The title of this Clinical Perspective has been borrowed from a song by Paul McCartney,
a song that emphasizes the difficulties of reaching one's dreams. If I choose that
title, it is because it describes quite well my own experience as wrist investigator.
Truly, my struggling to understand carpal mechanics has been like a long and winding
road; an exciting road, indeed, but one not devoid of unexpected curves and misleading
signposts: an endless road for a hopeless wrist enthusiast ([Fig. 1]).
Fig. 1 Preparing a specimen to investigate the effects of partial carpal fusions in the kinematics
of the wrist. Biomechanics Laboratory, Mayo Clinic, Rochester MN. October 1987.
I got “infected” by the carpal virus in the early 1980s, when I had the chance of
attending a seminar organized by Carlos Irisarri in Madrid about wrist injuries. The
program was unusual. I was expecting to learn some tips about the management of scaphoid
fractures, but I found myself diving in a pool of unknown terminology: carpal misalignment,
segmental instability, rotary subluxation. What a tsunami of thought-provoking concepts!
What a challenge for a poorly trained orthopedic surgeon from the suburbs of Barcelona
like me! I'll never forget the thrill of questioning Ron Linscheid and Julio Taleisnik
that day, Of course, I hardly understood their kind answers: I was too inexperienced
to comprehend that new world. Later that week I read the seminal papers of Drs. Linscheid,
Dobyns, and Taleisnik about carpal instability,[1]
[2] but I could not get the message. If I wanted to swim in that pool, I first needed
to learn the basics of swimming. So I went back to the Anatomy department and started
from scratch.
The history of how we all got to know the wrist is a long one. Vesalius, in the 16th
century, had already made precise drawings of the carpal bones.[3] Their function, however, was pretty much ignored for centuries. See, for instance,
the only two lines that Sir Charles Bell wrote in 1833 about the wrist in his classical
Bridgewater treatise.[4] “The carpal bones,” he said, “are so closely connected that they form a sort of
ball which moves on the end of the radius.” Surprisingly, only 8 years later, a 143-page
book about the functional anatomy of the wrist was published by Gustav Günther from
Hamburg in Germany.[5] Not only had he spent hours and hours in the laboratory dissecting and observing
wrist specimens, but he had measured radii of curvatures at both radiocarpal and midcarpal
levels at a time when X-rays were not available. As far as I know, this recently rediscovered
book was the first ever published about the wrist.
After Günther's publication, the carpus became a hot issue to explore, and luminaries
such as Wilhelm Henke[6] and Friedrich Henle[7] added new discoveries about intracarpal motion. Henke[6] was the first to suggest differential mobility between the proximal and distal rows,
while Henle[7] came out with the first description of the two major axes of wrist motion. The discovery
of X-rays triggered an explosion of new data in just few years. Bryce[8] was the first to recognize that there is also differential motion between scaphoid
and lunate. Corson[9] noticed how important the so-called dart-throwing rotation is in most daily activities.
Fick[10] realized that the two axes of wrist rotation were not orthogonal, intersecting on
the same plane, but oblique and biplanar. Destot[11] was the first to describe scapholunate dissociation. Yes, those were the early golden
years after which the wrist was no longer a block of fixed bones but a fascinating
mechanism of small joints, each with its own motion. Unfortunately, the First World
War put an end to all of that, and the carpus had to wait 50 more years until it again
drew some attention … but this is not the story I wanted to write about. I am not
a historian.
The story I promised to report on is my own experience: the story of my journey to
understand carpal stability. I could as well have told you about my struggles to understand
carpal motion, but the message would have been the same: Knowledge does not progress
if one is not willing to reconsider one's viewpoints when new evidence suggests them
to be untrue.
