Adipose Tissue as Pain Generator in the Lower Back and Lower Extremity: Application in Musculoskeletal Medicine

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Lee et al. HCA Healthcare Journal of Medicine (2020) 1:5
https://doi.org/10.36518/2689-0216.1102
257
Clinical Review
Adipose Tissue as Pain Generator in the Lower
Back and Lower Extremity: Application in
Musculoskeletal Medicine
Se Won Lee, MD ,1 Craig Van Dien, MD ,2 Sun Jae Won, MD, PhD3
Abstract
Description
Adipose tissue (AT) has diverse and important functions in body insulation, mechanical
protection, energy metabolism and the endocrine system. Despite its relative abundance in
the human body, the clinical significance of AT in musculoskeletal (MSK) medicine, partic-
ularly its role in painful MSK conditions, is under-recognized. Pain associated with AT can
be divided into intrinsic (AT as a primary pain generator), extrinsic (AT as a secondary pain
generator) or mixed origin. Understanding AT as an MSK pain generator, both by mechanism
and its specific role in pain generation by body region, enhances the clinical decision-making
process and guides therapeutic strategies in patients with AT-related MSK disorders. This
article reviews the existing literature of AT in the context of pain generation in the lower
back and lower extremity to increase clinician awareness and stimulate further investigation
into AT in MSK medicine.
Keywords
adipose tissue; fat pad; musculoskeletal pain; connective tissue; lipodystrophy; lipoma; obe-
sity; lipedema; pain generator
Author aliations are listed
at the end of this article.
Correspondence to:
Se Won Lee, MD
Department of Physical
Medicine and Rehabilitation
MoutainView Medical
Center
2880 N Tenaya Way, 2nd Fl,
Las Vegas, NV 89128
(sewlee2014@gmail.com)
www.hcahealthcarejournal.com
© 2020 HCA Physician Services, Inc. d/b/a
Emerald Medical Education
HCA Healthcare
Journal of Medicine
Introduction
Mounting evidence supports the various func-
tions of adipose tissue (AT), most notably its
link to obesity and metabolic dysfunction.1-3
Aside from the impact of obesity on the mus-
culoskeletal (MSK) system, the role of AT in
painful MSK conditions is less established.
Historically, AT masses/lipomas were consid-
ered common pain generators. However, the
high prevalance of asymptomatic lipomas,4,5
inconsistent responses to local injections and
increasing awareness of other neighboring pain
generators disputed their reputation in painful
MSK conditions. AT has recently re-entered
the focus of MSK clinicians, most notably for
its use in regenerative medicine.6 Moreover,
localization and evaluation with high resolution
imaging technologies has improved under-
standing of AT in other contexts, particularly
pain generation. Therefore, our objective is to
review the available literature on AT-related
painful MSK disorders in the lower back and
lower extremity, focusing on its pathogenic role
as a pain generator as well as practical diagno-
sis and management.
Distribution, Physiologic Changes
and Mechanical Properties of
Adipose Tissue
AT is largely located in subcutaneous regions,
followed by visceral regions. Ectopic areas
of deposition include bone marrow and the
retro-orbital, intramuscular, intermuscular
and periarticular regions.7 With aging, there is
global redistribution of AT from subcutaneous
to truncal/visceral regions.8 Local redistribution
also occurs, as seen in AT on the plantar aspect
of the heel and metatarsophalangeal joints.9 In
addition, aging AT cells undergo cellular senes-
cence, a process that promotes AT dysfunction
through dysregulation of extracellular remod-
eling, inflammation and pathologic angiogene-
sis.10

HCA Healthcare Journal of Medicine
258
AT is a highly expandable connective tissue
comprised of adipocytes (lipid-filled cells)
enclosed within collagen-based structures
(basement membrane and interlobular septa)
and smaller numbers of fibroblasts.11 It protects
the underlying MSK structures, contributes to
mechanical stability and resists shear strain.12
Nonetheless, the mechanical integrity of AT
varies between individuals and over an individ-
ual’s lifespan. For example, the stiness and
thickness of heel AT was found to be higher in
overweight and obese individuals as compared
to normal-weight individuals.12 This discovery is
partly explained by increased fibrosis, a process
that limits the ability of adipocytes to expand.13
Increased stiness can also reflect a degenera-
tive process, as repetitive microtrauma reduces
water content and elastic fibrous tissues.13-15
Furthermore, septal hypertrophy and frag-
mented elastic fibers in heel AT occurs with ag-
ing.12 These changes can negatively impact the
mechanical properties of AT and consequently
its functions in shock absorption and resistance
to compressive and sheer forces of gait.12
Adipose Tissue as an Intrinsic and
Extrinsic Pain Generator
Pain-related to AT falls into two categories: 1)
Intrinsic: pain originating directly from/within
AT and 2) Extrinsic: pain related to the interac-
tion of AT with surrounding structures. Mixed
processes are not uncommon.
