Sports and Performing Arts Medicine

Sports and Performing Arts Medicine:

2. Lower Extremity Injuries
Mark A. Harrast, MD, Seneca A. Storm, MD, Jonathan T. Finnoff, DO,
Stuart Willick, MD, Cedric K. Akau, MD

Objective: This self-directed learning module highlights lower limb sports and perform-
ing arts injuries. It is part of the study guide on sports and performing arts medicine in the
Self-Directed Physiatric Education Program for practitioners and trainees in physical
medicine and rehabilitation. Using a case vignette format, this article specifically focuses on
hip, knee and ankle pain in athletes and performing artists. The goal of this article is to
influence the learner’s existing practice techniques for evaluating and managing common
lower limb injuries in these populations.

2.1 Clinical Activity: Formulate a diagnostic approach to the identification of a

painful, snapping hip in a 28-year-old professional ballet dancer.
Snapping hip, an audible or palpable ‘snap’ during hip range-of-motion (ROM), has
intra-articular and extra-articular etiologies. The prevalence in ballet dancers approaches
90%, with an average onset at age 14-16 years. Eighty percent of cases occur bilaterally [1].
The snapping may develop atraumatically or may follow a specific traumatic event like
twisting or falling. Forced hip extension and external rotation is the mechanism for labral
injuries.
Intra-articular causes of hip snapping include loose bodies, labral tears, synovial chon-
dromatosis, osteochondral fractures, and femoral acetabular impingement (FAI)[1]. Any of
these diagnoses may lead to clicking with hip rotation. Long-standing labral tears may lead
to subchondral cysts and premature osteoarthritis [2].
Femoral acetabular impingement is due to abnormal contact between the anterosuperior M.A.H. Spine and Sports Fellowship, Depart-
ment of Rehabilitation Medicine, Department
femoral neck and the anterosuperior acetabulum (Figure 1) [3,4]. There are 2 primary of Orthopedics and Sports Medicine, University
mechanisms for FAI: (1) cam, and (2) pincer. The cam mechanism involves impingement of Washington, Box 356940, 1959 NE Pa-
between a dysmorphic (flattened) superior femoral head-neck junction and the acetabular cific, Seattle, WA 98195. Address correspon-
dence to: M.A.H.; e-mail: mharrast@u.
rim, whereas the pincer type is due to a prominent acetabular rim (eg, acetabular retrover- washington.edu
sion). FAI may lead to labral tears and premature osteoarthritis [4]. Disclosure: nothing to disclose
Extra-articular causes are categorized by medial (internal) or lateral (external) hip S.A.S. Department of Physical Medicine &
snapping. External snapping, the most common type, is caused by the iliotibial band (ITB) Rehabilitation, Michigan State University Col-
or gluteus maximus tendon snapping over the greater trochanter. Internal snapping local- lege of Osteopathic Medicine, Lansing Spine &
Extremity Rehabilitation, Lansing, MI.
izes over the anterior groin and involves the iliopsoas tendon snapping over deeper osseous Disclosure: nothing to disclose
structures (eg, iliopectineal eminence, femoral head, or lesser trochanter) [1,2]. J.T.F. Department of Physical Medicine and
Physical examination of hip snapping should include hip joint ROM and hip girdle Rehabilitation, College of Medicine, Mayo
strength and flexibility assessments. Having the patient demonstrate the snap may help Clinic, Rochester, MN
Disclosure: nothing to disclose
identify the mechanism [1]. Tests that suggest an intra-articular cause include pain with hip
flexion-abduction-external-rotation (FABER) testing, hip flexion-adduction-internal rota- S.W. Division of Physical Medicine and Re-
habilitation, University of Utah, Salt Lake City,
tion testing, or a positive scour test [4,5]. Labral tears may cause decreased hip propriocep- UT
tion and ROM [2]. Extra-articular internal snapping hip may be reproduced by moving the Disclosure: nothing to disclose
hip from a flexed-abducted-externally rotated position to an extended-adducted-internally C.K.A. Division of Physical Medicine and Re-
rotated position, thus moving the iliopsoas tendon across the anterior osseous hip struc- habilitation, University of Hawaii; Department
of Sports Medicine and Rehabilitation, Straub
tures. Hip snapping over the greater trochanteric region that is caused by hip flexion and Clinic and Hospital, Honolulu, HI
extension with the ITB under tension suggests extra-articular external snapping hip [1]. Disclosure: nothing to disclose
Plain radiographs are typically normal, but occasionally demonstrate osseous injury (eg, Disclosure Key can be found on the Table of
loose body) or findings suggestive of FAI (Figure 2). Real-time ultrasonography provides Contents and at www.pmrjournal.org

PM&R © 2009 by the American Academy of Physical Medicine and Rehabilitation

S60 1934-1482/09/$36.00 Suppl. 1, S60-S66, March 2009
Printed in U.S.A. DOI: 10.1016/j.pmrj.2009.02.001
PM&R
Figure 1. Femoacetabular impingement: (a) cam type, (b)
pincer type. From Hunt [3] and Manaster [4]. Reprinted with
permission [3,4].
