P1.ch3.2. hip
2. Historical reviews
Adduction Deformity
Adduction deformity is one of the most characteristic features
of the hip in cerebral palsy. This deformity leads to a scissors
posture, and disturbs activities of daily life, such as dressing and
toileting. This deformity also inhibits stable weight bearing,
causing a crouched posture. Many procedures have been proposed
for correction.
Adductor Release
Adductor release with anterior obturator neurectomy has been
widely used and recommended. Keats in 1957 presented resection
of all adductors and gracilis, combined with anterior obturator
neurectomy, as an useful procedure.54 Banks and Green also
described the effectiveness of the adductor release with anterior
obturator neurectomy in 1960.55 Many other authors have also
stressed the effectiveness of this procedure, for prevention and
treatment of subluxation and dislocation of the hip, and for the
correction of adduction deformity.120-128
However recently, instability of the hip, due to weakness of
adductors has been disclosed, as a serious complication, after
adductor release with anterior obturator neurectomy. The original
article in the literature, which noted the muscular insufficiency
after adductor release with obturator neurectomy, was presented by
Samilson and associates. They noted that in spite of large number
of satisfactory results observed in perineal care and in prevention of
hip problems, 66% of 30 patients were reported with unsatisfactory
results as far as gait improvements were concerned.123 This seems
to indicate that adductor release with obturator neurectomy is not
always an excellent procedure, in the aspect of obtaining hip
stability in weight bearing. Samilson also pointed out serious
pitfalls of the adductor release with anterior obturator neurectomy,
showing occurrence of postoperative abduction deformity in 13
patients.
We in 1986 reported instability of the hip during gait after
adductor tenotomy with anterior obturator neurectomy observed in
a comparative study of 42 children with cerebral palsy, initiating a
hypothesis that the short monoarticular adductor brevis is an
antigravity muscle which stabilizes the hip and subsequently the
whole body.26 We stressed the need to preserve this muscle, as an
important antigravity stabilizer, when correcting adduction
deformity. Recently, we have even noticed importance of the
adductor longus as another antigravity muscle. It is our observation
that hip stability is lessened when adductor longus tenotomy was
done unselectively.35,61 In our observations, antigravity stability is
much preserved in the patients in whom the intramuscular tendon
of the adductor longus is only selectively released and the extent of
release was minimized(Fig. 3, 6). In this situation, it seemed
necessary for us to find out other muscular factors to correct the
adduction deformity and at the same time preserve antigravity
stability of these short monoarticular muscles as much as possible.
35,61,129,130
It may seem quite paradoxical to correct the adduction
deformity, without releasing these adductor muscles. However,
short monoarticular muscles, such as the adductor longus and
brevis are theoretically more important, for preserving stability of
the hip in quadrupedal and bipedal locomotion. Hence, other
muscular factors should be addressed and identified. Clinically,
postoperative results of this selective release surgery are quite
satisfactory where the adductor longus and brevis are preserved and
other muscular factors are released.61
Adductor Transfer
Adductor transfer is another recommended procedure to
correct adduction deformity. Stephanson and associates reported the
results of adductor transfer in 87 patients with cerebral palsy, and
stated that it was an effective mode of treatment of the triad of hip
deformities consisting of flexion, adduction and internal rotation.131
Several authors have subsequently reported the superiority of the
transfer against adductor tenotomy, with or without anterior
obturator neurectomy.132-138 However, as Aronson stated, it has
not been clearly demonstrated whether the functional results of
adductor transfer and adductor release are different.137 Bleck stated
that adductor transfer appears to have no advantage.67
From the spasticity-control point of view, the most significant
concern is, whether the transferred adductor longus, adductor
brevis and the short muscle of adductor magnus can now act, as
body-supporting and antigravity muscles, to keep the pelvic girdle
in antigravity position. It is also usually mentioned that muscle
power of the transferred muscle will be reduced.
The other concern is, whether the antigravity power for
flexion, adduction and external rotation of the adductor longus and
brevis is maintained, or not by adductor transfer. The main
beneficial point of this transfer mentioned is to convert the
activities of flexion, adduction and external rotation of the adductor
longus and brevis to the activities of extension. Hence, adductor
transfer will result in total loss of the most important supporting
activities in adduction, flexion and external rotation of the hip.
