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Biomechanical and anatomical consequences of carpal tunnel release
Clinical Biomechanics 18 (2003) 685–693 www.elsevier.com/locate/clinbiomech
Review
Biomechanical and anatomical consequences of carpal tunnel release Jeffrey J. Brooks, Jonathan R. Schiller, Scott D. Allen, Edward Akelman
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Department of Orthopaedics and Division of Engineering, Rhode Island Hospital/Brown University School of Medicine, 593 Eddy Street, Providence, RI 02905, USA Received 26 February 2003; accepted 5 March 2003
Abstract Carpal tunnel syndrome is an exceedingly common orthopaedic problem in the United States. When conservative management is unsuccessful, most surgeons proceed to surgical treatment. Though the carpal tunnel release procedure is usually curative, many patients experience postoperative complications, such as scar sensitivity, pillar pain, recurrent symptoms, and grip weakness, regardless of whether the release was done through an open, mini-open, or endoscopic approach. The exact causes of these and other complications of carpal tunnel release remain unclear. Release of the carpal tunnel has an effect on carpal anatomy and biomechanics, including an increase in carpal arch width, carpal tunnel volume, and changes in muscle and tendon mechanics. We set out to review the morphological and biomechanical changes caused by carpal tunnel release with the goal of better understanding the root causes of postoperative complications. This article first reviews normal carpal tunnel anatomy and anatomic variations, then available surgical techniques for carpal tunnel release, and finally the literature on morphologic, physiologic and biomechanical alterations in the wrist after carpal tunnel release. Ó 2003 Elsevier Ltd. All rights reserved.
1. Introduction and clinical significance Carpal tunnel syndrome is one of the most common orthopedic conditions, with an estimated incidence of nearly 1% annually in the United States (Einhorn and Leddy, 1996), which translates into almost 2.8 million new cases per year. If conservative therapy fails, surgical release of the carpal tunnel is the preferred method of treatment. Though the majority of patients have relief of symptoms postoperatively, there are still a significant number of patients who experience disabling postoperative symptoms. Disabling loss of grip strength and pillar pain may be a result of anatomical or biomechanical alterations caused by carpal tunnel release (Gartsman et al., 1986; Ludlow et al., 1997). This article will review normal carpal tunnel anatomy and anatomic variations. The available surgical techniques for carpal tunnel release are reviewed. Finally, the literature on morphologic, physiologic, and biomechanical alterations in the wrist after carpal tunnel release will be summarized. An appreciation of these changes may improve the surgical and postoperative
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Corresponding author. E-mail address: [email protected] (E. Akelman).
0268-0033/$ - see front matter Ó 2003 Elsevier Ltd. All rights reserved. doi:10.1016/S0268-0033(03)00052-4
management of carpal tunnel syndrome and subsequent treatment of poor postoperative outcomes.
2. Anatomy The carpal bones and intercarpal ligaments at its medial, lateral, and posterior borders form the carpal tunnel. The anterior border is formed by the transverse carpal ligament and flexor retinaculum (Hoppenfeld Sd, 1984; Tanabe and Okutsu, 1997). The terms ‘‘flexor retinaculum’’ and ‘‘transverse carpal ligament’’ have been considered synonyms, however, Cobb et al. demonstrated that they are distinct structures (Cobb et al., 1993). The flexor retinaculum as a whole can be divided into three parts from proximal to distal. The antebrachial fascia forms the proximal part of the flexor retinaculum. A superficial fascial layer is inseparable from the thickened deep investing antebrachial fascia, which is anterior to the median nerve and continuous with the transverse carpal ligament distally. The two layers separate to enclose the flexor carpi radialis tendon radially and the contents of GuyonÕs canal and the flexor carpi ulnaris tendon ulnarly. Thus, the deep investing antebrachial fascia at this level is volar to the contents of the carpal tunnel and dorsal to GuyonÕs canal (Fig. 1)
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Fig. 1. Schematic illustration of the three parts of the flexor retinaculum (FR). D: The distal part is the aponeurosis from which the thenar and hypothenar muscles take origin. M: The middle part, or the transverse carpal ligament proper, also gives origin to the thenar and hypothenar muslces. P: The proximal part of the flexor retinaculum, courses deep to the flexor carpi ulnaris (FCU) and flexor carpi radialis (FCR) tendons.
(Cobb et al., 1993). The transverse carpal ligament proper represents the middle third of the flexor retinaculum and forms the palmar ‘‘roof’’ of the carpal tunnel. It inserts into the scaphoid tuberosity and ridge of the trapezium radially and the hamulus and pisiform ulnarly where it is narrowest between the hamate hook and trapezial ridge (Fig. 2). The distal third is the aponeurosis between the thenar and hypothenar muscles, from which these muscles originate. Tanabe maintains that the distal part of the flexor retinaculum described by Cobb is actually separated from the transverse carpal ligament by a layer of adipose tissue (Tanabe and Okutsu, 1997). The proximal to distal extent of the transverse carpal ligament proper runs from the level of the distal pisiform proximally (11 mm distal to the capitate–lunate joint) to the meta-diaphyseal junction of the third metacarpal distally (10 mm distal to the carpometacarpal joint of the long finger). The thickness of the flexor retinaculum over the carpal tunnel is 10 times that of the antebrachial fascia (Cobb et al., 1993). Contained within the carpal tunnel are the median nerve and the nine extrinsic flexor tendons of the thumb and fingers (flexor pollicis longus tendon, four flexor digitorum superficialis tendons, and four flexor digitorum profundus tendons). The median nerve normally divides into six branches at the distal end of the flexor retinaculum––the recurrent motor branch, three proper digital nerves and two common digital nerves. The motor branch of the median nerve usually innervates the thenar muscles and the index and middle finger lumbricals. Sensory branches usually innervate the thumb, index, middle, and radial half of the ring fingers. Lanz classified variations of median nerve anatomy in the carpal tunnel
Fig. 2. (a) Palmar and (b) axial views of the transverse carpal ligamne (TCL). (a) The three bands of the TCL are illustrated with their bony attachments. H ¼ hamate hook, P ¼ pisiform, T ¼ trapezium, S ¼ scaphoid.
into four groups. Division of the motor branch can be extraligamentous, subligamentous, transligamentous, supraligamentous, or can originate from the ulnar border of the median nerve. Furthermore, the motor branch may arise in the forearm, or may be separated by the persistent median artery or an aberrant muscle only to join distal to the transverse carpal ligament (Lanz, 1977). The transverse carpal ligament is that part of the flexor retinaculum in the mid-third that has bone-tobone attachments. The middle third is the transverse carpal ligament proper. The distal part is the aponeurosis between the thenar and hypothenar muscles, from which these muscles originate. It has been hypothesized that median nerve compression most likely occurs in wrist flexion at the proximal edge of the transverse carpal ligament where it joins the deep investing fascia of the forearm, the anatomic explanation for PhalenÕs sign (1996). Alternately, the median nerve may be compressed where the carpal tunnel is narrowest at the level of the hook of the hamate by either synovial hypertrophy or a space-occupying lesion (Cobb et al., 1993). Additionally, imaging studies of median nerve motion during wrist flexion have demonstrated that patients with carpal tunnel syndrome are more likely than normal patients to have
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limited median nerve motion in the carpal canal. The nerve in normal patients moved radially and posteriorly to a position interposed between the flexor tendons during wrist flexion. The nerve in patients with carpal tunnel syndrome was more likely to remain in position at the flexor retinaculum. The limited motion of the nerve in these cases may predispose the nerve to compression during wrist flexion leading to carpal tunnel symptoms (Allmann et al., 1997). Another study on patients with non-specific forearm pain associated with median nerve compression found that patients experiencing pain were more likely to have decreased median nerve motion during wrist flexion (Greening et al., 1999).
3. Carpal tunnel anatomic variations Phalen originally reported on his 17-year experience in 1966, suggesting that thickening of the flexor synovium was the most common direct cause of median nerve compression and carpal tunnel syndrome in his patients (Phalen, 1996). Tanzer, however, noted three of 21 patients with cystic masses in the carpal tunnel and seven of these 21 hands had various congenital anomalies (Tanzer, 1959). Singer retrospectively looked for anatomic variations in 147 hands undergoing carpal tunnel release via an extended exposure (Singer and Ashworth, 2001). The authors noted anatomic variations in 60 hands (41% of hands), one-third of which had anatomic variations intrinsic to the carpal tunnel. The intrinsic variations included anomalous lumbrical origins in nine hands (6%), which could crowd the carpal tunnel during grip and finger flexion, most commonly the long finger lumbrical. Siegel found that proximal lumbrical origin and/or lumbrical hypertrophy could cause median nerve compression by a space-occupying effect (Siegel et al., 1995). Cobb confirmed that lumbrical excision would reduce carpal tunnel pressure during simulated grip in cadavera (Cobb et al., 1995). Singer noted a flexor digitorum superficialis muscle belly present in six of 147 hands (4%) of patients undergoing carpal tunnel release (Singer and Ashworth, 2001). These variants may not likely be appreciated during limited-exposure carpal tunnel release.