dynamic imaging of soft tissue structures about the hip and
can frequently diagnose the cause of extra-articular snapping
hip [1]. However, for intra-articular snapping hip, magnetic
resonance arthrography (MRA) is the study of choice and is
more sensitive for capsulolabral injuries (95%) than is stan-
dard magnetic resonance imaging (80%) [2]. Magnetic reso-
nance arthrography testing presents increased patient risk
due to the use of gadolinium.
Nonsurgical treatments may benefit some types of snap-
ping hip, although specific therapeutic regimens have not
been well-studied. A 10-12 week trial of treatment including
anti-inflammatory medications, rest, modalities, massage, il-
iopsoas and ITB stretching, lumbopelvic stability exercises,
and proper warm-up may be adequate [4,5]. Injections and
other alternative treatments have been tried. Surgical referral
may be indicated depending upon the identified etiology and
Figure 2. Radiograph demonstrating cam type femoroac-
etabular impingement of the left hip. Note the decreased
femoral head-neck offset and lateral “bump” which rotates
into the acetabular rim, resulting in shear stress to the articular
cartilage and subsequent labral tear or detachment.
Vol. 1, Iss. 3, Supplement 1, 2009 S61
Figure 3. ACL sprain on MRI.
response to conservative measures. Intra-articular causes
typically require surgery for symptomatic relief and mini-
mally invasive techniques are improving [2]. Hip arthros-
copy may enable the physician to both identify and treat
intra-articular pathology [2]. However, hip neurovascular
structures are vulnerable to injury during portal placement
[2]. Several surgical techniques for external snapping hip
have reported varied success [5].
2.2 Clinical Activity: Analyze current information re-
garding ACL injury risk factors and injury preven-
tion programs in a 16-year-old female basketball
player.
Approximately 80,000 to 250,000 anterior cruciate ligament
(ACL) disruptions occur yearly in the United States with the
majority occurring in the 15- to 25-year-old age group (Fig-
ure 3) [7,8]. Females are 2 to 8 times more likely than males
to sustain an ACL injury [7,8]. A noncontact rather than
contact mechanism is more frequently responsible for ACL
injuries in both genders. An ACL disruption causes short-
term disability such as loss of time from athletic activities,
school, or work, and predisposes to the long-term disability
of posttraumatic osteoarthritis [7,8]. It is therefore impera-
tive that scientifically based ACL injury prevention programs
be initiated in high risk populations. The first step in this
process is the identification of noncontact ACL injury risk
factors.
There are several intrinsic and extrinsic risk factors asso-
ciated with noncontact ACL injuries. Extrinsic risk factors
include weather, sports surface, footwear, and knee braces.
ACL injuries occur more frequently during periods of high
evaporation and low-rainfall, which results in harder ground
S62 Harrast et al
conditions and increased shoe-surface traction [7,8]. The
new artificial turf installed for American football appears to
significantly reduce noncontact ACL injury rates [7,8]. Arti-
ficial floors in women’s team handball increase the risk of
noncontact ACL injury when compared to natural wood
floors, likely due to the increased shoe-surface traction as
documented by a higher coefficient of friction on artificial
floors [7,8]. Previous research has reported a lower risk of
knee injuries in athletes whose shoes had shorter cleats,
although further research on the role of footwear in noncon-
tact ACL injury risk is needed [7,8]. One study of intramural
tackle football athletes demonstrated a 3 times higher inci-
dence of ACL injury in athletes who did not wear a prophy-
lactic knee brace when compared to those who wore a brace
[7,8]. However, other studies have not reproduced these
results [7,8]. Therefore, the role of prophylactic knee bracing
in non-ACL injury prevention remains indeterminate.
