REVIEW

Joint Hypermobility Syndrome: Recognizing a

Commonly Overlooked Cause of Chronic Pain
Bharat Kumar, MD, Petar Lenert, MD, PhD
Division of Immunology, University of Iowa, Iowa City.

ABSTRACT

Joint hypermobility syndrome, also known as benign hypermobility syndrome, is a connective tissue
disease characterized by joint instability, chronic pain, and minor skin changes. It shares many clinical
features of Ehlers-Danlos syndrome, Hypermobility Type; enough so that many authorities consider them
as one disease process. Approximately 3% of the general population is believed to have joint hypermobility
syndrome, but despite this high prevalence, due to lack of awareness, heterogeneity of clinical presentation,
and reliance on physical examination for diagnosis, it is largely overlooked by primary care physicians as
well as by specialists. This leads to delayed or missed opportunities for diagnosis, and inappropriate
interventions that frustrate both providers and patients. We review the literature regarding the patho-
physiology, diagnosis, treatment options, and prognosis of joint hypermobility syndrome, and advocate for
primary care physicians to consider it in the differential diagnosis of patients with chronic pain.
Ó 2017 Elsevier Inc. All rights reserved.
The American Journal of Medicine (2017) 130, 640-647

KEYWORDS: Chronic pain; Connective tissue disease; Musculoskeletal condition

Joint hypermobility syndrome, also termed benign hyper-
mobility syndrome, is a connective tissue disorder charac-
terized by chronic musculoskeletal pain due to joint
hyperextensibility. Occasionally considered a milder
variant of Ehlers-Danlos syndrome, Hypermobility Type, it
is seen in up to 3% of the general population, a prevalence
rivaling fibromyalgia, gout, and rheumatoid arthritis.
Despite this, it is likely underdiagnosed by physicians due
to its highly variable clinical presentation, absence of a
confirmatory test, and controversies regarding its etiology
and pathogenesis.
The diagnosis of joint hypermobility syndrome is
largely clinical and can be established in the primary care
setting. Because patients have a high rate of concomitant
fatigue, headaches, orthostatic hypotension, anxiety, and
abdominal and genitourinary complaints, identifying these
patients and providing a more appropriate, unifying
Funding: None.
Conflict of Interest: The authors have no conflicts of interest to declare.
Authorship: Both authors had access to the data and had a role in
writing the manuscript.
Requests for reprints should be addressed to Bharat Kumar, MD, Di-
vision of Immunology, University of Iowa Hospitals and Clinics, 200
Hawkins Drive, Iowa City, IA 52242.
E-mail address: Bharat-Kumar@UIowa.edu
diagnosis is important. Additionally, identification of joint
hypermobility as a cause of chronic pain and fatigue may
help guide providers toward more appropriate manage-
ment strategies, including physical therapy and nonopioid
pain relievers.
EPIDEMIOLOGY
The prevalence of joint hypermobility syndrome is esti-
mated to be about 3%, based on a 2013 survey of 12,853
participants in the UK.1 However, joint hypermobility
syndrome is likely underdiagnosed and its prevalence is
expected to be much higher.2 Epidemiological studies sug-
gest that patients of all races and age groups are affected,
although it is more prevalent in children and adolescents,
who tend to have greater mobility of joints.3
Generalized joint hypermobility, that is, the finding of
hyperextensibility in multiple joints with or without other,
accompanying chronic musculoskeletal complaints, is even
more prevalent. Ten to twenty percent of individuals exhibit
joint hypermobility, particularly children, adolescents,
females, Asians, and West Africans.4 Indeed, a study among
female monozygotic and dizygotic twins suggested that
generalized joint hypermobility may be found in up to 20%
of females.5 Although large-scale epidemiological studies
are lacking, the rates of generalized joint hypermobility in

0002-9343/$ -see front matter Ó 2017 Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1016/j.amjmed.2017.02.013
Kumar and Lenert Joint Hypermobility Syndrome 641

competitive athletes may be even higher, given the inherent decreased joint momenta in the lower extremities, necessi-
advantages of increased flexibility in sports such as tating greater force to maintain equilibrium.10,11 However,
gymnastics, swimming, and track and field.6 their conclusions have been tempered by other studies that
have failed to reliably demonstrate such changes, and a
systematic review questioned the clinical relevance of dif-
PATHOPHYSIOLOGY ferences in gait.12
Because of this variable clinical Additionally, patients with joint
presentation and lack of specific hypermobility syndrome tend to
biomarkers, researchers have been CLINICAL SIGNIFICANCE lack proprioceptive acuity.13 Pro-
unable to identify a single patho-