In the early 1980s, I read everything about the subject, but my level of dissatisfaction
was still high. I wanted certainties, not speculations. Infected as I was by the carpal
virus, I needed to see things for myself. Cooney and Chao[12] had, not long before, demonstrated that the amount of force transmitted across the
carpus was much larger than previously thought. Indeed, the wrist resists substantial
amounts of load, but how can this little joint resist that without yielding? That
was one of the questions I was obsessed with. I spent 5 years in the anatomy laboratory
of the Universitat Autònoma de Barcelona, and I earned my PhD studying ulnar-side
carpal injuries. I struggled to find a mechanical model that could explain carpal
stability, and I found it. The scaphoid had to be the key to unveil that riddle. Of
course, as stated in Ecclesiastes, “there is nothing new under the sun”—most of my
thoughts had been thought already. My long and winding journey had just started. My
first stop would be the scaphoid.
The Scaphoid: The Key to Carpal Stability
The Scaphoid: The Key to Carpal Stability
Geoffrey Fisk,[13] in his Hunterian lecture delivered at the Royal College of Surgeons in 1968 (45
years ago now) had already stated that the wrist is a link system with a tendency
to collapse into a zigzag pattern, which he called the concertina effect. According
to that theory, the scaphoid was the key element preventing the concertina effect.
Certainly, when the carpus is axially loaded, the lunate tends to rotate into extension
while the capitate translates dorsally. That's the concertina effect. However, if
we have an intercalated scaphoid with proximal and distal links to the dorsum of the
lunate and to the palmar edge of the capitate, there is an obvious sense of elastic
stability that eliminates the risk of carpal collapse ([Fig. 2]). Unquestionably, the scaphoid as a bridge between the two carpal rows was a good
model to explain stability.
Fig. 2 According to Lambrinudi,[14] the scaphoid is the key element in preventing the “concertina” effect (white arrows),
as long as the palmar scaphocapitate and dorsal scapholunate links (yellow springs)
are intact.
That idea was not entirely new, however. It was derived from the teachings of Professor
Constantine Lambrinudi to his fellows Gilford and Bolton, who published a quite similar
theory several years before.[14] Later on, Linscheid and associates,[1] with their “slider-crank” mechanical model, further emphasized the importance of
the scaphoid for the wrist to be both mobile and stable. I must confess that, when
I carefully read those articles, I thought that I had finally understood the carpus.
But of course that explanation was not devoid of drawbacks. In a way, that theory
appeared to indicate that any alteration of the carpal alignment was the result of
intracarpal pathology. Yet, as demonstrated by Professor Allieu[15] at Montpellier, France, carpal malalignment is not always the result of intracarpal
pathology; it may occasionally be an adaptation to something wrong outside the carpus.
Needless to say, carpal malalignment and carpal instability are not equivalent terms.
A dorsally tilted radial fracture, for instance, may exhibit malalignment as an adaptive
phenomenon, which may disappear when the fracture is reduced. In other words, the
theory according to which the scaphoid was the key to normal carpal alignment was
not valid any more. My road to understanding carpal stability would not be a straight
one.
The Scapholunate Stabilization Model
The Scapholunate Stabilization Model
It was in the early 1980s that I got fascinated by the new concepts defended by Professors
Landsmeer[16] at Leiden in The Netherlands. Not long before, one of his associates Professor,
John Kauer,[17] had moved to the University of Nijmegen, also in The Netherlands, and became full
professor of anatomy. These two gentlemen had gone a step ahead by emphasizing the
role of the scapholunate ligaments in the stabilization of the wrist. The lunate,
they said, is wedge-shaped, being narrower dorsally than palmarly, and therefore,
under axial load, the lunate would always rotate into extension while the scaphoid
would go into flexion under the same type of load ([Fig. 3]). Based on this, they hypothesized that there is a dynamic, self-stabilizing mechanism
by which the two bones do not dislocate in differing directions thanks to the scapholunate
interosseous ligament, an important structure consisting of three distinct components:
palmar, proximal, and dorsal. If that linkage disappears, the carpus is likely to
collapse, with the scaphoid falling into full flexion and pronation, while the lunate
extends and supinates.
Fig. 3 The lunate tends to rotate into extension and translate palmarly (red arrow) under
axial load (white arrow) because it is wider palmarly than dorsally. The scaphoid,
by contrast, tends to collapse into flexion and dislocate dorsally (red arrow) owing
to its obliquity relative to the axis of the forearm.
