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Management of the Adult, Spastic, Equinovarus Foot Deformity

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Foot & Ankle International http://fai.sagepub.com/

Management of the Adult, Spastic, Equinovarus Foot Deformity

Steven J. Lawrence and Michael J. Botte
Foot Ankle Int 1994 15: 340
DOI: 10.1177/107110079401500610

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01 98-0211/94/1506-0340$03.00/0
FOOT8 ANKLEINTERNATIONAL
Copyright Q 1994 by the American Orthopaedic Foot and Ankle Society. Inc.
Current Topic Review
Management of the Adult, Spastic, Equinovarus Foot Deformity
ABSTRACT
Management of the persistent, acquired, neurogenic equi-
novarus foot may be a confounding rehabilitativedilemma.
Victims of cerebrovascularaccidents and traumatic brain
injury commonly develop this neurogenic deformity. The
plantarflexed and inverted foot position results from an
imbalanceof forces about the hindfoot due to exaggerated
muscle tone and hyperactive stretch reflexes. Significant
functional impairment may ensue if a plantigrade foot
position cannot be achieved and maintained. Surgical
correction may be necessary if conservative measures
fail. Determination of the dynamic and static components
contributing to the equinovarus deformity is difficult. Gait
analysis and dynamic electromyographic studies are val-
uable adjuncts for operative planning. The wide-ranging
goals of surgery vary from improving transfer and ambu-
lation skills, to assisting wheelchair positioning, to facili-
tating use of braces and/or shoe wear.
INTRODUCTION
Neurologic deficits following stroke and brain injury
frequently affect the sensibility, motor control, and po-
sition of involved extremities. An equinovarus foot po-
sition results from patterns of hypertonic muscular in-
volvement. The deformity may result in significant func-
tional impairment if left uncorrected. The persistent,
spastic equinovarus deformity is frequently difficult to
evaluate and treat.
ETIOLOGY
The most common etiology of an acquired, spastic,
adult equinovarus deformity is either traumatic brain
injury or cerebrovascular accident. Other neurologic
Foot and Ankle Fellow, University of California Medical Center,
San Diego, California. Currently in private practice with Orthopaedic
Associates of Allentown, Allentown, Pennsylvania 18104.
t Associate Professor of Orthopaedic Surgery and Chief, Foot and
Ankle Surgery, University of California Medical Center, and Chief,
Rehabilitation Medicine Service, Veteran’s Administration Hospital,
San Diego, California. To whom requests for reprints should be
addressed at Department of Orthopaedics, MCH 8894, UCSD Medi-
cal Center, 200 West Arbor Dr., San Diego, California 92103.
340
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Steven J. Lawrence, M.D.,’ and Michael J. Botte, M.D.t
San Diego, California
conditions with hypertonia, such as incomplete spinal
cord injury and multiple sclerosis, may result in a similar
equinovarus deformity.”
Traumatic brain injury and stroke involve a significant
portion of our population. In this country, 60% of an
estimated annual 500,000 stroke victims survive their
cerebrovascular infar~tion.~ The prevalence of stroke in
this country is nearly 1.7 m i l l i ~ nMany
. ~ of these survi-
vors are functionally limited by debilitating neurologic
deficits. Furthermore, an additional 500,000 traumatic
brain injuries occur each year, of which 50,000 to
70,000 cases are classified as “severe” inj~ries.~’ Over-
all, the cost of health care, shattered dreams, and
broken lives for these two subtypes of brain injury is
overwhelming.
Although the disabilities associated with stroke and
brain trauma may overlap, there are tremendous dis-
similarities. Whereas the brain trauma victim is stereo-
typed as a young male with injuries sustained in a
motor vehicle a~cident,~’ the stroke victim is character-
ized by one major distinction-advanced age.’ Hemi-
plegic involvement in stroke patients contrasts with the
variable hemiplegic, triplegic, or quadriplegic involve-
ment common to traumatic head injury patients. Finally,
the closed head injury victim too frequently displays a
formidable constellation of disabilities, including ex-
treme hypertonus, severe cognitive and perceptual def-
icits, and tumultuous behavioral aberrations-a com-
bination rarely observed in hemiplegics.
