe off.
Beginning with the loading response phase and throughout the remainder of the single leg stance phase of running, the hip is stabilized, extended, abducted and externally rotated by the concentric contraction of the hip muscles of the stance�leg (the gluteals, piriformis, obturator internus, superior gemellus and inferior gemellus). Weakness or fatigue in any of these muscles can result in internal rotation of the femur, adduction of the knee, internal rotation of the tibia, and over-pronation (see figure 5). Overpronation therefore, can be a result of muscle weakness or fatigue. If this is the case, the athlete may have a quite normal NDT, and yet when the hip muscles don�t function as needed, can overpronate.
In a runner who has significant over pronation, the foot may continue to pronate into mid stance, resulting in a�delayed supination response, and thus less power generation at toe off. The athlete may attempt two biomechanical fixes here that could contribute to the development of MTSS. Firstly, the tibialis posterior will strain to prevent the over pronation. This can add tension to the DCF and strain the medial tibia. Secondly, the gastroc-soleus complex will contract more forcefully at toe off to improve the power generation. Again, the increased force within these muscle groups can theoretically add tension to the medial tibia through the DCF and possibly irritate the periosteum.
Evaluating The Injured Athlete
Knowing that over pronation is one of the leading risk factors for MTSS, start your evaluation at the ground and work your way up. First, perform the NDT, noting if the difference is more than 10mm. Analyze the athlete�s running gait on a treadmill, preferably when the muscles are fatigued, as at the end of a training run. Even with a normal NDT, you may see evidence of over pronation in running (see figure 6).
Next evaluate the knee. Is it adducted? Notice if the hip is level or if either hip is more than 5 degrees from level. These are indications that there is likely weakness at the hip. Traditional muscle testing may not reveal the weakness; therefore, functional muscle testing is required.
Observe the athlete perform a one-legged squat with arms in and arms overhead. Does the hip drop, the knee adduct and the foot pronate? Test the strength of hip abductors in side lying, with hip in neutral, extended, and flexed, keeping the knee straight (see figure 7). Test all three positions with hip rotated in neutral, and at end ranges of external and internal rotation. Test hip extension in prone with the knee straight and bent, in all three positions of hip rotation: external, neutral and internal. The position where you find the weakness is where you should begin strengthening activities.
Treat The kinetic Chain
If there is weakness in the hip, begin by having the athlete perform isometric exercises in the position of weakness. For instance, if you find weakness in hip abduction with extension, then begin isolated isometrics in this position. Not until the muscles consistently fire isometrically in this position for three to five sets of 10 to 20 seconds should you add movement. Once the athlete achieves this level, begin concentric contractions, in that same position, against gravity. Some examples are unilateral bridging and side lying abduction. Eccentric contractions should follow, and then sport specific drills.
Keep in mind if there are other biomechanical compensations, they must also be addressed. If the tibialis posterior is also weak, begin strengthening there. If the calf muscles are tight, initiate a stretching program. Utilise whatever modalities might be helpful. Lastly, consider a stabilising shoe if the ligaments in the foot are over stretched. Using a stabilising shoe for a short time during rehabilitation can�be helpful in cuing the athlete to adopt new movement patterns.
Conclusion
The best way to prevent shin pain from MTSS is to decrease the athlete�s risk factors. Ideally, each athlete should have a basic running gait analysis and proper shoe fitting. Include hip strengthening in functional positions such as unilateral stance as part of the strengthening program. Pair inexperienced athletes with a more experienced mentor to ensure proper training, use of equipment, and investigation of pain at onset. They may be more likely to tell a teammate they are feeling pain than a coach or trainer. Progress the running schedule of heavier athletes more slowly to allow adaptation of the bone. Ensure that athletes fully rehabilitate before returning to play because the chances of recurrence of MTSS are high.
References
1. Am J Sports Med. 2015 Jun;43(6):1538-47
2. Br J Sports Med. 2015 Mar;49(6):362-9
3. Med Sci Sports Exerc. 2009;41(11):1991-1996
4. J Am Podiatr Med Assoc. 2007 Jan;97(1):31-6
5. J Sports Med. 2013;4:229-41
6. Gait and Posture. 1998;7:77�95
Chiropractor, Dr. Alexander Jimenez gives insight into the relevant anatomy and functional biomechanics of the piriformis muscle, highlights the role it plays in musculoskeletal dysfunction and looks at management options in cases of muscle dysfunction.