What I liked about that explanation was that it helped understand why scapholunate
dissociations displace the way they do, but also that it provided a guide to how to
solve carpal instabilities: you reconstruct the scapholunate connection, and the carpus
will be able to carry on again. This was a straightforward concept, and I got hooked
by its the simplicity. Unfortunately, the balm of believing that I knew the truth
did not last long; that model could explain only scapholunate instabilities. The pathomechanics
of most other carpal instability patterns remained unanswered. That meant more curves
in my road ahead.
The “Self-Stabilizing Spring” Theory
The “Self-Stabilizing Spring” Theory
In 1983, I bought and carefully read The Wrist by Julio Taleisnik,[18] another important person in my life. Dr. Taleisnik had always defended a modification
of Navarro's columnar theory,[19] in which the central column of the carpus was controlled not only by the scaphoid
on the lateral side but also by the triquetrum on the medial side. Both of them would
be important stabilizers, and their mechanism of action would be more or less as follows:
Under axial load, the obliquely oriented scaphoid is likely to rotate into flexion.
The triquetrum, by contrast, is likely to be pulled into extension by the palmar hamatotriquetral
ligament. Accordingly, if the ligaments connecting these bones are intact, the proximal
row is likely to become dynamically stable. Based on these concepts, I proposed comparing
the wrist to a spring with two prongs projecting in opposite directions ([Fig. 4]).[20] The more the spring is loaded from distal to proximal, the more stiff the spring
becomes, and the greater the stability. To achieve equilibrium between these two opposite
moments, all the ligaments in this system need to be intact, particularly the dorsal
scapholunate ligament, which prevents scaphoid flexion, and the palmar lunotriquetral
ligament, which prevents extension of the triquetrum. Not surprisingly, these are
the thickest, the strongest, and biomechanically the most important of all proximal
interosseous ligaments.[21] I must confess that I was immediately seduced by the simplicity of this model. I
looked at it from every perspective and could not find an objection against it. It
was the model I had been looking for, so I started disseminating it in my lectures.
Fig. 4 Photograph of a disarticulated proximal carpal row seen from distal to proximal.
The dorsal scapholunate ligament protects the scaphoid against excessive flexion,
while the palmar lunotriquetral ligament controls extension of the triquetrum.
The “Oval Ring Theory”
It was about that time that I was offered the opportunity of working as visiting scientist
at the Biomechanics laboratory of the Mayo Clinic in Rochester, Minnesota. That was,
no doubt, the most rewarding time of my professional life, and I'll always be thankful
to Drs. Green, Dobyns, and Chao for making it possible. Working with such great individuals
such as Drs. An, Linscheid, Cooney, Amadio, Berger, Bishop, Horii, and Schuind was
a big challenge, but also a beautiful experience. Once I got used to the Mayo Clinic
ways of doing things, I proposed testing the “self-stabilizing spring” model of carpal
stabilization in the cadaver. Tabloid journalists say, “Don't spoil a good story by
sticking to the facts.” That's exactly what happened when we tried to validate the
“self-stabilizing spring” model in the laboratory: we spoiled our “good story.” With
the late Dr. Kobayashi, we used stereoradiographic techniques to verify whether it
was true that the scaphoid flexes while the triquetrum extends when the neutrally
positioned wrist is axially loaded.[22] Much to my dismay, we found that what we had been teaching was not correct. We proved
instead that, under axial compression, all three bones rotate into flexion. Indeed,
when the wrist is axially loaded, the scaphoid flexion moment predominates over the
triquetrum extension moment, and a “volar intercalated segmental instability” pattern
of malalignment appears unless the two palmar midcarpal ligaments are intact: the
one binding the capitate to the triquetrum and hamate, and the other linking the capitate
to the scaphoid. Certainly, the more we looked into it, the more ligaments we found
to be involved, and the more reasonable appeared the so-called oval ring concept suggested
by David Lichtman ([Fig. 5]).[23] Yes, for the wrist to be stable there must be a mechanical interaction of joint
compressive forces and the constraining effects of several ligaments in both the lateral
and medial columns of the wrist ([Fig. 6]).