Intrinsic Pain Generation
Dye et al. described pain perception of dier-
ent intraarticular structures in a conscious in-
dividual by arthroscopic probing and found the
infrapatellar fat pad to be both highly localized
and sensitive compared to neighboring struc-
tures.16 In an alternative study, similar noxious
responses were induced by injecting hyperton-
ic saline (5%) into the infrapatellar fat pad.17
Such findings underscore the rich nociceptive
innervation of fat pads by substance-P and
calcitonin gene-related peptide nerve fibers
and lend credibility to pain originating directly
from AT.18 Moreover, AT is metabolically active
and produces proinflammatory adipokines
such as tumor necrosis factor-alpha, leptin,
vaspin, chemerin and interleukin-6.3,19,20 As an
example, pain syndromes due to inflamed fat
pads are well described in patients with HIV.
These pain syndromes include retrocalcaneal
pain from isolated inflammation of Kager’s fat
pad and nonspecific anterior knee pain related
to inflammation of the infrapatellar fat pad.21
AT torsion resulting in inflammation and/or
ischemic necrosis is amongst other proposed
mechanisms of AT-based pain.22
Extrinsic Pain Generation
Painful MSK conditions can be related to the
interaction of AT with surrounding structures,
i.e., extrinsic pain generator. Lipomas, for ex-
ample, are AT masses that can arise from any
location where fat is normally present. Local
pain in lipomas can result from irritation of a
fascial layer or other neighboring structures,
such as bursa and nerve.23 If nerve irritation oc-
curs, distant pain (either radiating or referred)
can be experienced.24 The pain characteristics
and presentation of painful fat pads/symp-
tomatic lipoma will vary based on the body
region and surrounding structures. (Table 1) As
another example, increased adiposity can cause
tendinopathy due to direct mechanical loading
and biochemical alterations caused by systemic
dysmetabolic factors.25 Rich neovasculariza-
tion and sensory innervation of AT surrounding
tendons may also play a role in chronic tendon
pain.26 In addition, there is evidence that AT can
contribute to the development of osteoarthri-
tis via adipokines, such as leptin, visfatin and
resistin.19 Other processes, such as the loss of
the AT structural integrity, can contribute to
pain generation. This loss is observed in plantar
fat pad atrophy.27
Mechanisms and Biomechanics of
Musculoskeletal Pain Generation:
Regional Approach
Lower Back and Buttock
Episacroiliac subcutaneous lipomas, or “back
mice,” are subfascial fat herniations that may
be encountered in patients with nonspecific
low back pain.4 These lipomas are oen bilat-
eral and located near the sacroiliac “dimple,”
posterior iliac crest and lumbar paraspinal area.