The piriformis muscle (PM) is well-known in the fraternity of sports medicine as a significant muscle in the posterior hip. It is a muscle that has a role in controlling hip joint rotation and abduction, and it is also a muscle made famous due to its �inversion of action� in rotation. Furthermore, the PM also grabs attention due to its role in the contentious �piriformis syndrome�, a condition implicated as a potential source of pain and dysfunction, not only in the general population but in athletes as well.
Relevant Anatomy
The name piriformis was first coined by Belgian Anatomist Adrian Spigelius in the early 17th century. Its name is derived from the Latin word �pirum� meaning �pear� and �forma� meaning �shape� � ie a pear shaped muscle (see Figure 1)(1).
The PM originates on the anterior surface of the sacrum and is anchored to it by three fleshy attachments between the first, second, third and fourth anterior sacral foramina(2). Occasionally its origin may be so broad that it joins the capsule of the sacroiliac joint above and with the sacrotuberous and/or sacrospinous�ligament below(3,4).
PM is a thick and bulky muscle, and as it passes out of the pelvis through the greater sciatic foramen, it divides the foramen into the suprapiriform and infra-piriform foramina(5). As it courses antero-laterally through the greater sciatic foramen, it tapers out to form a tendon that is attached to the superior-medial surface of the greater trochanter, commonly blending with the common tendon of the obturator internus and gemelli muscles(6).
The nerves and blood vessels in the suprapiriform foramen are the superior gluteal nerve and vessels, and in the infra- piriforma fossa are the inferior gluteal nerves and vessels and the sciatic nerve (SN)(5). Due to its large volume in the greater sciatic foramen, it has the potential to compress the numerous vessels and nerves that exit the pelvis.
PM is closely associated with the other short hip rotators that lie inferior such as the superior gemellus, obturator internus, inferior gemellus and obturator externus(2). The primary difference between the PM and other short rotators is the relationship to the SN. The PM passes posterior to the�nerve whereas the other otators pass anterior (see figure 2).
Variants
A few anatomical variants have been found with the PM:
1. Additional medial attachments to the first and fifth sacral vertebrae and to the coccyx(7).
2. The tendon may fuse with the gluteus medius or minimus above, or superior gemellus below(7).
3. In less than 20% of cases it is divided into two distinct portions through which part or all of the sciatic nerve may pass(7).
4. It may blend with the posterior hip joint capsule as a conjoined tendon with the obturator internus(8).
5. The distal attachment of the PM has shown to vary in dimensions and position on the supero-medial surface of the greater trochanter. It can span a distance of between 25-64% of the anterior-posterior length on the greater trochanter, with 57% attaching more anterior and 43% more posterior(9).
6. Pine et al (2011) studied the insertion point extensively and found that four types of insertion existed and these were classified based on the relationship to the obturator internus(10). The variability in position and breadth of the distal attachment of the PM muscle may influence the validity of the concept known as �inversion of action� (see below).
The other hotly debated issue is the relationship between the PM and the SN. The conclusion is that there are several anatomical variations of the PM and its SN relationship. The sub-types of this variation include(11-13):
Type 1 (A below). Typical pear shape muscle with the nerve running anteriorly and inferiorly to this (in 70%-85% of cases).
Type 2 (B below). The PM is divided into two parts with the common peroneal nerve running between the two parts and the tibial nerve running anterior and below (found in 10-20% of cases).
Type 3 (C below). The peroneal portion loops over the top of the muscle and the tibial portion is below (found in 2-3% of cases).
Type 4 (D below). Undivided nerve passing through the PM (occurs in about 1% of cases).
It is also believed that two other very uncommon variations occur (see E and F below).
Type A is the most common variation, showing the SN passing below the PM
Functional Considerations
The primary functional roles of the PM are;
1. Hip external rotation(15).
2. Abductor at 90 degrees of hip flexion(15).
3. In weight-bearing, the PM restrains the femoral internal rotation during stance phase of walking and running(2).
4. Assists the short hip rotators in compressing the hip joint and stabilising the joint(6).
5. As it can exert an oblique force on the sacrum, it may produce a strong rotary shearing force on the sacroiliac joint (SIJ). This would displace the ipsilateral base of the sacrum anteriorly (forward) and the apex of the sacrum posteriorly(16).
As the PM is the most posterior of the hip external rotators due to its attachment on the anterior surface of the sacrum, it has the greatest leverage to exert a rotation effect on the hip joint. It is often seen clinically that the PM appears to be tight and hypertonic, while the other short hip�rotators that are closer to the axis of rotation become inhibited and hypotonic.