Fig. 5 Wrist dissection showing the four links (yellow arrows) that determine intracarpal
stability, according to Lichtman's “oval ring model”[23] C: capitate; S: scaphoid; L:lunate; Tq: triquetrum.
Fig. 6 Under axial load (yellow arrow), the distal row tends to rotate into pronation, the
scaphoid into flexion, and the triquetrum toward extension (red curved arrows).
Role of Wrist Proprioception in Carpal Stability
Role of Wrist Proprioception in Carpal Stability
There was one moment, however, when I started to feel uneasy working with simplified
mechanical models, and I felt particularly uneasy thinking of ligaments as if they
were like cables providing the only means of stability to the joint. No, ligaments
could not be the only wrist stabilizers. If they were, how could gymnasts land on
their wrists from considerable heights without suffering any injury at all? If the
average yield strength of the dorsal scapholunate ligament is 260 newtons,[21] which is ∼58 pounds-force, how come it doesn't break more often? Of course, the
answer had to be in the forearm muscles. By and large, the vast majority of mechanical
models had ignored or underestimated the role of muscles in protecting these joints
from injury. It was time for us to change that. It was time to study neuromuscular
control of carpal stability.
First of all, we needed to know the mechanisms of wrist proprioception to clarify
why and how our muscles know when they are required. Two research teams have been
working on this: one led by Elisabet Hagert[24]
[25] at the Karolinska Institute in Stockholm, Sweden, and the other by Richard Berger[26] at the Mayo Clinic. The two teams had used sophisticated immunohistochemical analyses
to identify, qualify, and quantify mechanoreceptors in the carpal ligaments. At that
time, I was already in Spain, where in 1994, with my senior partner Alberto Lluch,
we founded the Institut Kaplan, the first private hand center in the country. We envisioned
a center emphasizing good-quality clinical practice, teaching, and research. The latter
was mostly done at the Anatomy Department of the University of Barcelona, where we
set up the URBES (Unitat de recerca de la biomecànica de l'extremitat superior) laboratory
under the patronage of Professor Manuel Llusá.
In 2007, we established a collaboration with Elisabet Hagert, who was kind enough
to spend time in our laboratory obtaining samples from the different wrist ligaments
to evaluate the density and distribution of mechanoreceptors in the carpus. Interestingly
enough, most ligaments inserted into the triquetrum were richly innervated with plenty
of receptors, while other ligaments behaved like blind structures.[25] Dr. Hagert's team had gone even further. Using ultrasound guidance, they inserted
fine wire electrodes into the dorsal scapholunate ligaments of normal volunteers.[24] After electrical stimulation of that ligament, the electromyographic activity in
specific forearm muscles was recorded in different wrist positions. That investigation
provided evidence of wrist ligamentomuscular reflexes, with early reactions being
interpreted as a joint-protective function, while later co-contractions probably indicating
supraspinal control of wrist stability ([Fig. 7]). Of course, activity changes were not restricted to one muscle for each wrist position.
Combined reactions were the rule. Unfortunately, we didn't have enough knowledge about
the mechanisms by which muscles could influence carpal bone alignment. Certainly,
there was a need for further research in this regard. That would be one of our main
lines of research ([Fig. 8]).
Fig. 7 Schematic representation of the ligamentomuscular reflexes that mediate proper neuromuscular
wrist stabilization. Afferent and efferent stimuli (red arrows) communicate the stressed
state of the ligament to the protective muscles.
Fig. 8 Photograph of a specimen set in a specially designed jig to investigate the effect
of individual muscle contraction in the alignment of the carpal bones. Black sensors
are attached to specific bones to assess three dimensional carpal rotations. (URBES
laboratory, Department of Anatomy, Universitat de Barcelona, Spain.)
