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VIII THE HAND AND UPPER LIMB
214  Management of the Spastic Hand
CHAPTER 214
Management of the Spastic Hand
ANN VAN HEEST, MD JAMES HOUSE, MD
OVERVIEW OF HAND SPASTICITY
ANALYSIS OF SPASTICITY IN THE HAND
TREATMENT GOALS
SURGICAL PRINCIPLES
Wrist Flexion Deformity
Thumb-in-Palm Deformity
Finger Swan-Neck Deformity
Authors' Preferred Method
COMPLICATIONS AND THEIR MANAGEMENT
OUTCOMES OF TREATMENT
OVERVIEW OF HAND SPASTICITY
Chapter Heading – Management of Spastic Hand
All of these disorders have in common a central nervous system injury causing an upper
motor neuron paresis or palsy. In an upper motor neuron disorder, the normal inhibitory
control of tone is lost, and the resultant peripheral manifestation is spasticity. Muscle
spasticity causes imbalance across joints with resultant loss of function
Hand spasticity is a disorder most commonly seen in association with traumatic
brain injury, cerebral vascular injury, cervical spine injury, and cerebral palsy.
All of these disorders have in common a central nervous system injury causing an upper motor neuron paresis or
palsy. In an upper motor neuron disorder, the normal inhibitory control of tone is lost, and the resultant peripheral
manifestation is spasticity. Muscle spasticity causes imbalance across joints with resultant loss of function. Cerebral
palsy has the added complexity that the central nervous system injury occurs in the perinatal period, so that the
effect of spasticity on the immature skeleton must be considered as well.
In the upper extremity, the typical pattern of spastic joint posturing includes shoulder internal rotation, elbow
flexion, forearm pronation, wrist flexion and ulnar deviation, thumb-in-palm, and finger swan-neck or clenched fist
deformities (Fig. 214-1). Although this pattern of deformity is the most common, the particular pattern and severity
are individual to each patient on the basis of the extent and area of the underlying central nervous system disorder.
Spasticity in the hand does not occur as an isolated problem. Motor involvement can take the form of spasticity
(increased tone), flaccidity (decreased tone), or athetosis (lack of or poor control of tone). The interplay of these
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various types of motor involvement is an important part of defining the problem. In evaluating a particular joint
deformity, several forces often work together to exacerbate the joint deformity (Fig. 214-2). For example, in a wrist
flexion/ulnar deviation deformity, the deformity can be due primarily to spasticity of the flexor carpi ulnaris muscle.
However, weakness or flaccidity of the extensor carpi radialis longus and brevis muscles can exacerbate the wrist
flexion/ulnar deviation deformity because there is no active antagonist (extension/radial deviation) to the spastic
flexor carpi ulnaris (flexor/ulnar deviation). The spasticity of the agonist (in this example, the flexor carpi ulnaris) as
well as the strength and control of the antagonist (in this example, the extensor carpi radialis longus and brevis) must
be assessed to evaluate the problem accurately.
Several disease processes that involve upper motor neuron lesions due to brain dysfunction are considered
together because they have a single final common pathway: spasticity in the hand (Fig. 214-3). Traumatic brain
injury is the most commonly seen in patients younger than 40 years and is typically secondary to motor vehicle
accidents. Major return of function can occur up to 18 months after traumatic brain injury with cognitive
improvements during many years after the injury.1 Cerebral vascular accidents affect 1 in 1000 individuals per year;
spastic hemiplegia is the most common sequela for the surviving patients. This is because the middle cerebral artery
is the most commonly involved vessel, with resultant sensory and motor system dysfunction. Cerebral palsy is most
commonly secondary to ischemic central nervous system injuries occurring in the perinatal period. This is most
commonly associated with low birth weight with prematurity, anoxic events, or cerebral vascular bleeds or emboli.
The incidence is 0.2% (2 children per 1000 live births), increasing to 10% in the premature, low-birth-weight child.
Spasticity of the hand is not the only manifestation of these central nervous system disorders. The pattern of
musculoskeletal spasticity is classified by the limb or limbs involved: monoplegia (one limb), hemiplegia (one arm
and one leg), diplegia (two legs), triplegia (one arm and two legs), and quadriplegia (all four extremities).
All individuals who present with spasticity in the hand need a further evaluation of their central nervous system.
