m. dupuytren: the cutaneous ligaments of the palmodigital...
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M. Dupuytren: The cutaneous ligaments of the
palmodigital junction of the hand.
A.T. Malsagova 1806203
Under the supervison of
P.M.N. Werker, M.D. Ph.D.
R.L. Zwanenbrug, drs.
University Medical Center Groningen, the department of Plastic Surgery (and the department
of Neuroscience, Anatomy)
Scientific internship January – June 2012
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Abstract
Introduction
Dupuytren’s Disease (DD) is a fibroproliferative disease of the normal palmar and digital
fascia of the hand, resulting in the formation of fibrous cords. Although this is a benign
disease, the fibrous cords can give rise to disabling flexion deformities of the fingers,
sometimes necessitating amputation in the advanced stages. Although the normal
microanatomy of the fascial structures of the hand is essential to the understanding of DD’s
progression and its treatment, the literature in unequivocal especially where it concerns the
transition of the palmar fascia into the digital fascia. The aim of this study was therefore to
elucidate the microanatomy of the palmodigital junction and its relation to palmar and digital
fascial structures.
Methods
To this end we performed a literature and a dissection study. We dissected a total number of
26 cadaveric digits, 13 middle fingers and 13 ring fingers from 13 fresh frozen human
cadaveric hands. A longitudinal midline incision was used on the volar aspect of the hand,
running from the midpalm to the tip of the finger. The characteristics of the palmodigital
structures were observed and their interrelations with palmar and digtal structures. The
proximal and distal borders of the palmodigital fibrous condensations were measured and
their width in the midline of the finger at origin and radially and ulnarly.
Results
At the palmodigital junction we found a structure which to our knowledge has not been
described before. This structure spirals around the neurovascular bundle at the palmodigital
junction and we therefore suggest to call it the palmodigital spiralling sheet (PSS). The
proximal border fibres of PSS originate from the pretendinous band and insert into the
natatory ligament (NL). The intermediate fibres originate from the flexor tendon sheath over
the A1 pulley and continue as Grayson’s fibres. The distal border fibres originate from the
flexor tendon sheath just distal to the proximal border of the A2 pulley and arch into Cleland’s
1B ligament while it attaches on the flexor tendon sheath at the proximal interphalangeal
joint. PSS forms the most proximal and inner part of the neurovascular tunnel. Additionally
three types of continuities between volar and dorsal fibres in the digit have been found,
possibly contributing to a spiralling arrangement of fibres in the neurovascular tunnel.
Conclusion
This study has provided new insights in the microanatomy of the palmar, digital and
especially the palmodigital fascia of the hand. The palmodigital spiralling sheet at the
palmodigital junction has been found to have an important linking function between the
palmar and the digital fascia. PSS and the continuities found between fibres in the digit make
the fascia of the palm and digit an intertwining continuum of fibres, instead of separate
anatomical structures. Therefore any part of this continuum has the potential of becoming
pathologic in DD.
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Introductie
De ziekte van Dupuytren is een fibroproliferatieve aandoening van de normaal aanwezige
fasciale structuren van handpalm en vingers, wat vaak resulteert in het ontstaan ven fibreuze
strengen. Hoewel deze aandoening benigne is, leiden deze fibreuze strengen vaak tot
invaliderende flexiecontracturen van de vingers. In een gevorderd stadium van deze ziekte
kan soms zelfs amputatie noodzakelijk zijn. Hoewel de normale microanatomie van de
fasciale structuren van de hand essentieel is voor inzicht in de progressie van de ziekte van
Dupuytren en de behandeling ervan, lijkt er in de literatuur geen consensus over te bestaan en
dat geldt vooral voor de anatomie van de palmodigitale overgang. Het doel van dit onderzoek
was daarom het verhelderen van de microanatomie van de palmodigitale overgang en diens
verbanden met palmaire en digitale fasciale structuren.
