POSTERIOR ANKLE IMPINGEMENT SYNDROME
Pain and restriction of motion at the posterior or posterolateral aspect of the ankle,
arising during forced plantar flexion of the tibiotalar joint,
as the posterior tibia margin impinges upon the posterior talar process (positive posterior impingement test),
are the clinical findings that characterizes posterior ankle impingement syndrome.
1 The posterior ankle impingement syndrome as also been referred to as “os trigonum syndrome” and “talar compression syndrome” in the literature.
2
Posterior ankle impingement syndrome is usually associated with activities that promotes repetitive forced plantar flexion of the ankle.
It is common among ballet dancers and soccer players,
for instance.
Symptoms can develop with normal anatomy or can be enhanced by anatomic variations,
osseous anomalies at the posterior aspect of the talus,
soft-tissue anomalies,
such as fibrosis or scarring of the posterior talar or subtalar joint capsule,
shortening of the flexor hallucis longus tendon and tendon sheath,
accessory muscles,
ganglion cysts or loose bodies in the posterior talar recess.
3
It can also result from acute injury,
such as posterior talofibular ligament avulsion,
lateral talar process fracture and lesion of os trigonum synchondrosis.4 Response to injury by thickening of the posterior capsule and adjacent soft tissue,
leads to development of symptoms 4-6 weeks later; also loose bodies,
by itself,
can result in this syndrome.
Anatomic considerations:
Although soft tissue anomalies may be the cause of posterior impingement syndrome,
bone abnormalities are more frequent,
and those include changes in the posterior tibia,
posterior talus and superior calcaneus.
5-11
The anatomic modification of the posterior talar anatomy is the main cause of posterior ankle impingement.
Between the articular surface of the subtalar dome and the posterior aspect of the subtalar joint,
we find the medial and lateral tubercles of the posterior process of the body of the talus,
holding between them the course of the flexor hallucis longus tendon.
Just posterior to the sustentaculum tali,
the lateral process,
usually more prominent,
is more prone to variation in morphology,
thus more commonly implicated in posterior impingement.
When it appears enlarged,
it is named “Stieda process”.
The failure in fusion of the secondary ossification nucleus at the lateral process,
results in the separation of a secondary ossicle between 8 and 11 years,
known as “os trigonum”, which presents in 7 to 14% of the population and is bilateral in about 1,4% of the population.
12 The os trigonum may be either entirely separated or may be united to the posterior talus by a synchondrosis or a syndesmosis.
Therefore,
four anatomic presentations can be identified at the posterolateral talus:
Type I: Normal lateral tubercle
Type II: Stieda process
Type III: Os trigonum (accessory bone)
Type IV: Synchondrotic or syndesmotic fusion of an os trigonum
Changes in morphology of the posterior articular surface of the tibia,
such as a downsloping configuration of the tibial epiphysis,
or post-traumatic hypertrophy of the posterior malleolus,
also favor ankle impingement at the posterior aspect of the tibiotalar joint.
13
Anomalies of soft tissues in the posterior ankle - ligaments,
joint capsule,
synovium and flexor tendon hallucis longus - can be related to posterior ankle impingement syndrome.
The ligament anatomy of the posterior aspect of the ankle is complex comprising the posterior inferior tibiofibular ligament (PITF),
the intermalleolar (transverse tibiofibular) ligament,
the “tibial split” and the posterior talofibular ligament (PTFL).
Thickening of the intermalleolar ligament,
sometimes called the “posterior labrum”,
can be associated with ankle posterior impingement.
During plantar flexion,
this ligament,
that extends from the medial malleolus to the superior margin of the fibular malleolar fossa,
can insinuate into the joint and cause pain.
14
Accessory muscles can,
less frequently,
be described as a cause of posterior ankle impingement syndrome.
15-18
Another anatomic variation,
the prominence of posterosuperior aspect of the calcaneus,
known as Haglund deformity,
can be associated to the development of posterior ankle impingement syndrome at the level of the distal Achilles,
as mentioned bellow.
13
Imaging findings
Posterior ankle impingement syndrome results in characteristic bone and soft tissue changes,
well depicted in MRI on T1-weighted and T2-weighted fat suppressed or short tau inversion recovery (STIR) images.
