Athletes
Sports Spine Specialist Chiropractic Team: Athletes strive to achieve their body’s maximum performance by participating in numerous training regimens consisting of strenuous exercises and physical activity and ensuring they meet all of their body’s nutritional requirements. Through proper fitness and nutrition, many individuals can condition themselves to excel in their specific sport. Our training programs are designed for athletes that look to gain a competitive edge in their sport.
We provide sport-specific services to help increase an athlete’s performance through mobility, strength, and endurance. Occasionally, however, the excess workouts can lead many to suffer injuries or develop underlying conditions. Dr. Alex Jimenez’s chronicle of articles for athletes displays in detail the many forms of complications affecting these professionals while focusing on the possible solutions and treatments to follow to achieve overall well-being.
by Dr Alex Jimenez | Diets, Fitness, Gastro Intestinal Health, Gut and Intestinal Health
When it comes to stomach discomfort during exercise, forget that old adage “no pain, no gain.” New research suggests that excessive strenuous exercise may lead to gut damage.
“The stress response of prolonged vigorous exercise shuts down gut function,” said lead author Ricardo Costa.
“The redistribution of blood flow away from the gut and towards working muscles creates gut cell injury that may lead to cell death, leaky gut, and systemic immune responses due to intestinal bacteria entering general circulation,” Costa added. He’s a senior researcher with the department of nutrition, dietetics and food at Monash University in Australia.
Researchers observed that the risk of gut injury and impaired function seems to increase along with the intensity and duration of exercise.
The problem is dubbed “exercise-induced gastrointestinal syndrome.” The researchers reviewed eight previously done studies that looked at this issue.
Two hours appears to be the threshold, the researchers said. After two hours of continuous endurance exercise when 60 percent of an individual’s maximum intensity level is reached, gut damage may occur. Costa said that examples of such exercise are running and cycling.
He said heat stress appears to be an exacerbating factor. People with a predisposition to gut diseases or disorders may be more susceptible to such exercise-related health problems, he added.
Dr. Elena Ivanina is a senior gastroenterology fellow at Lenox Hill Hospital in New York City. She wasn’t involved with this research but reviewed the study. She said that normal blood flow to the gut keeps cells oxygenated and healthy to ensure appropriate metabolism and function.
If the gut loses a significant supply of blood during exercise, it can lead to inflammation that damages the protective gut lining. With a weakened gastrointestinal (GI) immune system, toxins in the gut can leak out into the systemic circulation — the so-called “leaky gut” phenomenon, Ivanina said.
But, she underscored that exercise in moderation has been shown to have many protective benefits to the gut.
“Specifically, through exercise, patients can maintain a healthy weight and avoid the consequences of obesity,” she said. Obesity has been associated with many GI diseases, such as gallbladder disease; fatty liver disease; gastroesophageal reflux disease (GERD); and cancer of the esophagus, stomach, liver and colon. Regular moderate physical activity also lowers the risk of cardiovascular disease, type 2 diabetes and depression.
To prevent exercise-related gut problems, Costa advised maintaining hydration throughout physical activity, and possibly consuming small amounts of carbohydrates and protein before and during exercise.
Ivanina said preventive measures might help keep abdominal troubles in check. These include resting and drinking enough water. She also suggested discussing any symptoms with a doctor to ensure there is no underlying gastrointestinal disorder.
Costa recommended that people exercise within their comfort zone. If you have stomach or abdominal pain, “this is a sign that something is not right,” he said.
Individuals with symptoms of gut disturbances during exercise should see their doctor.
The study authors advised against taking nonsteroidal anti-inflammatory drugs — including ibuprofen (Advil, Motrin) or naproxen sodium (Aleve) — before working out.
Costa said there’s emerging evidence that a special diet — called a low FODMAP diet — leading up to heavy training and competition may reduce gut symptoms. FODMAP stands for fermentable oligosaccharides, disaccharides, monosaccharides, and polyols. FODMAPs are specific types of carbohydrates (sugars) that pull water into the intestinal tract.
