In the normal forearm, coordinated motion at the proximal and distal radioulnar joints allows the radius to rotate or “pivot” about the ulna, producing 80° of protonation and supination. The biceps and supinator muscles are responsible for forearm supination, while forearm protonation is achieved via the pronator teres (PT) and pronator quadratus. The wrist joint consists of the midcarpal and radiocarpal joints, the latter being an ellipsoid joint that permits overall wrist motion through 75° of flexion and extension, 15° of radial deviation, and 40° of ulnar deviation. The primary wrist flexors are the flexor carpi radialis (FCR), palmaris longus (PL), and flexor carpi ulnaris (FCU) muscles, while the primary wrist extensors are extensor carpi ulnaris (ECU), extensor carpi radialis longus (ECRL), and extensor carpi radialis brevis (ECRB) muscles. However, a total of 24 tendons cross or insert at the wrist, all of which may affect wrist ROM and produce a variety of deformities in the spastic upper extremity.

The characteristic forearm and wrist spastic deformities are excessive forearm protonation and wrist flexion. Supinator muscle spasticity may also be present, which can be unmasked by correction of the forearm protonation deformity. Wrist extensor paresis or paralysis can contribute to wrist flexion deformity and should be considered in surgical planning.

While forearm protonation deformity is addressed with interventions that target the PT and PQ muscles, correcting a wrist flexion deformity may require interventions to the FCR, PL, FCU, ECRB/L, flexor digitorum superficialis (FDS), flexor digitorum profundus (FDP), flexor pollicis longus (FPL), and/or the radiocarpal joint. ^,, When correcting a wrist flexion deformity, it is important to appreciate the biomechanical ramifications of each intervention in the context of the patient’s existing function and functional goals. For example, hyperflexion at the wrist reduces the resting length of finger flexor muscles, thus impairing grip strength in patients with volitional control. ^,, Therefore, interventions that lengthen the primary wrist flexors are expected to improve grip strength. However, in patients with myostatic contracture of the finger flexor muscles, addressing the wrist flexors in isolation may produce a clenched-fist deformity and inhibit the patient’s functional capacity, and create new hand hygiene issues. Similarly, in patients who rely on tenodesis for grip, procedures to address wrist flexion deformity should aim to preserve or enhance the patient’s capacity for wrist flexion and extension. As such, the surgical plan must be individualized based on the patient’s deformity, abilities, and shared treatment goals.

In patients with preserved active forearm rotation, a spastic protonation deformity may be treated with PT lengthening, flexor-pronator (F-P) proximal release, or PT rerouting. The condition of both the pronator and supinator muscles is used to inform surgical decision-making. In patients with myostatic contracture of the F-P muscle groups, an F-P proximal release can simultaneously address both forearm protonation and wrist flexion deformity, particularly when the involved spastic muscles exhibit significant contractures. ^,, The procedure involves elevating the PT, FCR, PL, FDS, and FCU from their origin at the medial epicondyle.

Where the supinator muscle is paretic or paralyzed, PT rerouting may be used to address forearm protonation deformity both by decreasing protonation forces and restoring supination. However, substantial passive forearm supination ROM and volitional control of the PT is necessary for rerouting to restore forearm supination. Additionally, overcorrection into a supination deformity can occur. As such, this procedure is typically performed in children, albeit cautiously, who typically have less muscle and joint contractures with preserved PT motor activation. ^,

More commonly, increased tone or contracture in the PT is addressed with tendon lengthening. This procedure is performed through a longitudinal incision in the volar-proximal forearm that exposes the pronator teres myotendinous and tendinous portion deep to the radial artery and adjacent to the brachioradialis muscle. Either a z-lengthening or a fractional lengthening of the PT is then performed.

In a study of 18 patients treated with F-P proximal release, Braun and colleagues observed a significant improvement in forearm protonation deformity when a distal muscle advancement of 2.5 to 4.5 cm was achieved. However, 4 patients developed supination deformity as a complication of their release. Supination deformity was associated with F-P muscle advancement of 5 cm or more. Similarly, Inglis and Cooper reported correction of forearm protonation deformity in 18 patients with spastic protonation deformity who underwent F-P release, with no recurrence.