If a child first presents to the hand surgeon, identification is most commonly around 1 year of age because of
delayed development of normal pinch and grasp function. In this scenario, a complete neurologic evaluation is
necessary, including evaluation of the lower extremities, before a diagnosis of cerebral palsy can be made. In most
other scenarios, the hand surgeon is consulted for management of hand spasticity after the initial central nervous
system lesion has been diagnosed. The hand surgeon must continue to work with the rehabilitation physicians and
neurologists, as well as with any physicians who may be involved in lower extremity care, to maintain a
multispecialty approach that appropriately coordinates services for the patient. Associated issues can include mental
retardation, seizures, and speech disorders as well as lower extremity involvement that affects mobility.
In this chapter, the focus is on spastic hemiplegia secondary to cerebral palsy as the most common form of
spasticity of the hand. Similar principles can be applied to other causes of hand spasticity as well.
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ANALYSIS OF SPASTICITY IN THE HAND
Assessment of the patient with spastic cerebral palsy starts with the history and physical examination. Because
cerebral palsy is associated with low birth weight and prematurity, associated medical problems should be noted,
particularly seizures and mental retardation as indicators of more global central nervous system involvement.
Developmental motor delays should be assessed. Children with spastic hemiplegia most commonly will show
premature hand dominance, favoring the unaffected side even as young as 6 months. Delay of normal pinch and
grasp function patterning at 1 year of age is evident. Overall use of the upper extremity should be characterized both
from the history obtained from the parents and by the physician's direct observation. Overall upper extremity
function in cerebral palsy is most commonly classified by a nine-level grading system (Table 214-1). General
categories include the following: does not use; passive assist (poor, fair, or good); active assist (poor, fair, or good);
and spontaneous use (partial or complete). Agreement with the parents on the child's present overall level of limb
function lays the groundwork against which outcome of subsequent treatments can be compared.
Physical examination starts with an observation of the extent to which the individual uses the limb as well as the
child's overall functional abilities. The dynamic positioning of the shoulder, elbow, forearm, wrist, fingers, and
thumb is noted, particularly for grasp and release as well as for pinch function. Age-appropriate tasks or toys that
require two-handed use are helpful in this assessment. The limb is then examined for passive range of motion of the
shoulder, elbow, forearm, wrist, and hand, evaluating for joint contractures. Even if only the wrist and hand are to be
treated, the shoulder, elbow, and forearm need to be assessed because they are essential for the individual to
effectively position the hand in space.
Muscle tone is noted through the passive evaluation of joint mobility. Passive range of motion needs to be done
slowly to overcome muscle spasticity with gentle sustained resistance. Assessment for muscle and joint contracture
is performed by passive mobility of the joint and passive stretch of the muscle. If there is a loss of range of motion at
both the finger and wrist joints unaffected by change in position of the wrist, both muscle and joint contractures are
present. If there is full passive mobility of the joints and muscle, no contracture exists. If there is muscle contracture
without joint contracture, this can be elicited by testing the effect of joint motion on a biarticular muscle such as the
finger flexors. The finger flexor muscles are biarticular muscles, meaning they cross over more than one joint (the
wrist joint and the finger joints). Thus, positioning of the wrist joint in flexion allows full finger extension if there is
no finger joint contracture; but positioning of the wrist joint in extension will not allow full finger extension if there
is finger flexor muscle contracture. This is analogous to the intrinsic tightness test. This is commonly graded as
described by Zancolli (Table 214-2).2
Active range of motion is assessed next, including specific muscle testing for voluntary motor control of
antagonist muscles. This is particularly important for muscles that are considered for tendon transfer, such as the
pronator teres (for pronator teres rerouting); the flexor carpi ulnaris, extensor carpi ulnaris, or brachioradialis (for
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wrist extension); the extensor pollicis longus (for extensor pollicis longus rerouting); and the extensor pollicis brevis
and abductor pollicis longus for control of antagonists to the thumb-in-palm deformity.
Appropriate consultation or multispecialty approach to care should be instituted before surgical intervention is
considered. Several alternatives to surgical intervention exist. Consideration of the treatment pros and cons may
require discussions that include the rehabilitation physicians, neurologists, and neurosurgeons to adequately explore
the options of tone-reducing medications (diazepam, baclofen), tone-reducing injections (botulinum toxin, phenol),
tone-reducing neurosurgery interventions (selective dorsal rhizotomy), and therapy interventions (splinting,
stretching programs). At our institution, a spasticity management team of specialists is involved with evaluation of
the patient for tone-reducing interventions and helps guide the hand surgeon to other treatment alternatives. If a
patient has global problems with tone (most commonly quadriplegics), overall tone control should be obtained with
tone-reducing medications or with selective dorsal rhizotomy, and control is stabilized before hand surgery
intervention. Selective dorsal rhizotomy has been shown in one study3 to have an indirect tone-reducing effect even
in the upper extremity in addition to its primary direct effect in the lower extremity.
