Dry Needling and Hypermobility

While the impact of dry needling (DN) has been established for various indications and body regions [1-21], it is not necessarily clear when or even whether dry needling of patients with systemic hypermobility is indicated. Hypermobile individuals may “create” muscle contractures, commonly known as “taut bands’ in the myofascial pain literature, to provide stability in otherwise unstable joints. It is conceivable that lowering the muscle tone of such contractures would increase joint instability, leading to an immediate decrease in function. Before deciding to use dry needling on a patient with hypermobile joints, a brief review follows, summarizing some of the main characteristics of hypermobility, Ehlers-Danlos Syndrome (EDS), and Hypermobility Spectrum Disorders (HSD).


Joint mobility is a prerequisite to movement and motor development. Physiotherapists and other healthcare providers commonly measure joint range of motion against suggested norms required for movement efficiency [22]. When joint range deviates from these normative values, clinicians characterize the joint as either hypo- or hypermobile and offer therapy to address impairments in joint mobility and improve movement efficiency [23].

Hypermobility is quite common in patients, ranging from having one or two hypermobile joints to having generalized HSD or EDS [24, 25]. Hypermobility is defined as excessive joint movement within a normal plane of motion. Although in the clinic, the terms hypermobility, hyperlaxity, and hyperextensibility are often used interchangeably, the terms are not equal as the latter refers only to movement in abnormal planes [26].

Hypermobility can be structural, constitutional, or hereditary, but it can also result from functional changes in the joint and surrounding tissues. Localized hypermobility may be due to training, excessive stretching, trauma, such as surgery or joint dislocation, among others, but it can also be hereditary. Generalized or systemic hypermobility involves more than five joints and is usually hereditary, with significant individual differences based on age, sex, and ethnic background [26].  The most common genetic conditions associated with systemic hypermobility include Ehlers-Danlos, Marfan, and Down Syndrome.  Physiotherapists may assess systemic hypermobility with the Beighton Score (Figure 1), which has acceptable interrater reliability but inconclusive validity [27].

Several other commonly used tests lack satisfactory reliability and validity [27]. The Five-Part Questionnaire (Table 1) is the most used questionnaire for adults with conflicting evidence of reliability and validity [27, 28]. Another commonly used test is the Bristol Impact of Hypermobility test, which measures the impact of hypermobility on a person’s life and showed excellent test-retest reliability (download here) [29].

Table 1 – The Five-Point Questionnaire [28]
Can you now (or could you ever) place your hands flat on the floor without bending your knees?
Can you now (or could you ever) bend your thumb to touch your forearm?
As a child, did you amuse your friends by contorting your body into strange shapes or could you do the splits?
As a child or teenager, did your shoulder or kneecap dislocate on more than one occasion?
Do you consider yourself “double-jointed”?

Systemic hypermobility usually does not pose any major problems until puberty. In clinical practice, many teenage girls with EDS experience their pain and major dysfunction within weeks or months after their first menses. Most children are hypermobile, with girls having greater joint mobility than boys. Range of motion increases until adolescence and tapers into adulthood and old age. Since joint mobility in children is far greater than in adults, diagnosing hypermobility in children is challenging as there are no age-related norms for range of motion. An Australian study of 1,584 subjects showed that 61% of girls and 37% of boys were hypermobile [30]. This does not necessarily indicate that these children had abnormal range of motion or experienced disproportionate pain or dysfunction. Javadi Parvaneh and Shiari (2016) modified the Beighton criteria to improve the identification of hypermobility in children [31], but this test is not commonly used as most children with hypermobility are not symptomatic.

It is important to realize that not all hypermobile people are symptomatic [27]. However, those with systemic hypermobility tend to have higher reports of pain.  A study of 466 subjects with EDS demonstrated that 99% suffered from joint pain, 91% suffered from extremity pain, and many common comorbidities, such as chronic fatigue (82%), anxiety (73%), and depression (69%) [32]. Joint hypermobility was a common precursor to pain hypersensitivity and central sensitization in 40 hypermobile adolescents [33].