4. Pressure changes and mechanism of relief after carpal tunnel release When considering complete release of the carpal tunnel, one must consider the relevant anatomy (Tanabe and Okutsu, 1997; Cobb et al., 1993); neglecting to release the distal part of the flexor retinaculum or the proximal part described above may fail to completely relieve pressure on the median nerve or may result in
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failure of surgery to relieve symptoms of carpal tunnel syndrome (Tanabe and Okutsu, 1997; Phalen, 1996; Cobb and Cooney, 1994). Tanabe noted that release of only the transverse carpal ligament caused the edges of the cut ligament to spread apart by 1.3 0.2 mm but that complete release of both the transverse carpal ligament and the distal aponeurosis between the thenar and hypothenar muscles caused more than 6.6 0.2 mm of separation of the transverse carpal ligament edges and a corresponding significant decrease in carpal tunnel pressure (Tanabe and Okutsu, 1997; Okutsu et al., 1996). Okutsu et al. did an elegant study in 1989 in which carpal tunnel pressures were measured in multiple positions through an endoscopically placed catheter inside the carpal tunnel of patients under local anesthesia (Okutsu et al., 1989). In patients without carpal tunnel syndrome the normal carpal tunnel pressure at rest was 14.3 10 mmHg. In patients with carpal tunnel syndrome, pressure in the carpal tunnel averaged 43.0 17.2 mmHg preoperatively in the resting position, and 206.2 51.6 mmHg with active grip. With passive flexion and extension the pressures were 191.9 64 and 222.4 44.2 mmHg, respectively. This represents a fivefold increase in pressure during grip or extremes of motion in patients with carpal tunnel syndrome. In contrast, immediately postoperatively the pressures were 6.2 5.5 mmHg in the resting position, and 88 65 mmHg with active grip, pressures in other positions were similarly decreased, documenting clearly the physiologic effect of carpal tunnel release. The pressure in GuyonÕs canal decreases after endoscopic or open carpal tunnel release. In a study by Ablove et al. (1996), the authors studied 20 patients with documented carpal tunnel syndrome. GuyonÕs canal pressures decreased from 12.7 7.1 to 4.2 4.6 mmHg after carpal tunnel release alone. This is consistent with a previous study noting that 90% of patients with both median and ulnar compressive neuropathies at the wrist have relief of the ulnar nerve symptoms after isolated carpal tunnel release (Silver et al., 1985).
5. Surgical techniques To serve as background for understanding the biomechanical and anatomic changes after different types of carpal tunnel release, a brief review is presented here. A thorough review of the methods for carpal tunnel release and their pros and cons is beyond the scope of this paper. 5.1. Open release Since the first carpal tunnel surgery in 1924 by Herbert Galloway, numerous advances have been made to
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refine this very common procedure (Amadio, 1995). In general, carpal tunnel release can be performed using open or endoscopic procedures. The classic open and limited-open carpal tunnel release techniques involve complete division of the transverse carpal ligament and the deep fascia of the forearm under direct visualization (Green et al., 1999). The lesser level of difficulty and shortened operative time make the open release the procedure of choice with numerous hand surgeons. In the majority of patients, open release techniques lead to symptomatic relief with a low complication rate. However, scar tenderness and grip weakness may occur after open release. In order to minimize these postoperative complications, a limited transverse incision (2.0 cm or less) is made in the same location as the classic open release, but ends approximately 1 cm distal to the distal wrist crease. Carpal tunnel release through a limited open incision was performed by Atik et al. (2001) without damage to any neurovascular structures, and when performed from distal to proximal allowed for precise identification of structures at risk of injury (the superficial palmar arch, third common digital nerve, and aberrant motor branches of the median nerve) and improves the safety of carpal tunnel release. 5.2. Endoscopic release In an attempt to reduce postoperative morbidity, endoscopic techniques were developed and have been evolving since the late 1980s. The Agee single portal and Chow two portal carpal tunnel release utilize smaller incisions and require less dissection of the subcutaneous tissue and structures overlying the transverse carpal ligament. However, since these are endoscopic procedures, visibility may be limited and incomplete release of the transverse carpal ligament, nerve injury (median, ulnar, digital, palmar cutaneous branch of the median nerve), arterial injury (ulnar, superficial palmar arch), hematoma, and flexor tendon injury have been reported (Lee et al., 1992; Van Heest et al., 1995; Rowland and Kleinert, 1994). With endoscopic release techniques, there may be less scar tenderness, and proponents suggest an earlier return to work and activities of daily living compared to the open procedure. Trumble published a prospective, randomized, multicenter trial comparing endoscopic versus open release. The endoscopic group had a more rapid improvement in strength and scar tenderness than the open group in the first three months after surgery. However, at one year follow-up there was no difference in patient satisfaction between the endoscopic and open release (Trumble et al., 2002). Brown et al. (1993) in a prospective, randomized trial of 145 patients found no significant difference in patient satisfaction and symptom relief between the two portal endoscopic and the classic open release at 84 days postoperatively. Additionally, no significant difference in sensibility, thenar
weakness or atrophy, and pillar pain was found between the groups. Scar tenderness was similar for both procedures at three weeks postoperatively, but differed significantly at week 11 with 61% of the open patients complaining of mild to severe tenderness. The endoscopic group returned to work around day 14, as opposed to day 28 for the open group. Both open and endoscopic carpal tunnel release are effective for relieving symptoms, however, endoscopic release of the transverse carpal ligament may shorten the recovery time, permitting an earlier return to work and resumption of activities of daily living.
6. Potential biomechanical complications of carpal tunnel release Generally reported complications of carpal tunnel release include incomplete release, neuropraxia or injury to the median or ulnar nerve, and inadvertent entrance into GuyonÕs canal, injury to digital nerves, the ulnar artery and the superficial palmar arch (Lee et al., 1992; Seiler et al., 1992). However, there exist several biomechanical changes after carpal tunnel release, which may be considered ‘‘complications’’, not merely ‘‘expected’’ postoperative, changes. The phenomenon of pillar pain is a frequent complication reported after both open and endoscopic surgical techniques with an incidence between 6% and 36% (Katz et al., 1995; Mirza et al., 1995). Division of the transverse carpal ligament through open or endoscopic techniques may lead to an increase in carpal arch width and carpal tunnel volume (Fig. 3), both of which may be responsible for postoperative pillar pain, and may also cause changes in other intercarpal articulations (Fisk, 1984; Fuss and Wagner, 1996; Kiritsis and Kline, 1995; Seradge and Seradge, 1989; Garcia-Elias et al., 1989a). ‘‘Pillar pain’’ can delay return to work and resumption of activities of daily living, foster emotional distress, increase cost to the health care system, and potentiate loss of grip strength (Seradge and Seradge, 1989). Pillar pain has been characterized as pain or tenderness in the thenar or hypothenar eminence, or radial and ulnar tenderness, and has been reported to subside by the third postoperative month (Ludlow et al., 1997). Pain most commonly originates in the piso-triquetral joint, possibly due to alteration of the forces over the joint and/or displacement of the pisiform after releasing the transverse carpal ligament (Seradge and Seradge, 1989). The etiology of pillar pain remains uncertain. There is currently no evidence that carpal tunnel release causes changes in the piso-triquetral articulation, although GuyonÕs canal does dramatically change in shape after carpal tunnel release (Richman et al., 1989). Current work has suggested four potential etiologies for pillar pain: muscular or ligamentous, neurogenic,
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1989; Garcia-Elias et al., 1989b). Thus, division of this ligament could alter the normal function of the wrist and contribute to such postoperative complications as pillar pain and grip weakness. 7.1. Carpal stiffness
Fig. 3. (a) The carpal arch width depicted on an axial view of the carpal tunnel (H ¼ hamulus, P ¼ pisifrom, T ¼ trapezium, S ¼ scaphoid). (b) Carpal tunnel volume (dark area) and the contents of the carpal tunnel––The tendons of the flexor digitorum profundus, flexor digitorum superficialis, flexor pollicis longus, and the the median nerve. The ulnar artery and nerve and the flexor carpi radialis tendon are shown for orientation.
edematous, and alteration of the carpal arch structure (Ludlow et al., 1997). Muscular or ligamentous causes of pillar pain may be related to relaxation of the intrinsic muscles of opposition and pinch with sectioning of the transverse carpal ligament, and subsequent migration of the transverse carpal ligament toward its osseous origins (Hunter, 1991). Cutaneous nerve branches in the palmar and subcutaneous tissue may be injured when incising in the ‘‘critical pillar rectangle’’, which was defined by Wilson as the wrist flexion crease proximally, 1 cm distal to the hook of hamate, ulnar border of the hamate ulnarly, and the scaphoid tubercle radially (Wilson, 1994). Postoperative edema superficial to the transverse carpal ligament may also cause pain in the thenar or hypothenar areas. Resolution of this swelling is usually coincident with relief of pillar pain (Green et al., 1999).