(Figure 1) There appears to be a female predi-
lection. Subfascial herniation to the myofascial
layer makes symptomatic lipoma dicult to
distinguish from myofascial pain syndrome. A
discrete, large and painful palpable nodule fa-
vors lipoma herniation rather than a myofascial
trigger point.23

Lee et al. (2020) 1:5. https://doi.org/10.36518/2689-0216.1102
259
Table 1. Classification of painful adipose tissue/fat pad disorders aecting lower back and lower
extremity
Location Common pathologies Characteristics and suggested mechanisms of pain
Systemic Adipose Tissue Disorders
General
Lipodystrophy
(congenital and
acquired)
Chronic pain with neuropathic pain most common, fol-
lowed by arthralgia, muscle pain Common chronic periph-
eral neuropathy
Partial
Lipedema
Pain and tenderness in the bilateral lower extremities,
skin hypersensitivity, neural tissue compression within the
septa surrounding fat lobules
Partial lipodystrophy
(acquired)
Hoa’s fat pad with anterior (infrapatellar) knee pain and
Kager’s fat pad with posterior heel pain, anterior to the
Achilles tendon in patients with HIV infection
Adiposis dolorosa
(Dercum’s disease)
Painful subcutaneous adipose tissues involving extremi-
ties, torso and even face
Adipose Tissue Pain Generation by Body Region
Lower back
and buttock
Subcutaneous painful
fat pad
Episacroiliac subcutaneous lipomas, “back mice”, irritating
myofascia, fascial herniation and torsion of fat pad, com-
monly in the episacral region, oen bilateral
Can cause neuropathic pain by irritation of cluneal nerves
Spinal lipoma
Lipomyelomeningocele (fatty mass in conus medullaris),
lipoma of the terminal ilum causing tethered cord/root
syndrome
Spinal epidural lipomatosis (primary and secondary) with
lumbosacral radiculopathy
Hip and
thigh
Painful fat pad
Femoral fat pad entrapment with femoroacetabular
impingement, anterior inferior iliac spine fat pad causing
adhesion of joint capsule and gluteal muscle
Lipoma Deep large intramuscular lipoma with thigh pain
Knee Painful fat pad
Hoa’s infrapatellar fat pad impingement, suprapatellar,
prefemoral fat pad impingement syndrome (hyperexten-
sion of knee) with anterior knee pain
Lipoma arborescens Involving suprapatellar recess
Ankel and
foot
Lipoma Retrocalcaneal bursitis
Painful fat pad Insertional Achilles tendinopathy
Fat pad atrophy and
migration
Nociceptive pain on the heel (plantar aspect) and forefoot
(metatarsalgia)
Piezogenic pedal
papules
Subcutaneous fat herniation in the heel, especially in
weight bearing
Lipomas of the spinal cord are rare tumors of-
ten associated with occult spinal dysraphism.24
Spinal lipomas are more commonly located in
the conus medullaris and called lipomyelome-
ningocele. Lipomyelomeningocele is character-
ized by a subcutaneous fibrofatty mass, lamina
defect, compressive myelopathy and tethered
cord syndrome.28 It can present with progres-
sive neurological deficit in the lower extremities
with the loss of bladder function.24 Lipoma of
the terminal filum is another common cause of
tethered cord syndrome with lower back pain as
the first presenting symptom.29 Spinal epidural
lipomatosis is extremely uncommon and can be
found incidentally or present symptomatically as
radiculopathy, neurogenic claudication and

HCA Healthcare Journal of Medicine
260
myelopathy.30 It has been associated with exog-
enous steroid use (epidural or chronic systemic
steroids), endogenous hypercortisolism (Cush-
ing’s syndrome), hypothyroidism, hyperprolac-
tinemia and protease inhibitors in patients with
HIV.31 Spinal epidural lipomatosis is most oen
localized to the thoracic spine followed by lum-
bosacral spine.30,32
Hip and Thigh
Femoral fat pads were recently recognized as
a source of pain in femoroacetabular impinge-
ment syndrome, with fat pad entrapment
occurring between the femoral head-neck
junction and labrum. In patients with cam-type
femoroacetabular impingement, Jayasekera
et al. observed similar clinical outcomes with
arthroscopic resection of the femoral fat pads
in the anterior head-neck junction with or
without creating a spherical femoral head.33 In
addition, anterior inferior iliac spine fat pads
have been implicated in anterior groin pain as a
consequence of inflammation, fibrosis, scar and
adhesion (between the joint capsule, rectus
femoris and gluteus muscles).34
Most lipomas in the thigh are asymptomatic
but can be painful when situated deep (under
the enclosing fascia, in the intramuscular and
intermuscular layers) or if they are large (usual-
ly due to the expansion of so tissue or com-
pression of the peripheral nerve).35,36
Knee
Infrapatellar or Hoa’s fat pad impingement
syndrome is a well-known cause of anterior
knee pain that occurs at either the infrapatellar
or peri-patellar region during knee hyperexten-
sion. Hoa’s fat pad can be impinged by any
combination of neighboring structures, includ-
ing the patella and patellar tendon anteriorly,
femoral condyle posteriorly and proximal tibia
caudally.37 (Figure 2) A minor injury to Hoa’s
fat pad, including hyperextension with or with-
out twisting and a direct trauma, can cause
swelling, inflammation, fibrosis and scarring
that contributes to the altered biomechanics
and increased pain perception.37 Anterior knee
pain can also result from anterior suprapatellar
fat pad impingement. This triangular-shaped
fat pad is located on the superior edge of the
patella (underneath the quadriceps tendon,
anterior/superficial to the suprapatellar re-
cess).38,39 Impingement occurs during maximal
knee flexion. Lastly, the prefemoral fat pad, lo-
cated proximal to the femoral trochlea, can be
impinged between the patella and anterolateral
surface of the distal femur during flexion and
extension of the knee.40,41
Lipoma arborescens is a benign, “tree-like”
AT lesion characterized by the replacement
of subsynovial connective tissue with AT and
synovial villous proliferation. This replacement
can result in intermittent painful swelling of
the knee joint, typically involving the suprapa-
Figure 1. Ultrasonographic figure of multiple fat pads on the lumbosacral region in a patient with
chronic low back pain.