Intrinsic risk factors that have been investigated include
the anatomic risks of a wide Q-angle, improper knee align-
ment during injury, foot pronation, high body mass index
(BMI), and narrow intercondylar notch size. Other risks are
hormonal factors, familial tendency, and neuromuscular fac-
tors. An increased static and dynamic Q-angle has been
associated with a higher incidence of ACL injury [7,8]. Foot
pronation, as measured by navicular drop, occurs more fre-
quently in athletes with ACL injuries when compared to
healthy controls, suggesting that pronation may contribute to
ACL injury [7,8]. Athletes with a higher BMI may be at higher
risk for noncontact ACL injury risk, because they tend to land
in a more extended knee position and have reduced knee
flexion angles [7,8]. A narrow intercondylar notch width may
predispose to noncontact ACL injury [7,8].
Estradiol inhibits fibroblast proliferation and type 1 pro-
collagen synthesis in vitro, and these effects are attenuated
with progesterone [7,8]. Thus, during the estradiol dominant
follicular phase of the menstrual cycle, it is possible that a
relative down regulation of collagen production occurs,
which is reversed during the luteal phase due to the increase
in progesterone. Clinical studies examining ACL laxity in
women have demonstrated the greatest knee laxity occurs in
the early luteal phase [7,8]. Interestingly, it appears that the
highest frequency of ACL injury in women occurs in the early
and late follicular phases, although these findings require
further study [6-8].
There are a multitude of noncontact ACL injury risk
factors in the female population. Women tend to have less
knee and hip flexion during jumping, cutting and pivoting
maneuvers when compared to men [7,8]. In addition, they
have an increase in knee valgus, hip internal rotation, tibial
external rotation, quadriceps muscle contraction, and less
knee joint stiffness during these activities [7,8]. Fatigue ex-
acerbates these abnormal movement patterns [7,8]. Women
also have a quadriceps dominated thigh muscle contraction
pattern when performing landing and cutting activities [7,8].
This results in an anterior tibial force vector and reduced
knee stiffness [6,7]. Female ACLs are smaller, less elastic, and
LOWER EXTREMITY INJURIES
tear at a lower strain and stress than their male counterparts
[7,8].
Athletes who sustain an ACL injury are twice as likely to
have a relative with an ACL injury when compared with
controls [7,8]. This finding suggests a possible familial pre-
disposition to ACL injury.
To date, 10 successful programs to prevent noncontact
ACL injury have been developed [7,8]. These successful
programs feature many different exercise and behavioral
strategies to correct modifiable risk factors. The programs
include improving the athlete’s coordination and movement
patterns by means of proprioception exercises on wobble
boards, increasing knee and hip flexion angles during land-
ing by means of “soft landing” drills, reducing dynamic knee
valgus through cutting and jumping technique drills, in-
creasing hamstring strength via hamstring strengthening ex-
ercises, and improving understanding of noninjury risk fac-
tors through risk awareness education [7,8]. The success of
these programs suggests that correcting the modifiable non-
contact ACL injury risk factors can reduce the incidence of
ACL injury. While further research on this subject is re-
quired, initiating a program aimed at preventing noncontact
ACL injury in high risk populations should be considered at
this time.
2.3 Clinical Activity: Develop a diagnostic and manage-
ment strategy for patellofemoral pain in a triathlete.
Patellofemoral pain (PFP) is one of the most common knee
disorders evaluated by sports medicine practitioners. It is
considered a syndrome because it consists of a constellation
of symptoms that are not explained by an isolated etiology.
However, the most commonly accepted source of pain is the
subchondral bone of the patellofemoral joint, since there are
no nerve endings in the overlying articular cartilage.
Athletes with PFP typically describe retropatellar and oc-
casionally medial or lateral patellar retinacular aching [8,9].
The pain is frequently exacerbated by hills, stairs, squatting,
and prolonged sitting, all of which increase patellofemoral
joint compressive forces. For triathletes, the event that exac-
erbates their pain (ie, running and/or biking) should be
identified. The knee examination should include inspection
with close attention paid to lower limb alignment and patellar
tracking. It should also include palpation, range-of-motion
tests, neurologic evaluation, and PFP provocative testing.