The International Foundation for Functional Gastrointestinal Disorders suggests consulting a dietitian familiar with FODMAP diets. Such diets can be difficult to initiate properly on your own, the foundation says.
Costa also said there’s no clear evidence that dietary supplements — such as antioxidants, glutamine, bovine colostrum and/or probiotics — prevent or reduce exercise-associated gut disturbances.
The study results were published online recently in the journal Alimentary Pharmacology & Therapeutics.
by Dr Alex Jimenez | Athletes, Complex Injuries, Physical Rehabilitation, PUSH-as-Rx
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
by Dr Alex Jimenez | Diets, Fitness
It’s no surprise — overweight children who don’t properly learn self-regulating habits likely become obese adults. What is surprising is that one of the most common ways to help — restricting children’s diets — actually compounds the problem.
That’s the thrust of a new study by University of Illinois researchers who point to a disturbing pattern: Parents shame by withholding food due to weight gain, then children cope with the negative emotions by overeating.
Further exasperating the trend, overweight children are often rewarded with food by parents, and as they grow older, the children reward themselves with food.
Researchers who studied the pattern added a genetic component as well to better understand obesity. They reported that a child’s genetics, relating to cognition and emotion, likely play a key role. They found that when biological conditions were just right, a nudge by the social aspect sets kids on a path to obesity.
Kelly Bost, co-author of the study (published in Pediatric Obesity), and professor of child development at the University of Illinois, said: “When parents offer food to children whenever they are upset, children may learn to cope with their negative emotions by overeating, and they start to develop this relationship with food early in life; eating — especially comfort food — brings a temporary soothing. People intuitively understand that.”
The findings support the team’s hypothesis that a correlation exists between all factors: parenting approaches, combined with a child’s genetic make-up and restrictive feeding, and the child’s weight and the child’s propensity to be obese.
Bost said that children can effectively learn control for themselves: “Some of the things parents do, they may not think are related to how children are developing their eating habits. The ways parents respond or get stressed when children get upset are related in an indirect way. The way we respond to that emotion can help children to develop skills for themselves, to self-regulate, so that everyday challenges don’t become overwhelming things that they have to manage with respect to food.”
Bost and her team used data from the “Strong Kids” program, outreach developed by The Oregon Resiliency Project, an organization that is based on “research, training, and outreach effort aimed at social and emotional learning, mental health promotion, and social-emotional assessment intervention” of children, according to the organization’s website.
The team examined information about parents’ feeding styles, and how they typically reacted to their children’s (ages 2.5 to 3 years) negative emotions. The researchers examined these factors in combination with genetic data.
For the genetic factor, they looked at the COMT gene, a gene known for regulating cognition and emotion. This gene is the gatekeeper for dopamine, which controls the brain’s reward and pleasure centers.
Bost and her team studied minute variances in the gene pool to determine which children might be more susceptible to negative emotions or stress. They based their genetic research on the breakdown of amino acids in proteins that could lead to personality differences. One of them is the change produced by genetics in the form of a single part of our DNA: the nucleotide polymorphisms (SNPs). There are many types of SNPs; some affect the composition of protein and, depending on the change, affect the amount of dopamine in the brain, as presented by Psychology Today. Dopamine controls the brain’s reward and pleasure centers.
One type of SNP can change an amino acid from valine (Val) to methionine (Met). While largely academic, these two types of proteins influence emotion. Bost explained it best in the study: “We all carry two copies of genetic information — one from Mom, and one from Dad. In a person with Val/Val, the COMT system works three to four times faster than those with other combinations do, and therefore accumulates less dopamine in the front of the brain. Children who have at least one copy of Val tend to be more resilient emotionally. Those who are Met carriers have the propensity to be more reactive to negative emotion or stress.”