Activities of flexion, adduction and external rotation of the
adductor longus and brevis are indispensable to elevate the pelvic
girdle against the lower extremity at the beginning of the turnover
activities, and also to flex the hip and raise the pelvis from the
on-abdomen posture to the on-knees posture. Even for gaining
stable standing and walking postures and for prevention of
backward tilt of the pelvic girdle, antigravity adduction and flexion
activities of the adductor longus and brevis are needed. Hence it is
our advice that antigravity activities of the adductor longus and
brevis should not be damaged. Therefore, we have questioned the
use of the transfer of the adductors in which flexion, adduction and
external rotation activities of the adductors is totally converted to
extension activities for the sole purpose of deformity correction.
The third concern is that there seems to be some
misunderstanding about the adductor longus and brevis being
internal rotators. The adductor longus and brevis have been
clinically considered, as internal rotators in the treatment of
adduction deformity in cerebral palsy. Hence the releases have
been recommended. Anatomically, Duchenne139 and Kapandji140
documented the adductor longus as an external rotator, while
Hollinshed described this muscle as an internal rotator.48
Clinically however, there are evidences that the adductor longus is
an external rotator. Kobara and associates documented that
obstinate internal rotation tendency was observed in the cases in
whom the adductor longus was totally sectioned in their hip
surgery, while this tendency was prevented in the cases in which
the adductors were not sectioned.141 Based on their clinical
observations, they stressed the importance of preserving the
adductor longus as an external rotator in patients who has a
possibility of independent gait. We also agree that more careful
preservation of these external rotator muscles would be needed.35,61
Discussions have to be carried out, whether release, or transfer of
these muscles can result in loss of external rotation power of the
hip causing obstinate internal rotation deformity or not.
Regarding the function of the adductor longus, there have
been many documents that this muscle is hypertonic, and
contributes to adduction and internal rotation deformity. However,
there has been little discussion on whether this muscle has
antigravity activities or not. After we reached the conclusion that
the adductor brevis is a very important antigravity muscle for
stable weight bearing on the lower extremity26, we carefully
analyzed whether the adductor longus too has antigravity activities
or not. We noticed clinically that stability is very much preserved
in patients with potential to walk independently, if the adductor
longus is protected and other hypertonic muscles are selectively
released. By proximal release of the medial hamstrings and distal
section of the hamstring part of the adductor magnus, adduction
deformity of the hip has been remarkably corrected, and much
release of the adductor longus has not been needed (Fig. 3AB,
5AB).42,61 By preserving the adductor longus, stability of the hip
has been enormously increased. On the basis of this observation,
we reached to the conclusion that the adductor longus as well as
the adductor brevis are important antigravity adductors, providing
stability in standing, walking, in quadrupedal locomotion and in
turnover activities.
Thus, our treatment views changed from the traditional one
where the section or transfer of the adductor longus was
unavoidable as it was a contributing factor for adduction deformity
is unavoidable, to the one where the adductor longus should be
preserved as it is the most important antigravity muscle and an
external rotator. This concept of preserving the adductor longus
and brevis as much as possible led us to revolutionize the
treatment, providing stability for patients in all motor levels of
development, and promising encouraging results for patients with
cerebral palsy.
Medial Hamstrings Release
There are many observations that the medial hamstrings are
one of the significant contributing factors for adduction deformity.
Baker pointed out that the medial hamstrings especially the
semitendinosus is one of the main causes of adduction deformity.142
He demonstrated the technique to identify the tightness and
contracture of each hamstring muscle and recommended
lengthening of these muscles.
Motor-function wise, the medial hamstrings are the main
internal rotators when the hip is in extension, and are quite
different from the adductor longus and brevis, which are external
rotators of the hip, when the hip is in flexion.
Anatomically, the medial hamstrings are the multiarticular
muscles whereas the adductor longus and brevis are monoarticular
muscles. Thus, theoretically as the first choice, it is reasonable and
understandable to lengthen these multiarticular medial hamstrings,
for correction of adduction deformity.
However, if we carry out lengthening of the medial
hamstrings distally, two serious problems can arise. One is, as
Baker stated, the postoperative genu recurvatum, due to muscular
imbalance between knee extensors and flexors with loss of
flexibility and stability of the knee, during standing and walking.