Joint hypermobility syndrome is a com- prioception, the ability to judge
physiologic mechanism by which position of joints, is essential for
patients develop joint hypermo- mon cause of chronic pain and fatigue
joint stabilization; therefore, pa-
bility syndrome. The fact that only seen in at least 3% of the general
tients with joint hypermobility
a small proportion of patients with population.
syndrome may be at greater risk for
generalized joint hypermobility,
Patients may also present with head- joint injuries, particularly in the
that is, hypermobility found on
aches, anxiety, orthostasis, and abdom- knees bilaterally. A 2010 system-
physical examination, go on to atic review and meta-analysis of 18
inal pain.
develop varying levels of muscu- studies concluded that there is an
loskeletal pain and fatigue sug-
Providers can use the Beighton Score and increased risk of knee injury, but
gests that there are a host of Brighton Criteria to screen for joint no such finding for ankle injuries.14
genetic and environmental factors hypermobility syndrome. Joint hypermobility syndrome
that contribute to its development.

Establishing a diagnosis is important patients also tend to have
decreased muscle mass and mus-
because lifestyle modification can help
Genetic Factors cle strength.15 This may be partly
to prevent further injury and pain.
The role of genetics in the devel- due to increased laxity of tendons,
Chronic use of narcotics is not which are unable to transmit po-
opment of joint hypermobility recommended.
syndrome is controversial, and wer produced by muscles.16
evolving with the rapid adoption Additionally, starting in child-
of genetic testing in research and clinical settings. The vast hood and early adolescence, the
majority of cases do not appear to be linked to any identi- fear of provoking pain and sustaining injury may lead to
fiable mutation, although pedigree studies have shown a decreased levels of physical activity, leading ultimately to
weak autosomal dominant inheritance pattern with variable deconditioning and exercise intolerance.17 This effect is
penetrance.7 even found in high-level athletes with generalized joint
In fewer than 10% of cases, a mutation in the gene hypermobility.3
TNXB, coding for the extracellular matrix glycoprotein In addition to these biomechanical perturbations, patients
Tenascin X, has been identified. These patients tend to have with joint hypermobility syndrome also have neurologic
more pronounced dermatologic signs, including skin hyper- disturbances that contribute to the diffuse musculoskeletal
8
extensibility, velvety skin, and easy bruisability. A host of pain. Generalized hyperalgesia is a common complaint, and
rarer mutations have also been identified in some patients is believed to be mediated by centralized sensitization.18
with joint hypermobility syndrome, but the clinical signifi- There do not appear to be any longitudinal studies on the
cance of genetic testing for these is, as of yet, unknown. 9,10 development of chronic musculoskeletal pain of neurologic
origin, but cross-sectional studies suggest that chronic
trauma reduces the pain threshold. Some authorities have
Environmental Factors even speculated that hyperalgesia may serve as a compen-
In addition to the genetic predisposition due to presumed satory mechanism, in the absence of functional mechanisms
difference in collagen structure, current theories emphasize to prevent joint instability such as intact proprioception.19
the importance of localized biomechanical overloading and Alternatively, the high prevalence of chronic pain in joint
chronic soft tissue injury due to joint laxity and instability. hypermobility syndrome may be attributed in part to the fact
Repetitive microtrauma may lead to altered kinematics, that those with chronic pain are more likely to see physi-
which, in turn, cause overload on other joints and further cians and obtain testing than those without pain.
soft tissue injury manifesting as arthralgias and diffuse Less well explored are the psychosocial aspects of joint
musculoskeletal pain. hypermobility syndrome. The higher rates of anxiety and
Studies have also demonstrated more widespread effects depression are hypothesized to be due to pain-related fear
on altered gait and posture. In 2 studies comparing patients and fear avoidance, but no studies have been performed
with asymptomatic generalized joint hypermobility to those specifically in joint hypermobility syndrome patients.20
with joint hypermobility syndrome, it was found that pa- Even less is understood about the autonomic dysfunction
tients with joint hypermobility syndrome tend to have seen in joint hypermobility syndrome. Patients frequently
642 The American Journal of Medicine, Vol 130, No 6, June 2017