This genetic component was combined with the researchers’ studies. “We know that how parents respond to their children’s negative emotions influences the development of children’s response patterns over time,” Bost said in the study. “There is a whole body of literature linking emotion dysregulation to emotional overeating, dysregulation of metabolism, and risk for obesity, even starting at early ages. We wanted to begin to integrate information from these various fields to get a more holistic view of gene-environment interactions at this critical time in life for developing self-regulation.”
They began their research with a group of 126 children who were studied for the social aspect. For the genetic component, saliva samples were taken. Parents filled out questionnaires, rating how they typically respond to their common situations, including emotional outbursts.
Bost and colleagues found that parents most likely to use restrictive feeding were those who reported more frequent use of unresponsive stress-regulating strategies with their children — punishing or dismissive —and had children who were higher weight status and tested positive for the Met amino acid. But the same was not necessarily true for children who were Val carriers.
Bost and her team determined that breaking the cycle did not begin with blaming parents but instead by encouraging them to develop positive reinforcement and other techniques that could help their kids respond better and also help develop positive eating habits that likely would carry into adulthood.
While there exist myriad programs that focus on providing good nutrition or how to plan less stressful mealtimes, Bost explains that parents should also learn emotion regulation strategies in response to children who display emotional breakdowns and are eating to soothe — especially if the parents are restricting foods.
She added, “Sometimes the way parents respond is based on their own stress, belief systems, or the way they were raised. Educating parents from a developmental perspective can help them to respond to their children’s emotions in ways that will help their children learn to self-regulate their emotions and their food intake . . . responsive parenting involves an understanding of what stress-reducing approaches are most effective for a particular child.”
by Dr Alex Jimenez | Diets, Fitness
A new diet plan that dictates that you eat only one food for several weeks to lose weight fast is drawing warnings from many experts who say it is dangerous and only successful in the short term.
The Mono Diet (sometimes called the Banana Island or Monotrophic Diet) was popularized by a YouTube star nicknamed “Freelee the Banana Girl” (real name: Leanne Ratcliffe) who claimed it helped her lose weight, the New York Post reports.
Ratcliffe claimed to have lost 40 pounds eating close to 30 bananas a day.
A new version, the Sweet Potato Diet, promises the spud can help you lose 12 pounds in just two weeks. The hashtag #monomeal on Instagram, which highlights pictures of people’s meals containing a single food, has more than 38,000 posts, and the diet was one of the most searched in 2016, according to Google.
Frances Largeman-Roth, a registered dietitian and author of “Eating in Color,” tells the Post you can lose weight by eating only one food, but it’s likely to result from eating less.
“Yes, this diet can produce weight loss,” she says “But, the weight loss is a result of caloric restriction — not because any particular food is magically producing weight loss. It’s an incredibly restrictive and unbalanced diet and I do not recommend that anyone follow it.”
Experts warn such diets can also cause symptoms like dizziness and lead to some serious health problems, including dangerous metabolic changes and muscle loss.
by Dr Alex Jimenez | Fitness, UTEP (Local) RSS
UTEP claimed two superlative Conference USA track and field honors as Emmanuel Korir and Tobi Amusan were named C-USA Male and Female Track Athletes of the Year, announced by the league office on Friday afternoon.
�Both athletes are very special and talented. He [Korir] was the best candidate for our league and would most likely do very well other top conferences as well,� head coach Mika Laaksonen stated. �A lot of work goes into these things and Tobi worked incredibly hard over these past two years and she absolutely deserves this award, they both do.�
Korir ran a world best 1:14.97 in the 600m earlier this year at the New Mexico Cherry & Silver meet, which was his first race on an indoor 200m banked track. The freshman followed that up by capturing the NCAA title in the 800m (1:47.48) at the same track in Albuquerque, N.M., with a time of 1:47.48. The freshman is one of three athletes in the world to run an outdoor sub-45 400m and a sub-1:44 in the 800m.
The Kenyan native won the NCAA outdoor title in the 800m (1:45.03) and is the first Miner to win both titles in the same year.