Inversion Of Action
The most contentious issue related to the function of the PM is its �reversal-of- function role� or �inversion of action� role. Many authors have suggested that as the hip approaches angles of 60-90 degrees and greater, the tendon of the PM shifts superiorly on the greater trochanter. As a result, its line of pull renders it ineffective as a hip external rotator; however it does contribute to internal hip rotation. Therefore it reverses its rotation role at high hip flexion angles(15,17,18).
The function of the PM at varying joint angles is an important consideration for the clinician who is evaluating and treating �piriformis syndrome�. Often it has been advocated to stretch the hip into flexion, adduction and external rotation to stretch the PM over the glutes by utilising the �reversal of function� concept.
However, more recent anatomical dissection studies have shown that the attachment of the PM onto the greater trochanter can be variable and in some instances it may insert in a position whereby it is unable to reverse its function, for example in a more posteriorly placed attachment(19). Therefore, stretching the PM into external rotation when the hip is flexed beyond 90 degrees � based upon reversal of function � would be ineffective as a treatment or misleading as an examination technique(19)
MSK Dysfunction & PM Syndrome
Many decades ago, the role that the PM played in creating sciatic-like symptoms was first suggested by Yeoman (1928) when it was considered that some cases of sciatica may originate outside the spine(20). This was supported soon after when Freiberg and Vinkle (1934) successfully cured sciatica by surgically dividing the PM(21). Based on cadaver dissections Beaton and Anson (1938) gave the hypothesis that the spasm of the PM could be responsible for the irritation of the SN(12).
The term �piriformis syndrome� was first coined by Robinson in 1947(22) and was applied to sciatica thought to be caused by an abnormality in the PM (usually traumatic in origin) with emphasis on ruling out more common causes of sciatica such as nerve root impingement from a disc protrusion. It soon became an accepted clinical entity � but with no consensus about the exact clinical signs and diagnostic tests to differentiate it from other sources of sciatica(23,24).
Piriformis syndrome can be defined as a clinical entity whereby the interaction�between the PM and SN may irritate the SN and produce posterior hip pain with distal referral down the posterior thigh, imitating �true sciatica�. Isolating the dysfunction to this region usually follows exclusion of the more common causes of buttock pain and sciatica.
More specifically, complaints of buttock pain with distal referral of symptoms are not unique to the PM. Similar symptoms are prevalent with the more clinically evident lower back pain syndromes and pelvic dysfunctions. Thus, a thorough evaluation of these regions must be performed to exclude underlying pathology(4). It has been suggested that piriformis syndrome� is responsible for 5-6% of cases of sciatica(25,26). In the majority of cases, it occurs in middle-aged patients (mean age 38 yr)(27) and is more prevalent in women(28).
Pathogenesis Of Piriformis Syndrome (PS)
PS may be caused by or relate to three primary causative factors;
1. Referred pain due to myofascial trigger points (see Figure 4)(2,28-30). Examples include tight and shortened muscle fibres precipitated by muscle overuse such as squat and lunge movements in external rotation, or�direct trauma(16). This increases the girth of the PM during contraction, and this may the source of the compression/entrapment.
2. Entrapment of the nerve against the greater sciatic foramen as it passes through the infrapiriform fossa, or within a variant PM(29,31).
3. SIJ dysfunction causing PM spasm(29,32).
Janvokic (2013) has presented a number of causative factors in PS(29);
1. Gluteal trauma in the sacroiliac or gluteal areas.
2. Anatomical variations.
3. Myofascial trigger points.
4. Hypertrophy of the PM or spasm of the PM.
5. Secondary to spinal surgery such as laminectomy.
6. Space occupying lesions such as neoplasm, bursitis, abscess, myositis. 7. Intragluteal injections.
8. Femoral nailing.
Symptoms
Typical symptoms reported in piriformis syndrome include:
A tight or cramping sensation in the buttock and/or hamstring(33).
Gluteal pain (in 98% of cases)(34).
Calf pain (in 59% of cases)(34).
Aggravation through sitting and squatting(35), especially if the trunk is inclined forward or the leg is crossed over the unaffected leg(36).
Possible peripheral nerve signs such as pain and paraesthesia in the back, groin, buttocks, perineum, back of the thigh (in 82% of cases)(34).
Physical Findings & Examinations
Palpable spasm in and around the PM and obturator internus and external tenderness over the greater sciatic notch (in 59-92% of cases)(34,35). The patient is placed in the Sims position. The piriformis line overlies the superior border of the PM and extends from immediately above the greater trochanter to the cephalic border of the greater sciatic foramen at the sacrum. The line is divided into equal thirds. The fully rendered thumb presses on the point of maximum trigger-point tenderness, which is usually found just lateral to the junction of the middle and last thirds of the line.