exhibit postural tachycardia syndrome (postural orthostatic

Table 1 Differential Diagnosis of Joint Hypermobility in
tachycardia syndrome) as well as bowel and bladder Adults*18
dysfunction, putatively due to connective tissue
abnormalities.21 Disease Associated Features
EDS Classic Type (Types I & II) Skin hyperextensibility
CLINICAL EVALUATION Bruising
Velvety skin
The role of the clinical examination in the diagnosis of joint EDS Hypermobility Type (Type III) Clinically indistinguishable
hypermobility syndrome is critical and cannot be overstated. from JHS
The history and physical examination serve 3 major goals: EDS Vascular Type (Type IV) Thin translucent skin
1) to screen for generalized joint hypermobility; 2) to Extensive bruising
determine the extent of disease burden; and 3) to help EDS Kyphoscoliotic Type (Type VIA) Scoliosis
exclude other connective tissue diseases characterized by Severe muscle hypotonia
generalized joint hypermobility. Scleral fragility
Generalized joint hypermobility is a relatively common Marfanoid habitus
phenomenon, and not all patients who have generalized joint EDS Musculocontractural Scoliosis
hypermobility go on to develop joint hypermobility syn- Type (Type VIB) Severe muscle dystonia
EDS Arthrochalasia Type Bilateral clubfoot
drome. Only about 3.3% of women and 0.6% of men will
(Type VIIA) Dysmorphic facies
develop chronic pain, fatigue, or other complaints that Developmental delays
closely resemble, and may be considered, a chronic pain/ Skin hyperextensibility
fatigue syndrome in its own right. In fact, patients with EDS Dermatosparaxis Type Skin fragility
generalized joint hypermobility may be advantaged in Easy bruising
certain competitive fields, such as dance and gymnastics.22 Large hernias
Another subset of patients seems to cope well with the EDS due to FKBP14 deficiency Severe muscle hypotonia
symptoms of generalized joint hypermobility and so never Developmental delays
come to medical attention.23 Scoliosis
At the same time, there are a variety of other connective Sensorineural hearing loss
tissue disorders that are characterized by generalized joint EDS due to TNXB deficiency Muscle weakness
Velvety skin
hypermobility (Table 1).24 Because joint hypermobility
Skin hyperextensibility
syndrome is a diagnosis of exclusion, it is of utmost impor- Marfan syndrome Muscle hypoplasia
tance to identify other signs of potential disease and to Ascending aorta dilation
carefully solicit a family history for connective tissue disor- Arachnodactyly
ders. In particular, Marfan syndrome and Ehlers-Danlos Scoliosis
syndrome, Vascular Type (although this type is not typi- Pectus excavatum
cally associated with generalized hypermobility) need to be High palate
ruled out because, unlike joint hypermobility syndrome, these Loeys-Dietz syndrome Muscle hypotonia
are associated with sudden demise. Although establishing the Hypertelorism
diagnosis of Ehlers-Danlos syndrome and other heritable Cleft palate/bifid uvula
connective tissue diseases is beyond the scope of this article, Arterial tortuosity
Limb-girdle muscular dystrophy 2E Developmental delay
recognition of associated congenital abnormalities listed in
Arrhythmias
Table 1 is essential in determining which cases need referral Scoliosis
to medical genetics for further testing and counseling. Osteogenesis imperfecta Blue sclerae
Joint hypermobility syndrome has a highly variable (non-deforming type) Repeated fractures
presentation but most patients come to attention because of
EDS ¼ Ehlers-Danlos syndrome; JHS ¼ joint hypermobility syndrome.
their joint complaints. Although joint hypermobility syn- *Selected differential diagnoses of joint hypermobility in adults.
drome manifests itself in childhood, symptoms may appear Please note that this is not an exhaustive list and that many of the
at any age. Therefore, the role of the history and physical above-mentioned conditions are highly variable in presentation.
examination are paramount because there are no laboratory
or radiographic tests to confirm the diagnosis, and general-
ized joint hypermobility may be seen in many other con-
nective tissue diseases. Primary care providers can be aided by a 5-point ques-
tionnaire devised by Hakim et al5 for the detection of joint
hypermobility; positive responses to 2 of these 5 questions
Generalized Joint Hypermobility had a sensitivity of 84% and specificity of 85% in 2 cohorts
Because generalized joint hypermobility is a prerequisite for of 382 patients (Table 2). Because range of motion
the diagnosis of joint hypermobility syndrome, providers decreases with advancing age, this questionnaire may be
should perform a thorough history and physical examination particularly helpful in older patients who may have once
to identify any symptoms and signs of hypermobility. been hypermobile but no longer appear to be so.25
Kumar and Lenert Joint Hypermobility Syndrome
Table 2 Questions to Ask Patients with Suspected Joint
Hypermobility

Do you consider yourself double-jointed?

