Ehler's-Danlos Syndrome III (Hypermobility Type) 

By Havilah Hoffman

Ehler's-Danlos Syndrome III (Hypermobility type) is a genetic condition that can lead to life-long chronic pain and recurrent injury. When combined with Joint Hypermobility Syndrome (which has similar diagnostic symptoms and treatment), it is estimated that 10 percent of the population suffers from this disorder.[1] The cost of medical treatments, work absenteeism, and loss of quality of life for EDS Type III patients points to a serious medical crisis that deserves greater attention in the medical community. EDS is classified as a connective tissue disorder. Because of this, the dominant amount of research and treatment has focused on the connective tissues and collagen formation. However, new research has shown a notable nerve disorder component to the syndrome. Initial evidence from case studies treating the nerve component of EDS Type III has proved promising and worthy of greater medical study. In this paper we will point to evidence of a nerve component to hypermobility and why CINK treatment may prove superior in alleviating hypermobility's negative symptoms.

Connective tissue abnormalities associated with Ehler's-Danlos Syndrome III such as soft velvety skin, poor wound healing, and hyper flexibility [2] have generally been the main focus of research and treatment for hypermobile patients. After all, the main complaints of those suffering from EDS III are chronic pain, joint dislocations and subluxations. But the assumption that the chronic pain and joint dislocations are a result of the connective tissue abnormalities ignores a possible nerve disorder with high and low fluctuations that may be causing muscle laxity in areas and spasm and tension in others.

Points of possible nerve dysfunction with low impulse may be shown by common hypermobility symptoms of: muscle weakness, hypotonia, easy fatigability, reduction in vibration sense, poor balance with increased incidence of falls, diminished joint position sense, slower than normal gait [3], axonal polyneuropathy, [4] neurally mediated hypotension, and postural orthostatic tachycardia syndrome.[5]Poor position and vibration sense, neurally mediated hypotension, and axonal polyneuropathy may show poor function that reduces nerve impulse and blood flow to the body and muscles.  In other words, the muscle weakness, fatigue, and coordination issues may be a result of the nerves and not just a problem in the muscle tissue itself. The lack of muscle development and proper blood flow create a weakened support structure more prone to degenerative disc issues and compression that can lead to pain and chronic injury. Additionally, a person with poor position sense and balance has a much greater risk of overstretching and dislocation.

But there is more to EDS III than the laxity of connective tissue and a nerve disorder creating underperformance diminished and structural sensitivity. Certain symptoms point to a heightened response such as: temporomandibular dysfunction ("TMJ syndrome"), headaches, especially migraines, cervical muscle tension, myofascial spasms, palpable spasms with tender points consistent with fibromyalgia,[6] an "over response" to physical and emotional stress leading to adrenaline surges as well as fluctuations in heart rate and blood pressure[7]. So, while certain diagnostic points may show laxity (i.e. low blood pressure, extreme range of motion in the fingers) other points of the body demonstrate extreme tension both in the muscles and surges of blood flow and pressure.

Further symptoms point to a fluctuation between these extremes. Many hypermobility patients suffer from irritable bowel syndrome, in essence a fluctuation in the body between laxity (diarrhea) and gripping (constipation and muscle cramping).[8] Adrenaline surges also follow similar highs and lows in hypermobile patients. Easy fatigability leads the body to produce more adrenaline. The excess adrenaline makes the person unaware of how tired they are and often leads to overextending oneself. The overextending in turn leads to fatigue and a vicious cycle.[9] During periods of adrenaline surges the body is more prone to TMJ, muscle spasms, and tendonitis. While periods of ebbs produce fatigue and lax muscles, whose weakened support can lead to pain from compression and overstretching. This cycle can begin from an overly low point, (extreme fatigue leading to an adrenaline surge), or a high point (stress and anxiety). This cycle can begin from an overly low point, (extreme fatigue), or a high point (stress and anxiety).  In the cycle a client may present at either extreme for extended periods leading to the mistaken assumption that it is simply this high or low that is the problem.