7. Biomechanical change after carpal tunnel release A number of studies have examined the effect of dividing the transverse carpal ligament on the carpal arch. The transverse carpal ligament has been shown to serve three functions: anchor thenar and hypothenar musculature, provide transverse stability to the carpus, and act as a pulley for the flexor tendons (Seradge and Seradge,
Carpal stiffness is obtained by differentiating strain energy with respect to displacement of centroids of adjacent rigid bodies. By applying a dorsopalmar compressive load, a calculated displacement force on adjacent carpal bones can be described. Dorsopalmar compression tests when the flexor retinaculum has been sectioned demonstrate that carpal stiffness decreased by an average of 7.8% (232–214 N/mm), indicating that the flexor retinaculum plays a minor role in transverse stability of the carpus and should be regarded as a pulley for the flexor tendons rather than an intercarpal stabilizer (Garcia-Elias et al., 1989b). The transverse intercarpal ligaments, especially the capito-hamate ligament, are essential in providing stability to the carpal tunnel, since their division in the presence of an intact flexor retinaculum leads to dorsopalmar compressive instability of the carpus under applied stress. 7.2. Muscular and tendon effects Fuss and Wagner dissected five fresh frozen forearms and hands to demonstrate muscle attachments to the flexor retinaculum prior to studying joint mechanics before and after carpal tunnel release. Bisection of the flexor retinaculum caused certain muscles to lose their anatomic attachments due to muscular pull shifted distally and radially or ulnarly (Fuss and Wagner, 1996). Muscle shortening occurred in the superficial head of the flexor pollicis brevis 25% (relative to rest length), the ulnar part of the abductor pollicis brevis 20% (opposition and adduction), the opponens pollicis 20%, and the opponens digiti minimi 10%. This causes a loss of muscle length leading to a loss of muscle strength. Additionally, release of the transverse carpal ligament may disrupt the alignment and tracking of the piso-triquetral joint causing pain (Seradge and Seradge, 1989). This piso-triquetral tracking or alignment problem could be a possible etiology of pillar pain. Another change noted by many authors is that the flexor tendons in the carpal tunnel displace palmarward after carpal tunnel release (Amadio, 1995). The transverse carpal ligament has been suggested as an important pulley in the flexor tendon system that prevents bowstringing. Division of the transverse carpal ligament through an open, limited open, or endoscopic release, may significantly increase flexor tendon excursion during wrist flexion. Increased excursion, or the distance the tendon travels relative to the jointÕs center of rotation, is noted after 20–30° wrist flexion (Kiritsis and Kline, 1995).
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Thus, as the distance increases between the tendon and the center of rotation in the wrist joint due to bowstringing, the distance the tendon travels with changing wrist position increases. The palmar displacement of the flexor tendons with wrist flexion could be another potential cause of postoperative wrist flexion weakness, and potentially reinforces the need for a short period of immobilization to allow sufficient time for intrinsic reconstitution of the transverse carpal ligament, although splinting after carpal tunnel release has not been proven beneficial (Bury et al., 1995). Conversely, functional gripping activities and maximum grip strength are accomplished with the wrist in an extended position, thus palmar displacement of the flexor tendons during wrist flexion is unlikely clinically significant.
8. Morphologic changes following carpal tunnel release 8.1. Carpal arch and carpal tunnel volume Cobb et al. (1993) determined normal carpal tunnel dimensions by injecting contrast material into the carpal tunnel and examining antero-posterior (AP) radiographs. On the AP view, the carpal tunnel is shaped like an hourglass (Fig. 4), with the narrowest part at the level of the hook of the hamate. The mean width of the carpal tunnel was 25 1.2 mm proximally, 20 1.2 mm at the hook of the hamate, and 25 1.5 mm at its distal extent, a significant difference ðP < 0:0001Þ. This is an important feature to note, as it is of utmost importance when measuring carpal arch width pre and postcarpal tunnel release––if axial slices are at different proximal–distal
Fig. 4. The carpal tunnel is hourglass-shaped, with the narrowest portion located between the hook of the hamate and trapezial ridge.
levels of the carpal tunnel significant error could be introduced into the measurements of carpal arch width. The transverse carpal ligament normally attaches on the pisiform, hook of the hamate, scaphoid and trapezium, maintaining a concavity to the carpal arch and carpal tunnel. When this ligament is divided, the concave arch flattens and the distance between the carpal insertions increases. Fisk demonstrated an average increase of 3 mm between the scaphoid and pisiform after carpal tunnel release (Fisk, 1984). Garcia-Elias measured the width of the carpal arch using the trapezio-hook of hamate distance before and after transverse carpal ligament release. When the ligament was intact, the distance decreased between these two bones in both wrist flexion and extension. However, when the transverse carpal ligament was released, the distance significantly increased an average of 11% (Garcia-Elias et al., 1992). Gartsman et al. (1986) did a retrospective review of patients who had undergone open carpal tunnel release and either had standardized carpal tunnel view radiographs taken before and after the procedure was done, or a radiograph of the unoperated side was used as a control. In this study, the lack of preoperative assessment of the operative wrist is the major criticism. The carpal arch width was measured between the palmar tips of the trapezial ridge and hook of the hamate with the wrist extended 50°. Range of motion did not change significantly after carpal tunnel release using the opposite side as a control. Of 50 operated wrists, 47 had widening of the carpal arch width and three had no change, ranging from 0% to 52% widening with an average widening of 13.6%, or 2.9 mm. The range of increase in absolute widening of the carpal arch was 0–8.5 mm. However, the authors did not examine variability or repeatability of measurements. This study differs from others in that it found a greater magnitude of arch widening after carpal tunnel release, perhaps because of the wrist position (50° extension) being different from wrist position in other studies using magnetic resonance imaging (MRI) or computed tomography (CT) in neutral or only slight extension positions. Gartsman found that an increase in carpal arch width greater than 20% over control correlated with a statistically significant decrease in grip strength of 25.85%. Patients with greater widening did not have an increased incidence of postoperative wrist pain. ‘‘Columnar pain’’ did not correlate with arch widening either. In 1992, Viegas et al. (1992) examined carpal tunnel radiographs before and after endoscopic carpal tunnel release using the same technique for measurement and radiographic documentation as Gartsman et al. The authors noted an increase of 1.7 mm (7% increase) in carpal arch width 10 days after surgery. In contrast to GartsmanÕs findings, most patients had an increase in arch width of 0–10%, with very few wrists increasing
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more than 20% in arch width postoperatively. One might conclude from comparing ViegasÕ and GartsmanÕs studies that fewer patients would be expected to have impaired grip after endoscopic carpal tunnel release compared with open carpal tunnel release, since fewer of the wrists in the former group had increases in arch width of more than 10%. In 1987 Richman et al. (1987) introduced MRI as a means of evaluating carpal tunnel volume. The study determined that there was no significant difference between MRI and direct cadaveric measurements of carpal tunnel volume (with a silicone injection technique) and carpal arch width (measured using calipers accurate to 0.5 mm), using a standard protocol for direct measurements on cadavera and MRI data from cadaver wrists. This indicated excellent intra and inter-observer reliability of this MRI measurement technique, and excellent reproduction by MRI of true direct measurements of volume and width of the carpal tunnel. Two years later, Richman examined the effect of open carpal tunnel release on carpal canal volume, carpal arch width, and position of the canal contents in 15 wrists assessed by MRI (Richman et al., 1989). Carpal canal volume in treated hands increased from 6.3 1.0 to 7.8 1.5 ml after surgery, while untreated hands had no change in volume of the carpal tunnel. These measurements were significant ðP < 0:001Þ. These volume differences persisted at an eight-month examination in eight hands as well. The volume increase seemed to come from a more circular shape of the carpal tunnel on axial images, with the transverse carpal ligament becoming more convex, while the distance between the trapezial ridge and the hook of the hamate increased to a lesser degree (more increase in the antero-posterior than in the medial–lateral dimension of the carpal tunnel). The median nerve displaced an average of 3.5 1.9 mm anteriorly postoperatively when compared with control wrists, which was significant. The carpal arch width increased a small amount after carpal tunnel release, by 6.3 4.6% which was statistically significant. However, in the eight hands studied eight months postoperatively, there was no difference in carpal arch width from preoperative values, implying that the carpal arch recoils somewhat by eight months postoperatively. However, the authors did not mention if the identical proximal–distal level was used for measurement of the pre and postoperative carpal arch width, introducing the possibility of error from comparing axial MRI cuts from different levels in the carpal tunnel which could hide or exaggerate differences in this parameter. The images in RichmanÕs paper clearly demonstrated a difference in shape of GuyonÕs canal from flat to oval after release of the transverse carpal ligament, a finding which is supported by the measurement of decreased pressure in GuyonÕs canal after carpal tunnel release (Ablove et al., 1996; Silver et al., 1985). The change in shape of Gu-
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yonÕs canal was also noted by Ablove et al. (1994). Silver noted resolution of ulnar compressive neuropathy at the wrist after isolated carpal tunnel decompression (Silver et al., 1985). Kato and colleagues used MRI before and after endoscopic carpal tunnel release in 10 hands to determine morphologic changes in the carpal tunnel after endoscopic release (Kato et al., 1994). The authors divided the carpal tunnel into a palmar part and a dorsal part using a line from the beak of the trapezium to the hamulus, the ‘‘H–T line’’. Of note, the majority of the increase in volume postoperatively was found to come from an increase in the palmar area, indicating that widening the carpal arch is not a major mechanism for increase in carpal tunnel volume after endoscopic carpal tunnel release. Specifically, the dorsal cross sectional area increased by about 3% (from 200 20 to 206 30 mm2 ). The palmar cross sectional area accounted for most of the volume increase: it was 32 8 mm2 preoperatively, and 114 13 mm2 postoperatively, and increase of 360%. This data implies that the volume increase after endoscopic carpal tunnel release comes from a palmar opening of the edges of the transverse carpal ligament, increasing the palmar area of the carpal tunnel, without much widening of the carpal arch. The findings of Kato et al. are different from previous authors (Gartsman et al., 1986) who did note an increase in carpal arch width (increased distance between the hamulus and trapezial ridge). Perhaps the carpal arch does widen a small amount, as other studies suggest, but KatoÕs sample size (10 hands) was too small to detect a significant difference. The authors did note and increase in arch width (H–T line) from 22.1 mm preoperatively to 23.8 mm postoperatively without statistical significance. Ablove et al. (1994) reported the MRI-documented morphologic changes of 18 wrists in 17 patients after Agee endoscopic (Agee et al., 1992) or subcutaneous, two-incision (Chow, 1989) (non-endoscopic) carpal tunnel release. The authors measured carpal arch width at the same level as other studies, at the level of the trapezial ridge and hamate hook. Carpal canal volume was nearly identical pre and postoperatively when endoscopically released wrists are compared with the results of Richman et al. (6.1 2.2 preoperatively and 7.5 2.5 ml postoperatively). Carpal arch width increased from 22.4 2.5 to 23.3 3.3 mm in the endoscopic group and from 23.5 2.0 to 24.1 2.1 mm in the subcutaneous group at final follow-up examination two years postoperatively, but the differences were not statistically significant. Of note, this study also noted palmar displacement of the median nerve measuring 0.6– 1.0 mm after endoscopic or subcutaneous carpal tunnel release, confirming the findings of Richman et al. However, the palmar displacement of the median nerve is less than that noted after open carpal tunnel release.