Lee et al. (2020) 1:5. https://doi.org/10.36518/2689-0216.1102
261
tellar bursa.42 Other reported locations include
the hip and ankle joints. It is more common
in males between the 5th and 6th decades of
life and is associated with osteoarthritis and
inflammatory arthropathy.43
Ankle and Foot
Kager’s fat pad is bordered by the Achilles
tendon, retrocalcaneal bursa and flexor hallucis
longus tendon in the posterior ankle.44 (Figure
2) It reduces tendon kinking and minimizes
pressure on the bursa.45 Patients with Kager’s
fat pad impingement can present with a painful
bulging mass at the retrocalcaneal space of the
posterior ankle. Symptoms are exacerbated by
ankle plantarflexion with a knee hyperextension
(recurvatum) momentum in a closed kinetic
chain movement. Pathologies of the neighbor-
ing structures and lipodystrophy (LD) of the
fat pad can also contribute to impingement.21
A lipoma beneath the flexor retinaculum of the
tarsal tunnel can cause tarsal tunnel syndrome.
It manifests with pain behind the medial malle-
olus that radiates to the plantar aspect of the
foot.46,47
Fat pad atrophy and migration occurs in the
sole of an aging foot at the superficial to me-
dial calcaneal tuberosity48 and under the meta-
tarsal heads. It is oen associated with plantar
heel pain, metatarsalgia and metatarsal sublux-
ation. In addition to normal age-related chang-
es, fat pad atrophy can occur as a consequence
of steroid injections.49,50
Piezogenic pedal papules are herniations of the
subcutaneous fat into the plantar fascia reti-
naculum. They are common incidental findings
in weight-bearing areas of the foot, particularly
the plantar heel fat pad.51 The papules may only
be visible in full weight-bearing. Although a
Figure 2. Ultrasonographic figures of fat pads (yellow colored line) in the anterior knee (right
upper corner) and the posterior ankle (le lower corner). Red arrows indicate proposed impinge-
ment mechanisms of these fat pads.

HCA Healthcare Journal of Medicine
262
majority of lesions are asymptomatic, papules
may be discretely tender on palpation. Irritation
of local nerves and blood vessels by repetitive
trauma can contribute to pain.52
Systemic Adipose Disorders
Although painful MSK conditions related to fo-
cal AT are the main focus of this paper, system-
ic adipose disorders, in particular lipedema and
lipodystrophy (LD), may likewise cause lower
back and lower extremity pain and, therefore,
will be briefly reviewed.
LD is a heterogeneous group of disorders
characterized by abnormal distribution of AT,
including AT loss or hypertrophy.53,54 LD can be
classified into primary (idiopathic or familial)
versus secondary depending on the underly-
ing etiology (HIV, panniculitis, autoimmune,
medication, trauma), or general versus partial
depending on the extent of involvement.55-57
More than 70% of patients with LD suer
from chronic pain, most commonly neuro-
pathic pain, followed by arthralgia and muscle
pain amongst others. Peripheral sensory-mo-
tor neuropathy is found in more than 60% of
patients with LD and diabetes.58 Underlying
mechanisms for peripheral neuropathy in LD
are not entirely clear but likely include a com-
bination of metabolic dysfunction and a failure
of the shock-absorbing function of peripheral
nerves. Specifically, loss of epineural fat com-
ponents is thought to contribute to chronic
trauma, inflammation/pressure palsies and
denervation.58-61 Muscle pain is common in
congenital LD, but readily apparent myopathy
is not common in LD other than a late compli-
cation of juvenile dermatomyositis.58
Lipedema, a type of LD, is characterized by
abnormal deposition of subcutaneous AT,
frequently involving the lower extremities
symmetrically.62-64 There is a demographic
predilection for females of a younger age and
commonly a family history.62 A typical patient
complaint is pressure,-mediated leg pain and
tenderness. These symptoms may be a conse-
quence of neural compression within the septa
surrounding fat lobules. Other potential mech-
anisms include hypersensitivity, mechanical
friction and skin irritation.62 As the hypertrophy
extends from hips to ankles, lipedema may
be misdiagnosed as lymphedema.62 In com-
parison, lymphedema is typically painless and