Two further observations point to a connection between these high and low fluctuations in the nerves and the connective tissues. Many athletes have hypermobility, as their sports require heightened range of motion. Their extreme range of motion is often viewed as an asset until one of two external factors throw their system off balance and the negative symptoms of EDS III appear. When these athletes take some time off or retire from their sport, the change in activity levels throws their body into a laxity pattern with accompanying joint aches and discomfort. These pains are often attributed to damage from their sport but prolonged rest increases the symptoms instead of lessening them. On the other end periods of heightened stress, either physical or emotional, often lead to muscle strain and gripping. In both cases symptoms of neurally mediated hypotension and syncope as well as neurally mediated hypertension and general dysautonomia are likely to peak. This could show the loss of equilibrium.

Additionally, areas of extreme laxity and hypermobility often transform into gripping points prone to muscle strain and spasm. This is true especially in areas that provide balance and support. CINK has found Sway Back structures to be the most commonly associated with EDS III. In Classic Sway Back structures, their main leaning point and center of gravity is at the trochanters. This is also the first place noted by both patients and CINK practitioners to transform into a gripping pattern that interferes with daily activities. As they transition to Compensated Sway Back Structures the hip flexors begin to grip to hold the body back from extensive leaning. Eventually the gripping becomes so extreme that the patients are unable to find positions in which the muscles do not grip. Common activities such as walking and sitting become painful due to muscle strain. Stretching only offers temporary relief but does not turn off the firing pattern. Often the hip maintains its extreme range of motion when tested though the hip flexors will appear shortened when standing due to the gripping pattern.

Structures may continue in a gripping pattern for extended periods added more and more locations of constant tension. These locations are almost always involving small muscles surrounding a joint or vertebrae reducing its range of motion. As diagnostic testing for EDS III classification focuses on low nerve impulse and extreme range of motion, these patients are often not included as suffering from EDS III despite history of previous laxity. Other clients fluctuate between periods of gripping and leaning often in the same location. For example, Sway Back structures often alternate between hip flexor gripping and extreme leaning in the hips leading to periods of muscle strain and periods of bursitis from the accompanying leaning.

The above information points to a problem of balance between high nerve impulse and low nerve impulse. The appropriate treatment would therefore try to normalize the structure. Current treatments, however, focus on drastically alternating the impulse from either low to high or high to low.

Diagnostic testing for EDS III classification has focused on what we could now consider symptoms of low nerve impulse-- i.e. abnormal flexibility and hypotonia. Likewise, treatments for EDS III have sought to reduce this range of motion and increase muscle tone. Physical therapy exercises such as those recommended by the University of Washington Orthopaedics and Sports Medicine, focus on the development and strengthening of the muscles through concentric flexion of these muscles in isolation.[10] By focusing on strength building exercises to increase muscle mass, the belief is the structure will be better supported and less likely to suffer from pain and injury. This focus makes three assumptions: the body can build muscle with focus; the structure is otherwise sound and responds normally; and, as a corollary, once the muscles have developed by any form of flexion, the body will naturally use the coordinated and correct movement of these muscles in its daily life. 

An example of the first assumption can be shown in the University of Washington Orthopaedics and Sports Medicine's recommended exercises of calf raises and toe flexing. Assuming the client is reasonably mobile, why have the muscles of the calf and foot not developed normally? The prescribed muscle building in the region would be appropriate for muscle atrophy from bed rest, prolonged wearing of a cast, or for training for a sport that requires superior foot and calf strength, but EDS III patients have repeatedly shown a weakened ability to gain muscle from normal activity. This points to the need of an additional or alternative approach to strength building than those required of muscularly normal patients.

The second assumption can be shown in the lack of more coordinated and whole body exercises as a bridging step between focused muscle flexion and correct muscle engagement on sports and daily activities. EDS III patients have more uniformity to their hypotonia pointing toward a systemic lack of general muscle engagement in daily activities. Thus, even if these isolated movements manage to develop added muscle tissue, there is no safeguarding that the extra muscle tissue will provide additional structural support throughout the day. This is especially concerning given EDS III patients' statistically weaker coordination and body awareness.