Role of Muscles in Carpal Stability
Role of Muscles in Carpal Stability
In my lectures, I was used to saying that the most likely dynamic scaphoid stabilizer
was the flexor carpi radialis (FCR). I had even worked on the hypothesis according
to which, if an axial load was about to disrupt the dorsal scapholunate ligament,
the mechanoreceptors contained in that ligament would detect such an unusual tension
and would generate a warning message to the spinal cord, which would be followed by
an almost automatic order to the FCR muscle, and a reactive contraction would correct
the malalignment or, at least, prevent further ligament damage.
The concept of the FCR being a dynamic scaphoid stabilizer was not new. In fact, it
was first published by Christian Jantea[27] in 1994, based on the fact that the tendon uses the scaphoid as a pulley to increase
its mechanical advantage. Moreover, because the FCR tendon angles around the scaphoid
tuberosity, any contraction was likely to generate a dorsally directed vector that
extends the scaphoid. It was such a nice explanation that I must admit that I felt
a bit disappointed when it was not confirmed by Dr. Hagert's in vivo experiments.
So we decided to do our own testing. With one of my doctoral fellows, Guillem Salvá,[28]
[29] we completed a cadaver study in which we loaded the FCR tendon while holding the
hand in neutral position. Scaphoid displacements were monitored using a highly accurate
electromagnetic motion-tracking system. Once again, our hypothesis—according to which
the FCR is able to induce extension to the scaphoid—was proved to be wrong. No matter
how we placed the wrist, the scaphoid always flexed when axially loaded. Indeed, when
forced against the scaphoid, the trapezium induces flexion, not extension as we had
hypothesized. Obviously, we will have to find new explanations for these findings,
and that is what we are doing right now in our laboratory.
Summary
Truly, my personal path toward understanding carpal kinetics has been characterized
by a series of curves motivated by misconceptions that proved not to be good enough
to explain reality. Indeed, there is no real advancement if one is not willing to
reconsider one's ideas when new evidence suggests these not to be completely true.
In the beginning I thought that the wrist was an enigmatic articulation, with funny-shaped
articular surfaces. Back then, the only bone that counted in providing stability was
the scaphoid. Truly, that bone was regarded as the essential link between the two
carpal rows. Then I learned about the importance of a precise interaction between
the scaphoid, which tended to rotate into flexion, and the lunate, which tends to
rotate into extension. And then I became convinced about the important stabilizing
role of both the scapholunate and lunotriquetral ligaments in providing stability.
The wrist was like a spring with two prongs directed in opposite directions. And then
I realized that the proximal row, by itself, was not enough to guarantee stability
to the wrist, and the oval ring concept came into place. But of course, when we studied
the elastic properties of all carpal ligaments, it was obvious that they were not
strong enough to be considered as cables holding bones in place. Stability could not
depend only on ligaments. But then we learned about the existence of mechanoreceptors
in those ligaments, and we had to admit that neuromuscular control had been by and
large underestimated. And here we are now trying to unravel new evidence suggesting
a complex system of ligamentomuscular reflexes. Indeed, for the wrist to be stable
in kinetic terms, not only does joint geometry need to be intact, but also the ligaments
must be mechanically and sensorily active to detect changes of tension to trigger
specific muscle activations or inhibitions to control carpal rotation.
If carpal knowledge were a mountain, I must say that the hiking until now has been
great. There have been times, however, when I thought that I was about to reach the
top of it. Of course, it looked as if the summit was right there.…but it was not!
I guess that, paraphrasing the ASSH past president Marybeth Ezaki, definitely, we
are not there yet. But I'll never forget those who inspired me to undertake—and those
who came along on—such an exciting journey ([Fig. 9]). To all of them, and particularly to Ron Linscheid and Jim Dobyns, God bless you!
Fig. 9 Short list of those who inspired me to undertake—and those who came along on—such
an exciting journey. From left to right, upper row: Drs Günther, Destot, Fisk, Dobyns,
Linscheid, Taleisnik, Allieu. Middle row: Drs. Kauer, Cooney, Berger, Amadio, Lichtman,
Saffar, Stanley. Lower row: Drs. Lanz, Horii, Heras-Palou, Hagert, Lluch, Ferreres,
Lluch-Bergadá, and many more.