Sagittal images play an important role in detecting os trigonum or a Stieda process,
as a cause of posterior ankle impingement,
as well as associated findings in posterior ankle impingement syndrome,
such as bone marrow edema,
bone cysts,
and adjacent fat pad and articular capsule edema.
Fat pad edema surrounding an os trigonum or lateral talar process,
is known as the “nutcracker phenomenon”.
(Fig.1,
2) Fat-suppressed fluid-sensitive images are particularly useful to detect edema.
(Fig.
3) A downsloping posterior malleolus may be found.
(Fig.
4)
Correlation between sagittal and axial images may show posterior capsular thickening,
synovitis and adjacent soft tissue edema,
sometimes associated with ligament thickening.
2,
8,19,20,21 The posterior intermalleolar ligament may increase in thickness and reach the same size or grow thicker than the adjacent posterior ankle ligaments (PITF and PTFL),
acquiring a meniscoid appearance and becoming known as the posterior labrum.
(Fig.
4)
Table 1 lists some different bone,
joint and soft tissue MR image findings associated with posterior ankle impingement syndrome.
Table 1
MR imaging findings associated with posterior ankle impingement syndrome
|
1- Bone or joint anomalies
|
Posterolateral talar tubercle:
Stieda process,
os trigonum (edema/ fragmentation/ pseudoarthrosis),
Shepherd`s frature
Posteromedial talar tubercle:
Prominence or fracture,
FHL tunnel ossification,
accessory ossicles.
Tibial:
Downward sloping posterior tibial plafond,
posterior malleolus fracture or malunion
Posterior subtalar joint:
Osteophytes,
loose bodies,
PVNS
|
2- Soft tissue findings
|
Synovitis with distension of the posterior recesses of the tibiotalar and subtalar joint
Thickening of posterior intermalleolar ligament (posterior labrum; meniscoid appearance) (same size or thicker to adjacent posterior ankle ligaments,
PITF and PTFL)
Flexor hallucis longus tenosynovitis
Edema of FHL myotendinous junction
Accessory muscle (peroneocalcaneus internus,
tibiocalcaneus,
long accessory of quadratus plantae,
peroneus quartus)
|
POSTEROMEDIAL ANKLE IMPINGEMENT SYNDROME
Less described in the literature,
posteromedial impingement syndrome is not yet completely understood.
A pronation-supination injury seems to be the starting point,
as it leads to disruption of the anterior talofibular ligament and compression of the deep component of the deltoid ligament,
between the medial malleolus and medial process of the talus,
with subsequent fibrosis and loss of compliance of the ligament.
22
Clinically,
pain at the posteromedial ankle with forced plantar flexion and inversion,
is more suggestive of posteromedial impingement,
rather than pure posterior tibial dysfunction or impingement from os trigonum or Stieda process.
Although prominence of the posteromedial talar process and posterior aspect of the medial malleolus can result in this clinical condition,
anomalies of the posteromedial soft tissues are more relevant in the posteromedial ankle impingement,
usually with fibrosis and edema in the medial tibiotalar recess and posteromedial corner of the ankle,
just medial to posterior talar process.
These soft-tissue changes include thickening,
scarring and edema of the posterior tibiotalar ligament,
which loses its normal fat-striated appearance,
hypertrophy of the posteromedial tibiotalar joint capsule,
and edema and fibrosis surrounding the posterior tibial tendon (less commonly the flexor digitorum longus or flexor hallucis longus).
(Fig.
5,
6) 23-25 Besides the soft-tissue changes,
bone marrow edema and bone cyst may be seen in the medial compartment of the ankle.
HAGLUND´S SYNDROME
Prominence of the posterosuperior aspect of calcaneal tuberosity,
well depicted in sagittal MR images,
is the hallmark of Haglund’s syndrome.
Repetitive traction imposed by gastrocnemius-soleus complex lead to chronic friction of the Achilles tendon,
with retrocalcaneal bursa and,
posterior Kager fat pad impaction,
resulting in Achilles tendinosis and retrocalcaneal bursitis,
known as Haglund´s syndrome.
(Fig.
7) 26-28