Other causes of knee pain, such as meniscal or ligamentous
injuries, should be ruled out. Strength and flexibility imbal-
ances should be identified. Particular attention should be
paid to ITB tightness since it may lead to lateral patellar
tilting, excessive lateral patellar pressure, and decreased pa-
tellar mobility [10].
While the focused knee examination is helpful to detect
diagnoses other than patellofemoral pain (eg, mensical tears),
the most important portion of the examination for patel-
lofemoral pain is the kinetic chain evaluation. The hip fre-
quently plays an important role in PFP. Dynamic MRI has
demonstrated lateral patellar displacement due to excessive
PM&R
femoral adduction and internal rotation during knee exten-
sion in PFP subjects [11]. In addition, several studies have
found hip abduction and external rotation weakness in run-
ners with knee injuries, including PFP [12,13]. The foot and
ankle may also contribute to PFP. Excessive subtalar joint
pronation can lead to tibial internal rotation and compensa-
tory femoral internal rotation, thus increasing patellofemoral
joint stress.
The kinetic chain evaluation should begin with a static
standing evaluation of the athlete for femoral anteversion,
genu valgum, and pes planus, the hip, knee, ankle, and foot
motion should be inspected during gait for signs of increased
patellofemoral joint stress. A double leg squat can be used to
detect dysfunctional lower limb movement patterns. This
maneuver will also reveal restrictions in functional hip and
knee flexion, and in ankle dorsiflexion motion. The single leg
squat is a great test of functional hip strength, femoral control
(ie, presence or absence of excessive femoral adduction and
internal rotation), and ankle-foot motion (ie, presence or
absence of excessive pronation). For triathletes with PFP
from running, video running technique analysis should be
performed. If their pain is due to cycling, their bicycle fit and
pedaling technique should be evaluated.
Radiologic imaging is rarely helpful during the initial PFP
evaluation. Radiographs may detect bony lesions or osteoar-
thritis of the patellofemoral joint. An MRI can evaluate the
menisci, ligaments, and articular cartilage.
Historically, PFP treatment focused on correction of pa-
tellar malalignment and tracking abnormalities. It typically
included strengthening of the medial thigh (vastus medialis),
stretching of the lateral structure (ITB), patellar taping tech-
niques (eg, McConnell taping), patellar bracing, patellar mo-
bilizations, and surgical procedures such as lateral patellar
retinacular releases and realignment procedures. While some
of these treatments may still be employed, current treatments
are more functional and focus on correcting kinetic chain
deficits.
Treatment begins with pain reduction through activity
modification and judicious use of physical modalities, med-
ications (eg, acetaminophen and/or -nonsteroidal anti-in-
flammatory drugs), McConnell taping, and patellofemoral
joint bracing. Examples of activity modifications for running
athletes include deep water running, elliptical machines, and
running on softer surfaces. If the proximal kinetic chain
evaluation revealed weak hip abductors and external rota-
tors, strengthening of this musculature should take place.
Excessive femoral adduction and internal rotation during
weight bearing activities can be corrected through neuro-
muscular reeducation and strengthening of the dynamic
lumbopelvic stabilizing muscles. Excessive subtalar joint
pronation can be corrected through strengthening of the foot
intrinsic muscles and ankle support muscles, stretching the
calf, and utilizing orthotics. In addition to calf tightness,
inflexibility of the hip flexors, quadriceps, ITBs and ham-
strings should be corrected. Running and bicycling tech-
nique and bicycle fit abnormalities should be corrected.
Vol. 1, Iss. 3, Supplement 1, 2009 S63
2.4 Educational Activity: Describe the various etiol-
ogies of ankle pain following a traumatic ankle
injury sustained by a 35-year-old man while he was
playing basketball.
The ankle is the most frequently injured joint in athletes,
accounting for 20% to 35% of total time lost to injury in
running and jumping sports [14]. Thus, it is important for
the physiatrist to understand the various etiologies of trau-
matic ankle injuries.