Ehlers Danlos Syndrome and Hypermobility Spectrum Disorders

As summarized in the 2017 EDS clinical classifications, Ehlers-Danlos Syndromes are a heterogeneous group of thirteen different but overlapping connective tissue disorders featuring joint hypermobility, skin hyperextensibility, and fragile tissues (Table 2) [24]. Many patients with EDS experience persistent pain, autonomic dysfunction, and gastrointestinal dysmotility [34]. Each subtype has its own specific major and minor criteria. For all subtypes, except the hypermobile subtype, the definitive diagnosis must be made by molecular confirmation with identification of the involved gene(s), which implies that the diagnosis of hypermobile EDS is made based on history, examination, and a clinical impression [24].

Table 2 – Clinical Classification of the Ehlers-Danlos Syndromes, Genetic Basis, and Protein Type [24]


Clinical Subtype
Genetic basis
Classical EDS
Major: COL5A1, COL5A1
Rare: COL1A1
Type V collagen
Type I collagen
Classical-like EDS
Tenascin XB
Cardiac-valvular EDS
Type I collagen
Vascular EDS
Major: COL3A1
Rare: COL1A1
Type III collagen
Type I collagen
Hypermobile EDS
Arthrochalasia EDS
Type I collagen
Dermatosparaxis EDS
Kyphoscoliotic EDS
Brittle Cornea syndrome
Spondylodysplastic EDS
Musculocontractural EDS
Myopathic EDS
Type XII collagen
Periodontal EDS

Several patients with hypermobility do not meet any of the new criteria, and for these individuals, the term Hypermobility Spectrum Disorders (HSD) was coined [24]. Patients with HSD usually have musculoskeletal symptoms, although some may have limited multisystem involvement. Both hEDS and HSD patients feature a myofibroblast-like phenotype with several abnormal extracellular matrix components (ECM), such as different expressions of CCN1/CYR61 and CCN2/CTGF inflammation mediators, an altered organization of α-smooth muscle actin cytoskeleton, and increased levels of the ECM-degrading metallo-proteinase-9, among others [35]. HSDs are divided into generalized (G-HSD), peripheral (P-HSD), localized (L-HSD), and historical (H-HSD) subtypes. The genetic basis, prevalence, and incidence of HSDs are not known.

Historically, EDS and HSD have been poorly recognized by healthcare providers. In 2005, only 10% of physicians referring their hypermobile EDS patients to rheumatology clinics realized that joint hypermobility was the underlying cause of their patients’ pain [36]. Many physiotherapists are unaware of the condition [37], although EDS is a common, heritable trait seen in up to 10%–30% of males and 20%-40% of females [38]. Ehlers Danlos Syndrome is the most common inherited connective tissue disorder with approximately 1 in 5000 births [39], compared to 1 in 3000-10000 for Marfan Syndrome [40], and 1 in 10000 -15000 for Osteogenesis Imperfecta [41, 42].  The hypermobile type of EDS is characterized not only by hypermobility but also by chronic pain, dysautonomia, chronic fatigue, anxiety, and other associated symptoms and represents at least 80%-90% of all EDS cases [39]. Many patients with hypermobile EDS experience significant levels of disability, which is highly correlated with both physical and psychological factors [43].

As part of the differential diagnostic process, patients must be screened for possible neurological complications resulting from tissue weakness, biophysical deformative stresses, entrapments, and tissue deformations [44]. Comorbid conditions reported with hypermobile EDS include Chiari malformations with or without tethered cord syndrome [45] and craniocervical instability with or without ventral brainstem compression [46]. Other common comorbidities include mast cell activation syndrome [47], gastrointestinal dysfunction [48], and postural orthostatic tachycardia syndrome (POTS) [49].

Dry Needling

Since pain is very common in patients with EDS and HSD, DN may seem like an excellent treatment option, but some caution is warranted. Managing pain in hypermobile patients can be quite challenging and often requires a multimodal, interdisciplinary approach [50, 51] that may include manual therapy, such as trigger point therapy and soft tissue mobilizations [52], pain science education [53], cognitive, emotional, and behavioral therapy [54], and external-focus exercise therapy [55, 56]. The role of DN for hypermobile patients has not been scientifically confirmed. Still, based on our extensive clinical experience with hypermobile patients, DN can be an important aspect of physiotherapy for patients with HSD and EDS, especially for reducing pain [57]. Our physiotherapy center, Bethesda Physiocare (Bethesda, Maryland, USA), is one of only 22 centers globally recognized as EDS Centers & Networks of Excellence (Figure 2). We have treated thousands of patients with EDS/HSD.