Methode
Met dit doel hebben wij een literatuur en een dissectie studie uitgevoerd. In totaal zijn er 26
vingers gedisseceerd, waarvan 13 ring- en 13 middelvingers, afkomstig van 13 handen van
fresh frozen cadaver materiaal. Er is een longitudinale midlijn incisie van de midpalm tot aan
de vingertop gebruikt. Er is gelet op de karakteristieken van de palmodigitale structuren en
hun anatomische relaties met palmaire en digitale structuren. De proximale en distale grenzen
van de palmodigitale structuren zijn gemeten als ook de breedte in de midlijn, aan de radiale
en de ulnaire zijde.
Resultaten
Op de palmodigitale overgang hebben wij een structuur gevonden die voor zover wij weten
nog nooit eerder beschreven is. Deze structuur spiraliseert als een geheel om de
neurovasculaire bundel. Daarom stellen wij voor om deze structuur de palmodigital spiralling
sheet (PSS) te noemen. De proximale grens vezels van PSS hebben hun origo in de
pretendineuze band en insereren in het natatorium. De intermediaire vezels hebben hun origo
op de flexorpeesschede, voornamelijk ter hoogte van de A1 pulley, en insereren in Grayson’s
ligament. De distale grens vezels van PSS hebben hun origo ook op de flexorpeesschede, net
distaal van de proximale grens van de A2 pulley, en buigen mee met Cleland’s 1B ligament
richting de flexorpeesschede bij het proximale interfalangeale gewricht. Zodoende vormt PSS
het meest proximale en binnenste deel van de neurovasculaire tunnel. Daarbij zijn er ook drie
soorten continuïteit gevonden tussen volaire en dorsale vezels in de vinger. Deze dragen
mogelijk bij aan de oriëntatie van vezels binnen de neurovasculaire tunnel.
Conclusie
Dit onderzoek heeft nieuwe inzichten gegeven in de microanatomie van de palmaire, digitale
en vooral de palmodigitale fascies van de hand. De palmodigital spiralling sheet op de
palmodigitale overgang heeft een belangrijke verbindende functie tussen de palmaire en de
digitale fasciale structuren. PSS en de eerder genoemde drie soorten continuïteiten verenigen
de palmaire en digitale fascies tot een doorlopend continuüm ven vezels, waarin geen aparte
anatomische structuren zijn aan te wijzen. Daarom kan ieder onderdeel van dit continuüm
potentieel pathologisch worden bij de ziekte van Dupuytren.
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Contents
Abstract 2
Contents 3
Introduction 5
Materials and Methods 16
Results 19
Discussion 39
Conclusion 45
Acknowledgements 46
References 47
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Introduction
This study has been performed to elucidate the microanatomy of the hand, focusing on the
fascial structures of the palmodigital junction. Although the microanatomy of the hand is
essential to the understanding of how Dupuytren’s Disease (DD) progresses and to its surgical
treatment, the literature is incomplete and gives different accounts on the same fascial
structures. Prior to getting into this particular aspect of DD, we shall give a detailed overview
of the current knowledge of DD.
Dupuytren’s contracture or Dupuytren’s Disease, also known as palmar fibromatosis, is a
fibroproliferative disease of the normal palmar and digital fascia resulting in the formation of
noduli and cords in the palm and fingers of the hand. Although this disease is a benign
process, the fibrous cords may gradually give rise to disabling flexion contractures of the
metacarpophalangeal (MCP), proximal interphalangeal (PIP) and distal interphalangeal (DIP)
joints next to web space contractures. The flexion contractures can overtime become so
severe, as to make the patient dependant on others in his daily activities. Surgery is the
treatment of choice in most cases of Dupuytren’s contracture, but recurrence and or extension
into unaffected areas is almost inevitable. There is no cure for DD, in the worst case scenario
the flexion contractures necessitate amputation of one or multiple fingers for the lack of better
treatment.