The corollary of this assumption believes that the patient can naturally re-coordinate muscle movements from how they were trained by these exercises into how they should move for daily life. As previously stated, these exercises focus on concentric contraction. Given EDS III patients' propensity for muscle spasm and gripping, this body training can be damaging. Particularly problematic are exercises like straight leg raises and quadriceps flexing. These movements can teach the hip flexors to grip tight when engaged (an area especially prone to spasm in Sway Back EDS III structures). Teaching the body that muscles only operate in tight contraction or complete laxity makes the body's tendency to alternate between high and low impulse more extreme. Movements in which the hip flexors can easily grip (walking, hiking, cycling, and even elliptical use) may become painful due to muscle strain and spasm. The more the client engages in these activities, the more the ingrained reflex of muscle gripping strains the muscles and the more pain it can cause. Ironically when the body is in pain it tends to grip exacerbating this problem. If the patient reduces their engagement in these activities without increasing alternate activities like swimming, the body will weaken. The weakened state can throw the patient back into a low impulse pattern or the body will grip the spasmed muscles tighter to make up for the decrease in muscular support from the atrophied muscles. These clients often appear weak with marked hypotonia but show locations of very tight muscles, generally surrounding joints or the spine, such as hip and neck tension. These clients may also be diagnosed with fibromyalgia. While these clients may be less prone to injuries like subluxation and dislocation, due to the tense muscles surrounding the joints, their daily pain is not reduced and may actually increase. The low impulse factors may increase symptoms fatigue and muscle weakness, while the fluctuations between the high and low impulses can increase symptoms of heart palpitations and pre-syncope. So, the client becomes locked into a pattern with no good alternatives. The more they move, the more they grip. The less they move, the weaker they become although the gripping pattern may remain. In this respect such prescriptive exercises may be a net negative for the patient. To reduce the high impulse gripping, physical therapists may prescribe stretching. We will discuss this in the high to low treatments.

Prolotherapy is another approach that seeks to counter the low impulse of joint laxity and reduce its negative effects like subluxation and dislocation. Prolotherapy involves injecting an irritant into a ligament or tendon to induce inflammation and stimulate healing. The healing process produces scar tissue that thickens the ligament or tendon.[11] By focusing only on the lax ligaments and tendons, prolotherapy treats a symptom and does not try to address the overall syndrome. And while tightened ligament tissue may reduce the risk of over stretching and subluxation, it ignores the hypotonia. Without muscular support the patient may still experience joint and spinal compression from leaning patterns. Prolotherapy only seeks to reduce one form of low impulse so it does not address high impulse symptoms like gripping. The procedure itself being a trauma may produce a muscular gripping pattern in the region while healing and would simply alternate the area from low impulse to high. Improvement results from prolotherapy have been variable with more research needed.[12] The main concern is that it is only treating a symptom instead of the disorder.

On the other end are treatments that seek to treat high impulse symptoms. Physical therapists counter gripping patterns through stretching exercises. The arm behind the back exercise recommended by UW Medicine is particularly problematic as a hypermobile patient could easily sublux their shoulder while performing the task. The risk of injury from stretching of the joints is great enough that most experts now advise against it.[13] Likewise certain exercises that involve extreme stretching and positions (such as certain yoga poses) should also be avoided. But why then do many EDS III patients seek out such activities? Pulling or stretching an area can temporarily stop a muscle grip in the region offering relief. Also, unlike activities involving extreme strength and heavy lifting, EDS III patients are generally "good" at movements required in yoga, which can be an ego boost. Unfortunately, the type of stretching further loosens the joints. The body sensing this instability will respond by gripping the muscle around the region tighter. The more muscle gripping, the more the patient will want to stretch locking them into a stronger high impulse pattern and more pain. Therefore, stretching is not considered a viable treatment for high impulse symptoms like muscle gripping and spasm.

A similar problem can occur from dry needling. Dry needling is when a needle is inserted into a "trigger point," or spasmed muscle that has been causing the patient pain. The needle will produce a twitch response that causes the muscle to cramp and tighten even more. When the needle is removed, the muscle contraction is reduced to a more relaxed state than before the needle insertion. With the muscle "turned off" the pain is lessened. Dry needling does not look to why the muscle was gripped in the first place and here in lies the problem. For example, a client has dry needling performed in a number of areas around her hips. If these muscle stay turned off the body becomes especially loose in the area and is prone to falls, bursitis, and dislocations. More commonly the muscle gripping will quickly return and can become even more severe. The patient can then become dependent on the treatment without lasting benefit. This reaction is because the gripped muscles were actually serving a purpose. We previously stated that case studies show gripping patterns first emerge at points of extreme laxity creating instability. The gripping muscles counteract this instability. When these muscles get turned off the body becomes unstable. Recognizing this instability, the body will quickly turn the muscle back on, sometimes more strongly than before. For this reason, the dry needling treatment for EDS III can prove problematic.