Sprains are the most common ankle injury, comprising
about 40% of all sports-related injuries [15]. The most fre-
quent mechanism of injury is plantarflexion and inversion
[16]. In this position, the bony constraints of the ankle
mortise around the talus are reduced and the lateral liga-
ments are susceptible to injury. The anterior talofibular liga-
ment (ATFL) is injured first, followed by the calcaneofibular
ligament (CFL), and finally the posterior talofibular ligament
(PTFL) [15]. The patient’s history should include the mech-
anism of injury, history of previous ankle sprains, the pres-
ence of a “pop” at the time of the injury, pain intensity, ability
to immediately weight-bear, neurological symptoms, and the
length of time postinjury until the onset of swelling [15].
Localized tenderness over the ankle ligaments assist in iden-
tifying the presence of a tear [15]. Laxity of the ATFL and CFL
can be detected by the anterior drawer and talar tilt tests,
respectively, with the contralateral ankle serving as a control
[16]. The Ottawa Ankle Rules for patients ages 18-55
years recommend radiographs only when there is ankle pain
and 1 of the following findings: bone tenderness at the base of
the fifth metatarsal, inability to bear weight immediately after
the injury or for 4 steps in the emergency room, or bone
tenderness at the tip or posterior edge of either malleolus
[17]. Subtle physeal injuries can also occur in pediatric
athletes [15].
Syndesmotic or “high” ankle sprains account for only
10%-20% of all ankle sprains. However, they result in more
lost playing time and disability than lateral ankle sprains
[16]. The usual mechanism of injury is dorsiflexion and
external rotation [15,16]. Athletes present with difficulty in
weight-bearing and pain in the region of the distal syndes-
mosis. They are tender to palpation over the anterior ankle.
Their pain is exacerbated by passive external rotation of the
foot with the ankle in a neutral position or by squeezing the
mid tibia and fibula (Figure 4) [14,15]. Radiographs are
necessary to evaluate for ankle mortise widening. More than
5 mm of mortise widening on radiographs of plantar flexion
and external rotation views is deemed abnormal [14]. MRI
may be helpful if radiographs are normal [15].
Achilles tendon rupture usually occurs during a sudden
jump or push off. It is most common in 30-year-old men,
with 75% of the ruptures occurring during an athletic activity
like basketball and soccer [16]. The tendon usually ruptures
in a hypovascular zone located 2-6cm proximal to the calca-
neal insertion [16]. The athlete usually feels a pop and
sudden pain, and is unable to continue activity. Physical
examination frequently reveals a palpable tendon gap, posi-
S64 Harrast et al
Figure 4. External rotation stress test (a) and Squeeze test (b)
for syndesmotic ankle sprains.
tive Thompson test (Figure 5), and inability to perform a
single heel raise [16]. In equivocal cases, ultrasound or MRI
may be useful in making the diagnosis [16].
In athletes with chronic ankle pain and mechanical symp-
toms, particularly adolescent athletes, osteochondral lesions
of the talus should be considered. Symptoms may include
pain, swelling, instability, catching, or locking [14,15]. Os-
LOWER EXTREMITY INJURIES
teochondral lesions occur on the lateral talar dome 43% of
the time and often develop following ankle trauma [14,15].
Medial lesions are less commonly associated with trauma and
are often difficult to see on standard radiographs. Plantar-
flexed oblique views of the ankle mortise facilitate lesion
identification, and MRI can provide additional information
required for appropriate treatment recommendations [15].
Subluxing peroneal tendons can cause lateral ankle pain.
The acute clinical presentation includes a history of a pop or
snap followed by pain, swelling, and tenderness posterior to
the lateral malleolus. Provocative testing consists of resisting
eversion with the ankle dorsiflexed [15]. In equivocal cases,
MRI or ultrasound is helpful [15]. Peroneal tendons can
occasionally tear following lateral ankle sprains in young
athletes [15]. The presentation includes tenderness and
swelling posterior to the distal fibula with no evidence of
subluxation. Magnetic resonance imaging or ultrasound can
confirm the diagnosis [15].
Fractures of the ankle should always be suspected in cases
of significant trauma [15]. Further, overuse injuries of the
ankle such as anterior tibiotalar impingement, posterior an-
kle impingement, posterior tibial tendinopathy, medial mal-
leolus stress fractures, chronic lateral ankle instability and
nerve entrapment syndromes should be considered in the
differential diagnosis of ankle pain [14-17].
2.5 Educational Activity: Discuss the causes of lower
leg pain in a 33-year-old marathon runner.
The differential diagnosis of leg pain in a marathoner in-
cludes muscle/tendon overload, bone overload, chronic ex-
ertional compartment syndrome, and vascular causes [18].