Correction of forearm protonation deformity with PT rerouting has also yielded favorable results. ^, In their study of 22 patients with cerebral palsy who underwent pronator teres rerouting, Sakellarides and colleagues reported that 82% had a good to excellent result, with an average of 46° degrees of active supination gained as compared with the preoperative range of motion. Using a modified version of the surgical approach described by Sakellarides, Strecker and colleagues performed 42 PT rerouting procedures in 41 children with cerebral palsy. The authors reported an average gain in supination of 78° and no surgical complications after a mean follow-up of 21 months.

In patients without volitional control of the forearm, pronator teres z-lengthening is used to correct forearm protonation deformity. Pronator teres tenotomy is not recommended due to the risk of unmasking or creating a supination deformity.

Wrist flexion deformity is addressed in conjunction with finger flexion deformities since the extrinsic finger flexors span the wrist and can contribute to the wrist deformity. In patients with volitional control, the contributions of the FCR, PL, and FCU to wrist flexion deformity are treated with either F-P proximal release or individual tendon lengthening. F-P origin release, as previously described, permits distal migration of the muscles without denervating or transecting the muscle. This shortens the resting length of the muscle, thereby decreasing its force of contraction, modulates spasticity by decreasing afferent signals to suppress the overactive spinal reflex, yet does not eliminate function.

In a study of 9 patients with spastic hemiplegia after cerebrovascular accident, F-P proximal release resulted in a mean increase in active wrist extension by 65° (range, 30° to 120°). More recently, Thevenin-Lemoine and colleagues reported improvement in wrist extension and global hand function after F-P proximal release in 50 patients (54 wrists) with UMN injury. At an average follow-up of 26 months, the mean gain in wrist extension with the fingers fully extended was 67° (range, −10° to 110°), and hand function increased significantly as compared with preoperatively. However, the authors noted partial recurrence of wrist flexion deformity in 22% of this population.

Alternatively, spasticity in one or both of FCR and FCU may be treated with z-lengthening or fractional lengthening, and PL spasticity treated with tenotomy. The choice of lengthening procedure depends on the “useful zone” of the individual muscle’s myotendinous junction, which is defined as the extent of muscle-tendon overlap available for effective and safe fractional lengthening, where a greater length or “useful zone” has less risk for rupturing the muscle-tendon unit. If the myotendinous junction “useful zone” is narrow or short with more than 1 to 2.5 cm of lengthening required to correct the wrist flexion deformity, z-lengthening should be considered. ^,, Lengthening procedures are performed through a volar forearm incision through which the spastic and/or contracture muscle tendons are exposed and identified ( Fig. 1 ). Based on the contribution of each wrist flexor to the deformity and the magnitude of contracture, z-lengthening is employed over fractional lengthening if greater correction or length is required.

Volar forearm incision to expose the pronators, wrist, and finger flexors. A curvilinear incision can be utilized to expose the myotendinous junctions and tendons of the wrist and finger flexors. Note the more proximal longitudinal incision to expose the pronator teres myotendinous junction.

In a study by Keenan and colleagues, the authors reported improved hand function in 91% and increased use of the upper extremity in 77% of 22 patients with spasticity who underwent Z-lengthening of the FCR and FCU tendons, fractional lengthening of the FDS and FDP, and tenotomy of the PL tendon. While no complications were observed in this population after a mean follow-up of 33 months, lengthening procedures have been associated with under-correction of deformity, as well as muscle-tendon rupture with subsequent loss of grip strength. ^,,

In certain cases, the FCU or the ECU can be utilized to correct the flexed wrist posture and restore active wrist extension. ^,,, The FCU produces wrist flexion and ulnar deviation deformities. Releasing the FCU from its insertion on the pisiform removes its contribution to both the flexion and ulnar deviation postures. However, if volitional FCU control is present, it can be routed around the subcutaneous border of the ulna and transferred to the ECRB to restore active wrist extension and correct the excessive ulnar deviation by recentering or centralizing the wrist extensor. Thometz and colleagues reported on 25 patients with cerebral palsy who underwent the FCU to ECRL or ECRB transfer at a mean age of 8 years. At a mean follow-up of 8.7 months, the mean active wrist motion was a 44.2° extension and a 19.0° flexion. Due to the added supination force afforded by the transfer, mean active supination was 40.2° and protonation was 53.4°. The authors noted that the outcomes were excellent in 6, good in 9, fair in 5, and poor in 5 patients. Poor results were often due to the development of a forearm supination and wrist extension deformity.