STAGES OF RECOVERY
Recovery Phase
After a severe cerebrovascular accident, an initial,
but short-lived, period of flaccidity ensues. At a later
time, spasticity develops. It results from loss of cortical
modulation over primitive motor and postural reflexes
emanating from the spinal cord and brain~tem.’.~.~’.~’
Spasticity is manifested as increased muscle tone, hy-
peractive stretch reflexes, and possibly clonus or rigid-
it^.^ Active motion, if and when it returns, typically
occurs in characteristic flexor or extensor patterns.
Foot & Ankle International/Vol. 15, No. 6IJune 1994
Fig. 1. Photograph of longstanding equinovarus deformity of the
right foot in a brain-injuredpatient. The hindfoot deformity was nearly
fixed, and redundant skin behind the Achilles tendon caused chronic
maceration. A forefoot adductus position accompanies the hindfoot
deformity.
Fig. 2. A lateral radiograph of the foot demonstrating a severe
equinovarus position. The anterior portion of the talar dome is irreg-
ular, indicating tibiotalar arthrosis. Disuse osteopenia is evident.
These patterns of muscle involvement produce pre-
dictable limb posturing. In flexor posturing, the hip is
typically held in flexion, adduction, and internal rotation,
the knee is flexed, and the foot is held in equinovarus.
Ambulation is difficult or impossible with severe flexor
patterning. In contrast, with extensor patterning, the
hemipelvis of the spastic hemiplegic limb becomes el-
evated and retracted; the hip is extended, internally
rotated, and adducted; the knee is extended; and the
foot is held in equino~arus.~ This more functional, ex-
tension pattern is accentuated by an upright position
and weightbearing through the
In the acute recovery phase, intensive physical, oc-
cupational, and speech therapies are concentrated to
allow for spontaneous, neurologic recovery and to fa-
cilitate residual motor control. Lower extremity therapy
focuses on the long-term goal of ambulation; active and
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MANAGING EQUINOVARUS FOOT DEFORMITY 341
passive mobilization, stretching exercises, neuromus-
cular reeducation, biofeedback techniques, balance re-
actions, and gait training are used to affect functional
gains.
Prevention of fixed soft tissue contractures through
mobilization of the spastic limb is a central goal in the
management of hypertonus. Range of motion exer-
cises, splinting, and phenol blocks may be used to
inhibit spasticity. Open, dilute, intraneural phenol injec-
tions into motor branches may be an effective, albeit
temporary, means to decrease h y p e r t ~ n i a . ~ ~ ~ ~
Phenol produces a chemical axon~tmesis.~ Spasticity
may return after 2 to 6 months following successful
axonal regenerati~n.~’ An external support may be
necessary to place the foot into a plantigrade position-
a polypropylene ankle-foot orthosis is commonly uti-
lized.17Calf weakness, proprioceptivedeficits, or ataxia
may necessitate long-term use of an o r t h o s i ~ . ~
Moderate to severe spasticity, manifested as exces-
sive plantarflexion prior to heel strike, may require an
aluminum double upright brace with a plantarflexion
stop; concomitant hindfoot varus may require a medial
T-~trap.”.~ Severe
~ spasticity, clonus, or soft tissue
contractures may prevent attempts to control the de-
formity with an orthosis.
Postrecovery Phase
The postrecovery phase is marked by the end of
spontaneous neurologic improvement. Neurologic re-
covery generally plateaus within 6 months for stroke
victims and 18 months for brain injury victim^.^ Addi-
tional spontaneous recovery beyond these periods of
time usually does not occur. However, at this time,
surgical intervention may be considered. Reconstruc-
tive surgery may permit additional functional gains
which would otherwise be unattainable.
ASSESSMENT
Physical Examination
Although the most common site of neurogenic de-
formity is the foot and ankle, the examination must
entail the entire body.” The equinovarus deformity is
usually the most prominent portion of spastic lower
limb involvement. lpsilateral hip and knee limb deform-
ities (and other extremity deformities) may require eval-
uation and management. Careful preoperative planning
is necessary to ensure a reproducible corrective out-
come.