Muscle/tendon overload can occur in any muscle/tendon
unit. Muscle/tendon overload is often caused by errors in
training technique and/or biomechanical problems. The
most common training error that leads to tissue overload is
increasing running volume too fast. Hard running surfaces
and incorrect running shoes can also play a role. Biomechani-
cal issues associated with muscle/tendon overload in runners
include pes planus, rigid pes cavus, toe running, and im-
paired function of the larger, stronger hip muscles, including
gluteus medius and the hip external rotators. Impaired ec-
centric control of the hip external rotators allows the femur to
internally rotate after heel strike, which promotes hyper-
pronation and overload of tibialis posterior.
Muscle/tendon overload in the leg of endurance runners is
most commonly seen in the posterior compartments of the
leg. Overload of tibialis posterior and the gastrocnemius/
soleus/Achilles complex is commonly seen in hill runners
and toe runners, who place excessive concentric and eccen-
tric loads on these structures. Achilles tendon pain is often
felt between 2 and 6 centimeters above the insertion onto
calcaneus, but can also be felt at the insertion itself. Overload
of tibialis posterior can be appreciated anywhere along the
course of the muscle and tendon. Often, it is felt along the
medial tibia. The term “shin splints”---although commonly
used for anterior and medial leg pain in runners---is nonspe-
PM&R
Figure 5. Thompson test for Achilles tendon rupture. Upon squeezing a healthy calf, the foot will passively plantar flex (arrow) (ie,
test result is negative). A lack of plantar flexion upon squeezing the calf is indicative of a positive test.
cific and is discouraged. The preferred term, “medial tibial
stress syndrome” refers to a continuum of overload pathology
involving tibialis posterior, medial soleus, the tibial perios-
teum and the tibia itself. Early on, symptoms are often
present at the beginning of a run and then may improve as the
heel cord loosens up. As the condition worsens, symptoms
start earlier in the run and do not improve. Later, symptoms
may be present even with walking.
Runners who have a sudden increase in downhill running
are at risk for eccentric overload of the anterior leg muscles,
principally tibialis anterior. Pain is usually of insidious onset
and can be present anywhere along the course of the muscle/
tendon unit.
The peroneal muscles can become strained when trying to
control a sudden inversion ankle sprain. They can also be-
come chronically overloaded, and longitudinal split tears can
be seen in the peroneal tendons on MRI. If the lateral retinac-
ulum of the ankle is incompetent, the peroneal tendon can
sublux over the lateral malleolus. Occasionally a peroneal
muscle can herniate through a defect in the lateral fascia of
the leg. Peroneal muscle pain can be reliably diagnosed by
reproducing concordant pain with resistance testing of foot
eversion.
Bone overload is also common in endurance runners. The
spectrum of bone overload includes periostitis, stress reac-
tion, and stress fracture. High volume running can cause
overload of normal bone. Low and medium volume running
can cause overload of bone with abnormal mineralization,
structure or metabolism. Risk factors for stress fractures
include high volume running, improper training technique
such as increasing running volume too quickly, inadequate
caloric and protein intake and hormonal imbalance, as seen
with amenorrhea in the female athlete triad [19]. Symptoms
Vol. 1, Iss. 3, Supplement 1, 2009 S65
of bone stress can be difficult to distinguish from symptoms
of tendinopathy on clinical grounds alone. Magnetic reso-
nance imaging is the criterion standard for diagnosing bone
stress.
Chronic exertional compartment syndrome (CECS),
while less common than tendinopathies, is nonetheless fre-
quently encountered in running clinics. Although the under-
lying pathophysiology of CECS has not yet been clarified, the
end result is increased pressure during exercise within 1 or
more of the 4 compartments of the leg. The increased com-
partment pressure can cause pain, impaired function, and
temporary ischemia to muscles and nerves. The CECS is
diagnosed by intramuscular compartment pressure testing.
The most commonly involved compartment is the anterior
compartment, followed by the posterior compartments. In-
tramuscular pressures that are diagnostic for CECS are: rest-
ing ⬎ 15 mm Hg; 1 minute postexercise ⬎ 30 mm Hg; 5
minutes postexercise ⬎ 20 mm Hg.