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?
Positive responses to 2 of these questions have a sensitivity of 84%
and specificity of 85% for joint hypermobility syndrome (JHS), as
characterized by the Brighton Criteria for JHS.
Adapted from Hakim AJ, Cherkas LF, Grahame R, et al. The genetic
epidemiology of joint hypermobility: a population study of female twins.
Arthritis Rheum. 2004;50(8):2640-2644.5
The degree of hypermobility can be assessed and docu-
mented by the Beighton Score, which incorporates 5 simple
maneuvers to calculate a score between 0 and 9 (Figure 1). A
Beighton Score 4, in addition to arthralgias for longer than 3
months in 4 or more joints, constitutes the major criteria for the
Brighton Criteria (Figure 2).26 The Beighton Score should be
used in the context of the Brighton Criteria, because the
Beighton Score only documents the degree of hypermobility.
Additionally, joints should be examined for tenderness,
swelling, redness, and deformities in addition to assessing
range of motion in major joints. While frank swelling is rare,
some patients may have small noninflammatory effusions
resulting from meniscal or cartilaginous irritation. Similarly,
the presence of correctable deformities like swan neck de-
formities of the fingers may also resemble conditions like
rheumatoid arthritis.27
Furthermore, these patients may also have scoliosis,
lordosis, pes planus, genu valgum, patellar subluxation,
marfanoid habitus, varicose veins, rectal or uterine prolapse,
or thin skin.24 Many of these are considered minor criteria in
the Brighton Criteria.
Musculoskeletal Pain
There does not appear to be a specific pattern of joint
involvement, and some patients may have generalized and
symmetric polyarthralgias closely resembling inflammatory
arthritis. The pain is typically described as dull, and may be
self-limited or constant. Weight-bearing joints like the knees
and ankles appear to be more commonly involved. Unlike
classic descriptions of inflammatory arthritis, the joint pain
in joint hypermobility syndrome seems to be exacerbated by
repetitive use or physical activity. As a result, prolonged
morning stiffness (lasting >30 minutes) is rare, and the pain
usually occurs later in the day.20
Fatigue
Accompanying the diffuse musculoskeletal pain is often
very severe fatigue, seen in up to 84% of patients.28 In fact,
643
the fatigue can be so substantial that it can meet criteria for
chronic fatigue syndrome. Although the underlying cause is
unclear, muscle weakness is believed to be a key factor,
because this fatigue is associated with worsening with ac-
tivity, delayed recovery from physical exertion, and alter-
ations in gait.29 With advancing disease, postexertional
malaise and exercise intolerance become more of a back-
ground sensation of fatigue; over 90% of adults over the age
of 40 complain of fatigue, compared with only 28% in the
second decade of life.21
Additionally, there may be other contributors, including
sleep disturbance, concentration problems, and symptomatic
cardiovascular dysautonomia. Sleep disturbance is a
particularly common complaint in patients with joint
hypermobility syndrome, and may be linked to nocturnal
musculoskeletal pain, as well as periodic limb movement
and restless leg syndrome. While obstructive sleep apnea
has not been reported in joint hypermobility syndrome, in
other, related connective tissue diseases such as Ehlers-
Danlos syndrome and Marfan syndrome, hypotonia of the
upper respiratory passages may lead to upper airway resis-
tance, predisposing to hypopneic episodes.30 Altogether,
these sleep disturbances may contribute to poor sleep quality
and worsening fatigue.
Dysautonomia
About 75% of patients with joint hypermobility syndrome
appear to have impaired autonomic reflexes.31 Although
previously underappreciated, the decreased quality of life
due to severe dysautonomia can be as high as in patients
with congestive heart failure.22 Evidence suggests that there
is increased sympathetic tone, but decreased sympathetic
reactivity to stimuli. As a result, patients tend to have
orthostatic intolerance, gastrointestinal discomfort (such as
early satiety, bloating, postprandial nausea/vomiting), and
secretomotor complaints, including Raynaud phenomenon,
abnormal sweating, and sicca-like symptoms.32
Therefore, practitioners should solicit any history of
orthostatic symptoms, such as lightheadedness immediately
after rising from a seated position or an inability to remain in
an upright posture, and elicit objective signs in the clinic for
orthostasis.
While the cause of this dysautonomia remains uncertain,
speculation rests on peripheral neuropathy, increased
vascular distensibility leading to orthostasis, concurrent
depression, and low-level pain-induced sympathetic arousal
as potential causes.33
Headache
Headache is a particularly troublesome symptom experi-
enced by patients with joint hypermobility syndrome, with
75% of female patients suffering from migraines. This may
be due to intracranial vasculopathy causing reversible ce-
rebral vasoconstriction.34
However, patients tend to have a host of other primary
and secondary headaches, including those due to tension,
644 The American Journal of Medicine, Vol 130, No 6, June 2017