If physical examination reveals a joint or muscle contracture, particularly in a hemiplegic patient or in a patient
with isolated problems to the upper extremity, initial treatment includes splinting, stretching, and therapy
interventions. Electrical stimulation of the antagonist muscles has been advocated in the upper extremity of patients
with cerebral palsy, but lasting outcomes and improved function have not been reported. 4 Electrical stimulation has
been shown neither to improve digital extension nor to decrease finger flexor tightness in stroke patients. 5 If joint
positioning due to spasticity significantly compromises limb function, diagnostic and possible therapeutic injections
can be considered. Phenol has been described as a useful diagnostic adjuvant for 3 to 6 months of reduced spasticity
but requires an open procedure to ensure application to the motor nerve. 6,7 It has largely been discontinued at our
institution because of the risk of long-term pain in association with sensory nerve application as well as because of
its unpredictable results. Nerve blocks with local anesthetic agents can be useful diagnostically. For example, in a
stroke patient with minimal hand function but persistent skin breakdown secondary to clenched fist deformity, an
ulnar nerve block at the wrist can help assess whether severe spasticity in the intrinsic muscles of the hand
contributes to the deformity. Another injection modality used more recently is botulinum toxin type A (Botox),
which works by local blockage of the release of acetylcholine at the neuromuscular junction; the reversible action
lasts on average 3 to 4 months. With a reduction of tone in the specific muscles injected with botulinum toxin, a
better assessment of functional control of the antagonist muscles can be performed. Therapy during the period of
reduced tone has been reported to benefit functional use of the hand as well as allowing increased stretch on spastic
muscles.8,9 In the spastic mouse model, muscles have been shown to have a 15% increase in length with stretching
after botulinum toxin type A injections.10 If joint or muscle contracture exists, treatment should begin with splinting
and stretching exercises for at least 6 months, before consideration of surgical intervention.
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If the patient may be a possible candidate for surgical intervention and is not a candidate for the alternative
treatments or if the treatments did not resolve the patient's upper limb dysfunction, the examiner should review the
history and physical examination and answer the following questions to determine the next step in treatment:
 How old is the patient?
Although some series have reported early intervention in tendon transfer surgery, results have been favorable
only in surgeries involving release of severe spastic deforming muscles. A child usually needs to be at least 7 years
of age to consistently cooperate with a preoperative assessment of muscle tone and control as well as with
postoperative therapy protocols imperative to a successful result. Most series report tendon transfer surgeries at ages
averaging 14 years (range, 4 years to adult).
 What is this patient's overall limb function as classified by House? (see Table 214-1)
Surgical intervention has been shown to improve limb function by 2.6 functional levels, particularly for children
with an average baseline functional level of 2 to 3.
 What muscles are spastic and causing joint imbalance leading to limb dysfunction?
The spastic muscles may need to be released or weakened by lengthening.
 What muscles are flaccid or have poor motor control, leading to joint imbalance with resultant limb
dysfunction?
The flaccid or poorly controlled muscles need to be augmented, usually through tendon transfer.
 What muscles are under good voluntary control and are available for tendon transfer?
The muscles with good voluntary control are best for good results with tendon transfer.
 Is there significant athetosis or incoordination?
In general, athetosis is associated with poor results after surgical intervention. Surgical treatment in the athetoid
patient is rarely performed and usually would only involve joint stabilizations, such as fusion of the
metacarpophalangeal joint of the thumb in the face of dislocation or subluxation.
TREATMENT GOALS
Treatment of the hand dysfunction centers on improving muscle balance to maximize hand function consistent
with the quality of voluntary control retained. The primary lesion in the brain is not treated and remains the limiting
factor to the success of the surgery. The goal is not normalization of hand use but rather improvement of joint
positioning to maximize assistive hand function. Surgical treatment is indicated for patients with spastic deformity
and contractures, unresponsive to nonsurgical treatment, that produce specific functional impairment and could be
improved by better joint positioning.