Historical background
Although Dupuytren’s Disease bears the name of baron Guillaume Dupuytren, who was head
surgeon at Hôtel-Dieu in Paris from 1816 to 1835, the first descriptions of this condition date
back to much earlier. The oldest written descriptions of DD found, date back to 1614. In his
Observations Felix Plater from Basel describes the case of a stonemason with the
pathognomic flexion contractures of the ring and little fingers and ridging of the palmar skin,
which contemporary plastic surgeons would undoubtedly recognize as DD. But Felix Plater
misinterpreted it for contracted tendons which ruptured form their sheaths (1). It is suggested
that DD has its origin in Northern Europe. McFarlane believes DD to originate in Germanic
tribes between 1200 and 200 BC and that it was spread by their migration and also later by
Vikings through their international raids and conquests (2). This seems to be in accordance
with the high incidence of DD in north-east England and the north and west of Scotland,
which were invaded and colonized by Norsemen. Although no reports of DD have been
found, the presence of the disease in Scotland is illustrated by the legend of the Curse of the
MacCrimmons. These renowned bagpipe players were associated with a disease bending the
little finger.
Henri Cline probably was the first one to describe that the underlying cause of DD was to be
found in the palmar fascia, after he performed two dissections on cadaveric hands with
Dupuytren’s contracture in 1777. In his notes he also associates DD with manual labour.
Astley Cooper, one of Henri Cline’s former students, was the first one to introduce
fasciotomy as treatment for the thickened palmar fascia in DD (1). It was only on the 5th
of
December 1831, not long before his death, that Guillaume Dupuytren made his famous
contribution to this disease. He gave a lecture presenting his findings to Hôtel-Dieu and
demonstrating the case of a coachman Mr. Demarteau, on which he performed a palmar
fasciotomy at the same lecture cutting the diseased cords to release the flexion contracture
after which a splint was applied (3). Afterwards many publications criticizing Dupuytren’s
work followed. One of his severest critics was Goyrand, he denied any involvement of the
palmar fascia in DD. Sanson, one of the members of Dupuytren’s staff, defending his work
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against Goyrand, still believed the pathological tissue in DD to arise from normally present
palmar fascia. In spite of Goyrand’s contributions to DD, Dupuytren and Sanson were in the
right about the involvement of the palmar fascia in DD (4, 5).
Epidemiology
The prevalence of DD varies between 0.2 and 56%, depending on age, population group and
method of data collection (6). Mostly older Caucasian men of Northern European descent are
affected (5, 7). Epidemiological research has shown the prevalence of DD to vary
considerably among different races and it is uncertain whether the cause is genetic,
environmental or a combination of both. The prevalence of DD in the Norwegian population
aged over 60 years, has been reported to be 30% (6). Dupuytren’s contraction does exist in the
black population, but is extremely uncommon (8). As it is in the Asian population, though
some parts of Japan and Taiwan show similar prevalences to those of Northern Europe. But
the expression of DD is less extensive there, constituting only nodules without cord
formation, which usually makes surgery unnecessary (5). The existing data on the prevalence
of DD are still inconclusive in many respects. For instance although DD is said to be most
prevalent in the North-Western part of Europe, the highest prevalence rates of DD have been
found in Bosnia and Canada. Several studies have shown the prevalence of DD to increase
with age (6). Men are more frequently affected than women, with a 5.9:1 ratio, and children
rarely present with DD (6,9). The incidence rises for men in their 5th
decade and for women in
their 6th
decade. But the incidences in men and women seem to equalize as they approach the
9th
decade (5).
Aetiology
The aetiology of Dupuytren’s contracture is largely unknown, but research so far suggests that
the aetiology is most likely multifactorial, a combination of several genetic as well as
environmental factors. If the general belief that Dupuytren’s disease originates in the Vikings
and was spread through their conquest of new lands and migration in mainly Northern Europe
is true, one can conclude that there is probably a genetic component involved in the origin of
Dupuytren’s Disease. This would also explain why DD is uncommon in populations of
African, Middle-Eastern and Asian descent. DD is believed to have an autosomal dominant
inheritance pattern (6, 10). In fact Dolmans et al. have through a Genome Wide Association
Study identified nine genes associated with DD, of which six encoded proteins in the Wnt-
signaling pathway (11). This pathway regulates cellular proliferation and has been therefore
linked to DD. When over stimulated this pathway can through the effects of β-catenin lead to
fibroblast proliferation, nodule formation and eventually DD (12).