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Roger et al. (1985) studied axial CT scans at three levels and in three wrist positions in 34 wrists immediately before and two to three months after carpal tunnel release. They concluded that carpal tunnel release increased the carpal canal volume at all positions of flexion and extension, while the bony anatomy remained unchanged. Thus, the mechanism of increased volume of the carpal tunnel was by an increase in convexity of the transverse carpal ligament and not by an increase in carpal arch width. Similar CT scan results were noted by Schmitt et al. (1988), who noted an anterior ‘‘prolapsed’’ of the volar boundary of the carpal tunnel in most patients to account for the increase in carpal tunnel volume after carpal tunnel release in 90% of patients in their study. However, 10% of patients also had an increase in carpal arch area (increased distance of a line from the hamate hook to the trapezial ridge on axial CT scan cuts), suggesting that there is a small minority of patients who experience increase in carpal tunnel volume by this additional mechanism. As Gartsman noted a significant decrease in grip strength in patients whose carpal arch width increases more than 20%, perhaps there is a subset of patients at risk for this ‘‘pathologic’’ widening of the arch.
9. Conclusion Carpal tunnel surgery has been performed for nearly 80 years, yet despite the majority of patients who recover without complication, there are still a significant number that suffer postoperative pain and weakness. A successful decompression of the median nerve provides symptomatic relief of carpal tunnel symptoms, and generally allows patients to return to activities of daily living and employment. However, complete release of the carpal tunnel probably has a small but significant effect on carpal biomechanics and morphology. The small but appreciable increase in carpal arch width, as well as increased tendon excursion may have consequences on carpal kinematics. Postoperative complications of pillar pain and grip weakness may be attributed to a change in the carpal articulation or changes in the flexor tendon pulley system. Do the changes described warrant repair of the transverse carpal ligament or should a limited release of the carpal tunnel be performed to prevent troublesome postoperative complications? It is generally accepted that transverse carpal ligament lengthening, rather than simple division, is unnecessary to stabilize the carpal arch, however, it may be reasonable to prevent flexor tendon bowstringing. Perhaps excessive carpal morphologic change is preventable by ligament-preserving procedures? A study of carpal kinematics after carpal tunnel release is warranted to answer these questions.
Acknowledgement We would like to thank Ted Trafton for his tireless illustrative effort.
References Ablove, R.H., Moy, O.J., Peimer, C.A., Wheeler, D.R., Diao, E., 1996. Pressure changes in GuyonÕs canal after carpal tunnel release. J. Hand Surg. [Br.] 21, 664–665. Ablove, R.H., Peimer, C.A., Diao, E., Oliverio, R., Kuhn, J.P., 1994. Morphologic changes following endoscopic and two-portal subcutaneous carpal tunnel release. J. Hand Surg. [Am.] 19, 821–826. Agee, J.M., McCarroll Jr., H.R., Tortosa, R.D., Berry, D.A., Szabo, R.M., Peimer, C.A., 1992. Endoscopic release of the carpal tunnel: a randomized prospective multicenter study. J. Hand Surg. [Am.] 17, 987–995. Allmann, K.H., Horch, R., Uhl, M., et al., 1997. MR imaging of the carpal tunnel. Eur. J. Radiol. 25, 141–145. Amadio, P.C., 1995. The first carpal tunnel release? J. Hand Surg. [Br.] 20, 40–41. Atik, T.L., Smith, B., Baratz, M.E., 2001. Risk of neurovascular injury with limited-open carpal tunnel release: defining the ‘‘safe-zone’’. J. Hand Surg. [Br.] 26, 484–487. Brown, R.A., Gelberman, R.H., Seiler III, J.G., et al., 1993. Carpal tunnel release A prospective, randomized assessment of open and endoscopic methods. J. Bone Joint Surg. [Am.] 75, 1265–1275. Bury, T.F., Akelman, E., Weiss, A.P., 1995. Prospective, randomized trial of splinting after carpal tunnel release. Ann. Plast. Surgery 35, 19–22. Chow, J.C., 1989. Endoscopic release of the carpal ligament: a new technique for carpal tunnel syndrome. Arthroscopy 5, 19–24. Cobb, T.K., Cooney, W.P., 1994. Significance of incomplete release of the distal portion of the flexor retinaculum. Implications for endoscopic carpal tunnel surgery. J. Hand Surg. [Br.] 19, 283–285. Cobb, T.K., An, K.N., Cooney, W.P., 1995. Effect of lumbrical muscle incursion within the carpal tunnel on carpal tunnel pressure: a cadaveric study. J. Hand Surg. [Am.] 20, 186–192. Cobb, T.K., Dalley, B.K., Posteraro, R.H., Lewis, R.C., 1993. Anatomy of the flexor retinaculum. J. Hand Surg. [Am.] 18, 91–99. Einhorn, N., Leddy, J.P., 1996. Pitfalls of endoscopic carpal tunnel release. Orthop. Clin. North Am. 27, 373–380. Fisk, G.R., 1984. The influence of the transverse carpal ligament (flexor retinaculum) on carpal stability. Ann. Chir. Main. 3, 297– 299. Fuss, F.K., Wagner, T.F., 1996. Biomechanical alterations in the carpal arch and hand muscles after carpal tunnel release: a further approach toward understanding the function of the flexor retinaculum and the cause of postoperative grip weakness. Clin. Anat. 9, 100–108. Garcia-Elias, M., An, K.N., Cooney III, W.P., Linscheid, R.L., Chao, E.Y., 1989a. Stability of the transverse carpal arch: an experimental study. J. Hand Surg. [Am.] 14, 277–282. Garcia-Elias, M., An, K.N., Cooney, W.P., Linscheid, R.L., Chao, E.Y., 1989b. Transverse stability of the carpus. An analytical study. J. Orthop. Res. 7, 738–743. Garcia-Elias, M., Sanchez-Freijo, J.M., Salo, J.M., Lluch, A.L., 1992. Dynamic changes of the transverse carpal arch during flexionextension of the wrist: effects of sectioning the transverse carpal ligament. J. Hand Surg. [Am.] 17, 1017–1019. Gartsman, G.M., Kovach, J.C., Crouch, C.C., Noble, P.C., Bennett, J.B., 1986. Carpal arch alteration after carpal tunnel release. J. Hand Surg. [Am.] 11, 372–374.