Trigger point injections were recommended in a case report from India [58].  Studies comparing TrP injections with DN show many similarities in outcomes, but these studies are usually non-pragmatic with limited clinical applicability and methodological flaws [59-64].  As mentioned in the introduction, there is a risk that DN may reduce the patient’s joint stability, especially when that patient uses contractures for stabilization. Because it is sometimes difficult to predict how a patient with EDS will respond to DN, we recommend treating only a few muscles or maybe just a few TrP points during the first treatment sessions combined with pain science education [65-67]. Once a patient’s pain level has reduced, therapy must include progressive or graded loading, improving loading tolerance, and reducing kinesiophobia [68-70]. Another question is whether physiotherapists should needle stiffer areas, for example, sections of the spine, in hypermobile individuals. The stiffer areas may be more “normal” or functional, yet the relatively stiffer areas are also common causes of myofascial pain [57].

Another aspect to consider with needling patients with EDS is that connective tissues, especially fascia, are organized differently than in patients without hypermobility [71]. In hypermobile EDS patients, the extracellular matrix changes exhibit reduced inter-fascial plane gliding [72], which is a bit surprising as, previously, decreased fascial gliding was primarily associated with a loss of flexibility [73]. Type I collagen and hyaluronan are important for fascial force transmission and gliding, promoting sliding of adjacent fascial tissue layers [74], but excessive hyaluronan can lead to stiffness of the ECM [75]. Hyaluronan or hyaluronic acid is a key component of the ECM found in vertebrate tissues [76], including in articular joint synovial fluid, providing lubrication and viscoelasticity to protect cartilage surfaces. The reduced gliding ability found in EDS patients may explain at least partially the widespread pain, but it may also impact proprioception and the ability to generate force and contract muscles efficiently [76, 77].

Up to 40% of muscle force is transmitted via fascia, especially the epimysium, and not through tendons [78, 79]. When connective tissues have significant laxity, forces may not get transmitted to adjacent fascial layers [57]. The changes in fascial gliding may be due to an increase in type I collagen and pathologic changes in matrix metalloproteinases in the ECM [80], which likely results in increased viscosity, reduced lubrication, and sliding movement of fascia [76]. It is conceivable that fascial needling approaches, including winding fascial needles in fascial tissues [81, 82], or Fu Subcutaneous Needling [83-85], may benefit patients with EDS. The theoretical basis for using needles in the treatment of fascial adhesions and scar tissue has developed sufficiently to consider its use in the clinic [86-91], and conceivably, these techniques may also be useful for patients with EDS, but there is no research to support this notion.

As hypermobile patients get older, they will likely become less hypermobile, mostly because the percentage area of collagen 1 increases significantly with aging [92]. There is some evidence that part of aging is associated with a decrease in the percentage of elastic fibers in the perimysium and a decrease in hyaluronan [92]. Older skin has less hyaluronan than younger skin [93]. Another contributing factor is the Yes-associated protein (YAP), expressed particularly in the deep fascia, where it is involved with fascial mechanotransduction, remodeling, regeneration, and fibrogenesis [94].

Jan Dommerholt, PT, DPT and Nathan Mayberry, PT, DPT

The Obvious Choice for Dry Needling Education

Dry Needling Course Series

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The Dry Needling 1 course is an excellent starting point for learning the fundamentals of dry needling therapy. With a focus on the safe and effective application of dry needling techniques, you will gain a solid understanding of myofascial trigger points, needling techniques, precautions, and how to apply these techniques in clinical practice.

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The Dry Needling 2 course is an intermediate-level course that provides in-depth knowledge and hands-on training for dry needling techniques of the extremities, including the upper and lower body. By completing this course, you will expand upon the skills you acquired in the DN-1 course and better understand the application of dry needling for managing musculoskeletal pain and dysfunction.

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The Dry Needling 3 course is the final course in the series and the last step before becoming a Certified Myofascial Trigger Point Therapist – Dry Needling (CMTPT/DN). This course offers an in-depth study of advanced dry needling techniques for hand muscles, several lower extremity and foot muscles, the craniofacial and craniomandibular muscles, and more.

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