To prevent this problem and decrease occurrence of the stiff-legged
knee, intramuscular lengthening of the semimembranosus has
been. However, in spite of this effort, stiff-legged knee or
recurvatum deformity is still a serious complication after the distal
release procedure of the medial hamstrings, as the hypertonicity of
knee extensors predominate. Trometz and associates used
intramuscular lengthening of the semimembranosus and biceps
femoris combined with Z lengthening of the semitendinosus and
gracilis, with marked improvements, preventing too much
extension of the knee during the stance phase of gait. But, he still
reported three genu recurvatum deformities in 31 patients.59
The another problem of distal release of the medial
hamstrings is that it acts indirectly on the hip and hence is not so
effective in correcting hip adduction deformity although correction
can be obtained to some extent. So to correct the adduction
deformity, a direct approach at the hip joint would be needed.
We conducted proximal lengthening of the semimembranosus
for correction of adduction and internal rotation deformity. In our
experience, selective proximal lengthening of the
semimembranosus is quite effective for correction of adduction
deformity, as compared to distal lengthening, and also preserves
activity of the knee flexors, preventing recurvatum and stiff-legged
knee.35,61
Anatomically, the semimembranosus is different from the
semitendinosus in form and function, although both are hip
extensors and knee flexors. The semimembranosus has a long
tendon at its proximal end/insertion in the hip and a short tendon at
its end/origin in the knee. According to our hypothesis, the
muscle fibers with long tendon fibersare propulsive and hyperactive,
whereas the muscle fibers without tendon fibers or with short tendon
fibers have antigravity activities and are less hyperactive. From this
point of view, it can be deduced that muscle fibers of the
semimembranosus with long tendon fibers are more propulsive and
hyperactive at the hip and subsequently contribute to adduction and
internal rotation deformity of the hip, whereas the muscle fibers
with short tendon fibers act as stabilizers of the knee. On the other
hand, the semitendinosus has a long tendon at its distal end/
insertion and has no or least tendon fibers at its proximal end/origin.
This means that the semitendinosus is hyperactive at the knee, and
subsequently contributes to the flexion deformity of the knee. It acts
as a stabilizing extensor and adductor of the hip as the muscle has no
or least tendon fibers at its origin.
These analyses led us to the conclusion that the
semimembranosus should be released at the proximal and should
not be lengthened at the distal, for correction of hip deformity.
The site for release of the semitendinosus is different from t
hat of the semimembranosus. Proximal origin of this muscle is
mostly with muscle fibers and therefore, acts to prevent flexion
collapse of the hip and anterior tilt of the pelvis. So, total section
of the proximal muscle origin of the semitendinosus should not be
considered for correction of hip adduction deformity in patients
with potentials of crutch gait or dependent gait. Distal release can
be considered for control of spasticity if there is a flexion
deformity of the knee in patients with some potential for crutch
walking. If there is no flexion deformity of the knee with potential
for crutch gait, sliding lengthening of the semitendinosus at its
distal tendon is only considered in some conditions where
concomitant intramuscular lengthening of the antagonist rectus
femoris is combined at its distal portion. Of course, in the totally
involved patients with markedly extended and adducted hip and
with scissors posture, total transection of proximal muscular origin
of the semitendinous can be considered.35,61
Proximal section of the gracilis tendon has been
recommended, as an established procedure for adduction
deformity. There is least controversy, regarding release of this
muscle.
Fig. 87A: Before OSSCS
Fig. 87B: After OSSCS
Fig. 87: Effect of OSSCS for hip deformity
Under construction
Adductor Magnus Release
There has been little documentation, regarding hypertonicity
of the adductor magnus. Kawada and associates in 1994 advocated
tenotomy of condylar tendon of the adductor magnus.53 Until
today, about 209 procedures have been conducted as a routine
procedure in our department.35,61 The adductor magnus, as a
whole, is one of the most important hip-extensors, which supports
the trunk upright in sitting, crawling and standing postures. This
muscle is an adductor and internal rotator when the hip is in
extension, and acts similar to the medial hamstrings.140 Here, it
must be emphasized that this muscle can be the most contributing
factor to adduction and internal rotation deformity of the hip.
While analyzing this muscle anatomically, we noted the fact that
this muscle is divided into two parts.
One is the adductor part with some short tendon fibers and
mostly muscle fibers. This part can be considered to participate in
adduction of the hip, supporting and keeping the trunk upright. The
other is the hamstring part with a long tendon. This part adducts
and extends the hip and acts as a propelling force during various
kinds of locomotion, but does not have antigravity activities.