J.J. Brooks et al. / Clinical Biomechanics 18 (2003) 685–693 Green, D, Hotchkiss, R.N., Pederson, W.C., 1999. In: GreenÕs Operative Hand Surgery, vol. 2. Churchill Livingstone, Philadelphia, pp. 1406–1417. Greening, J., Smart, S., Leary, R., Hall-Craggs, M., OÕHiggins, P., Lynn, B., 1999. Reduced movement of median nerve in carpal tunnel during wrist flexion in patients with non-specific arm pain. Lancet 354, 217–218. Hoppenfeld Sd, P., 1984. Surgical Exposures in Orthopaedics, The Anatomic Approach. JB Lippincott, Philadelphia, pp. 162–165. Hunter, J.M., 1991. Recurrent carpal tunnel syndrome, epineural fibrous fixation, and traction neuropathy. Hand Clin. 7, 491–504. Kato, T., Kuroshima, N., Okutsu, I., Ninomiya, S., 1994. Effects of endoscopic release of the transverse carpal ligament on carpal canal volume. J. Hand Surg. [Am.] 19, 416–419. Katz, J.N., Fossel, K.K., Simmons, B.P., Swartz, R.A., Fossel, A.H., Koris, M.J., 1995. Symptoms, functional status, and neuromuscular impairment following carpal tunnel release. J. Hand Surg. [Am.] 20, 549–555. Kiritsis, P.G., Kline, S.C., 1995. Biomechanical changes after carpal tunnel release: a cadaveric model for comparing open, endoscopic, and step-cut lengthening techniques. J. Hand Surg. [Am.] 20, 173– 180. Lanz, U., 1977. Anatomical variations of the median nerve in the carpal tunnel. J. Hand Surg. [Am.] 2, 44–53. Lee, D.H., Masear, V.R., Meyer, R.D., Stevens, D.M., Colgin, S., 1992. Endoscopic carpal tunnel release: a cadaveric study. J. Hand Surg. [Am.] 17, 1003–1008. Ludlow, K.S., Merla, J.L., Cox, J.A., Hurst, L.N., 1997. Pillar pain as a postoperative complication of carpal tunnel release: a review of the literature. J. Hand Ther. 10, 277–282. Mirza, M.A., King Jr., E.T., Tanveer, S., 1995. Palmar uniportal extrabursal endoscopic carpal tunnel release. Arthroscopy 11, 82– 90. Okutsu, I., Hamanaka, I., Tanabe, T., Takatori, Y., Ninomiya, S., 1996. Complete endoscopic carpal tunnel release in long-term haemodialysis patients. J. Hand Surg. [Br.] 21, 668–671. Okutsu, I., Ninomiya, S., Hamanaka, I., Kuroshima, N., Inanami, H., 1989. Measurement of pressure in the carpal canal before and after endoscopic management of carpal tunnel syndrome. J. Bone Joint Surg. [Am.] 71, 679–683. Phalen, G.S., 1996. The carpal-tunnel syndrome. Seventeen yearsÕ experience in diagnosis and treatment of six hundred fifty-four hands. J. Bone Joint Surg. [Am.] 48, 211–228. Richman, J.A., Gelberman, R.H., Rydevik, B.L., et al., 1989. Carpal tunnel syndrome: morphologic changes after release of the transverse carpal ligament. J. Hand Surg. [Am.] 14, 852–857. Richman, J.A., Gelberman, R.H., Rydevik, B.L., Gylys-Morin, V.M., Hajek, P.C., Sartoris, D.J., 1987. Carpal tunnel volume determi-
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nation by magnetic resonance imaging three-dimensional reconstruction. J. Hand Surg. [Am.] 12, 712–717. Roger, B., Chaise, F., Laval-Jeantet, M., 1985. X-ray computed tomographic analysis of structural changes of the carpal bones, after section of the anterior annular ligament. J. Radiol. 66, 693– 697. Rowland, E.B., Kleinert, J.M., 1994. Endoscopic carpal-tunnel release in cadavera. An investigation of the results of twelve surgeons with this training model. J. Bone Joint Surg. [Am.] 76, 266–268. Schmitt, R., Lucas, D., Buhmann, S., Lanz, U., Schindler, G., 1988. Morphometry using computerized tomography of the wrist in idiopathic carpal tunnel syndrome. Comparison of pre- and postoperative findings. Handchir. Mikrochir. Plast. Chir. 20, 41– 46. Seiler III, J.G., Barnes, K., Gelberman, R.H., Chalidapong, P., 1992. Endoscopic carpal tunnel release: an anatomic study of the twoincision method in human cadavers. J. Hand Surg. [Am.] 17, 996– 1002. Seradge, H., Seradge, E., 1989. Piso-triquetral pain syndrome after carpal tunnel release. J. Hand Surg. [Am.] 14, 858–862. Siegel, D.B., Kuzma, G., Eakins, D., 1995. Anatomic investigation of the role of the lumbrical muscles in carpal tunnel syndrome. J. Hand Surg. [Am.] 20, 860–863. Silver, M.A., Gelberman, R.H., Gellman, H., Rhoades, C.E., 1985. Carpal tunnel syndrome: associated abnormalities in ulnar nerve function and the effect of carpal tunnel release on these abnormalities. J. Hand Surg. [Am.] 10, 710–713. Singer, G., Ashworth, C.R., 2001. Anatomic variations and carpal tunnel syndrome: 10-year clinical experience. Clin. Orthop., 330– 340. Tanabe, T., Okutsu, I., 1997. An anatomical study of the palmar ligamentous structures of the carpal canal. J. Hand Surg. [Br.] 22, 754–757. Tanzer, R., 1959. The carpal-tunnel syndrome: A clinical and anatomical study. J. Bone Joint Surg. [Am.] 41A, 626–634. Trumble, T.E., Diao, E., Abrams, R.A., Gilbert-Anderson, M.M., 2002. Single-portal endoscopic carpal tunnel release compared with open release: a prospective, randomized trial. J. Bone Joint Surg. [Am.] 84-A, 1107–1115. Van Heest, A., Waters, P., Simmons, B., Schwartz, J.T., 1995. A cadaveric study of the single-portal endoscopic carpal tunnel release. J. Hand Surg. [Am.] 20, 363–366. Viegas, S.F., Pollard, A., Kaminksi, K., 1992. Carpal arch alteration and related clinical status after endoscopic carpal tunnel release. J. Hand Surg. [Am.] 17, 1012–1016. Wilson, K.M., 1994. Double incision open technique for carpal tunnel release: an alternative to endoscopic release. J. Hand Surg. [Am.] 19, 907–912.
Review
Biomechanical and anatomical consequences of carpal tunnel release Jeffrey J. Brooks, Jonathan R. Schiller, Scott D. Allen, Edward Akelman
*
Department of Orthopaedics and Division of Engineering, Rhode Island Hospital/Brown University School of Medicine, 593 Eddy Street, Providence, RI 02905, USA Received 26 February 2003; accepted 5 March 2003
Abstract Carpal tunnel syndrome is an exceedingly common orthopaedic problem in the United States. When conservative management is unsuccessful, most surgeons proceed to surgical treatment. Though the carpal tunnel release procedure is usually curative, many patients experience postoperative complications, such as scar sensitivity, pillar pain, recurrent symptoms, and grip weakness, regardless of whether the release was done through an open, mini-open, or endoscopic approach. The exact causes of these and other complications of carpal tunnel release remain unclear. Release of the carpal tunnel has an effect on carpal anatomy and biomechanics, including an increase in carpal arch width, carpal tunnel volume, and changes in muscle and tendon mechanics. We set out to review the morphological and biomechanical changes caused by carpal tunnel release with the goal of better understanding the root causes of postoperative complications. This article first reviews normal carpal tunnel anatomy and anatomic variations, then available surgical techniques for carpal tunnel release, and finally the literature on morphologic, physiologic and biomechanical alterations in the wrist after carpal tunnel release. Ó 2003 Elsevier Ltd. All rights reserved.
1. Introduction and clinical significance Carpal tunnel syndrome is one of the most common orthopedic conditions, with an estimated incidence of nearly 1% annually in the United States (Einhorn and Leddy, 1996), which translates into almost 2.8 million new cases per year. If conservative therapy fails, surgical release of the carpal tunnel is the preferred method of treatment. Though the majority of patients have relief of symptoms postoperatively, there are still a significant number of patients who experience disabling postoperative symptoms. Disabling loss of grip strength and pillar pain may be a result of anatomical or biomechanical alterations caused by carpal tunnel release (Gartsman et al., 1986; Ludlow et al., 1997). This article will review normal carpal tunnel anatomy and anatomic variations. The available surgical techniques for carpal tunnel release are reviewed. Finally, the literature on morphologic, physiologic, and biomechanical alterations in the wrist after carpal tunnel release will be summarized. An appreciation of these changes may improve the surgical and postoperative
*
Corresponding author. E-mail address: [email protected] (E. Akelman).
0268-0033/$ - see front matter Ó 2003 Elsevier Ltd. All rights reserved. doi:10.1016/S0268-0033(03)00052-4
management of carpal tunnel syndrome and subsequent treatment of poor postoperative outcomes.
2. Anatomy The carpal bones and intercarpal ligaments at its medial, lateral, and posterior borders form the carpal tunnel. The anterior border is formed by the transverse carpal ligament and flexor retinaculum (Hoppenfeld Sd, 1984; Tanabe and Okutsu, 1997). The terms ‘‘flexor retinaculum’’ and ‘‘transverse carpal ligament’’ have been considered synonyms, however, Cobb et al. demonstrated that they are distinct structures (Cobb et al., 1993). The flexor retinaculum as a whole can be divided into three parts from proximal to distal. The antebrachial fascia forms the proximal part of the flexor retinaculum. A superficial fascial layer is inseparable from the thickened deep investing antebrachial fascia, which is anterior to the median nerve and continuous with the transverse carpal ligament distally. The two layers separate to enclose the flexor carpi radialis tendon radially and the contents of GuyonÕs canal and the flexor carpi ulnaris tendon ulnarly. Thus, the deep investing antebrachial fascia at this level is volar to the contents of the carpal tunnel and dorsal to GuyonÕs canal (Fig. 1)
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Fig. 1. Schematic illustration of the three parts of the flexor retinaculum (FR). D: The distal part is the aponeurosis from which the thenar and hypothenar muscles take origin. M: The middle part, or the transverse carpal ligament proper, also gives origin to the thenar and hypothenar muslces. P: The proximal part of the flexor retinaculum, courses deep to the flexor carpi ulnaris (FCU) and flexor carpi radialis (FCR) tendons.