Hip flexion with active external rotation or passive internal rotation may exacerbate the symptoms(36).
Positive SLR that is less than 15 degrees the normal side(37).
Positive Freiberg�s sign (in 32-63% of cases)(34,35). This test involves reproducing pain on passive forced internal rotation of the hip in the supine position � thought to result from passive stretching of the PM and pressure on the sciatic nerve at the sacrospinous ligament.
Pacers sign (in 30-74% of cases)(34,35). This test involves reproducing pain and weakness on resisted abduction and external rotation of the thigh in a sitting position.
Pain in a FAIR position(34). This involves the reproduction of pain when the leg is held in flexion, adduction and internal rotation.
An accentuated lumbar lordosis and hip flexor tightness predisposes one to increased compression of the sciatic nerve against the sciatic notch by a shortened piriformis(38).
Electro-diagnostic tests may prove useful (see below).
Investigations
Conventional imaging such as X-ray, CT scan and MRI tend to be ineffective in diagnosing piriformis syndrome.
However, some value may exist in electro- diagnostic testing.
It is beyond the scope of this paper to discuss in detail the process of electro- diagnostic testing; the reader is directed to references for more a more detailed description of how these tests are administered(35,36,39). However the purpose of these tests is to find conduction faults in the SN. Findings such as long-latency potentials (for example the H reflex of the tibial nerve and/or peroneal nerve) may be normal at rest but become delayed in positions where the hip external rotators are tightened(27,36,39).
It is accepted that the tibial division of the SN is usually spared, the inferior gluteal nerve that supplies the gluteus maximus may be affected and the muscle becomes atrophied(40). However testing of the peroneal nerve may provide more conclusive results as is more likely to be the�impinged portion of the SN. The H-wave may become extinct during the painful position of forced adduction-internal rotation of the affected leg(36).
The �Myth� Of Piriformis Syndrome
Stewart 2003 argues that piriformis syndrome is an often over-used term to describe any non-specific gluteal tenderness with radiating leg pain(41). He argues that only in rare cases is the PM implicated in nerve compression of the SN to truly qualify as a piriformis syndrome. He cites only limited evidence and cases where the diagnosis of piriformis syndrome can be made.
1. Compressive damage to the SN by the PM. Stewart cites studies whereby in few isolated studies, the SN was seen to be compressed by the PM in instances such as hypertrophy of the muscle,�usual anatomical anomalies such as a bifid PM, and due to compression by fibrous bands.
2. Trauma and scarring to the PM leading to SN involvement; it is possible that rare cases of true Piriformis Syndrome have been caused by direct heavy trauma to the PM due to a blunt trauma to the muscle. This is termed �post- traumatic PS�.
McCory (2001) supports this argument by stating that it is more likely that (given the anatomical relationship of the PM to the various nerves in the deep gluteal region) the buttock pain represents entrapment of the gluteal nerves, and the hamstring pain entrapment of the posterior cutaneous nerve of the thigh, rather than the SN alone(33). This would explain the clinically observed phenomenon in the absence of distal sciatic neurological signs. Whether the PM is the cause of the compression has not been clearly established. It is possible that the obturator internus/gemelli complex is an alternative cause of neural compression. He suggests using the term �deep gluteal syndrome� rather than piriformis syndrome.
Treatment
When it is believed that a piriformis syndrome exists and the clinician feels that a diagnosis has been made, the treatment will usually depend on the suspected cause. If the PM is tight and in spasm then initially conservative treatment will focus on stretching and massaging the tight muscle to remove the PM as being the source of the pain. If this fails, then the following have been suggested and may be attempted(23,36):
Local anaesthetic block � usually performed by anaesthesiologists who have expertise in pain management and in performing nerve blocks.
Steroid injections into the PM.
Botulinum toxin injections into the PM.
Surgical Neurolysis.
Here, we will focus on therapist-directed interventions such as stretching of the PM and direct trigger point massage. It has always been advocated that PM stretches are done in positions of hip flexion greater than 90 degrees, adduction and external rotation to utilize the �inversion of action� effect of the PM to isolate the stretch to this muscle independent of the other hip external rotators.