On the basis of these observations, we have carried out
section of the hamstring part of the adductor magnus, for correction
of adduction and internal rotation, with excellent results.35,42,53,61
With selective combined releases of adductor magnus, medial
hamstrings and psoas, adduction deformity is effectively corrected,
and we can now save most of the adductor longus. The adductor
part of the adductor magnus should be carefully preserved, as they
are important antigravity hip-adductors (Fig. 3AB, 6AB, 60AB,
87AB, 88AB, 95AB).
Iliopsoas Release
The iliopsoas is also an important muscular factor causing
adduction and internal rotation deformity. There is little in the
literature mentioning about this muscle as an adductor. However,
there is consensus among orthopaedic surgeons that the iliopsoas is
an important adductor and flexor of the hip. In clinical studies
during past 20 years, we have noticed the fact that in the group in
which psoas tendon was sectioned or lengthened, adduction and
internal rotation was more effectively corrected. Based on these
observations, we confirmed that the iliopsoas is one of the main
adductors, and contributes to adduction and internal rotation
deformity.
Based on these findings, we are enumerating the main factors
causing adduction deformity:
1) Medial hamstrings
Semitendinosus
Semimembranosus
Gracilis
2) Psoas and iliacus
3) Adductor magnus
Hamstring part
4) Tendinous part of adductor longus
Combined hypertonicity of these muscles are considered to
cause adduction deformity. So one has to consider how to relieve
the combined hypertonicity of these muscles appropriately, by
release of these muscles.
Flexion Deformity
The iliopsoas, rectus femoris, sartorius, tensor fascia lata,
pectineus, gracilis and adductor longus and brevis are all
considered, as flexors of the hip. Various surgical approaches have
been undertaken to reduce the flexion deformity contributing
factors.
The Soutter's muscle slide operation, which releases the
origin of the sartorius, rectus femoris, tensor fascia lata, and
gluteus medius from the iliac crest and the outer surface of the iliac
bone and displaces them distally was commonly used in treatment
of flexion contracture of the hip due to poliomyelitis.143
Roosth in 1972, reported similar muscle slide operation, in
which the sartorius, tensor fascia lata, rectus femoris and anterior
part of the gluteus medius are detached. This muscle slide
operation probably diminishes the hypertonicity of the flexors to
some extent.144 However, the problem caused would be that of
weakness of the abductors (gluteus medius) of the hip. The gluteus
medius is a short monoarticular abductor, and an important
supporter of the pelvis, on the femur. Bleck also pointed out
importance of pelvic stabilization by the gluteus medius during
gait.67 Loss of function of the abductors by these sliding
operations may not be acceptable, even if the damage is minimal,
as it causes pelvic obliquity and an ineffective gait called
Trendelenburg gait.
Iliopsoas release is another procedure to correct flexion
deformity. Keats and associates in 1969 advocated iliopsoas
tenotomy through the anteromedial approach, which they
developed as a result of experiences in adductor release and
anterior obturator neurectomy.145 Bleck noticed that the iliopsoas
was the main and powerful flexor of the hip, and reported
experiences of the iliopsoas tenotomy for correction of flexion
deformity of the hip.146 In follow-up study of the patients in whom
iliopsoas tenotomy was conducted, he noted postoperative
weakness in hip flexion, and hence advocated his new approach
called as "iliopsoas recession," for correction of flexion deformity.
147
We observed many patients in whom flexion and adduction
deformity was well corrected, after iliopsoas recession. Weakness
in upward flexion of the lower extremity at the hip was however
observed after iliopsoas recession, especially when it was
combined with adductor tenotomy.
