Mathes & Hentz, 2/e, ISBN 0-7216-8811-X Chapter 214 (edited file)—"Management of the Spastic Hand" 4／5／2018, Page 1 of 16, 3 Figure(s), 4 Table(s), 0 Box(es)

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 Mathes & Hentz, 2/e, ISBN 0-7216-8811-X Chapter 214 (edited file)—"Management of the Spastic Hand" 4／5／2018, Page 2 of 16, 3 Figure(s), 4 Table(s), 0 Box(es)

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. Mathes & Hentz, 2/e, ISBN 0-7216-8811-X Chapter 214 (edited file)—"Management of the Spastic Hand" 4／5／2018, Page 3 of 16, 3 Figure(s), 4 Table(s), 0 Box(es)

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 Mathes & Hentz, 2/e, ISBN 0-7216-8811-X Chapter 214 (edited file)—"Management of the Spastic Hand" 4／5／2018, Page 4 of 16, 3 Figure(s), 4 Table(s), 0 Box(es)

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. Mathes & Hentz, 2/e, ISBN 0-7216-8811-X Chapter 214 (edited file)—"Management of the Spastic Hand" 4／5／2018, Page 5 of 16, 3 Figure(s), 4 Table(s), 0 Box(es)

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. Mathes & Hentz, 2/e, ISBN 0-7216-8811-X Chapter 214 (edited file)—"Management of the Spastic Hand" 4／5／2018, Page 6 of 16, 3 Figure(s), 4 Table(s), 0 Box(es)

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 Mathes & Hentz, 2/e, ISBN 0-7216-8811-X Chapter 214 (edited file)—"Management of the Spastic Hand" 4／5／2018, Page 7 of 16, 3 Figure(s), 4 Table(s), 0 Box(es)

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 Mathes & Hentz, 2/e, ISBN 0-7216-8811-X Chapter 214 (edited file)—"Management of the Spastic Hand" 4／5／2018, Page 8 of 16, 3 Figure(s), 4 Table(s), 0 Box(es)

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 Mathes & Hentz, 2/e, ISBN 0-7216-8811-X Chapter 214 (edited file)—"Management of the Spastic Hand" 4／5／2018, Page 9 of 16, 3 Figure(s), 4 Table(s), 0 Box(es)

 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 Mathes & Hentz, 2/e, ISBN 0-7216-8811-X Chapter 214 (edited file)—"Management of the Spastic Hand" 4／5／2018, Page 10 of 16, 3 Figure(s), 4 Table(s), 0 Box(es)

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 thumb- in-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); Mathes & Hentz, 2/e, ISBN 0-7216-8811-X Chapter 214 (edited file)—"Management of the Spastic Hand" 4／5／2018, Page 11 of 16, 3 Figure(s), 4 Table(s), 0 Box(es)

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 Mathes & Hentz, 2/e, ISBN 0-7216-8811-X Chapter 214 (edited file)—"Management of the Spastic Hand" 4／5／2018, Page 12 of 16, 3 Figure(s), 4 Table(s), 0 Box(es)

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 Mathes & Hentz, 2/e, ISBN 0-7216-8811-X Chapter 214 (edited file)—"Management of the Spastic Hand" 4／5／2018, Page 13 of 16, 3 Figure(s), 4 Table(s), 0 Box(es)

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 House28 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.

REFERENCES 1. Teasdale G, Skene A, Parker L, Jennett B: Age and outcome of severe head injury. Acta Neurochir Suppl Wien 1979;28:140-143. 2. Zancolli EA, Zancolli ERJ: Surgical management of the hemiplegic spastic hand in cerebral palsy. Surg Clin North Am 1981;61:395. 3. Loewen P, Steinbok P, Holsti L, MacKay M: Upper extremity performance and self-care skill changes in children with spastic cerebral palsy following selective posterior rhizotomy. Pediatr Neurosurg 1998;29:191-198. Mathes & Hentz, 2/e, ISBN 0-7216-8811-X Chapter 214 (edited file)—"Management of the Spastic Hand" 4／5／2018, Page 14 of 16, 3 Figure(s), 4 Table(s), 0 Box(es)