However, recent evidence from Waldner (2015) using ultrasound investigation discovered that there was no interaction between hip flexion angle and the thickness of the PM tendon in both internal and lateral hip rotation stretching � suggesting that the PM does not invert its action(19). Furthermore, Pine et al (2011)(9) and Fabrizio et al (2011)(10) in their cadaveric studies found that the PM insertion is a lot more complex and varied than first thought. It is possible that the PM may invert its action only in some subjects but not others.
Therefore, due to the disagreements and confusions over the �inversion of action� concept, it is recommended that the clinician �covers all bases� and performs two variations of a PM stretch � stretches in flexion, adduction and external rotation and stretches in flexion, adduction and internal rotation. Examples of these stretches are given in figures 5-7 below.
Trigger Points & Massage
(see Figure 8)
The best approach to palpate the PM trigger points is in the position suggested by Travel and Simons(2) and this is shown below. In this position, the clinician can feel for the deep PM trigger points and apply a sustained pressure to alleviate the trigger�points � and also apply a flush massage to the muscle in this position.�In this position the large gluteus maximus is relaxed and it is easier to feel the deeper PM.
Summary
The PM is a deep posterior hip muscle that is closely related anatomically to both the sacroiliac joint and the sciatic nerve. It is a hip external rotator at hip flexion angles of neutral to 60 degrees of hip flexion, an abductor when in flexion and also contributes to hip extension.
It has been previously accepted that the PM will �invert its action� or �reverse its function� after 60 degrees of flexion to become a hip internal rotator. However, recent ultrasound and cadaveric studies has found conflicting evidence that this �inversion of action� may in fact not exist.
PM is a muscle that is a dominant hip rotator and stabiliser, and thus has a tendency to shorten and become hypertonic. Therefore, stretching and massage techniques are best utilised to reduce the tone through the muscle. Furthermore, it has also been implicated in compression and irritation of the sciatic nerve � often referred to as piriformis syndrome�.
References
1. Contemp Orthop 6:92-96, 1983.
2. Simons et al (1999) Travell and Simons� Myofascial Pain and Dysfunction. Volume 1 Upper Half of the Body (2nd edition). Williams and Wilkins. Baltimore.
3. Anesthesiology; 98: 1442-8, 2003.
4. Joumal of Athletic Training 27(2); 102-110, 1996.
5. Journal of Clinical and Diagnostic Research. Mar, Vol-8(3): 96-97, 2014.
6. Clemente CD: Gray�s Anatomy of the Human Body, American Ed. 30. Lea & Febiger, Philadelphia, 1985 (pp. 568-571).
7. Med J Malaysia 36:227-229, 1981.
8. J Bone Joint Surg;92-B(9):1317-1324, 2010.
9. J Ortho Sports Phys Ther. 2011;41(1):A84, 2011.
10. Clin Anat;24:70-76, 2011.
11. Med Sci Monit, 2015; 21: 3760-3768, 2015.
12. J Bone Joint Surg Am 1938, 20:686-688,1938.
13. Journal of Clinical and Diagnostic Research. 2014 Aug, Vol-8(8): 7-9, 2014.
14. Peng PH. Piriformis syndrome. In: Peng PH, editor. Ultrasound for Pain Medicine Intervention: A Practical Guide. Volume 2. Pelvic Pain. Philip Peng Educational Series. 1st ed. iBook, CA: Apple Inc.; 2013 .