To remedy this situation, various procedures have been
proposed. Tylkowski in 1986 reported aponeurotic lengthening of
the iliopsoas at the pelvic brim, for spastic hip flexion deformity.148
Hajime and associates in 1985 51 and Kawamura and associate in
1986 52, and myself in 1987 26 proposed selective lengthening of
the psoas at the inguinal level for reduction of hip dislocation and
correction of hip deformity. In the reports, we separated the
multiarticular psoas, from the monoarticular iliacus, and
recommended selective lengthening of the psoas tendon, while
preserving the iliacus as an important antigravity muscle. Our
inguinal level approach where release of the iliopsoas is done at the
inguinal level seems more effective than the one at pelvic brim
level proposed by Tylkovski, because release at the distal level
reduces whole spasticity of the psoas and most of the spasticity of
the iliacus appropriately. Although postoperative weakness of the
flexors could be a problem, our combining proximal
semimembranosus tendon lengthening could minimize and
compensate the weakness of the iliopsoas by reducing extensor
spasticity of the hip. There has been no serious loss of flexion
power after the inguinal level release(Fig.3AB, 6AB, 87AB,
100AB,101AB, 102AB. Rang in 1986 described
Fig.101: Before OSSCS
Fig101B: After OSSCS
Fig.101AB: Effects of OSSCS for flexion
deformity of the hips
5-year-old girl
selective sectioning of the psoas tendon at the inguinal level, for
correction of flexion deformity of the hip. He also preserved the
iliacus muscle.66 Recently, Sutherland and associates conducted
gait analysis in ambulatory patients after selective psoas release at
the pelvic brim and reported excellent results.149 These papers
make sense, since monoarticular iliacus is eventually preserved,
and the hyperactive psoas is only selectively released. However,
problem in psoas release at pelvic brim is that only proximal parts
of the psoas tendon are released, and the rest of the psoas and the
entire muscle-tendon units of the iliacus cannot be released, as the
level of release is more proximal than that of inguinal approach. As
a result, spasticity of the unreleased fibers is left unreduced, and
can cause residual flexion deformity. The effect of control of
spasticity could be limited in psoas release at pelvic brim.
Thus, selective release of the psoas has become popular and
effective for correction of flexion, adduction and internal rotation
deformity, and relieving the hypertonicity. However, level of the
release is still debatable.
Hypertonicity of the rectus femoris also contributes to the
flexion deformity of the hip, although little has been documented
about hypertonicity of this muscle. Since this muscle is a
multiarticular muscle with long tendon proximally, hypertonicity in
it directly causes flexion deformity. Lengthening of this muscle
should be a concomitant procedure in correction of hip flexion
deformity.26,35,61 The sartorius is another multiarticular
muscle, which can contribute to hip-flexion. However, it is still not
clear, how much this muscle contributes to the flexion deformity.
For correction of flexion deformity, selective release of the
hypertonic flexors, such as the psoas, rectus femoris, and sartorius,
are considered to be essential, while facilitating short
monoarticular muscles, such as the iliacus, gluteus medius,
minimus and maximus, adductor magnus, longus and brevis, and
short periarticular rotators, and increasing weight bearing stability
(Fig. 3AB,6AB,17AB,23AB,25AB,40AB,87AB,100AB,101AB,
102AB)).
Fig.102A: Before OSSCS
Fig.102B: After OSSCS
Fig.102AB: Effect of OSSCS for hip and knee deformities
Internal Rotation Deformity
Internal rotation deformity is one of the most characteristic
hip deformities, and many findings have been presented, as causes
of this deformity.
Adductor Longus, Adductor Brevis and Gracilis
Keats, Banks and Green described that the adductor longus,
adductor brevis, and gracilis are the main adductors and internal
rotators, so proposed release of these muscles combined with
anterior obturator neurectomy, for achieving correction.54,55
Transfer of the adductor longus and brevis have also been
recommended as a preferable procedure.131-137 However clinically,
internal rotation deformity seems to remain in most of the patients
postoperatively when the patients begin to move and walk (Fig.
2AB). Sutherland and associates described in their
electromyographic study that the adductors showed inconclusive
and varied correlation with the abnormal internal rotation
movement.150
Anatomically, the adductor longus and brevis arise from the
wide posterior portion of the femoral bone and are inserted to the
anterior portion of the pubic bone [Please change your viewpoint].
Thus, theoretically from the anatomical point of view, when they
contract, they will adduct and externally rotate the femur.
As described earlier, it seems logical to me to consider that the
adductor longus and brevis are external rotators.
On the other hand, the gracilis, which arises from posterior
portion of the pubic bone, and is inserted to the anterior aspect of
proximal tibia, seems to rotate the lower extremity internally when
it contracts. Clinically too, adduction and internal rotation
deformity can be considerably relieved, with proximal release of
the gracilis, without any loss of stability (Fig. 3AB, 6AB, 82AB).
Thus gracilis can be considered to be an internal rotator of the hip.
Medial Hamstrings
The medial hamstrings consist of the semitendinosus,
semimembranosus and gracilis. Clinically, the medial hamstrings
have been given much attention, as the main contributing factor for
internal rotation deformity.