The final group of common treatments for EDS III are medications. There are a wide variety of medications. NSAIDS provide both pain relief and are anti-inflammatories. Opioids provide stronger pain relief for when NSAIDS prove ineffective. Skeletal muscle relaxants provide pain relief and mild sedation. Antidepressants also relieve pain and offer mild sedation. Steroids relieve inflammation. Finally, nerve blocks can be injected into points of extreme pain to offer relief be interrupting the nerve signals. These are the most common medical treatments though there are many others.

Pain medication often comes with side effects. NSAIDS can cause gastrointestinal problems. Opioids can create dependency and narcotic bowel syndrome. Antidepressants can trigger serotonin syndrome with symptoms including agitation, hyperreflexia, diarrhea, and hypotension. Multiple steroid injections may damage the cartilage. In cases of severe pain, these medications offer relief and should be utilized. In periods of severe gripping, these medications can calm the body down, lowering the high impulse, and placing the patient in a state where they can receive further treatment. However, they are not on their own restorative treatment for EDS III.  Lowering a high impulse artificially does not teach the body to produce a balanced impulse and may produce a boomerang effect when the medication in tapered off.  Remaining indefinitely on these medications puts the patient at greater risk of their negative side effects and masks the symptoms that would point towards progress or worsening of the syndrome. Sedation and nerve blocks can also directly retard and inhibit progress by giving the patient less sensation and control of their nerves. For these reasons they should be used sparingly as an assistant to other treatments and not as a complete treatment in themselves.

The main problem with all of these treatments from physical therapy to medication, is that they seek to eliminate a symptom rather than balance the system and treat the entire syndrome. CINK takes a more direct approach to EDS III by teaching the body to produce a consistent moderate impulse, instead of alternating between high and low. But what is CINK? CINK, or Corrective Integrated Neuro-Kinetics, is a method that uses the concept of energy lines and structures to identify and predict points of positive, negative, high and low neuro-muscular impulses. It then uses a technique of reflex induction to generate more beneficial neuro-muscular impulses. 

An energy line is a sequence and trajectory of neuro-muscular nerve impulses that happen often enough to be a reflex active in daily life. While the body creates many reflexes from repeated movement patterns, most are isolated to that activity. A baseball player will develop a reflex for his swing, however, the complicated movement pattern and muscle firing of the reflex will be isolated to that activity. An energy line is a firing pattern that is on most of the waking day and used for common activities like breathing, sitting, standing, and walking as well as more complicated activities that haven't yet developed an isolated reflex. Points of the body without an energy line will default to a relaxed or low impulse state unless the body consciously chooses to engage the muscles in this region. If a body does not have an energy line running through their abdominals, their default will be to have a relaxed abdomen. Thus, a client may do abdominal exercises as part of a strengthening regimen, but these muscles will not naturally engage to support their structure throughout the day without direct conscious effort. Because most of person's day is preoccupied with tasks that take focus away from the body, the majority of the day the abdominal muscle group will be lax. Further, if the body has an energy line that stretches the abdominal region, engagement of these muscles will be difficult and weak because the body is fighting against an ingrained reflex.

Energy lines themselves can be either positive or negative. A positive energy line will run through large muscle groups in a way that creates eccentric muscle engagement to support the body's structure without rigidity with an angle that promotes proper balance. Energy lines are deemed negative if they: create a reliance on smaller muscles for structural integrity; engage individual muscles in a concentric or a gripped fashion, or by placing the muscle in a complete stretch/slack position; or have trajectories that throw the body out of proper alignment disrupting balance and placing undue strain on portions of the vertebrae and joints. The deeper the reflex of the firing pattern, the stronger the energy line. 

Because of the limited physics of the human body, there are determinate variations in energy lines and combinations thereof. A set of cohesive energy lines makes up a structure. While a body may present without all the possible energy lines of a structure, they will not present with an energy line common to a different structure.  A Classis Sway Back will not have any Military structure energy lines and vice versa. There are nine total structures. Four Classic structures: Classic Sway Back, Classic Military, Classic Kyphosis-Lordosis, and Classic Flat Back. These have four corresponding Compensated structures: Compensated Sway Back, Compensated Military, Compensated Kyphosis-Lordosis, and Compensated Flat Back. The final structure is Ideal.