15. Kapandji IA. The Physiology of Joints. 2nd ed. London: Churchill Livingstone; 1970: 68.
16. J Am Osteopath Assoc 73:799-80 7,1974.
17. J Biomechanics. 1999;32:493-50, 1999.
18. Phys Therap. 66(3):351-361, 1986.
19. Journal of Student Physical Therapy Research. 8(4), Article 2 110-122, 2015.
20. Lancet. 212: 1119-23, 1928.
21. J Bone Joint Surg Am 16:126�136, 1934.
22. Am J Surg 1947, 73:356-358, 1947.
23. J Neurol Sci; 39: 577�83, 2012.
24. Orthop Clin North Am; 35: 65-71, 2004
25. Arch Phys Med Rehabil; 83: 295-301,2002.
26. Arch Neurol. 63: 1469�72, 2006.
27. J Bone Joint Surg Am; 81: 941-9,1999.
28. Postgrad Med 58:107-113, 1975.
29. Can J Anesth/J Can Anesth;60:1003�1012, 2013.
30. Arch Phys Med Rehabil 69:784, 1988.
31. Muscle Nerve; 40: 10-8, 2009.
32. J Orthop Sports Phys Ther;40(2):103-111, 2010.
33. Br J Sports Med;35:209�211, 2001.
34. Man Ther 2006; 10: 159-69, 2006.
35. Eur Spine J. 19:2095�2109, 2010.
36. Journal of Orthopaedic Surgery and Research, 5:3, 2010.
37. Muscle & Nerve. November. 646-649, 2003.
38. Kopell H, Thomnpson W. Peripheral Entrapment Neuropathies. Huntington, NY: Krieger, 1975:66.
39. Arch Phys Med Rehabil;73:359�64, 1992.
40. J Bone and Joint Surg, 74-A:1553-1559, 1992.
41. Muscle & Nerve. November. 644-646, 2003
Corticosteroid injections are widely used to aid injury rehabilitation but we still understand very little about their mechanism. Chiropractor, Dr. Alexander Jimenez examines the current thinking and discusses how this potentially impacts treatment options…
Corticosteroids are used for their anti- inflammatory and pain reducing effects. They can also reduce muscle spasms and influence local tissue metabolism for faster healing. Injection therapy is now widely available from specially trained general practitioners, physiotherapists and consultants, and can be offered for a wide range of clinical conditions. Because of this wide availability and the growing desire for injury �quick fixes�, it is important that they are used correctly and the full consequences are understood prior to injection.
The main indications for corticosteroid injection use are(1):
Acute and chronic bursitis
Acute capsulitis (tight joint capsule)
Chronic tendinopathy
Inflammatory arthritis
Chronic ligament sprains
Steroid injections of hydrocortisone are a synthetic form of a naturally produced hormone within the body called cortisol. Cortisol is important for regulating carbohydrate, protein and fat metabolism. It is also involved in metabolic responses in times of stress such as emotional problems, trauma, and infection, where levels of inflammation are elevated. Steroid injections work on the immune system by blocking the production of chemicals that activate the inflammatory reactions, therefore reducing inflammation and pain within injury locations.
Steroid injections can be directed into a joint, muscle, tendon, bursa, or a space around these structures. Figure one shows an injection aiming for the bursa within the shoulder joint. This is often a source of irritation and causes impingement when the shoulder moves. The location will depend on what tissue is causing the symptoms. When injected locally to the specific structure, the effects are primarily only produced there and widespread detrimental effects are minimal(2).
When To Use
Identifying the correct time to issue a steroid injection following injury requires careful consideration. The mechanical status of the tissue is important because this will vary depending on the stage of healing and therefore the effectiveness of the injection will also vary.
Figure 2 shows the different stages that a tendon can progress through following trauma. This is equally applicable to muscles, fascia, and other tissues too. A reactive tendinopathy (tendon degeneration/damage) will present shortly after injury/trauma/stress/ excessive loading, and will display acute swelling and inflammation. The initial care should be 2-3 weeks of rest, analgesia, ice application and gentle physiotherapy. If symptoms have not significantly improved after this period, then the introduction of a corticosteroid injection is appropriate for providing symptomatic relief by reducing inflammation and eliminating the occurrence of further damage because mechanical normality will be quickly restored(3).
If the tendon continues to be placed under excessive load, swelling and inflammation will remain or escalate, and continuous loading will eventually cause micro trauma and further tendon degeneration. If this is prolonged for long enough then the tendon will fail structurally(4).
The use of corticosteroids here is questionable because there is unlikely to be inflammation present to combat, and the injection alone will not repair this physical damage. Injection treatment at this stage may only be indicated if the athlete is in too much pain to participate in any significant rehabilitation. The symptomatic relief the injection may bring at this point could allow exercises to be performed, which can help accelerate the repair of physical damage. Ultimately, physical exercise is a key component in recovery following corticosteroid injections.
Impact On Treatment & Performance
For the best outcome, post-injection care � particularly with respect to timing � is important. Relative rest is recommended for the first two weeks post-injection. During this first two weeks the tissues are weakened and their failing strengths are reduced by up to 35%; this means the strength at which they would fail (tear) is much lower and more susceptible to rupturing(8).
By six weeks the bio-mechanical integrity is reestablished and the tissues are deemed �normal� again, with increased strength and function(8). Benefits are optimal within this 6-week period and often short-lived; therefore the athlete must comply strictly to a rehabilitation program to gradually load the tissues and ensure the correct load is applied during this period(9). Research has also shown that at twelve weeks post-injection�there is little significance in the difference between those who received a steroid injection and those who focused on exercise therapy alone, suggesting this early symptom relief should be used to enhance rehabilitation(10). If loading is accelerated in the early stages the athlete risks re-aggravation of the injury, delayed healing, further weakening and thus rupture.