Functional examination of the hypertonic lower ex-
tremity requires assessment of the deformity, its sever-
ity, associated muscle tone, and passive correction of
the deformity. Furthermore, voluntary control of both
selective and synergistic patterned motion should be
342 LAWRENCE AND BOTTE
assessed. Unfortunately, manual muscle testing is dif-
ficult and unreliable in the presence of spasticity.” A
local anesthetic may be injected to temporarily paralyze
spastic or rigid muscles and permit delineation of the
contributions of hypertonus and structural contracture
to the d e f ~ r m i t y . ~ - ’ ~ * ~ ~
Sensory testing is a vital component of the physical
examination. Impairment of tactile sensibility frequently
follows injury to the brain or spinal cord. However,
peripheral nerve injuries may also be present, especially
in patients with prolonged coma.32Loss of protective
sensation on the plantar aspect of the foot is a relative
contraindication for either bracing or joint fusion. Pro-
prioception should also be assessed, since severe im-
pairment may preclude ambulation or necessitate the
use of a total contact orthosis to enhance perception
of limb position through tactile feedback."^^^
Neurosensory Testing
A battery of neurosensory testing is frequently com-
pleted by various therapists or psychologists. These
tests serve to measure cognitive, perceptual, and com-
municative deficits. Impairments such as apraxia, bal-
ance deficits, body neglect, and impulsiveness may be
devastating deterrents to rehabilitative efforts.
Soft Tissue Contractures
Deformity may result from either dynamic influences
or soft tissue contracture. An unrelieved spastic de-
formity will eventually become contra~tual.’~ Contrac-
tures of skin, muscle, neurovascular structures, and
the joint capsule may occur and prevent full intraoper-
ative correction, or necessitate more extensive soft
tissue releases. These “secondary” contractures are
uncommon; however, they may be encountered in se-
verely involved individuals with longstanding, fixed de-
formities.
Osseous and Articular Involvement
Although surgical soft tissue lengthenings and re-
leases are sufficient for the correction of a majority of
recalcitrant deformities, the presence of bony and artic-
ular pathology should be considered. Forms of involve-
ment include (1) premorbid conditions, (2) previously
unrecognized, concomitant skeletal injury, (3) recog-
nized, concomitant skeletal trauma, (4) heterotopic
bone formation,6 and (5) arthrosis of the ankle or sub-
talar joint complex. Arthrosis may result from lack of
adequate cartilage nourishment or pressure-related ne-
crosis secondary to immobilization from spasti~ity.~
Standard radiographs are recommended to ascertain
the presence of these abnormalities.
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Foot & Ankle InternationallVol. 15, No. 6IJune 7 994
GAIT AND DYNAMIC ELECTROMYOGRAPHIC
ANALYSIS
An understanding of the normal phasic activity of
each muscle in stance and swing phases of gait is
necessary before pathologic gait can be analyzed. The
determination and quantification of each spastic struc-
ture’s temporal contribution to the deformity requires
considerable knowledge and expertise. Visual analysis
of the patient’s gait should be undertaken with and
without assistive devices and/or braces.29 This fre-
quently will accentuate deficiencies. The individual com-
ponents of gait, such as cadence, stride length, limb
and joint position, balance, and stability, need to be
analy~ed.~~-~~
Gait analysis studies utilizing video analysis and dy-
namic electromyography performed at motion analysis
centers are helpful to confirm clinical findingsz5 High
speed video analysis permits a detailed computer analy-
sis of the alignment and position of the extremities and
its subsegments in the gait cycle.3oThe findings are
documented by visual and graphic means.
One must realize that spasticity is a dynamic entity.
It may vary with body position, emotional stress, and
painful stimulation. Electromyography (EMG) may
“quantify” spasticity by recording the amplitude and
temporal firing patterns of individual muscles. Further-
more, patterns of pathologic muscle firing can be clas-
sified as being either (1) in phase, (2) out of phase, (3)
continuous, or (4) totally absent.30The temporal firing
pattern of the seven muscles controlling the hindfoot
during the gait cycle can be quantified. Preoperative
dynamic EMGs may permit assessment of muscle ten-
don unit suitability for transfer, since the pattern of
activation is usually constant after transfer proce-
dures?,36
SPASTIC MUSCULAR IMBALANCE
Effects of Spasticity on the Hindfoot
In stroke victims, an equinus deformity is caused by
hyperactive stretch reflexes (often demonstrated by
clonus), an overfiring of the triceps surae, and hyper-
activity of the flexor hallucis longus (FHL) and flexor
digitorum longus (FDL) muscles.13.25-3e Normally, the
gastrocnemius-soleus complex is activated in mid-
stance to control the position of the ankle; however, in
hemiplegia, premature firing is frequently present in
either late swing or at floor c ~ n t a c t .Isolated
~ ~ , ~ ~spastic
involvement of the gastrocnemius or the soleus may be
present; however, both are typically ~ v e r a c t i v e . ~ ~ , ~ ~
Pathologic activity of the tibialis posterior muscle in
hemiplegic limbs has been It may
contribute to hindfoot inversion. Its firing pattern is
Foot & Ankle International/Vol. 15, No. 6IJune 1994
considered too weak or short-lived to be of significant
clinical importance by some investigator^^^.^^; however,
others advocate, in select instances, that transfer or
lengthening is i n d i ~ a t e d . ’ ~ -In
~ ’ general,
*~~ the tibialis
posterior muscle seems to be much less involved in
varus deformity than the tibialis anterior in traumatic
brain and stroke, as compared with cerebral palsy.