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SURGICAL PRINCIPLES
Surgical procedures to satisfy these treatment goals follow specific surgical principles (Table 214-3) to be
described as they apply to wrist flexion deformity, thumb-in-palm deformity, and finger swan-neck deformity. A
vast array of options exist for the surgeon treating the wrist, thumb, and fingers and a constellation of associated
deformities (Table 214-4). This requires the surgeon to carefully think through the type of deformity at each joint
separately and then synthesize them into a comprehensive reconstructive plan. If evaluation of the upper limb
revealed significant shoulder, elbow, or forearm deformity that precludes appropriate positioning of the limb in
space, treatment of these joint deformities should be included as part of the overall treatment plan. Because this is
beyond the scope of this text, the reader is referred to other sources if this situation is present. 2,11,12
Wrist Flexion Deformity
1. Release or lengthen the spastic muscle or muscles:
 Fractional lengthening of the flexor carpi ulnaris or flexor carpi radialis
 Flexor pronator slide
Most patients with hemiplegia have significant wrist flexion deformity, often accompanied by ulnar deviation. If
the wrist flexion deformity is mild and wrist extensor control exists, weakening the wrist flexors through fractional
lengthening may be sufficient. The wrist flexors can also be effectively lengthened by moving their origin distally, a
procedure termed a flexor pronator slide.13,14 This is particularly effective if there is concomitant finger flexor and
pronator tightness because the common origin of all of these muscles is released and allowed to move distally during
this procedure.
2. Augment the weak or flaccid muscle (tendon transfers):
 Brachioradialis to extensor carpi radialis brevis
 Extensor carpi ulnaris to extensor carpi radialis brevis
 Flexor carpi ulnaris to extensor carpi radialis brevis
 Flexor carpi ulnaris to extensor digitorum communis (if finger extension is inadequate)
In some cases, the wrist flexion deformity is more severe, and the principal wrist extensor muscles are not
functional. This may be evident on physical examination, or it may require use of a diagnostic motor nerve block or
a diagnostic botulinum toxin injection to temporarily weaken the spastic wrist flexor, most commonly the flexor
carpi ulnaris, to assess the patient's cortical control for wrist extension. Muscles that can be transferred to augment
wrist extension include the brachioradialis, extensor carpi ulnaris, and flexor carpi ulnaris (Green transfer). 15-17 Use
of the brachioradialis or extensor carpi ulnaris has the advantage of leaving both flexors intact (although they may
need to be concomitantly lengthened to diminish their spastic deforming force), thus minimizing the risk of
overcorrection. Use of the extensor carpi ulnaris has the advantage of diminishing the ulnar deviation forces as well
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for patients with concomitant ulnar deviation deformity. Use of the flexor carpi ulnaris to remove its effect as a
spastic wrist flexor and to transfer its force as a wrist extensor is reserved for the most severe cases.
In all cases of transfer into the wrist extensors, the finger function must be assessed preoperatively with the wrist
maintained in a neutral position. As mentioned, the finger flexor muscles are biarticular muscles so that changes in
the wrist position may change finger tone and function; this needs to be evaluated preoperatively. If the finger
flexors are so shortened that a clenched fist deformity ensues when the wrist is brought into extension, the finger
flexors will need to be fractionally lengthened as part of the surgical procedure. If the patient does not have
sufficient finger extensor control to extend the fingers (release) with the wrist in flexion, a transfer of one of these
muscles into the finger extensors (extensor digitorum communis) may be indicated. If the patient does not have
sufficient digital control or has too much tone with the wrist in an extended position, a tendon transfer into the wrist
extensors may result in an "extensor habitus" that will diminish, rather than help, grasp and release function.
Balance of the wrist is the goal, and it is important to recognize that wrist flexion facilitates finger extension by the
tenodesis effect.
3. Stabilize the joint for severe instability or contracture:
 Proximal row carpectomy
 Wrist fusion
If the patient has a severe wrist joint contracture limiting functional use of the hand refractory to at least 6 months
of nonsurgical intervention, consideration can be given to either a proximal row carpectomy, to shorten the skeleton,
or a wrist fusion, to hold the wrist in a fixed position. The proximal row carpectomy is used in combination with
releases and tendon transfer surgeries if the wrist lacks sufficient mobility passively; shortening the skeleton through
proximal row carpectomy can improve the wrist flexion deformity by 30 or 40 degrees of extension. This may be
useful in selected cases if the wrist is fixed in 10 to 20 degrees of flexion and the surgeon wishes to preserve wrist
motion to maintain the tenodesis effect. Wrist fusion has the advantage of being a predictable procedure in which the
wrist is positioned and fixed intraoperatively. It is indicated only for improved cosmesis and use of the hand as a
paperweight, in the skeletally mature individual, although it is possible to fuse the wrist in the skeletally immature
patient if care is taken to remove only cartilaginous surfaces. The proximal carpal row may be removed as part of
the wrist fusion procedure to allow some relaxation of the flexors and to facilitate positioning into slight wrist
extension. The finger position must be addressed as in tendon transfer surgery (described earlier).