involves the foot, whereas lipedema commonly
spares the foot with a step-o (cu sign) at
the ankle.65 The absence of pain and edema can
dierentiate lipohypertrophy from lipedema.64
Adiposis dolorosa, also known as Dercum’s
disease, shares similar clinical features with
lipedema, such as painful subcutaneous AT and
a predominance in females between the ages
of 35–50 years.66,67 Fat involvement of the torso
in early stages of the disease, greater pain
severity and comorbidities such as fibromyalgia
and metabolic disease distinguishes adiposis
dolorosa from lipedema.68,69
Evaluation with Imaging
Modalities
A majority of MSK disorders related to AT are
clinically diagnosed. Imaging modalities are
helpful to confirm the clinical diagnosis, evalu-
ate dierential diagnoses and aid in the iden-
tification of indiscrete masses in patients with
larger body habitus. With the increasing avail-
ability of ultrasonography (US) in outpatient
clinics, lipomas can be easily visualized in-oce
(Figure 1). Typical findings include a partially
or well-encapsulated mobile mass with similar
echogenicity to the neighboring fat (hypoecho-
ic or isoechoic depending on the heterogenicity
of AT and water components) and absence of
acoustic shadowing.70,71 Dierential diagnoses
for subcutaneous AT masses include epidermal
cyst, ganglion cyst and malignant neoplasm.
Epidermal cysts are isoechogenic, which is
similar to subcutaneous lipomas. However,
post-acoustic enhancement and lateral shad-
owing are dierentiating characteristics. Gan-
glion cysts typically demonstrate anechogenic-
ity within the cyst, with protrusion towards a
neighboring joint.72 US imaging of so tissue
malignant neoplasms, most commonly pleo-
morphic sarcoma and liposarcoma, can mimic
a lipoma. However, they typically demonstrate
larger size (≥ 5 cm), are intramuscular, have an
infiltrative border, grow rapidly and violate tis-
sue planes.71 Dierential diagnoses for deep-ly-
ing lipomas in US evaluation are extensive and
vary depending on mass location. These dier-
ential diagnoses may include congenital cysts,
ganglion cyst, heterotopic ossification, heman-
giomas, angiolipoma, hematoma, lymph nodes,
normal muscle/muscle herniation and malig-
nant tumors, amongst others.36,73 Sonoelastog-
raphy provides information on intrinsic tissue

Lee et al. (2020) 1:5. https://doi.org/10.36518/2689-0216.1102
263
properties. This information aides in the delin-
eation of malignant tumors, which are generally
stier than benign masses.74,75 Any suspicion for
malignant neoplasm requires further imaging
studies and the definite diagnosis with histo-
pathologic and molecular examination.
MRI is useful when US assessment is di-
cult. Examples include deeper, intraarticular
or intracortical lesions.76 On both T1 and T2
weighted images, lipomas demonstrate high
signal intensity, while fat-suppression sequenc-
es show decreased signal intensity.36 Increased
lipoma signal intensity on fat-suppression
sequences may indicate edema/fluid, necrosis
or mass heterogeneity (as seen in an atypical
tumor or liposarcoma).77 An MRI can also eval-
uate neighboring structures such as ganglion
cyst, plica, synovium, ligament, meniscus, bony/
tendon edema or any neoplastic lesions.37 A CT
can similarly be utilized to evaluate lipomas,
which would appear as a hypodense mass with
attenuation similar to fat tissue. A CT can be
particularly useful to delineate subtle ossifica-
tion/calcification and associated cortical bony
lesions.78 An x-ray is limited in the evaluation
of so tissue lesions (lipoma) in general but
serves utility in the identification of intraosse-
ous lipomas mimicking other diseases such as
fibrous dysplasia, aneurysmal bone cysts, sim-
ple cysts, bone infarcts and chondral tumors.79
Clinicians should be aware of the limitation
of imaging modalities, including inconsistent
relationships between the imaging findings and
the local pain.80
Management
The first step for the successful management
of symptomatic AT is to recognize AT as a
pain generator and investigate the underlying
mechanisms for the pain. This review primarily
focuses on the management of focal AT-related
painful MSK disorders; LD will be briefly cov-
ered.