Other structures may influence the varus component
of the deformity. In general, the most prominent deform-
ing structure is the tibialis a n t e r i ~ r .Frequently,
~ ~ , ~ ~ it
fires continuously throughout the gait cycle. Further-
more, when spastic involvement of the soleus is pres-
ent, it contributes to both equinus and v a r u ~ . ~The ’ present: (1) the deformity causes significant functional
long toe flexors, especially the FHL, may play a signifi-
cant role in effecting an inverted h i n d f ~ o t .A~clawtoe
~.~~
or curly toe deformity of the hallux and/or lesser toes
may accompany the equinovarus deformity if the con-
tributions of the FHL or FDL are ~ignificant.~’ Finally,
the peroneals, especially the peroneus brevis, are func-
tionally paralyzed and therefore play a passive role in
the hemiplegic foot posturing.25
The pattern of muscle overactivation in traumatic
brain injury frequently mimics those seen in hemiplegia,
despite a more global and multifocal brain injury pattern.
Specifically, in a series of 33 brain injury patients with
severe equinovarus deformities, Keenan and
colleague^'^ noted patterns of involvement recorded
with dynamic EMG showed no significant differences
from those of stroke patient^.'^ Abnormalities of the
activation of the tibialis posterior tendon were noted in
20 patients, silence was found in 10, and normal param-
eters were seen in one patient^.'^ Nevertheless, suc-
cessful surgical correction to a plantigrade position was
afforded without Z-plasty or fractional lengthening of
the tendon.13 In Keenan et al.’s13 series, a split anterior
tibialis tendon transfer (SPLATT) procedure, tendo
achillis lengthening (TAL), and long toe flexor releases
were used successfully in 90% of cases, with no evi-
dence of recurrence at 4-year f~llow-up.’~ Therefore,
as stated before, the role of the tibialis anterior is
probably more significant than the role of the tibialis
posterior muscle in brain injury patients in causing a
equinovarusdeformity. In addition, unwarranted length-
ening of the tendon should be discouraged, since cal-
caneovalgus and painful collapse of the longitudinal
arch may ensue.38
Effects of Spasticity on the Forefoot and Midfoot
The same structures that cause hindfoot imbalance
may, similarly, effect forefoot and midfoot imbalance.
An overactive tibialis posterior may, for example, result
in forefoot adductus. “Weakness” of the peroneus lon-
gus may permit forefoot varus and/or midfoot supina-
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MANAGING EQUINOVARUS FOOT DEFORMITY 343
tion. Finally, spastic extrinsic toe flexors may cause
curly toes or anterior cavus. These associated deform-
ities of the midfoot and forefoot may serve to confirm
the presence and magnitude of these structures’ con-
tribution to hindfoot deformity.
SURGICAL INTERVENTION
Indications
It is estimated that 1 in 10 spastic patients are
suitable candidates for reconstructiveeff orts.12Surgical
correction is indicated when the following criteria are
impairment, (2) rehabilitative efforts and bracing at-
tempts have been unsuccessful, and (3) the period of
spontaneous neurologic recovery has ended.