Sutherland and associates confirmed with
electromyographic study that the medial hamstrings showed
evidences of spasticity and were consistently contracted in a
definite synchrony with internal rotation movement, which begins
just before heel strike and continues through the stance phase. On
the basis of this electromyographic analysis, they carried out
transfer procedures of the semitendinosus, semimembranosus and
gracilis to the lateral distal aspect of the femur in 7 patients,
with good results. Thus, they clearly demonstrated that
hyperactivity of the medial hamstrings is the main factor to cause
internal rotation mostly in the stance phase.150 This view is quite
reasonable.
Ray and associates carried out similar procedures in which
they transferred the semitendinosus to the lateral intermuscular
septum and the semimembranosus to the fascia of the biceps
femoris, and reported decrease in internal rotation in 15 of the 17
hips.151 Thus, the medial hamstrings have caught enough
attention, as significant internal rotators, and hence transfer of
these muscles has been advocated.
Reduction of hypertonicity of semimembranosus and
semitendinosus appear to be essential for correction of internal
rotation deformity. However, release or transfer at the distal tendon
insertion seems to present serious problems.
The most serious problem of release or transfer is occurrence
of genu recurvatum deformity or occurrence of stiff-legged knee.
Sutherland and associates reported occurrence of recurvatum in
one patient with ataxia, and described that their gait was less
stable.150 Ray and associates also reported of a child who had genu
recurvatum in one knee after the operation, and stated that his gait
had not improved overall.151
Thometz reported effect of lengthening of the medial
hamstrings on gait in 31 patients, and noted genu recurvatum
developed in 3 cases 59, although he attempted to prevent
stiff-legged-knee, by intramuscular lengthening of the
semimembranosus. Therefore, they became reluctant to lengthen
the medial hamstrings, in patients who had only internal rotation
deformity, unless there was in addition excessive flexion deformity
of the knee in stance phase.
The second problem is postoperative medial instability of the
knee, after Z- or sliding lengthening of the semimembranosus.
With weakness of medial restraint mechanism of the
semimembranosus, instability of the knee can occur, causing
persistent pain in the medial joint space due to degenerative
changes in late adulthood. Distal attachment of the
semimembranosus is important for stability of the knee, as a
medial protective restraint. Therefore, we should be careful when
carrying out distal sliding or Z lengthening of the
semimembranosus, in order to preserve this joint-support
mechanism.
Another aspect is that distal release of the semimembranosus
can be more effective for correction of knee deformity, since the
main activity of the distal tendon is to flex the knee whereas it is
less effective in correction of hip deformity such as internal
rotation of the hip. There exists a clear functional difference
between the proximal and the distal tendon of the
semimembranosus. It is considered that the proximal tendon
extends, adducts and internally rotates the hip directly, whereas the
distal tendon flexes the knee.
On this basis, proximal lengthening of the semimembranosus
is considered to be the most effective way for correction of hip
internal rotation, and also for preserving the supporting restraint
mechanism of the knee joint.35 Thus, proximal lengthening of the
semimembranosus is recommended as an essential procedure, for
correction of internal rotation deformity of the hip.51,52,61
Hypertonicity relieving procedure of the semitendinous is
another complex issue. In the severely involved patients with
extended or dislocated hips, total section of proximal origin of the
semitendinosus is very effective for achieving correction. However
since the proximal origin has a muscular origin and is considered
to have some supportive activities, direct proximal release can
cause loss of these activities in hip-extension, which could be
serious in ambulatory patients inducing hip flexion deformity and
consequent anterior tilt of the pelvis with lumbar lordosis. Thus, in
order to decrease internal rotation activities of the semitendinosus
in patients with potentials of independent and crutch gait,
combined lengthening with intramuscular tenotomy of the
proximal origin and sliding lengthening of the distal tendon seems
to be the only way to be done, without losing supporting activities
of the proximal muscular part. Thus, the semimembranosus and
semitendinosus including the gracilis can be recognized as the
main contributing factors of internal rotation and release of these
muscles can be proposed. Site, level and amount of the release
should be carefully analyzed.
Iliopsoas
It is debatable whether the iliopsoas muscle acts, as an
internal, or an external rotator. It is obvious that it acts as an
external rotator, in such conditions as in developmental
hip-dislocation and femoral neck fracture in which center of
rotation of the femur is not located in the center of the femoral
head. So, contraction of the iliopsoas directly pulls on the lesser
trochanter to the forward with external rotation of the femur.
However, it is questionable, if the iliopsoas always acts as an
external rotator in conditions where the femoral head is centered in
the hip.