4. Carmick J: Clinical use of neuromuscular electrical stimulation for children with cerebral palsy. Part II: upper extremity. Phys Ther 1993;73:514-527. 5. Hines AE, Crago PE, Villian C: Functional electrical stimulation for reduction of spasticity in the hemiplegic hand. Biomed Sci Instrum 1993;29:259-266. 6. Keenan MAE, Thomas E, Stone L: Percutaneous phenol block of musculocutaneous deformity in cerebral palsy. J Bone Joint Surg Am 1990;15:236. 7. Braun RM, Hoffer MM, Mooney V, et al: Phenol nerve block in the treatment of acquired spastic hemiplegia in the upper limb. J Bone Joint Surg Am 1973;55:580-585. 8. Wall SA, Chait LA, Temlett JA, et al: Botulinum A chemodenervation: a new modality in cerebral palsied hands. Br J Plast Surg 1993;46:703. 9. Van Heest AE: Applications of botulinum toxin in orthopaedics and upper extremity surgery. Techniques Hand Upper Extremity Surg 1997;1:27-34. 10. Goldner JL, Koman LA, Gelberman R, et al: Arthrodesis of the metacarpophalangeal joint of the thumb in children and adults: adjunctive treatment of thumb-in-palm deformity in cerebral palsy. Clin Orthop 1990;253:75-89. 11. Manske PR, Strecker WB: Cerebral palsy, stroke, brain injury. In Peimer CA, ed. Surgery of the Hand and Upper Extremity. New York, McGraw-Hill, 1995:1517. 12. Waters PM, Van Heest A: Spastic hemiplegia of the upper extremity in children. Hand Clin 1998;14:119-134. 13. Inglis AE, Cooper W: Release of the flexor-pronator origin for flexion deformities of the hand and wrist in spastic paralysis. J Bone Joint Surg Am 1966;48:847-857. 14. White WF: Flexor muscle slide in the spastic hand: the Max Page operation. J Bone Joint Surg Br 1972;54:453-459. 15. House JH, Gwathmey FW: Flexor carpi ulnaris and the brachioradialis as a wrist extension transfer in cerebral palsy. Minn Med 1978;61:481-484. 16. McCue FC, Honner R, Chapman WC: Transfer of the brachioradialis for hands deformed by cerebral palsy. J Bone Joint Surg Am 1970;52:1171-1180. 17. Green WT: Tendon transplantation of the flexor carpi ulnaris for pronation-flexion deformity of the wrist. Surg Gynecol Obstet 1942;75:337-342. 18. Matev I: Surgical treatment of spastic "thumb-in-palm" deformity. J Bone Joint Surg Br 1963;45:703-708. 19. Manske PR: Redirection of extensor pollicis longus in the treatment of spastic thumb-in-palm deformity. J Hand Surg Am 1985;10:553. 20. Filler BC, Stark HH, Boyes JH: Capsulodesis of the metacarpophalangeal joint of the thumb in children with cerebral palsy. J Bone Joint Surg Am 1976;58:667-670. 21. Smith RJ: Flexor pollicis longus abductor-platy for spastic thumb-in-palm deformity. J Hand Surg Am 1982;7:327. 22. Littler JW: The finger extensor mechanism. Surg Clin North Am 1967;47:415-432. Mathes & Hentz, 2/e, ISBN 0-7216-8811-X Chapter 214 (edited file)—"Management of the Spastic Hand" 4／5／2018, Page 15 of 16, 3 Figure(s), 4 Table(s), 0 Box(es)

23. Van Heest A: Lateral band re-routing in the treatment of swan-neck deformities due to cerebral palsy. Techniques Hand Upper Extremity Surg 1997;1:*** 24. Tonkin MA, Hughes J, Smith KL: Lateral band translocation for swan-neck deformity. J Hand Surg Am 1992;17:260-267. 25. Swanson AB: Surgery of the hand in cerebral palsy and the swan neck deformity. J Bone Joint Surg Am 1960;42:951-964. 26. Thometz JG, Tachdjian MO: Long-term follow-up of the flexor carpi ulnaris transfer in spastic hemiplegic children. J Pediatr Orthop 1988;8:407. 27. House J, Gwathmey F, Fidler M: A dynamic approach to the thumb-in-palm deformity in cerebral palsy. J Bone Joint Surg Am 1981;63:216-225. 28. Van Heest AE, House JH, Cariello C: Upper extremity surgical treatment of cerebral palsy. J Hand Surgery Am 1999;24:323-330. 29. Mital MA: Lengthening of the elbow flexors in cerebral palsy. J Bone Joint Surg Am 1979;61:515-522. 30. Strecker WB, Emanuel JP, Dailey L, Manske PR: Comparison of pronator tenotomy and pronator rerouting in children with spastic cerebral palsy. J Hand Surg Am 1988;13:540-543. 31. Zancolli EA: Structural and Dynamic Bases of Hand Surgery, 2nd ed. Philadelphia, JB Lippincott, 1968. 32. Sakellarides HT, Mital MA, Lenzi WD: Treatment of pronation contractures of the forearm in cerebral palsy by changing the insertion of the pronator radii teres. J Bone Joint Surg Am 1981;63:645-652. 33. Green WT, Banks HH: Flexor carpi ulnaris transplant and its use in cerebral palsy. J Bone Joint Surg Am 1962;44:1343-4352. 34. Omer GE, Capen DA: Proximal row carpectomy with muscle transfers for spastic paralysis. J Hand Surg Am 1976;1:197-204. 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. Mathes & Hentz, 2/e, ISBN 0-7216-8811-X Chapter 214 (edited file)—"Management of the Spastic Hand" 4／5／2018, Page 16 of 16, 3 Figure(s), 4 Table(s), 0 Box(es)

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.