Amusan was the leading scorer for the Miners with 25 points at the C-USA Indoor Championships and notched a meet record in the 60m hurdles with a time of 8.01. The sophomore helped her team win its third consecutive conference title. Amusan qualified to the NCAA Indoor Championships in the 60m hurdles where she notched a sixth-place showing.
The outdoor season started with a bang, as she set a school record (12.63) in the 100m hurdles at the UTEP Springtime meet. She followed that with a first-place finish at the 2017 Clyde Little Field Texas Relays in the 100m hurdles, setting a meet record time of 12.72. The Nigerian native scored 24.5 points at the C-USA Outdoor Championships leading the women�s team to its first ever outdoor conference title.
Both athletes were named semifinalists for college track and field�s high individual honor, The Bowerman Award. The women�s three finalists will be announced on Wednesday, June 21 and the men�s finalists will be announced Thursday, June 22.
For more information on UTEP track and field, follow the Miners on Twitter (@UTEPTrack) and on Instagram (uteptrack).
by Dr Alex Jimenez | Diets, Fitness
Bathing suit season is here, and for many of us that means no longer being able to hide those extra pounds beneath a chunky sweater. Fortunately, there are some small and easily implemented lifestyle adjustments that can quickly shrink your waistline.
Here are 10 ways to slim down for swimsuit season. The best part? None involve the gym.
Plan ahead: Making meals ahead of time can save you calories in the long run. Try cooking up large-batch dinners over the weekend and simply reheat throughout the week. Lisa Lillien, author of the “Hungry Girl” Website, featuring advice on guilt-free eating, suggests emphasizing lean proteins and veggies. Commit time on the weekend to meal prep and all you have to do is throw the ingredients in the pan during the week.
Drink more: Water, that is. Staying hydrated is important for your overall body function and can prevent you from feeling hungry. Sometimes the body confuses dehydration with the sensation of hunger. This problem comes with an easy solution — drink more water. Bring a travel water bottle with you when you’re on the go so you can remember to stay hydrated.
Limit or avoid alcohol: Cutting out alcohol is one of the quickest ways to lose weight. Alcohol triggers a process in the body similar to sugar. It can set off the same insulin resistance that can cause weight gain. For six days of the week, cut out alcohol.
Snack on healthy foods: Keep a variety of healthy snacks around to satisfy cravings. Protein bars and nuts are great snacks that will satisfy your hunger and prevent you from making poor food decisions at meal times. Fresh fruit and veggies are another great snack option.
Banish stress: Maintaining a healthy diet isn’t about never indulging. It’s about eating healthy foods the majority of the time and treating yourself on occasion. Don’t stress out if you veer off course. Instead, do what you can to get back on track. Stress can actually be a source of weight gain, so try to focus on the positive.
Careful with carbs: Processed white carbs are a no-no. They spike blood sugar levels and cause the pancreas to produce insulin, which causes the accumulation of fat. Instead, opt for refined carbs like brown rice and oats.
Start with soup: According to research from Penn State University, soup is a great diet food. The combination of liquids and solids helps make you feel full faster. Eat it before a meal and you may be able to decrease your overall calorie intake by up to 20 percent.
Consider your coffee: Black coffee isn’t a diet buster — it’s the milk and sugar that go in it. A latte from your favorite coffee shop can be a hidden source of fat and calories. Try swapping your usual espresso for a plain black or green tea.
Stop multitasking: A recent study in the American Journal of Clinical Nutrition found that multitasking while you eat will leave you feeling unsatisfied. Instead, slow down and enjoy your time savoring your meal without the distractions.
Spice it up: According to a recent study led by David Heber, a professor of medicine and director of the Center for Human Nutrition at the University of California-Los Angeles, capsaicin — the compound found in chili peppers — speeds metabolism and helps burn calories. Participants in the study were given a capsaicin supplement or a placebo for four weeks. The group who received capsaicin burned more fat for several hours after the meal for a total of 100 to 200 more calories a day. Spicy foods may also make you feel fuller more quickly than bland foods.
by Dr Alex Jimenez | Athletes, Complex Injuries, PUSH-as-Rx
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