Vascular causes of leg pain are far less common in younger
runners. One clinical entity of note, however, is popliteal
artery entrapment syndrome. This relatively rare condition
affects women more than men. Causes include a hypertro-
phied medial gastrocnemius muscle and abnormal tissue
bands associated with plantaris, popliteus and gastrocne-
mius, which can potentially compromise the popliteal artery.
Two physical examination maneuvers that suggest popliteal
artery entrapment if symptoms are reproduced are (1) repet-
itive activation of the plantar flexors with the knee extended
and (2) prolonged passive stretch of the hamstring and heel
cord. More definitive diagnosis is usually made by dynamic
vascular ultrasound or arteriogram with and without the
appropriate provocative maneuvers.
S66 Harrast et al
ACKNOWLEDGMENT
The authors thank Mark S. Collins, MD, for providing the
MRI showing the ACL sprain.
REFERENCES
*1. Winston P, Awan R, Cassidy JD, Bleakney RK. Clinical examination
and ultrasound of self-reported snapping hip syndrome in elite ballet
dancers. Am J Sports Med 2007;35:118-126.
2. Kelly BT, Williams RJ 3rd, Philippon MJ. Hip arthroscopy: current
indications, treatment options, and management issues. Am J Sports
Med 2003;31:1020-1037.
3. Hunt D, Clohisy J, Prather H. Acetabular labral tears of the hip in
women. Phys Med Rehabil Clin N Am 2007;18:497-520.
4. Manaster BJ, Zakel S. Imaging of femoral acetabular impingement
syndrome. Clin Sports Med 2006;25:635-657.
5. Motta-Valencia K. Dance-related injury. Phys Med Rehabil Clin N Am
2006;17:697-723.
6. White RA, Hughes MS, Burd T, Hamann J, Allen WC. A new operative
approach in the correction of external coxa saltans: the snapping hip.
Am J Sports Med 2004;32:1504-1508.
*7. Griffin LY, Albohm MJ, Arendt EA, Bahr R, Beynnon BD, Demaio M,
et al. Understanding and preventing noncontact anterior cruciate
ligament injuries: a review of the Hunt Valley II meeting, January
2005. Am J Sports Med 2006;34:1512-1532.
8. Hewett T, Shultz SJ, Griffin LY. Understanding and Preventing Non-
contact ACL Injuries. Champaign, IL: Human Kinetics; 2007.
* Indicates key references.
LOWER EXTREMITY INJURIES
*9. Fredericson M, Powers CM. Practical management of patellofemoral
pain. Clin J Sport Med 2002;12:36-38.
10. Fredericson M, Yoon K. Physical examination and patellofemoral
pain syndrome. Am J Phys Med Rehabil 2006;85:234-243.
*11. Powers CM. The influence of altered lower-extremity kinematics on
patellofemoral joint dysfunction: a theoretical perspective. J Orthop
Sports Phys Ther 2003;33:639-346.
12. Ireland ML, Willson JD, Ballantyne BT, Davis IM. Hip strength in
females with and without patellofemoral pain. J Orthop Sports Phys
Ther 2003;33:671-676.
13. Niemuth PE, Johnson RJ, Myers MJ, Thieman TJ. Hip muscle weak-
ness and overuse injuries in recreational runners. Clin J Sport Med
2005;15:14-21.
14. Baumhauer JF, Nawoczenski DA, DiGiovanni BF, Flemister AS.
Ankle pain and peroneal tendon pathology. Clin Sports Med
2004;23:21-34.
*15. Simons SM. 2007. pClinical sports medicine; Frontera E, Herring S,
Micheli L, Silver J, editors. 459-471.
16. Title CI, Katchis SD. Traumatic foot and ankle injuries in the athlete.
Orthop Clin North Am 2002;33:587-598.
17. DiGiovanni BF, Partal G, Baumhauer JF. Acute ankle injury and
chronic lateral instability in the athlete. Clin Sports Med 2004;23:
1-19.
*18. Edwards PH Jr, Wright ML, Hartman JF. A practical approach for the
differential diagnosis of chronic leg pain in the athlete. Am J Sports
Med 2005 Aug;33:1241-1249.
19. Mattila VM, Niva M, Kiuru M, Pihlajamaki H. Risk factors for bone
stress injuries: a follow-up study of 102,515 person-years. Med Sci
Sports Exerc 2007;39:1061-1066.