Lanz and associates stated that the iliopsoas could act as an
external as well as an internal rotator, alternately, according to the
position of the lower extremity.152 Clinically, in cerebral palsy,
it seems that the iliopsoas acts as an internal rotator, along with
other internal rotators. In the hip in which the iliopsoas, adductors
and medial hamstrings are released, internal rotation seems to
decrease (Fig. 3AB, 82AB). Bleck emphasized that internal
rotation deformity decreases after iliopsoas recession.147 Rang who
also recommended selective release of the psoas tendon, noted
decrease in the internal rotation deformity.66
We also presented selective lengthening of the psoas tendon
n our previous study.27 Recently, we have proposed psoas
tenotomy and aponeurotic tenotomy of the iliacus at the inguinal
level of the hip for severe flexion deformities. Our conclusion is
that iliopsoas is an important internal rotator causing internal
rotation in most patients with cerebral palsy. Selective release of
the psoas tendon and aponeurotic tendon of the iliacus at inguinal
level is essential, for correction of internal rotation deformity.
35,61,129,130
Tensor Fascia Lata and Gluteus Medius and Minimus
Anatomically, the tensor fascia lata has been considered as
an internal rotator.48 Anterior portions of the gluteus medius and
minimus are also considered as internal rotators. Thus, for
correction of internal rotation deformities, release of these muscles
has been proposed.
In 1972, Roosth reported the release of tensor fascia lata and
anterior part of the gluteus medius and minimus from the outer
wall of the pelvis, for correction of flexion and internal rotation
deformity of the hip.144
We have had experiences with section of the tensor fascia
lata at the insertion to the iliotibial tract in eight hips. However,
there was no improvement in internal rotation in all these hips. We
also have a diplegic patient for whom release of the fascia lata at
the insertion to the iliotibial tibial was done only on one side. In
this patient, we noted an increase of internal rotation on the
released side in W sitting posture, whereas there was no increase in
internal rotation on the unreleased side. This comparison seemed
to demonstrate that the tensor fascia lata acts as a restraint to
internal rotation in W sitting posture. After these observations, we
abandoned release of the tensor fascia lata for correction of internal
rotation. Thus, clinically, internal rotation activity of the tensor
fascia lata is still uncertain, and needs to be more carefully
analyzed clinically, functionally and anatomically.
Adductor Magnus
Contribution of the adductor magnus for internal rotation
deformity has not been specifically mentioned. Anatomically, the
adductor magnus consists of two muscle groups. The one is a short
adductor part, and the other is a long hamstring part. The adductor
part is a short monoarticular muscle with a short tendon or without
tendon, and therefore, considered as an antigravity muscle of the
trunk and pelvis against the thigh in hip extension. The adductor
part should be carefully preserved.
The hamstring part though also a monoarticular muscle, is
quite different in form and style from the short adductor part. It has
a long tendon distally. Anatomically, these two groups of the
adductor magnus are considered as internal rotators. We consider
the hamstring part of the adductor magnus, as an internal rotator
with propulsive activities. It is considered to be hyperactive in
cerebral palsy. We have conducted tenotomy of this muscle with
significant improvement, and without any loss of stability.35,53,61
Thus, clinically, the hamstring part of the adductor magnus can be
identified, as a muscle, which contributes to internal rotation
deformity (Fig. 87AB, 100AB,101AB,102AB).
Anteversion and Internal Rotation
In the human hip joint, existence of anteversion of the femur
in babies and infants has been well documented. It is also
emphasized that this excessive anteversion usually decreases in the
normal process of weight bearing in standing and gait, with
external rotation activities of the external rotators such as gluteus
maximus. On the other hand in cerebral palsy, this external rotator
mechanism does not function, resulting in uncorrected excessive
anteversion of the femur. Bleck measured anteversion of the femur
in CP patients, and concluded that certain degree of excessive
anteversion was observed.147 Similar observations have also been
reported by other investigators.153-159
Theoretically and anatomically, existence of anteversion
means that the distal part of the femur is internally rotated against
the proximal part of the femur, when the latter is kept in neutral
position. So, this anteversion of the femur can be considered one of
the main causes of internal rotation. In order to decrease internal
rotation during gait, external rotation osteotomy of the femur was
carried out.159
Hoffer and associates proposed supracondylar derotation
osteotomy of the femur.155 Derotation osteotomy of the femur in
subtrochanteric region is also another recommended procedure.