Thumb-in-Palm Deformity
1. Release or lengthen the spastic muscle or muscles:
 Adductor pollicis
 Flexor pollicis brevis
 Flexor pollicis longus
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If the primary deformity is adduction of the first metacarpal, without significant metacarpophalangeal or
interphalangeal joint deformity, the primary deforming force is the adductor pollicis. Treatment includes a partial
tenotomy or myotomy near its insertion (often in conjunction with a first web Z-plasty for individuals with
concomitant skin contracture) or a release of its origin off the third metacarpal as described by Matev. 18
If the primary deformity is adduction of the first metacarpal with metacarpophalangeal joint flexion deformity,
without significant interphalangeal joint deformity, the primary deforming forces are the adductor pollicis and the
flexor pollicis brevis. Treatment includes a surgical release of the adductor, through either a first web Z-plasty or a
palmer incision as described before, with the release of the flexor pollicis brevis through the same incision.
If the primary deformity is adduction of the first metacarpal with both metacarpophalangeal and interphalangeal
joint flexion deformity, the primary deforming forces are the adductor pollicis, the flexor pollicis brevis, and the
flexor pollicis longus. Treatment includes a surgical release of the adductor and flexor pollicis brevis, as described
before, as well as a lengthening of the flexor pollicis longus through a separate volar incision. Depending on the
degree of contracture, either a fractional lengthening at the musculotendinous level (for the less severely contracted)
or a Z-lengthening of the tendon (for the more severely contracted) may be performed.
2. Augment the weak or flaccid muscle (tendon transfers):
 Donors: brachioradialis, flexor carpi radialis (if flexor carpi ulnaris is not transferred), palmaris longus, flexor
digitorum superficialis
 Recipients: abductor pollicis longus, extensor pollicis brevis (if metacarpophalangeal joint is stable), extensor
pollicis longus
 Rerouting: extensor pollicis longus
For the milder deformity with antagonists present, the surgical releases (adductor, flexor pollicis brevis, flexor
pollicis longus) alone are sufficient. For the more severe deformity without antagonists present, the surgical releases
need to be augmented by tendon transfers. Tendons to be transferred can be the brachioradialis, flexor carpi radialis,
palmaris longus, or flexor digitorum superficialis. The choice of donor tendon is primarily based on the synthesis of
the entire reconstructive plan, noting particularly that use of the flexor carpi radialis tendon is contraindicated if the
flexor carpi ulnaris is used as a wrist extension tendon transfer. The recipient tendon most commonly chosen is the
abductor pollicis longus because this augments first metacarpal abduction. Transfer into the extensor pollicis brevis
is contraindicated if the metacarpophalangeal joint is unstable (type III thumb). Rerouting of the extensor pollicis
longus tendon is used commonly, particularly if the patient has good control of the interphalangeal joint extension.19
The extensor pollicis longus is transferred from the third dorsal compartment into the first dorsal compartment, thus
changing its vector from extension/adduction of the thumb to extension/abduction of the thumb.
3. Stabilize the joint in the presence of severe instability or contracture:
 Metacarpophalangeal joint fusion or volar capsulodesis
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 Interphalangeal joint fusion
If the primary deformity of the thumb is one of first metacarpal adduction with secondary metacarpophalangeal
hyperextension deformity (subluxation or dislocation), the metacarpophalangeal joint will need to be stabilized to
provide an adequate base for pinch function. The metacarpophalangeal joint can be stabilized by a volar
capsulodesis as described by Filler et al20 or by fusion.10 In the skeletally immature individual, a fusion can be
performed if the epiphysis of the proximal phalanx is significantly ossified; the distal end of the metacarpal is fused
to the proximal phalanx epiphysis by use of smooth K-wires with careful technique protecting the proximal phalanx
physis to preserve longitudinal growth. Another combination available, particularly for the patient with severe flexor
pollicis longus spasticity and interphalangeal joint flexion deformity, includes release of the flexor pollicis longus
tendon at its insertion, transfer onto the radial aspect of the thumb (palmar abduction), and fusion of the
interphalangeal joint for stabilization.21
Finger Swan-Neck Deformity
1. Release or lengthen the spastic muscle or muscles:
 Intrinsic slide
 Ulnar motor neurectomy
For patients with mild swan-neck deformity secondary to intrinsic spasticity, an intrinsic slide procedure has been
described to lengthen these muscles by use of two dorsal incisions to elevate and slide the interossei origins. For
patients with concomitant thumb adductor spasticity, a diagnostic injection of the motor branch of the ulnar nerve
with local anesthetic or phenol can be used to assess its effect on both thumb-in-palm and intrinsic spasticity
disorders. If the results are favorable, an ulnar motor neurectomy can be performed just distal to Guyon canal.