Local, non-pharmacological interventions that
may improve AT-related disorders in the lower
back and lower extremities include orthotics,
taping and modification of daily activity. For
fat pad atrophy and migration in the foot, heel
cups (rubber or felt pad) and low dye taping
can be tried for heel pain and a metatarsal pad
for metatarsalgia.81 Repeat steroid injections
through the plantar fat (during plantar fascia
and intermetatarsal bursa/neuroma injec-
tions) should be avoided to prevent atrophy.
Ethanol-based nerve fiber ablation has been
previously attempted to mitigate pain associ-
ated with AT. However, caution is required as
AT scarring and denaturing can occur. Biome-
chanical evaluation and avoiding faulty training
(with repetitive trauma) should be considered
a means to alleviate pain and prevent progres-
sion and recurrence. Symptomatic Hoa’s fat
pad impingement with pes cavus may respond
to heel li placement by mitigating knee ex-
tension moments known to aggravate symp-
toms.82 Placing a pillow under the knee avoids
full knee extension, relieving pain associated
with sleeping in the supine position.
Weight loss should also be emphasized to
decrease metabolic dysfunction and the bio-
mechanical disadvantages associated with
increased weight. Weight loss has favorable
impacts on pain and biomechanics of the lower
extremity, including decreased foot plantar
loading pressure, increased ankle plantarflex-
ion, knee joint motion (maximal knee flexion),
compressive force and peak moments around
the hip and knee.83-85 However, evidence re-
flecting the impact of weight loss in AT-related
painful MSK disorders is scarce and unclear.
Okifuji and Hare suggested obesity may not
impact pain response in the absence of in-
flammation or nerve injury, though obesity can
potentiate inflammatory response.86 Dodet et
al.87 and Zahorska-Markiewicz et al.88 reported
higher pain thresholds among the obese pop-
ulation compared to the nonobese population.
Although the exact mechanisms were not clear,
ghrelin and galanin were suggested for mod-
ulation of the obesity-induced change in pain
threshold.89,90 Regardless of the direct impact
of obesity and weight loss on AT-related pain,
aerobic endurance exercise is important to
decrease complications related to chronic MSK
pain and to improve metabolic dysfunction.91
Surgical options can be considered in patients
who fail conservative treatment and have dis-
abling pain. Potential interventions include fat
pad resection in impingement syndrome. These
interventions include intraarticular or extraar-
ticular fat pad resection in anterior groin pain,
Hoa’s fat pad resection in anterior knee pain
and Kager’s fat pad resection in retrocalcaneal

HCA Healthcare Journal of Medicine
264
heel pain.34,9 2,9 3 Scarring of the surgical site and
the impact of regional stability can be challeng-
ing postoperatively. Alternatively, US guided
scraping of vascularized fat pads can relieve
pain from neighboring chronic tendinopathy.26
A few studies highlight the non-cosmetic im-
plantation of fat for fat pad atrophy, such as
fat graing for metatarsalgia and chronic heel
pain.27,94,9 5
As it pertains to LD, management should focus
on symptomatic manifestations and metabolic
syndrome. Recombinant human leptin (me-
treleptin) is considered for generalized LD, with
low serum leptin levels to improve metabolic
syndrome and weight loss.96,97 In secondary LD,
recognizing and managing the underlying etiol-
ogy is useful for successful treatment.98
Conclusion
AT should be recognized as one of the pain
generators in painful musculoskeletal disorders.
Therapeutic strategies for adipose tissue-re-
lated pain disorders could be better guided by
understanding the mechanism by which AT-re-
lated pain is occurring.
Conflicts of Interest
The authors declare they have no conflicts of
interest.
Dr. Lee is an employee of Sunrise Health GME
Consortium, a hospital aliated with the
journal’s publisher.
This research was supported (in whole or in
part) by HCA Healthcare and/or an
HCA Healthcare aliated entity. The views
expressed in this publication represent those of
the author(s) and do not necessarily represent
the ocial views of HCA Healthcare or any of
its aliated entities.
Author Aliation
1. Department of Physical Medicine and Reha-
bilitation, Sunrise Health GME Consortium,
Las Vegas, NV
2. Department of Physical Medicine and
Rehabilitation, JFK Johnson Rehabilitation
Institute, Edison, NJ
3. Department of Rehabilitation Medicine,
Yeouido St. Mary’s Hospital, College of
Medicine, The Catholic University of Korea,
Seoul, South Korea
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