(Cobb et al., 1993). The transverse carpal ligament proper represents the middle third of the flexor retinaculum and forms the palmar ‘‘roof’’ of the carpal tunnel. It inserts into the scaphoid tuberosity and ridge of the trapezium radially and the hamulus and pisiform ulnarly where it is narrowest between the hamate hook and trapezial ridge (Fig. 2). The distal third is the aponeurosis between the thenar and hypothenar muscles, from which these muscles originate. Tanabe maintains that the distal part of the flexor retinaculum described by Cobb is actually separated from the transverse carpal ligament by a layer of adipose tissue (Tanabe and Okutsu, 1997). The proximal to distal extent of the transverse carpal ligament proper runs from the level of the distal pisiform proximally (11 mm distal to the capitate–lunate joint) to the meta-diaphyseal junction of the third metacarpal distally (10 mm distal to the carpometacarpal joint of the long finger). The thickness of the flexor retinaculum over the carpal tunnel is 10 times that of the antebrachial fascia (Cobb et al., 1993). Contained within the carpal tunnel are the median nerve and the nine extrinsic flexor tendons of the thumb and fingers (flexor pollicis longus tendon, four flexor digitorum superficialis tendons, and four flexor digitorum profundus tendons). The median nerve normally divides into six branches at the distal end of the flexor retinaculum––the recurrent motor branch, three proper digital nerves and two common digital nerves. The motor branch of the median nerve usually innervates the thenar muscles and the index and middle finger lumbricals. Sensory branches usually innervate the thumb, index, middle, and radial half of the ring fingers. Lanz classified variations of median nerve anatomy in the carpal tunnel
Fig. 2. (a) Palmar and (b) axial views of the transverse carpal ligamne (TCL). (a) The three bands of the TCL are illustrated with their bony attachments. H ¼ hamate hook, P ¼ pisiform, T ¼ trapezium, S ¼ scaphoid.
into four groups. Division of the motor branch can be extraligamentous, subligamentous, transligamentous, supraligamentous, or can originate from the ulnar border of the median nerve. Furthermore, the motor branch may arise in the forearm, or may be separated by the persistent median artery or an aberrant muscle only to join distal to the transverse carpal ligament (Lanz, 1977). The transverse carpal ligament is that part of the flexor retinaculum in the mid-third that has bone-tobone attachments. The middle third is the transverse carpal ligament proper. The distal part is the aponeurosis between the thenar and hypothenar muscles, from which these muscles originate. It has been hypothesized that median nerve compression most likely occurs in wrist flexion at the proximal edge of the transverse carpal ligament where it joins the deep investing fascia of the forearm, the anatomic explanation for PhalenÕs sign (1996). Alternately, the median nerve may be compressed where the carpal tunnel is narrowest at the level of the hook of the hamate by either synovial hypertrophy or a space-occupying lesion (Cobb et al., 1993). Additionally, imaging studies of median nerve motion during wrist flexion have demonstrated that patients with carpal tunnel syndrome are more likely than normal patients to have
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limited median nerve motion in the carpal canal. The nerve in normal patients moved radially and posteriorly to a position interposed between the flexor tendons during wrist flexion. The nerve in patients with carpal tunnel syndrome was more likely to remain in position at the flexor retinaculum. The limited motion of the nerve in these cases may predispose the nerve to compression during wrist flexion leading to carpal tunnel symptoms (Allmann et al., 1997). Another study on patients with non-specific forearm pain associated with median nerve compression found that patients experiencing pain were more likely to have decreased median nerve motion during wrist flexion (Greening et al., 1999).
3. Carpal tunnel anatomic variations Phalen originally reported on his 17-year experience in 1966, suggesting that thickening of the flexor synovium was the most common direct cause of median nerve compression and carpal tunnel syndrome in his patients (Phalen, 1996). Tanzer, however, noted three of 21 patients with cystic masses in the carpal tunnel and seven of these 21 hands had various congenital anomalies (Tanzer, 1959). Singer retrospectively looked for anatomic variations in 147 hands undergoing carpal tunnel release via an extended exposure (Singer and Ashworth, 2001). The authors noted anatomic variations in 60 hands (41% of hands), one-third of which had anatomic variations intrinsic to the carpal tunnel. The intrinsic variations included anomalous lumbrical origins in nine hands (6%), which could crowd the carpal tunnel during grip and finger flexion, most commonly the long finger lumbrical. Siegel found that proximal lumbrical origin and/or lumbrical hypertrophy could cause median nerve compression by a space-occupying effect (Siegel et al., 1995). Cobb confirmed that lumbrical excision would reduce carpal tunnel pressure during simulated grip in cadavera (Cobb et al., 1995). Singer noted a flexor digitorum superficialis muscle belly present in six of 147 hands (4%) of patients undergoing carpal tunnel release (Singer and Ashworth, 2001). These variants may not likely be appreciated during limited-exposure carpal tunnel release.
4. Pressure changes and mechanism of relief after carpal tunnel release When considering complete release of the carpal tunnel, one must consider the relevant anatomy (Tanabe and Okutsu, 1997; Cobb et al., 1993); neglecting to release the distal part of the flexor retinaculum or the proximal part described above may fail to completely relieve pressure on the median nerve or may result in
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failure of surgery to relieve symptoms of carpal tunnel syndrome (Tanabe and Okutsu, 1997; Phalen, 1996; Cobb and Cooney, 1994). Tanabe noted that release of only the transverse carpal ligament caused the edges of the cut ligament to spread apart by 1.3 0.2 mm but that complete release of both the transverse carpal ligament and the distal aponeurosis between the thenar and hypothenar muscles caused more than 6.6 0.2 mm of separation of the transverse carpal ligament edges and a corresponding significant decrease in carpal tunnel pressure (Tanabe and Okutsu, 1997; Okutsu et al., 1996). Okutsu et al. did an elegant study in 1989 in which carpal tunnel pressures were measured in multiple positions through an endoscopically placed catheter inside the carpal tunnel of patients under local anesthesia (Okutsu et al., 1989). In patients without carpal tunnel syndrome the normal carpal tunnel pressure at rest was 14.3 10 mmHg. In patients with carpal tunnel syndrome, pressure in the carpal tunnel averaged 43.0 17.2 mmHg preoperatively in the resting position, and 206.2 51.6 mmHg with active grip. With passive flexion and extension the pressures were 191.9 64 and 222.4 44.2 mmHg, respectively. This represents a fivefold increase in pressure during grip or extremes of motion in patients with carpal tunnel syndrome. In contrast, immediately postoperatively the pressures were 6.2 5.5 mmHg in the resting position, and 88 65 mmHg with active grip, pressures in other positions were similarly decreased, documenting clearly the physiologic effect of carpal tunnel release. The pressure in GuyonÕs canal decreases after endoscopic or open carpal tunnel release. In a study by Ablove et al. (1996), the authors studied 20 patients with documented carpal tunnel syndrome. GuyonÕs canal pressures decreased from 12.7 7.1 to 4.2 4.6 mmHg after carpal tunnel release alone. This is consistent with a previous study noting that 90% of patients with both median and ulnar compressive neuropathies at the wrist have relief of the ulnar nerve symptoms after isolated carpal tunnel release (Silver et al., 1985).
5. Surgical techniques To serve as background for understanding the biomechanical and anatomic changes after different types of carpal tunnel release, a brief review is presented here. A thorough review of the methods for carpal tunnel release and their pros and cons is beyond the scope of this paper. 5.1. Open release Since the first carpal tunnel surgery in 1924 by Herbert Galloway, numerous advances have been made to
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refine this very common procedure (Amadio, 1995). In general, carpal tunnel release can be performed using open or endoscopic procedures. The classic open and limited-open carpal tunnel release techniques involve complete division of the transverse carpal ligament and the deep fascia of the forearm under direct visualization (Green et al., 1999). The lesser level of difficulty and shortened operative time make the open release the procedure of choice with numerous hand surgeons. In the majority of patients, open release techniques lead to symptomatic relief with a low complication rate. However, scar tenderness and grip weakness may occur after open release. In order to minimize these postoperative complications, a limited transverse incision (2.0 cm or less) is made in the same location as the classic open release, but ends approximately 1 cm distal to the distal wrist crease. Carpal tunnel release through a limited open incision was performed by Atik et al. (2001) without damage to any neurovascular structures, and when performed from distal to proximal allowed for precise identification of structures at risk of injury (the superficial palmar arch, third common digital nerve, and aberrant motor branches of the median nerve) and improves the safety of carpal tunnel release. 5.2. Endoscopic release In an attempt to reduce postoperative morbidity, endoscopic techniques were developed and have been evolving since the late 1980s. The Agee single portal and Chow two portal carpal tunnel release utilize smaller incisions and require less dissection of the subcutaneous tissue and structures overlying the transverse carpal ligament. However, since these are endoscopic procedures, visibility may be limited and incomplete release of the transverse carpal ligament, nerve injury (median, ulnar, digital, palmar cutaneous branch of the median nerve), arterial injury (ulnar, superficial palmar arch), hematoma, and flexor tendon injury have been reported (Lee et al., 1992; Van Heest et al., 1995; Rowland and Kleinert, 1994). With endoscopic release techniques, there may be less scar tenderness, and proponents suggest an earlier return to work and activities of daily living compared to the open procedure. Trumble published a prospective, randomized, multicenter trial comparing endoscopic versus open release. The endoscopic group had a more rapid improvement in strength and scar tenderness than the open group in the first three months after surgery. However, at one year follow-up there was no difference in patient satisfaction between the endoscopic and open release (Trumble et al., 2002). Brown et al. (1993) in a prospective, randomized trial of 145 patients found no significant difference in patient satisfaction and symptom relief between the two portal endoscopic and the classic open release at 84 days postoperatively. Additionally, no significant difference in sensibility, thenar
weakness or atrophy, and pillar pain was found between the groups. Scar tenderness was similar for both procedures at three weeks postoperatively, but differed significantly at week 11 with 61% of the open patients complaining of mild to severe tenderness. The endoscopic group returned to work around day 14, as opposed to day 28 for the open group. Both open and endoscopic carpal tunnel release are effective for relieving symptoms, however, endoscopic release of the transverse carpal ligament may shorten the recovery time, permitting an earlier return to work and resumption of activities of daily living.