2. Augment the weak or flaccid muscle (tendon transfers):
 Lateral band rerouting
Swan-neck deformities are due to subluxation of the lateral band dorsal to the axis of rotation of the proximal
interphalangeal joint.22 This deformity can be corrected dynamically through transfer of the lateral band volar to the
proximal interphalangeal joint axis, into the proximal interphalangeal volar plate by a midlateral incision as
described by Tonkin.23,24 This procedure is indicated for patients with moderate swan-neck deformities, usually 30
to 40 degrees of hyperextension, causing locking of the joint with grasp.
3. Stabilize the joint for severe instability or contracture:
 Flexor digitorum superficialis tenodesis of the proximal interphalangeal joint
For more severe swan-neck deformity, tenodesis of the proximal interphalangeal joint can be performed through
a volar incision. A distally based slip of the flexor digitorum superficialis tendon is secured into the volar aspect of
the proximal phalanx as described by Swanson.25
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Authors' Preferred Method
This example describes the authors' preferred methods of evaluation, treatment, surgical technique, and
postoperative care. Note that the joints can be evaluated separately for treatment options, with a final reconstructive
treatment plan synthesizing the complexities of the entire upper limb deformity.
A 10-year-old child presents with a wrist flexion/ulnar deviation and thumb-in-palm deformity interfering with
her grasp-release and pinch function. She uses her hand as a poor passive assist. On passive range of motion, she has
no evidence of muscle or joint contracture. On active range of motion, she demonstrates severe spasticity of the
flexor carpi ulnaris with no extensor carpi radialis brevis or longus activity notable on examination. On observation
of grasp and release, she can use the hand only passively by placing objects into the hand to hold because her wrist
is dynamically in such a severely flexed position. She has good digital control in flexion and extension. Her thumbin-palm posture is secondary to isolated adduction of the first metacarpal with metacarpophalangeal joint
hyperextension deformity. Her thumb adducts across the palm of the hand so that the thumb sits between the index
and long finger. She demonstrates good voluntary control of her extensor pollicis longus but not of her extensor
pollicis brevis or abductor pollicis longus.
She was considered a possible surgical candidate for the following reasons. She is old enough to cooperate in her
examination (10 years old). She has overall limb function graded as a "poor passive assist." She has spastic
imbalance leading to joint deformity that limits function—the wrist flexion/ulnar deviation posturing limits her
grasp and release function, and the thumb-in-palm posturing limits her pinch function.
At her thumb, the adductor is spastic, the extensor pollicis brevis and abductor pollicis longus are poorly
controlled, and the metacarpophalangeal joint is unstable. By application of the surgical principles outlined before,
we recommended
1. a partial adductor pollicis tenotomy (to weaken the spastic muscle);
2. a tendon transfer into the abductor pollicis longus tendon (to augment the weak muscle); note that a tendon
transfer into the extensor pollicis brevis will only exacerbate the metacarpophalangeal hyperextension deformity,
and so it should not be performed; and
3. a volar metacarpophalangeal joint capsulodesis (to stabilize the severely unstable joint).
Similarly at her wrist, the flexor carpi ulnaris is spastic, the extensor carpi radialis brevis/longus is poorly
controlled, and the wrist joint is subtle. Diagnostic testing would be performed by injection of botulinum toxin into
the flexor carpi ulnaris to better test voluntary control of the extensor carpi radialis brevis/longus as an antagonist to
the flexor carpi ulnaris muscle when it is less spastic. If findings indicate that the patient has no extensor carpi
radialis brevis/longus control despite diminished flexor carpi ulnaris spasticity, on application of the surgical
principles outlined before we would recommend
1. fractional lengthening of the flexor carpi ulnaris (to weaken the spastic muscle);
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2. a tendon transfer into the extensor carpi radialis brevis; and
3. no joint stabilizations necessary.