Figure 1 Maneuvers used to calculate the Beighton Score. The Beighton Score is calculated by adding the points
obtained through each maneuvers, yielding a total maximum score of 9. A Beighton Score of 4 or higher is a major
criterion for the Brighton Criteria (Figure 2).

temporomandibular joint dysfunction, unilateral myofascial
pain, idiopathic cerebrospinal fluid leak, Chiari malforma-
tion, cervicogenic headache, and neck-tongue syndrome.
Pain amplification, local muscle hyperalgesia, and neck
motion are also contributors to persistent chronic
headache.35
Abdominal and Pelvic Pain
Unexplained abdominal pain is a very common complaint,
seen in up to 86% of patients.36 Both dysautonomia, as
mentioned above, and laxity in collagen comprising the
gastrointestinal tract, may underlie increased pain genera-
tion. Iturrino et al37 demonstrated that up to 25% of varia-
tion in gas and pain sensation in healthy subjects could be
associated with colonic compliance. Due to the reduced pain
thresholds in patients with joint hypermobility syndrome,
this gas and pain sensation may be further amplified.
Abdominal and pelvic pain also might be due to other
causes. Abnormal laxity may cause pelvic prolapse as well;
the rate of joint hypermobility in females with pelvic
Kumar and Lenert Joint Hypermobility Syndrome 645

Major Criteria Comments

Beighton Score > 4 See Figure 1 for calculaƟon of Beighton Score
Polyarthralgias Arthralgias for longer than 3 months in 4 or more joints
Minor Criteria Comments
Beighton Score < 4 Beighton score of 1,2, or 3 if younger than 50 years of age
Beighton score of 0,1,2 or 3 if older than 50 years of age
Oligoarthalgias Joint pain greater than 3 months in 1 to 3 joints, or
Back pain for greater than 3 months, or
Spondylosis, spondylolysis, spondylolisthesis
DislocaƟon or subluxaƟon In more than one joint, or
In one joint on more than one occasion
SoŌ Ɵssue lesions Three or more soŌ Ɵssue lesions,
e.g. epicondyliƟs, tenosynoviƟs, bursiƟs
Marfanoid habitus Armspan greater than height (>1.03 raƟo), or
Upper segment less than lower segment (<0.89 raƟo), or
Arachnodactyly
Skin abnormaliƟes Skin striae, or
Hyperextensibility, or
Thin skin, or
Abnormal scarring
Ocular signs Drooping eyelids, or
Myopia, or
AnƟmongoloid slant
Varicose veins, hernia, or uterine/rectal
prolapse
Mitral valve prolapse
Exclusion
Presence of Marfan Syndrome
Presence of Ehlers-Danlos Syndrome Other than EDS-Hypermobility Type (type III)

Figure 2 The Revised Brighton Criteria. In order to establish the diagnosis of joint hypermobility
syndrome, the individual must satisfy any one of the following: 1) 2 major criteria; 2) 1 major and 2 minor
criteria; 3) 4 minor criteria; or 4) 2 minor criteria and unequivocally affected first-degree relative in the
family. Figure adapted from Grahame R, Bird HA, Child A. The revised (Brighton 1998) Criteria for the
diagnosis of benign joint hypermobility syndrome (BJHS). J Rheumatol. 2000;27(7):1777-1779.26

prolapse has been reported to be as high as 54%.38
Additionally, females with joint hypermobility syndrome
are more likely to have polycystic ovaries, endometrial
cysts, uterine leiomyomas, endometrial hypertrophy, and
endometriosis.39
anxiety or depression, and nearly 7 times more likely to
have a panic disorder, compared with those without joint
hypermobility syndrome. This may partly be due to the fear
and anxiety associated with potential re-injury, but the na-
ture of this relationship remains largely uncharacterized.42