If this rehabilitation protocol is followed, the athlete will likely maximise their outcome. They can return to training, and with the severity of their symptoms reduced, this can allow progression to the next stage of training. If the injury is severe enough that surgery may be considered within three months, a steroid injection should not be performed as this can affect the success of the surgery.
Evidence For Sports Injuries
Here we will consider some of the more common sports injuries and summarize what the current evidence regarding steroid injection suggests.
Shoulders
Injection therapy is indicated in subacromial impingement or bursitis (as in Figure 3 below) to allow the inflammation reduction and restoration of normal movement. It is also indicated in rotator cuff pathology where the tendons are again inflamed, but also damaged and unable to undergo exercise therapy. Shoulder injections are shown to produce early improvements in pain and function with a high level of patient satisfaction(10). Symptoms are similar to those without injection at 12 weeks however, suggesting physical therapy is also important(10). Injection is not appropriate for shoulder instability as it can make the joint more unstable. Exercise therapy alone is recommended for this condition.
Hip Pain
Two soft tissue conditions that benefit the most from injection are piriformis syndrome (muscle tightness running deep to the buttock muscles), and greater trochanter pain syndrome (affecting the bursa surrounding the hip joint, or the gluteal tendons that are all in close proximity to the lateral hip)(11). Injection success is reported to be approximately 60-100% if the diagnosis is accurate and the correct protocols are adhered to(12). Other regions such as the adductor and hamstring tendons can also be treated for tendinitis or groin pains. However, injections into these�regions are deep and painful, and require extensive rest afterwards.
Knee Pain
Knee joint injections for arthritic conditions are most commonly used, with injection to the soft tissues much less common due to the complex diagnosis, and risk of detrimental side effects. The various bursa around the knee, the iliotibial band, and quadriceps and patellar tendons have all been shown to significantly benefit in the short-term; however accurate location is essential to ensure the tendon itself is not penetrated � only the surrounding regions(13).
Plantar Fasciitis
This is a painful injection to receive, and pain can last for well over one week post- injection (see figure 4). There is an approximate 2-4% risk that the fascia can rupture. In addition, there�s a risk of local nerve damage and wasting of the fat pad within the heel. Studies have demonstrated that at 4 weeks post-injection pain and thickness of the injured plantar fascia are reduced and these benefits remain three months later, suggesting a good outcome if the risks are avoided(14).
The majority of clients that present to the clinic with anterior knee pain over the coming year will more often than not have a patellofemoral (PF) problem.
It may be a slight bit of biomechanical mal-alignment that has stirred up the knee cap – this is the good, or they may have started to wear the cartilage behind the knee cap and as a result it has softened – chondromalacia � this is the bad. They may even have worn a hole into the knee cap cartilage and they now have a chondral defect, or worse still an osteochondral defect – the downright ugly.
These problems affect runners, cross fitters, group exercise enthusiasts (PUMP classes) and simple recreational walkers who spend a lot of time on hills and stairs.
How These Extremes Are Managed Will Differ
The biomechanical irritations and the chondromalacia versions can be managed conservatively with a combination of local treatment modalities and correcting the biomechanical faults. The more serious chondral/osteochondral defects often need some surgical intervention as often the pathology is too advanced to respond to conservative treatment alone.
Understanding the exact mechanical contributions of the knee cap in relation to the femur is critical for the therapist to effectively manage these problems.
At the local PF level, the fault is usually a malposition of the patella in the femoral trochlear groove. Often the knee cap is being pulled too far laterally and superiorly in the groove, creating an uneven contact situation between the knee cap and the femur. The PF compression force during loaded knee flexion (squats, lunges etc.) is no longer optimal and usually a smaller portion of the patella cartilage is taking all the load. This wears the cartilage down and creates pain and pathology. This is most noticeable as the knee flexes to 30 degrees and onwards as it is this knee flexion angle where the knee cap enters the femoral trochlear groove.
The more distant (but often dominant) faults lie at the hip/pelvis and at the feet. Below is a breakdown of common biomechanical faults that may contribute to PF pain syndromes.
1. Overpronation
If the foot pronates (rolls in) for too long or too much, the pronated midfoot forces the tibia to remain internally rotated. The femur follows the tibia and also internally rotates. This creates a mal-alignment at the knee whereby the PF arrangement is altered and the knee cap shifts laterally. We are all familiar with the Q angle of the knee and how this affects the PF alignment.