Only the Ideal structure is without points of overuse and points of underuse. The Ideal structure is strong and supported because energy lines run through all the major muscle groups in a trajectory that elicits eccentric contraction and proper balance. A person with Ideal structure does not have to think to engage their core when standing as the muscles are engaged in a default position. All the other structures are unstable and prone to strain and injury. All bodies begin with ideal structure. Then, in childhood or adolescence, many morph into one of the classic structures for a variety of factors--temperament, social mirroring, physical training, genetic conditions, external traumas, etc. The inherent instability of the Classic structures leads the body to add Compensation lines to shore up structural support. All Compensation lines create concentric contraction in an effort to increase muscular support, though in reality they create rigidity and muscle strain. If retained into adulthood or reintegrated as an adult, an Ideal structure is unlikely to alter except for cases of disease or external trauma. CINK practitioners use the knowledge of energy lines and structure to predict points of instability, strength, rigidity, as well as future gripping points as structures transition from Classic to Compensated forms.

But how does CINK help those with EDS III? The joint hypermobility of EDS III creates a greater risk of injury and increases the rate and severity of compression and disk degeneration in low impulse areas without healthy energy lines. This vulnerability also leads to earlier development of compensation lines and with it, the polar extremes of high and low impulses. The instability of these extremes also make EDS III patient more likely to develop negative reflexes from strength training and stretching than people without the disorder.

CINK focuses directly on changing the nerve impulse. In this way, it targets the extreme high and low impulses that are the center of EDS III syndrome. CINK focuses on altering reflexes through the most simplistic movements, beginning with just breathing, sitting, and standing so the body connects the reflex to all its daily activities and not just while exercising. The consistency of the firing pattern throughout the day helps temper the syndrome's inclination towards high and low impulse. Energy lines running through large muscle groups support the weight of the structure and protect the joints and vertebrae, while the eccentric contraction prevents gripping patterns and their corresponding pain. The greater level of structural support also allows the smaller muscles to soften their contraction relieving muscle strain without sacrificing stability. Case studies have shown increased muscle development and pronounced and lasting pain reduction. CINK training also improves structural alignment and increases body placement awareness generating a reduction in trips and falls. 

EDS III patients undergoing CINK treatment have also shown improvement in symptoms beyond the muscular-skeletal system. The reflex nerve impulse training has been shown to improve performance of the smooth muscles of the intestines, reducing IBS symptoms.  Symptoms of fluid pooling and pre-syncope have also shown marked improvement. Patients also show an increased ability to focus throughout the day and a decrease in anxiety and hyperactivity levels, due to the concentration level that is a necessary component to the CINK treatment.

CINK's unique approach to EDS III patients has shown great promise in case studies. It is now time to open up treatment to the broader population of EDS III sufferers with a program that finally addresses the syndrome and not just part of its symptoms. 

[1] Dyna Kids, Pocinki, Alan G. MD, "Joint Hypermobility and Joint Hypermobility Syndrome,"

[2] UW Medicine Orthopaedics And Sports Medicine. "Ehler's-Danlos Syndrome," last modified March 21, 2011,

[3] NCBI, "Ehler's-Danlos Syndrome, Hypermobility Type," last modified September 13, 2012,

[4] OMIM, "Ehler’s-Danlos Syndrome Type III,

[5] NCBI, "Ehler's-Danlos Syndrome, Hypermobility Type,"

[6] NCBI, "Ehler's-Danlos Syndrome, Hypermobility Type,"

[7] Dyna Kids, Pocinki, Alan G. MD, "Joint Hypermobility and Joint Hypermobility Syndrome,"

[8] NCBI, "Ehler's-Danlos Syndrome, Hypermobility Type,"

[9] Dyna Kids, Pocinki, Alan G. MD, "Joint Hypermobility and Joint Hypermobility Syndrome,"

[10] UW Medicine Orthopaedics and Sports Medicine, "Ehler's-Danlos Syndrome," last updated March 21, 2011, Linked to UW Medicine Orthopaedics and Sports Medicine, "Exercise and Arthritis," last updated September 23, 2011,

[11] "What is Prolotherapy,"

[12] NCBI, "Ehler's-Danlos Syndrome, Hypermobility Type,"

[13] Dyna Kids, Pocinki, Alan G. MD, "Joint Hypermobility and Joint Hypermobility Syndrome,"