Mitral Valve Prolapse PROGNOSIS

The relationship between joint hypermobility syndrome and
mitral valve prolapse is a matter of contention. Some of the
earlier studies did suggest an association,40 but with the
advent of stricter echocardiographic criteria, this has not
been validated.41 Regardless, cardiology consultation
should be considered for patients with suspected mitral
valve prolapse and joint hypermobility syndrome, because
many other connective tissue diseases can present with
mitral valve prolapse.
Psychosomatic Features
Evidence also suggests a strong psychosomatic component
to joint hypermobility syndrome. Patients with joint hyper-
mobility syndrome are 4 times more likely to develop
Establishment of the diagnosis of joint hypermobility syn-
drome is important because, unlike many other causes of
chronic musculoskeletal pain, joint hypermobility syndrome
is a nonprogressive and noninflammatory condition.
Because joint laxity decreases with advancing age, some
symptoms may attenuate later on in life.
However, patients should be aware that there are
sequelae to joint hypermobility syndrome. The increased
joint laxity may predispose patients to premature osteoar-
thritis, but this association has not been consistently
demonstrated.43,44 In at least one study, articular hypermo-
bility was found to be protective for progression of radio-
graphic hand osteoarthritis.45 For unclear reasons,
premenopausal joint hypermobility syndrome patients are
also at 1.8-fold increased risk of developing osteoporosis.46
646
MANAGEMENT
Lifestyle modification is considered the most important
intervention, although rigorous studies evaluating the effi-
cacy of any particular intervention is lacking. Patients
should be advised that excessive joint movement may
aggravate symptoms and lead to joint, meniscal, and carti-
lage injury. Regular exercise is important, but overtraining,
poor pacing, and excessive focus on joint flexibility may
also lead to injury. Low-cost interventions, like neuromus-
cular taping and bracing, may help to prevent injury and
improve gait.47,48 Importantly, patients should consider
strengthening programs for periarticular musculature in or-
der to stabilize joints.
Prior to strenuous activity, stretching techniques to
isolate tight muscles without stressing the joints may
improve balance and control. For those who engage in
athletic competition, nonsteroidal anti-inflammatory drugs
prior to physical activity may help reduce symptoms.49
Referral to physical therapy may be particularly useful in
tailoring and personalizing exercise regimens.50,51 Because
some patients may have extreme fear and anxiety of pro-
voking re-injury, cognitive behavioral therapy may be
required in certain cases.
Nutritional supplementation has also been proposed as an
important modality in the treatment of joint hypermobility
syndrome, but there is a lack of any studies investigating its
role specifically in joint hypermobility syndrome. Vitamin C
may be useful in addressing some cutaneous features, and
vitamin D supplementation may be required in those with
reduced bone mineral density.52
Importantly, there is no evidence available regarding the
use of opioids for the treatment of chronic pain due to
hypermobility. Because the pathogenesis of pain in hyper-
mobility relates more to chronic stresses, it does not stand to
reason that opioids will help promote long-term alleviation
of pain. Moreover, because opioid medications carry very
significant risks, including the development of central pain
sensitization, dependency, and the potential for abuse, these
should not substitute for physical therapy and lifestyle
modification.
CONCLUSION
Joint hypermobility syndrome is a relatively common cause
of chronic pain in the general population. Because its
diagnosis requires a high level of clinical suspicion and the
performance of specific physical examination maneuvers, it
is often overlooked by providers. This is unfortunate,
because establishment of the diagnosis allows for more
appropriate management and care. In addition to providing
an explanation to patients about their disease process, pa-
tients with joint hypermobility syndrome can also be
counseled about ways to protect their joints and to undergo
lifestyle modification in order to prevent further damage.
Providers should be cognizant that patients with chronic
musculoskeletal pain may have joint hypermobility and that
it may be related to a series of other, seemingly unrelated
The American Journal of Medicine, Vol 130, No 6, June 2017
symptoms such as headache, abdominal pain, fatigue, and
anxiety.
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