In spite of the genetic factor in DD, research indicates that environmental factors also make a
significant contribution to the development of DD. Srivastava et al. report ten cases of DD
from India, which all have been residing in the United Kingdom for a considerable amount of
time (6, 13). Smoking and alcohol abuse have been associated to DD, but may not be the
direct causes of DD (14). For instance although the alcohol consumption has doubled the last
40 years, the prevalence rates of DD have not. This contradicts a direct causative effect (6).
Dupuytren has in his time suspected an association of manual labour and hand trauma with
the development of DD (3), in present day there are as many studies acknowledging this
connection as rejecting it (7). A meta-analysis by Descatha et al. reports high levels of manual
labour and vibration to be associated with DD, in favour of the manual labour hypothesis (15).
If true, DD can be a reaction to the rupturing of fibrils in the collagen after trauma to the
palmar fascia. There is also a number of conditions which have been said to occur frequently
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with DD, though again not proved to be causative factors: diabetes mellitus,
hypercholesterolemia, cirrhosis of the liver, epilepsy and the use of anticonvulsant drugs
(5,7).
Presentation and Diagnosis
Although DD is generally known for the fibrous cords leading to flexion contractures, which
are relatively easy to diagnose, the early beginnings of DD are very hard to discern and can be
easily mistaken for other diseases. These early beginnings usually constitute the fibrosis of the
Grapow fibres, vertical fibres attaching the skin to the underlying palmar fascia. This results
in pitting and thickening of the palmar skin (16, 17). DD usually becomes easier to diagnose
once the pathognomonic nodules appear which in the natural course of the disease are
followed by fibrous cords. These nodules usually are located near the distal palmar crease (5),
but later can appear in the finger or at the level of the MCP joint of the thumb. When facing
skin pits and nodules, one should not forget to consider a differential diagnosis, consisting of
ganglia, inclusion cysts, occupational hyperkeratosis, callous formation and tenosynovitis
among others. Epithelioid sarcoma can also easily be mistaken for DD (18). As DD
progresses, the nodules transform into cords and cords also arise independently through
myofibroblast contraction. These cords mostly give rise to flexion contractures of the MCP
and PIP joints. The duration of the transition of the early nodules to the clinically relevant
flexion contractures may be variable, varying from as short as a year to more than two
decades (19). MCP flexion contractures usually precede PIP flexion contractures (17). Most
cords have their initiation points in the palm and can pass all the way to the distal phalanx,
giving the appearance of pseudotendons. DD rarely involves the DIP joint, but if it does, there
is usually a Boutonnière deformity, hyperextending the DIP joint. The most frequently
affected finger is the ring finger, followed by in decreasing order, the little finger, the middle
finger, the index finger and the thumb, being the least affected. DD has the tendency to start
in the palm of the hand and progress distally into the fingers, but it can also be isolated in the
palm or in the digits alone. Bilateral DD is very common, with one hand mostly being more
severely affected than the other. Hand dominance has not been reported to play any part in the
hand most affected by DD (20).
The lesions caused by DD are painless in most cases, although the nodules in the early stages
of DD can be painful on compression. But this sensation passes as the disease progresses.
There are also no signs of inflammation. As stated previously DD patients are mostly men and
they also have an earlier symptom onset than women. Another typical finding is blanching of
the skin overlying the cord on extension. Patients typically experience thickening of the
palmar skin, palmar nodules, stiffness and most importantly loss of the range in motion in one
or more fingers, leading to severe functional impairment. When the contractures become
severe (a MCP contracture of 30° or more), the patient is unable to put the palm of the
diseased hand on the table, which gives a positive tabletop test (21).