Surgical Considerations
Classification of the deformity should be undertaken,
since it may dictate surgical management. The severity
of the deformity, presence of unilateral versus bilateral
involvement, level of ambulatory and transfer skills,
cognitive and perceptual deficits, and the medical sta-
tus of the patient assist in determining the type and
extent of surgery. Patient motivation and cooperation
are other considerations. Realistic surgical goals and
the postoperative rehabilitative course must be under-
stood by the patient. Therefore, the goals and expec-
tations of surgery for a severely brain-damaged tetra-
plegic with a longstanding, bilateral equinovarus hind-
foot deformity differ from those of an ambulatory,
brace-dependent hemiplegic.
Surgical Goals
The primary surgical objectives are threefold: (1) to
neutralize hindfoot imbalance, (2) to increase active
function, or (3) a combination of the first two objectives.
While surgical soft tissue corrective releases are un-
dertaken to achieve and maintain a plantigrade position,
tendon transfers are intended to improve function by
providing volitional ankle dorsiflexion.
Specifically, attaining a plantigrade position is crucial
since it may allow the patient to wear normal shoes,
tolerate an orthosis, improve position in a wheelchair,
prevent decubiti, or assist transfer skills and ambula-
t i ~ n . ’ ~ Similarly,
’’~ tendon transfers are intended to
permit ambulation, improve gait patterns, or eliminate
bracing.5-27
Surgical Options
A considerable armamentarium of surgical options
should be available to the surgeon. The main surgical
options include tendon lengthening, tendon releases,
tendon transfers, muscle recessions, bony resection,
344 LAWRENCE AND BOlTE
and arthrodesis. The mainstay of operative correction
at the Ranchos Los Amigos Rehabilitation Center is a
combination of procedures featuring: (1) a percuta-
neous TAL, (2) SPLATT, and (3) long toe flexor re-
leases,18,25.36.38
Tendon Lengthening
A percutaneous triple-cut tenotomy, commonly
termed the Hoke procedure, allows for safe, effective,
Achilles tendon elongation. The 90” rotation of the
Achilles tendon permits this unique hemisection tech-
nique. This percutaneous procedure has been de-
scribed by numerous a ~ t h o r s . ~ Some
~ , ’ ~ form
- ~ ~ of open
Achilles tendon lengthening procedure is necessary
when previous operative procedures have been under-
taken on the Achilles tendon.
Open Achilles lengthenings in the form of a Z-plasty
or fractional lengthening are also possible. Either of
these techniques may be applied to the tibialis posterior
or the Achilles tendon. Fractional lengthening of the
tibialis posterior is undertaken in the retromalleolar
region at the musculotendinousjunction.’6,26Fractional
lengthening of the Achilles tendon is essentially a distal
gastrocnemius muscle recession.
Muscle Recessions
The Achilles tendon is the conjoined tendon of the
gastrocnemius and soleus. Therefore, elongation pro-
cedures of the tendon affect the strength of both the
soleus and gastrocnemius muscle. Isolated gastrocne-
mius lengthening may be undertaken without affecting
the soleus. Muscle lengthening may occur at origin of
the gastrocnemius or at its musculotendinousjunction.
The Strayer procedure permits an isolated distal gas-
trocnemius muscle release followed by proximal reat-
tachment without affecting the length-tension charac-
teristics of the so leu^.^^ Alternately, the Silverskiold
procedure combines the release of both heads of the
gastrocnemius muscle from the femoral condyles with
partial gastrocnemius denervation to weaken the spas-
tic gastrocnemius and correct e q ~ i n u s . ~ ’
Tendon Releases
Tendon releases (transection) are primarily used to
correct forefoot deformities. Curly toe or clawtoe de-
formities may be readily apparent, or, alternately, may
result from extrinsic toe flexor contractures unmasked
by operative hindfoot correction. Recently, the release
of the lumbricales, in addition to the long and short toe
flexors, has been recommended to prevent recurrent
painful toe flexion deformities caused by spastic intrin-
s i c ~The
. ~ release
~ is made through a plantar incision
at the base of each toe.’4-15*26
Although tendon releases
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Foot & Ankle InternationallVol. 15, No. 6IJune 7 994
allow for the theoretic possibility of overcorrection, this
complication has not been evident.”
Tendon Transfers
The reliability and utility of tendon transfer proce-
dures largely result from experience derived from cor-
recting similar deformities in cerebral palsy. The fun-
damental principles of correction are similar in both
subpopulations. The purpose of a tendon transfer is to
correct a dynamic deformity or to restore balance after
release of a fixed deformity.”