Bleck pointed out that anteversion of the femur is a cause for
internal rotation gait and recommended the derotation osteotomy at
the proximal part of the femur.67 We also have experiences in
which derotation subtrochanteric osteotomy was conducted to
correct severe internal rotation without dislocation or subluxation
of the hip. Internal rotation was corrected adequately in 17 of 18
hips. Appropriate derotational osteotomy technique, which does
not cause insufficiency of the quadriceps and gluteus maximus,
would be desirable. Intertrochanteric or subtrochanteric derotation
osteotomy can be other choices of site for correction of the internal
rotation deformity.
For internal rotation deformity, the hypertonicity of internal
rotators should be firstly reduced by selective muscle release and
then the intertrochanteric or subtrochanteric derotation osteotomy
of the femur could be used as a supplemental procedure.
Extension Deformity
Extension deformity is one of the special deformities, which
have often been neglected, as a lesser important deformity.
However, recently, serious concerns regarding this deformity have
been raised.
Extension deformity is mostly caused by hypertonicity of the
hamstrings, adductor magnus and gluteus maximus, shortens the
stride length, and induces a short steppage gait, as in cerebral palsy.
Hyperextension of the hip causes difficulties in sitting. Difficulties
are also seen in crawling due to inhibition of alternate
extension-flexion movements. In supine position, hyperextension
of the hips inhibits activities of the adductor longus and
brevis, hampering turnover movement. So, extension
hypertonicity of the hip inhibits fundamental activities of the body
in various phases of basic motor functions and activities of daily
living. Reduction of this hypertonicity is necessary for improving
functions in severely involved patients with cerebral palsy.
Recently, some surgeons have noticed the significance of this
problem and have presented papers. Silverskiold 1923 reported
transfer of the hamstrings from its proximal origin to the femur, for
relieving hyperextension in the hip.160 Seymour
proposed release of the proximal origin of the hamstrings to
increase stride in gait.161 These reports have led us to believe that
considerable hypertonicity in extensors of the hip exist, even in
mildly involved patients who are ambulatory, as well as in severely
involved with hyperextension of the hip.
Szalay and associates reported that hyperextension deformity
of the hip is observed in severely involved patients, and noted that
release of the proximal hamstrings and gluteus maximus were
needed to attain flexion of the hip.162 So in order to activate
sitting stability, they released the proximal hamstrings, gluteus
maximus, external rotators and posterior capsule. Their report
showed that hyperactivity of the hamstrings are the main
contributing factor of extension deformity of the hip. Elmer and
associates noticed the tightness of the hamstrings are responsible
for the hip extensor thrust and increased kyphosis, and carried out
proximal hamstrings lengthening in non ambulatory children with
spastic quadriplegia to improve hip and spine positioning.163 This
proximal hamstrings release could be recognized as a revolutionary
approach with broadened indications for extensor thrust of the hip.
We have also noted that hypertonicity of the hamstrings and
adductor magnus cause extension attitude of the hip, that is
observed in various forms in cerebral palsied patients, such as short
stride in gait, difficulty in alternate movements of lower extremity
in crutch gait, mermaid crawl and four point crawl, and difficulty
in sitting and turnover activities. So, we have carried out proximal
release of the hamstrings and hamstring part of the adductor
magnus to lessen extension deformity with internal rotation, for
ambulatory patients with crouched posture and short stride, for
patients with difficulty in sitting, and those with difficulties in
basic motor functions such as turnover, crawling and crutch gait
(Fig. 88AB, 95AB).53,61
Thus, proximal releases of the hamstrings in the hip have
been an indispensable procedure for inhibiting extensor pattern in
cerebral palsy. Now, proximal release of the hamstrings also play
important role in controlling all abnormal postural reflex such as,
asymmetric tonic neck reflex, symmetric tonic neck reflex and
tonic labyrinthine reflex.
Fig 88. Effect of proximal release of the hamstrings
for sitting difficulty due to extensors-spasticity
Top: Before OSSCS
Bottom: After OSSCS
External Rotation
Flexion, abduction and external rotation deformity is called
as a froglegged posture and is often seen in severely involved
patients. This is characterized by hypertonicity of the abductors
such as the gluteus maximus and paralysis of the adductors. In this
deformity, adductor longus and brevis do not act well. Turnover
movements are inhibited by flexed, abducted and externally rotated
hip. Treatment of external rotation deformity has not been well
documented. Szalay's approach of release of the gluteus maximus
and posterior pericapsular external rotator gives us a useful solution
to solve this difficult problem.162
To Contents
Back
Next