6. Potential biomechanical complications of carpal tunnel release Generally reported complications of carpal tunnel release include incomplete release, neuropraxia or injury to the median or ulnar nerve, and inadvertent entrance into GuyonÕs canal, injury to digital nerves, the ulnar artery and the superficial palmar arch (Lee et al., 1992; Seiler et al., 1992). However, there exist several biomechanical changes after carpal tunnel release, which may be considered ‘‘complications’’, not merely ‘‘expected’’ postoperative, changes. The phenomenon of pillar pain is a frequent complication reported after both open and endoscopic surgical techniques with an incidence between 6% and 36% (Katz et al., 1995; Mirza et al., 1995). Division of the transverse carpal ligament through open or endoscopic techniques may lead to an increase in carpal arch width and carpal tunnel volume (Fig. 3), both of which may be responsible for postoperative pillar pain, and may also cause changes in other intercarpal articulations (Fisk, 1984; Fuss and Wagner, 1996; Kiritsis and Kline, 1995; Seradge and Seradge, 1989; Garcia-Elias et al., 1989a). ‘‘Pillar pain’’ can delay return to work and resumption of activities of daily living, foster emotional distress, increase cost to the health care system, and potentiate loss of grip strength (Seradge and Seradge, 1989). Pillar pain has been characterized as pain or tenderness in the thenar or hypothenar eminence, or radial and ulnar tenderness, and has been reported to subside by the third postoperative month (Ludlow et al., 1997). Pain most commonly originates in the piso-triquetral joint, possibly due to alteration of the forces over the joint and/or displacement of the pisiform after releasing the transverse carpal ligament (Seradge and Seradge, 1989). The etiology of pillar pain remains uncertain. There is currently no evidence that carpal tunnel release causes changes in the piso-triquetral articulation, although GuyonÕs canal does dramatically change in shape after carpal tunnel release (Richman et al., 1989). Current work has suggested four potential etiologies for pillar pain: muscular or ligamentous, neurogenic,
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1989; Garcia-Elias et al., 1989b). Thus, division of this ligament could alter the normal function of the wrist and contribute to such postoperative complications as pillar pain and grip weakness. 7.1. Carpal stiffness
Fig. 3. (a) The carpal arch width depicted on an axial view of the carpal tunnel (H ¼ hamulus, P ¼ pisifrom, T ¼ trapezium, S ¼ scaphoid). (b) Carpal tunnel volume (dark area) and the contents of the carpal tunnel––The tendons of the flexor digitorum profundus, flexor digitorum superficialis, flexor pollicis longus, and the the median nerve. The ulnar artery and nerve and the flexor carpi radialis tendon are shown for orientation.
edematous, and alteration of the carpal arch structure (Ludlow et al., 1997). Muscular or ligamentous causes of pillar pain may be related to relaxation of the intrinsic muscles of opposition and pinch with sectioning of the transverse carpal ligament, and subsequent migration of the transverse carpal ligament toward its osseous origins (Hunter, 1991). Cutaneous nerve branches in the palmar and subcutaneous tissue may be injured when incising in the ‘‘critical pillar rectangle’’, which was defined by Wilson as the wrist flexion crease proximally, 1 cm distal to the hook of hamate, ulnar border of the hamate ulnarly, and the scaphoid tubercle radially (Wilson, 1994). Postoperative edema superficial to the transverse carpal ligament may also cause pain in the thenar or hypothenar areas. Resolution of this swelling is usually coincident with relief of pillar pain (Green et al., 1999).
7. Biomechanical change after carpal tunnel release A number of studies have examined the effect of dividing the transverse carpal ligament on the carpal arch. The transverse carpal ligament has been shown to serve three functions: anchor thenar and hypothenar musculature, provide transverse stability to the carpus, and act as a pulley for the flexor tendons (Seradge and Seradge,
Carpal stiffness is obtained by differentiating strain energy with respect to displacement of centroids of adjacent rigid bodies. By applying a dorsopalmar compressive load, a calculated displacement force on adjacent carpal bones can be described. Dorsopalmar compression tests when the flexor retinaculum has been sectioned demonstrate that carpal stiffness decreased by an average of 7.8% (232–214 N/mm), indicating that the flexor retinaculum plays a minor role in transverse stability of the carpus and should be regarded as a pulley for the flexor tendons rather than an intercarpal stabilizer (Garcia-Elias et al., 1989b). The transverse intercarpal ligaments, especially the capito-hamate ligament, are essential in providing stability to the carpal tunnel, since their division in the presence of an intact flexor retinaculum leads to dorsopalmar compressive instability of the carpus under applied stress. 7.2. Muscular and tendon effects Fuss and Wagner dissected five fresh frozen forearms and hands to demonstrate muscle attachments to the flexor retinaculum prior to studying joint mechanics before and after carpal tunnel release. Bisection of the flexor retinaculum caused certain muscles to lose their anatomic attachments due to muscular pull shifted distally and radially or ulnarly (Fuss and Wagner, 1996). Muscle shortening occurred in the superficial head of the flexor pollicis brevis 25% (relative to rest length), the ulnar part of the abductor pollicis brevis 20% (opposition and adduction), the opponens pollicis 20%, and the opponens digiti minimi 10%. This causes a loss of muscle length leading to a loss of muscle strength. Additionally, release of the transverse carpal ligament may disrupt the alignment and tracking of the piso-triquetral joint causing pain (Seradge and Seradge, 1989). This piso-triquetral tracking or alignment problem could be a possible etiology of pillar pain. Another change noted by many authors is that the flexor tendons in the carpal tunnel displace palmarward after carpal tunnel release (Amadio, 1995). The transverse carpal ligament has been suggested as an important pulley in the flexor tendon system that prevents bowstringing. Division of the transverse carpal ligament through an open, limited open, or endoscopic release, may significantly increase flexor tendon excursion during wrist flexion. Increased excursion, or the distance the tendon travels relative to the jointÕs center of rotation, is noted after 20–30° wrist flexion (Kiritsis and Kline, 1995).
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Thus, as the distance increases between the tendon and the center of rotation in the wrist joint due to bowstringing, the distance the tendon travels with changing wrist position increases. The palmar displacement of the flexor tendons with wrist flexion could be another potential cause of postoperative wrist flexion weakness, and potentially reinforces the need for a short period of immobilization to allow sufficient time for intrinsic reconstitution of the transverse carpal ligament, although splinting after carpal tunnel release has not been proven beneficial (Bury et al., 1995). Conversely, functional gripping activities and maximum grip strength are accomplished with the wrist in an extended position, thus palmar displacement of the flexor tendons during wrist flexion is unlikely clinically significant.