With chronic flexion posture of the wrist, the ECU can volarly subluxate or dislocate due to attenuation of the 6th extensor compartment, and produce a primary wrist flexion posture without excessive ulnar deviation. An unstable ECU can paradoxically cause wrist flexion during attempted active wrist extension. Thus, releasing the ECU from its insertion onto the 5th metacarpal base and transferring it to the ECRB can recentralize the wrist extensors and restore active wrist extension if volitional control of the ECU is present ( Fig. 2 A, B ).

( A , B ) ECU to ECRB transfer. The ECU [ red arrow ] can contribute to a flexed wrist and/or ulnarly deviated posture. The ECU can be released from its insertion on the 5th metacarpal and re-routed or transferred to the ECRB to restore wrist extension. ECRB, extensor carpi radialis brevis; ECU, extensor carpi ulnaris.

For spastic flexed wrist deformities in patients without meaningful motor control, isolated FCR, PL, and FCU tenotomies are not recommended in isolation as they create an imbalance toward a wrist extension deformity. To produce a stable wrist in the neutral position, once the spastic or contracted wrist and finger flexors have been corrected, paralyzed wrist extensors such as the ECRL/ECRB can be tenodesed or anchored to the distal radius to serve as a tether to maintain the wrist in a neutral position while preserving some limited passive motion at the radiocarpal joint. Similarly, a non-functional FCU or ECU can be transferred to the ECRL/ECRB as a static transfer or tether to produce a stable, neutral wrist.

However, in cases of severe wrist flexion deformities that cannot be corrected with muscle-tendon lengthening, tendon transfer, or tenodesis, total wrist arthrodesis remains a viable option. This is particularly useful when severe soft tissue contracture, radiocarpal remodeling, and/or wrist arthritis are present; in such cases, proximal row carpectomy and wrist arthrodesis may be necessary. ^, Excising the proximal carpal row decreases the tension on the extrinsic finger flexors, which can aid in the correction of a concomitant clenched-fist deformity. Although seemingly morbid and extensive, obtaining a neutral and stable wrist is paramount to correcting concomitant spastic hand deformities.

The biomechanics of the hand are arguably the most complex in the human body. A delicate balance of intrinsic and extrinsic finger flexor relative to extensor muscles acting across the carpometacarpal (CMC), metacarpophalangeal (MCP), and interphalangeal (IP) joints permits normal hand movement and posture. The actions of these muscles are influenced by static constraints such as the ligaments and joint capsules, which may attenuate, rupture, or contract, impacting hand function. Given the complex constellation of anatomic influences, it is unsurprising that several distinct hand deformities may be seen in patients with UMN injuries. Most frequently, the spastic hand presents with a so-called “clenched-fist” and “thumb-in-palm” (TIP) deformities. ^,

Clenched-fist deformity occurs due to a mechanical imbalance created by extrinsic finger flexor spasticity and/or contracture, extrinsic finger extensor weakness and/or paralysis, or both. The result is a flexed posture at the MCP and IP joints, which can markedly limit function. Poor palmar sensation, difficulty with nail trimming, and skin maceration create an environment conducive to ulceration and infection. Therefore, the overarching goal of muscle- and tendon-based procedures to address spastic hand deformities is to improve the resting posture of the digits.

To preserve extrinsic finger flexion in patients with a clenched-fist deformity, spasticity of the FDS and FDP can be addressed with fractional lengthening, z-lengthening, or F-P origin release. Extrinsic finger flexor spasticity can be effectively treated with fractional or z-lengthening through the utilitarian volar distal forearm exposure that was previously described to expose the wrist flexor muscles and tendons (see Fig. 1 ). Individual fractional or z-lengthening can be performed for the more superficial FDS muscles based on the amount of correction required. Correction or lengthening that can be achieved with fractional lengthening is dependent upon the capacity of muscle lengthening, which is a combination of the “useful zone,” described earlier, and the magnitude of contracture within the muscle ( Fig. 3 A, B ). The FDP to the fingers have a shared muscle, while the index finger FDP often is a single and separate muscle; thus, the FDP to the fingers are ideally lengthened with a more global or whole muscle-tendon unit fractional lengthening (see Fig. 3 ).

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