Available tendon transfers could include brachioradialis to the abductor pollicis longus for thumb abduction
(appropriate vector and strength) and extensor carpi ulnaris to extensor carpi radialis brevis. Transfer of the extensor
carpi ulnaris would help correct the ulnar deviation deformity by removing the ulnar deviation forces of the extensor
carpi ulnaris, and it would help augment wrist extension by tensioning the transfer so that the wrist lay in neutral at
rest.
Surgery is carried out in conjunction with the lower extremity surgeons, who removed plates placed as part of her
previous lower extremity reconstruction. A tourniquet is used intraoperatively after appropriate preparation and
draping.
The wrist is approached first through a curvilinear ulnar-sided incision. The extensor carpi ulnaris tendon is
divided just distal to the extensor retinaculum and delivered into the proximal end of the wound by freeing its fascial
attachments. Its excursion is checked; usually, approximately 3 to 4 cm indicates adequate excursion. A
subcutaneous tunnel is created to a second dorsal incision made over the second dorsal compartment just proximal to
the extensor retinaculum. In the interval distal to the thumb outcropper muscles (abductor pollicis longus and
extensor pollicis brevis) but proximal to the extensor retinaculum, a fascial window is made, and the tendons of the
extensor carpi radialis longus and brevis are identified. These tendons are usually fairly adherent because they are
not under good cortical control and have not had much differential excursion. If this is found, the extensor carpi
ulnaris will be transferred into both to prevent unnecessary dissection and subsequent adhesions.
Attention is now turned to the tendon transfer for the thumb. Through the radiodorsal wrist incision, the extensor
pollicis brevis and abductor pollicis longus are identified. It is verified that tension on the extensor pollicis brevis
tendon exacerbates the metacarpophalangeal hyperextension deformity, so this tendon is left in place. It is verified
that tension on the abductor pollicis longus tendon abducts the first ray. The brachioradialis tendon is then dissected
off into insertion onto the radial metaphysis, through the same incision; it is freed from its fascial insertions by
extensive proximal dissection, verifying 2 to 3 cm of excursion.
Attention is now turned to release of the thumb adductor. The Matev palmer incision is made, using the distal
portion of an extended carpal tunnel incision. The recurrent motor branch of the median nerve is identified and
protected, as well as the palmar arch. The origin of the transverse head of the adductor pollicis muscle is then
released off the third metacarpal while the deep ulnar nerve passing through the muscle near its origin is protected.
Any fascial bands are released until the muscle origin is seen to "slide" radially as the thumb is brought into
abduction.
Attention is now turned to the metacarpophalangeal capsulodesis. A radial midlateral incision is then made with
dissection carried down onto the metacarpophalangeal joint. A radial midlateral capsulotomy is performed. The
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volar capsule is identified and usually found to be significantly attenuated off its volar metacarpal origin. The
sesamoid bones are identified and denuded, with a corresponding area on the metacarpal neck area denuded as well.
Bone suture anchors or drill holes through bone are then placed in the volar metacarpal neck with nonabsorbable
suture placed through the sesamoid bones or adjacent volar plate. Tying the suture should bring the
metacarpophalangeal joint into approximately 30 degrees of flexion. Slight force on the repair may allow the neutral
position; assessment is made to verify that hyperlaxity or excessive flexion is not present. The metacarpophalangeal
joint is pinned with a 0.045-inch K-wire to protect the repair.
Attention is now turned to sewing in and tensioning the tendon transfers, starting first with the most proximal
joint. The extensor carpi ulnaris transfer is woven three times by a Pulvertaft weave through the extensor carpi
radialis brevis and longus tendons. A test suture for tensioning is placed and adjusted until the wrist sits at rest in
neutral. Final nonabsorbable 3-0 suture is placed. The brachioradialis tendon is then woven end-to-end into the
abductor pollicis longus tendon. Because of the significant size mismatch, use of Pulvertaft weaves of the abductor
pollicis longus into the brachioradialis is usually most effective. A test suture for tensioning is placed and adjusted
until the thumb sits in slight abduction with the wrist at neutral, in full abduction with the wrist in flexion, and in key
pinch with the wrist in full extension. Final nonabsorbable 2-0 suture is placed. Because the brachioradialis is also
biarticular, crossing both the elbow and wrist joints, the effect of elbow position is checked; it should help with
thumb abduction as the elbow extends (e.g., reaching out for an object) and allow key pinch with elbow flexion.