8. Morphologic changes following carpal tunnel release 8.1. Carpal arch and carpal tunnel volume Cobb et al. (1993) determined normal carpal tunnel dimensions by injecting contrast material into the carpal tunnel and examining antero-posterior (AP) radiographs. On the AP view, the carpal tunnel is shaped like an hourglass (Fig. 4), with the narrowest part at the level of the hook of the hamate. The mean width of the carpal tunnel was 25 1.2 mm proximally, 20 1.2 mm at the hook of the hamate, and 25 1.5 mm at its distal extent, a significant difference ðP < 0:0001Þ. This is an important feature to note, as it is of utmost importance when measuring carpal arch width pre and postcarpal tunnel release––if axial slices are at different proximal–distal
Fig. 4. The carpal tunnel is hourglass-shaped, with the narrowest portion located between the hook of the hamate and trapezial ridge.
levels of the carpal tunnel significant error could be introduced into the measurements of carpal arch width. The transverse carpal ligament normally attaches on the pisiform, hook of the hamate, scaphoid and trapezium, maintaining a concavity to the carpal arch and carpal tunnel. When this ligament is divided, the concave arch flattens and the distance between the carpal insertions increases. Fisk demonstrated an average increase of 3 mm between the scaphoid and pisiform after carpal tunnel release (Fisk, 1984). Garcia-Elias measured the width of the carpal arch using the trapezio-hook of hamate distance before and after transverse carpal ligament release. When the ligament was intact, the distance decreased between these two bones in both wrist flexion and extension. However, when the transverse carpal ligament was released, the distance significantly increased an average of 11% (Garcia-Elias et al., 1992). Gartsman et al. (1986) did a retrospective review of patients who had undergone open carpal tunnel release and either had standardized carpal tunnel view radiographs taken before and after the procedure was done, or a radiograph of the unoperated side was used as a control. In this study, the lack of preoperative assessment of the operative wrist is the major criticism. The carpal arch width was measured between the palmar tips of the trapezial ridge and hook of the hamate with the wrist extended 50°. Range of motion did not change significantly after carpal tunnel release using the opposite side as a control. Of 50 operated wrists, 47 had widening of the carpal arch width and three had no change, ranging from 0% to 52% widening with an average widening of 13.6%, or 2.9 mm. The range of increase in absolute widening of the carpal arch was 0–8.5 mm. However, the authors did not examine variability or repeatability of measurements. This study differs from others in that it found a greater magnitude of arch widening after carpal tunnel release, perhaps because of the wrist position (50° extension) being different from wrist position in other studies using magnetic resonance imaging (MRI) or computed tomography (CT) in neutral or only slight extension positions. Gartsman found that an increase in carpal arch width greater than 20% over control correlated with a statistically significant decrease in grip strength of 25.85%. Patients with greater widening did not have an increased incidence of postoperative wrist pain. ‘‘Columnar pain’’ did not correlate with arch widening either. In 1992, Viegas et al. (1992) examined carpal tunnel radiographs before and after endoscopic carpal tunnel release using the same technique for measurement and radiographic documentation as Gartsman et al. The authors noted an increase of 1.7 mm (7% increase) in carpal arch width 10 days after surgery. In contrast to GartsmanÕs findings, most patients had an increase in arch width of 0–10%, with very few wrists increasing
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more than 20% in arch width postoperatively. One might conclude from comparing ViegasÕ and GartsmanÕs studies that fewer patients would be expected to have impaired grip after endoscopic carpal tunnel release compared with open carpal tunnel release, since fewer of the wrists in the former group had increases in arch width of more than 10%. In 1987 Richman et al. (1987) introduced MRI as a means of evaluating carpal tunnel volume. The study determined that there was no significant difference between MRI and direct cadaveric measurements of carpal tunnel volume (with a silicone injection technique) and carpal arch width (measured using calipers accurate to 0.5 mm), using a standard protocol for direct measurements on cadavera and MRI data from cadaver wrists. This indicated excellent intra and inter-observer reliability of this MRI measurement technique, and excellent reproduction by MRI of true direct measurements of volume and width of the carpal tunnel. Two years later, Richman examined the effect of open carpal tunnel release on carpal canal volume, carpal arch width, and position of the canal contents in 15 wrists assessed by MRI (Richman et al., 1989). Carpal canal volume in treated hands increased from 6.3 1.0 to 7.8 1.5 ml after surgery, while untreated hands had no change in volume of the carpal tunnel. These measurements were significant ðP < 0:001Þ. These volume differences persisted at an eight-month examination in eight hands as well. The volume increase seemed to come from a more circular shape of the carpal tunnel on axial images, with the transverse carpal ligament becoming more convex, while the distance between the trapezial ridge and the hook of the hamate increased to a lesser degree (more increase in the antero-posterior than in the medial–lateral dimension of the carpal tunnel). The median nerve displaced an average of 3.5 1.9 mm anteriorly postoperatively when compared with control wrists, which was significant. The carpal arch width increased a small amount after carpal tunnel release, by 6.3 4.6% which was statistically significant. However, in the eight hands studied eight months postoperatively, there was no difference in carpal arch width from preoperative values, implying that the carpal arch recoils somewhat by eight months postoperatively. However, the authors did not mention if the identical proximal–distal level was used for measurement of the pre and postoperative carpal arch width, introducing the possibility of error from comparing axial MRI cuts from different levels in the carpal tunnel which could hide or exaggerate differences in this parameter. The images in RichmanÕs paper clearly demonstrated a difference in shape of GuyonÕs canal from flat to oval after release of the transverse carpal ligament, a finding which is supported by the measurement of decreased pressure in GuyonÕs canal after carpal tunnel release (Ablove et al., 1996; Silver et al., 1985). The change in shape of Gu-
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yonÕs canal was also noted by Ablove et al. (1994). Silver noted resolution of ulnar compressive neuropathy at the wrist after isolated carpal tunnel decompression (Silver et al., 1985). Kato and colleagues used MRI before and after endoscopic carpal tunnel release in 10 hands to determine morphologic changes in the carpal tunnel after endoscopic release (Kato et al., 1994). The authors divided the carpal tunnel into a palmar part and a dorsal part using a line from the beak of the trapezium to the hamulus, the ‘‘H–T line’’. Of note, the majority of the increase in volume postoperatively was found to come from an increase in the palmar area, indicating that widening the carpal arch is not a major mechanism for increase in carpal tunnel volume after endoscopic carpal tunnel release. Specifically, the dorsal cross sectional area increased by about 3% (from 200 20 to 206 30 mm2 ). The palmar cross sectional area accounted for most of the volume increase: it was 32 8 mm2 preoperatively, and 114 13 mm2 postoperatively, and increase of 360%. This data implies that the volume increase after endoscopic carpal tunnel release comes from a palmar opening of the edges of the transverse carpal ligament, increasing the palmar area of the carpal tunnel, without much widening of the carpal arch. The findings of Kato et al. are different from previous authors (Gartsman et al., 1986) who did note an increase in carpal arch width (increased distance between the hamulus and trapezial ridge). Perhaps the carpal arch does widen a small amount, as other studies suggest, but KatoÕs sample size (10 hands) was too small to detect a significant difference. The authors did note and increase in arch width (H–T line) from 22.1 mm preoperatively to 23.8 mm postoperatively without statistical significance. Ablove et al. (1994) reported the MRI-documented morphologic changes of 18 wrists in 17 patients after Agee endoscopic (Agee et al., 1992) or subcutaneous, two-incision (Chow, 1989) (non-endoscopic) carpal tunnel release. The authors measured carpal arch width at the same level as other studies, at the level of the trapezial ridge and hamate hook. Carpal canal volume was nearly identical pre and postoperatively when endoscopically released wrists are compared with the results of Richman et al. (6.1 2.2 preoperatively and 7.5 2.5 ml postoperatively). Carpal arch width increased from 22.4 2.5 to 23.3 3.3 mm in the endoscopic group and from 23.5 2.0 to 24.1 2.1 mm in the subcutaneous group at final follow-up examination two years postoperatively, but the differences were not statistically significant. Of note, this study also noted palmar displacement of the median nerve measuring 0.6– 1.0 mm after endoscopic or subcutaneous carpal tunnel release, confirming the findings of Richman et al. However, the palmar displacement of the median nerve is less than that noted after open carpal tunnel release.
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Roger et al. (1985) studied axial CT scans at three levels and in three wrist positions in 34 wrists immediately before and two to three months after carpal tunnel release. They concluded that carpal tunnel release increased the carpal canal volume at all positions of flexion and extension, while the bony anatomy remained unchanged. Thus, the mechanism of increased volume of the carpal tunnel was by an increase in convexity of the transverse carpal ligament and not by an increase in carpal arch width. Similar CT scan results were noted by Schmitt et al. (1988), who noted an anterior ‘‘prolapsed’’ of the volar boundary of the carpal tunnel in most patients to account for the increase in carpal tunnel volume after carpal tunnel release in 90% of patients in their study. However, 10% of patients also had an increase in carpal arch area (increased distance of a line from the hamate hook to the trapezial ridge on axial CT scan cuts), suggesting that there is a small minority of patients who experience increase in carpal tunnel volume by this additional mechanism. As Gartsman noted a significant decrease in grip strength in patients whose carpal arch width increases more than 20%, perhaps there is a subset of patients at risk for this ‘‘pathologic’’ widening of the arch.
9. Conclusion Carpal tunnel surgery has been performed for nearly 80 years, yet despite the majority of patients who recover without complication, there are still a significant number that suffer postoperative pain and weakness. A successful decompression of the median nerve provides symptomatic relief of carpal tunnel symptoms, and generally allows patients to return to activities of daily living and employment. However, complete release of the carpal tunnel probably has a small but significant effect on carpal biomechanics and morphology. The small but appreciable increase in carpal arch width, as well as increased tendon excursion may have consequences on carpal kinematics. Postoperative complications of pillar pain and grip weakness may be attributed to a change in the carpal articulation or changes in the flexor tendon pulley system. Do the changes described warrant repair of the transverse carpal ligament or should a limited release of the carpal tunnel be performed to prevent troublesome postoperative complications? It is generally accepted that transverse carpal ligament lengthening, rather than simple division, is unnecessary to stabilize the carpal arch, however, it may be reasonable to prevent flexor tendon bowstringing. Perhaps excessive carpal morphologic change is preventable by ligament-preserving procedures? A study of carpal kinematics after carpal tunnel release is warranted to answer these questions.
Acknowledgement We would like to thank Ted Trafton for his tireless illustrative effort.
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