Ectopic lesions of DD or lesions associated with DD can be found on the dorsum of the hand,
in the form of the so called knuckle pads or Garrod’s nodes at the level of the PIP joints.
These knuckle pads are associated with bilateral disease, and also with a higher simultaneous
occurrence of other forms of ectopic disease (22). These are plantar and penile fibromatosis,
Ledderhose’s Disease and Peyronie’s Disease respectively. Knuckle pads however do not
correlate with the severity of the disease, because they do not give rise to flexion contractures.
The appearance of knuckle pads precedes that of palmar nodules and they can regress as the
palmar disease progresses (19). Ledderhose’s disease does not result in flexion contractures
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either, but the thickening of the plantar fascia and the consequent development of nodules
make walking painful. Peyronie’s disease leads to penile curvature through the formation of
fibrotic lesions on the dorsum of the penis, sometimes impeding sexual function (17, 19).
Ledderhose’s as well as Peyronie’s diseases haven been found to be frequently present
concurrently with knuckle pads (22). Peyronie’s Disease has been found to share genetic
susceptibility with DD through the WNT2 locus (23).
The term Dupuytren’s diathesis was first introduced by Hueston in 1963 to describe a set of
features in the presence of which an individual had a greater predilection for Dupuytren’s
contracture (21). Currently Dupuytren’s diathesis constitutes the following criteria: male sex,
early disease onset (before 50 years of age), Northern European descent, more affected family
members, bilateral involvement and the presence of knuckle pads. There is no consensus
between different authors though on what this list of criteria should be. People with several of
the requirements for Dupuytren’s diathesis have an increased recurrence risk and a worse
prognosis. Hindocha et al. also showed the recurrence risk in people with Dupuytren’s
diathesis as defined by them, to be 71% in comparison to 23% in people without Dupuytren’s
diathesis (24).
Pathophysiology and histology
The pathophysiological processes underlying DD are fibroblastic proliferation and
disorganized collagen deposition, resulting in thickening of the palmar fascia, the formation
of nodules and transition to fibrous cords. Nodules consist of hypercellular and hypervascular
tissue, while cords are hypocellular and organized collagen structures, mostly collagen type
III. Myofibroblasts have been identified as the engine behind the development of Dupuytren’s
disease. The hypercellularity in the nodules constitutes mainly these myofibroblasts. These
are fibroblasts producing α-smooth muscle actin, which makes them resemble smooth muscle
cells (25, 26). The contractile property of myofibroblasts causes the fibrous cords in DD to
contract and result in flexion deformities of the fingers. As the disease progresses, the nodules
are replaced by cords through myofibroblast contraction, concurrently the nodulair
hypercellularity is replaced by the relative acellularity of the cords. The collagen in these
cords follows the lines of stress as exerted by the hand. Luck has described three phases in the
development of Dupuytren’s contracture. A proliferative phase which is characterized by
fibroblastic proliferation clinically presenting itself as the early nodules in DD. Secondly an
involutional phase follows which constitutes the contracting myofibroblasts and type I and III
collagen deposition. Finally a residual phase which is marked by relatively acellular scar-like
tissue constituting the fibrotic cords (27, 28). These stages in cord formation resemble those
of other forms of repair, such as wound healing. For instance both DD and the wound healing
process have collagen type III deposition in common. Furthermore the culpable cell in DD,
the myofibroblast, also plays an important role in granulation tissue, assisting wound closure
through its contractile properties (29, 30). For the time being it is unclear what triggers this
repair like response, some believe smoking, alcohol abuse and microtrauma to result in
microvascular disease and ischemia (17). Subsequently released free oxygen radicals are
suggested to be the inflicting agents triggering the tissue repair response (31).
Treatment
The early stages of DD do not necessarily warrant treatment. Nodules do not always progress
to cords and flexion contractures may be non progressive as well. Therefore observation is the
best policy for static forms of DD without impairment of function (17). Treatment indications
largely depend on the patient’s personal perception of impairment and on measured flexion
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contractures. Invasive treatment before functional limitations is usually not practiced.