Standard postoperative management includes long-arm cast immobilization (to protect the brachioradialis
transfer) in slight wrist extension/radial deviation (to protect the extensor carpi ulnaris transfer and stretch the flexor
carpi ulnaris lengthening) with the first metacarpal in extension/abduction (to protect the thumb transfer and stretch
the adductor pollicis lengthening) and pinning of the metacarpophalangeal joint in approximately 20 degrees of
flexion (to protect the metacarpophalangeal joint capsulodesis). For tendon transfers alone, 4 weeks of complete
protection is sufficient; however, in this case, 6 weeks of complete protection is necessary to allow
metacarpophalangeal joint healing. After 4 to 6 weeks of immobilization, the transfers are protected in a similar
position in a forearm-based splint, with active range of motion and light activities of daily living (showers, eating)
with the splint off three to five times per day. At 8 to 10 weeks after surgery, the splint is worn only at night and
for protection during high-risk activities (recess, gym, play), and strengthening exercises commence.
COMPLICATIONS AND THEIR MANAGEMENT
Balance is the key, and it can be difficult to obtain. Overcorrection is due to excessively tight tendon transfers or
excessive release (instead of lengthening) of spastic muscles and should be avoided through careful preoperative
planning and attention to surgical technique. A key surgical principle is to leave an option to reverse the surgical
correction if this is possible. Undercorrection occurs in the circumstances of release without concomitant tendon
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transfer, insufficient release, and undertensioned tendon transfers. If the initial procedure has resulted in
undercorrection of the deformity, undercorrection is easier to manage with a subsequent additional procedure to
obtain balance.
Recurrence can develop with skeletal growth,26 but it is rare in our experience if balance is achieved at the time
of surgery. Arthrodesis cannot be reversed, but "balance" or wrist position is set definitively at the time of surgery
without risk of overcorrection or undercorrection. Wrist arthrodesis risks loss of function if adequate assessment of
digital control is not considered as the tenodesis effect of the wrist is lost. Wrist arthrodesis should be reserved for
those with the lowest level of limb function.
Lack of improved function despite better position can be due to the underlying limitations of the surgery, namely,
central nervous system dysfunction and lack of selective voluntary control. These surgical corrections do not change
the primary etiology (i.e., the defective central nervous system), so overall surgical results will never yield a
"normal" limb. However, even better position without improved function is often a significant improvement from
the patient's perspective because the limb will look more "normal" even if does not function as normal. Sensibility is
also important, particularly as a predictor of spontaneous active use of the hand.
OUTCOMES OF TREATMENT
It is difficult to assess outcome as a measure of surgical results by use of functional measures such as range of
motion, grip strength, or standardized testing because patients with spastic hand deformities have such varying
levels of functional use, varying degrees of central nervous system involvement, and varying pictures of spasticity.
By the House Upper Extremity Functional Use Classification (see Table 214-1), House et al27 reported at least one
functional grade of improvement with surgical treatment of thumb-in-palm deformities. In another review of all
upper extremity surgical procedures, Van Heest and House 28 reported an average improvement of 2.6 functional
levels for individuals with an average preoperative use of fair passive assist (level 2). Patients with fair to good
voluntary control had the greatest functional improvement.
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FIGURE 214-1.
Typical spastic hemiplegic posturing in the upper extremity includes shoulder internal rotation,
elbow flexion, forearm pronation, wrist flexion and ulnar deviation, thumb-in-palm, and
clenched fist deformities.
FIGURE 214-2.
A, Normal anatomy of proximal interphalangeal joint extensors in the dorsal and lateral view.
The extrinsic finger extensors (EDC, EDQ, EIP) divide over the proximal phalanx to form the
central slip and two lateral bands. The finger intrinsics are the interossei and the lumbricals. The
intrinsics join the extrinsic lateral band to form the conjoined lateral band, commonly referred to
as the lateral band. In the normal state, dorsal subluxation of the lateral band is prevented by the
volar tethering effect of the transverse retinacular ligament. B, Muscle imbalance causing joint
deformity. Joint deformity occurs secondary to muscle imbalance. In the wrist joint, the wrist
extensors are often flaccid with poor rotational control, whereas the wrist flexors are often
spastic, causing wrist flexion deformity.
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FIGURE 214-3.
Sequence of events leading to limb dysfunction. Surgical treatment can address joint deformity
and dysfunction at the shoulder, elbow, forearm, wrist, thumb, and fingers.