The SPLATT procedure appears to be the most
frequently used transfer in equinovarus deformity cor-
rection. The transfer of one half to two thirds of the
anterior tibialis tendon to the cuboid or lateral cuneiform
is designed to restore balance and, possibly, function
to the hindfoot. The transfer, according to Hsu and
Edwards,” is indicated when dynamic EMG demon-
strates: (1) premature firing of the soleus, (2) midstance
firing of the anterior tibialis, and (3) diminished activity
of the peroneus brevis.
The transfer acts to redistribute excessive hindfoot
inversion produced by an overactive anterior tibialis to
the lateral column of the foot, thereby correcting fore-
foot varus and allowing for spontaneous correction of
a flexible varus h i n d f ~ t . ~Although
’ intended to add
volitional dorsiflexion to the ankle, the transfer often
functions as a tenodesis. Regardless, the SPLATT
procedure appears to be a successful, reliable proce-
dure in stroke, brain injury, and spinal cord-injured
It may also permit brace-free am-
patients.’3-’9*25*26.29.38
bulation in individuals previously requiring an external
~ u p p o r t .The
’ ~ ~surgical
~~ technique of the SPLATT has
been well described.” *15-18526938
A second type of split-tendon transfer involves the
tibialis posterior tendon. It is usually combined with a
TAL. The tendon is routed behind the tibia and directed
to the lateral portion of the midfoot or peroneus brevis
tendon.” Successful rebalancing appears to be de-
pendent on “in-phase firing” of the tibialis posterior.”
Although the tendon transfer is used to correct equi-
novarus deformities in children with cerebral palsy,’ it
has not gained widespread acceptance in the correction
of adult equinovarus feet.
Transfer of tendons from the plantar (flexor) surface
to the dorsal (extensor) surface of the foot has also
been attempted to increase dorsiflexor function. These
transfer procedures include the tibialis poste-
rior,28.35-39141
the FHL,25-36.38 and the FDL
Primary considerationsfor transfer include: (1) the mus-
cle is a primary component of the deformity and (2) the
muscle is active in swing phase.36This latter require-
ment facilitates active ankle dorsiflexion and theoreti-
Foor & Ankle In?ernational/Vol. 15, No. 6IJune 1994
cally converts an “out-of-phase’’ muscle to “in phase.”
In general, these “deformity neutralizing procedures”
are frequently combined with other soft tissue and bony
procedures, such as a TAL or triple arthrodesis.
Resection Arthroplasty
Bony resection, in the form of a talectomy, has limited
indications. However, a neglected, nonambulatory, se-
verely impaired patient with bilateral deformities and
bony involvement may be a suitable candidate. Talec-
tomy may also be an effective salvage procedure for
recurrence.
Bony resection allows for correction since it function-
ally lengthens all tendons traversing the hindfoot. A
talectomy may be combined with appropriate tendon
releases or a tibiocalcaneal fusion. The latter permits
precise control of foot alignment and recurrence. Spe-
cific recommendations for talectomy have been de-
scribed by Holmdahl.’o
Arthrodesis
A triple arthrodesis may be indicated in a severe
deformity with ankylosis or deformity of the subtalar
joint complex and deformity such as supination and/or
severe cavus. Modifications of the triple arthrodesis
such as the Lambrinudi may help achieve correction of
hindfoot and midfoot d e f ~ r m i t y . ~
SUMMARY
Management of a spastic equinovarus deformity may
be a challenging undertaking. Persistent deformity that
is resistant to stretching and bracing often requires
surgical correction. The underlying pathomechanics of
the complex deformity is difficult to assess. Gait analy-
sis and dynamic EMG studies should be an integral
part of a complete assessment. Patterns of limb spas-
ticity tend to be similar in traumatic head injury and
stroke patients.
When refractory deformity has not responded to
therapy in a comprehensive rehabilitation program, and
the patient is beyond the period of expected neurologic
recovery, surgical reconstruction should be considered.
The combination of an Achilles tendon release, the
SPLAlT procedure, and release of the long toe flexors,
short toe flexors, and lumbricales appear to provide a
dependable means to afford long-lasting correction of
the acquired, adult, equinovarus foot.
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MANAGING EQUINOVARUS FOOT DEFORMITY 345
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