Common causes of overpronation may be structural flatfoot problems that can be corrected with orthotics and shoe selection. However, tight soleus (that limits dorsiflexion) or a tight and overactive peroneal system that everts the foot and flattens the foot can also be a cause.
Stretching and loosening the soleus and peroneals along with strengthening the anti-pronation muscles such as tibialis posterior, flexor hallucis longus and flexor digitorum longus may help fix this problem.
FADDIR represents a flexed, adducted and internally rotated hip joint at foot strike. This is often caused by tight and overactive hip flexors such as TFL and the adductors and weakness in the abductors (gluteus medius) and external hip rotators (gemellus, obturator muscles). This hip posture forces the femur to roll inwards and as a result the knee is deviated medially and away from the vertical line drawn up from the foot. This also increases the Q angle and PF misalignment results and perpetuates the local knee imbalance of tight and overactive lateral quadriceps and lateral hamstrings along with ITB tightness. As a result the VMO weakens.
Loosening the overactive TFL, adductors, lateral quad, ITB and lateral hamstring whilst strengthening the gluteus medius, hip external rotators and VMO may help this biomechanical mal-alignment.
3. Pelvic Trendelenburg
Defined as lateral pelvic shift whereby at stance phase the opposite side of the pelvis drops down below the height of the pelvis on the stance side. This is usually caused by a weak gluteus medius complex that is unable to hold the pelvis stable during stance phase. The implications again are that this causes the knee to roll in and increase the Q angle. The solution is to muscle up the gluteus medius.
This often forgotten about imbalance creates a situation whereby the individual finds it difficult to attain hip extension at the end of stance phase. The hip remains locked in a degree of flexion.
The knock on effect is that the knee also stays locked in some flexion. With the knee in flexion, the knee cap is now compressed against the femur, compression on the underside of the kneecap may result. To fix this the therapist needs to stretch/loosen the hip flexors and strengthen the gluteus maximus to promote more hip extension.
IFM's Find A Practitioner tool is the largest referral network in Functional Medicine, created to help patients locate Functional Medicine practitioners anywhere in the world. IFM Certified Practitioners are listed first in the search results, given their extensive education in Functional Medicine
So as to advance through the six clarified stages, the athlete may undergo extensive physiotherapy, focusing on hip range of movement exercises, manual therapy and trigger point releases, active stretching, potentially deloaded activities like hydrotherapy or Alta G walking/ running and strong hip rotator and gluteal strengthening exercises. Much of this will be ‘controlled’ and led by the wishes of the surgeon as they will provide the framework on if and what happens concerning loading.
Hip Muscle Control
Summary
In this phase it’s anticipated that the athlete will remain relatively quiet for 2-3 weeks post surgery. This allows for full tissue recovery to happen, including scar tissue maturation. The athlete is allowed to completely mobilize in full weight-bearing; however care needs to be taken using any flexion and rotation motions and no lifting will be allowed.
Early Loading & Foundation
The primary feature of this phase is that the athlete can start early and low-load strength exercises focusing on muscle activation in a neutral spine position, along with a progressive selection of motion program to improve lumbar spine flexion, extension and rotation. In this stage that the physiotherapist will guide the athlete through safe and gentle stretches to your hip quadrant muscles like the hip flexors, gluteals, hamstrings and adductors. The athlete also lasts gentle neuro-mobilization exercises to advance the freedom of the sciatic nerve — an issue in this condition as neurological tethering is a chance as a result of scar tissue formation caused by the surgical procedure.
Progressive Loading
In this phase the athlete continues with a variety of movement progression along with the physiotherapist progresses manual therapy to the pelvis and lumbar spine. Neuro-mobilization techniques can also be progressed. The significant change in this phase is that the progression of load on many of the strength and muscle control exercises.�
Load Accumulation
This is the stage where the athlete begins to advance the load in strength-based exercises. Resistance is used in the form of barbell load and band resistance. Three exceptional exercises performed here are the ‘kneeling hip thruster’, ‘deadbug antirotation press’ and also the ‘quadruped walkout’ (Figures 6-8 — explained in detail in the online database of exercises).
The athlete also begins running drills at this phase and it might be expected that as well as building running Amount, the athlete should progress over four weeks to close to full sprint speeds. This is also the stage whereby they would initiate mild to moderate sports special skills drills. Another characteristic of this stage is that the athlete starts the ‘Sorensen test’ exercise (Figure 9) and it will be expected that they can maintain the position for no less than 90 seconds before advancing to the next phase.
Variants
Trigger Points & Massage
Hip Pain