However nodules in the early stages of DD can give rise to pain and discomfort. Fingerless
gloves with silicone padding across the palm can be worn to relief the pain until the painful
nodules resolve. Also intralesional steroid injections can possibly be used in the nodular stage
of the disease. One study has shown significant regression of the disease in 97% of the hands
after an average of 3.2 injections per nodule (32). Surgical treatment is the most commonly
used treatment for the advanced stages of DD with the aim to restore function. A flexion
contracture of 20-30° or more of the MCP joint or the interphalangeal joints is the general
indication for surgery (33), corresponding with the aforementioned positive table top test.
The most commonly used intervention for DD is fasciectomy which is the complete or partial
excision of the diseased fascia. Radical fasciectomy (RF) entails the complete excision of the
fascia in the palm and fingers, including both healthy and affected fascial structures. The
reasoning behind this was that seemingly unaffected fascia has the potential for causing
recurrence. Some believe this cancer operation for an in fact benign disease is inappropriate
(28). RF has become obsolete, because of its higher complication rate and similar recurrence
rate in comparison to limited fasciectomy (34). The most widely used surgical procedure to
treat DD is the limited or partial fasciectomy (LF) and entails the removal of diseased tissue
only. This approach allows proper exposure of the pathologic cord and possible involvement
of the neurovascular bundle (33). Segmental fasciectomy (SF) involves the excision of only
small one centimetre segments of pathologic tissue, by means of a series of C-shaped
incisions. The rate of recurrences and extensions of the disease after SF have been shown to
be similar to other surgical approaches (35, 36), which makes SF a plausible alternative for
LF. Finally with dermofasciectomy (DF) next to pathologic tissue the overlying skin is also
removed and replaced with skin-grafts from the ipsilateral extremity or the groin area (37).
The proponents of DF believe the skin to also be involved in the diseased tissue and therefore
advocate its removal. This method in some hands reduces the recurrence rate of DD (38, 39)
or at least prolongs the time till recurrence. This aggressive surgical approach is therefore
mostly used for recurrent and primary DD with diathesis when the skin is adherent to the
underlying pathologic tissue (16). One of the drawbacks in skin-grafting is that there is risk
for graft rejection and donor site morbidity. Although surgery does not cure DD, it does
release flexion contractures to the extent of significantly improving overall hand function
(40).
The great counterpart of fasciectomy is fasciotomy, which constitutes the division of the
contracture inflicting cord without excision, described by baron Dupuytren himself.
Nowadays this procedure is implemented in the form of percutaneous needle fasciotomy
(PNF). This procedure is less invasive than open surgery, for the skin is not cut. Disposable
needles are used for repetitive puncturing motions to divide the cord through the skin. The
finger is then passively stretched to further rupture the cord. PNF is a popular procedure,
because of its limited invasiveness, low complication rate and fast return of motion (usually
within one week) (33). PNF only requires local anaesthesia for the skin, for the cords are not
innervated. Damage to the digital nerve, tendon ruptures and skin tears are possible
complications of PNF. Recurrence rates are high, one study reported a 58% recurrence rate at
3 years (41) and another a 85% at 5 years (42). Van Rijssen et al. have conducted a
comparative study between LF and PNF (42, 43). They have found the results of PNF to be
similar to those of LF for early stages of DD but not for the advanced stages of DD. Their
conclusion is that PNF is unsuitable for advanced DD. PNF however remains a good
alternative for elderly, sickly patients not able to endure the physical strain of surgery.
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Advocates of fasciectomy and fasciotomy still argue especially on the issue of the digital
nerve being at considerable peril or not with the ‘blind’ procedure of PNF.
Additionally there is an open palm technique in which transverse incisions at the level of
palmar and digital creases can be left open to heal by secondary intention, introduced by
McCash (44). The only requirement is for the flexor tendons not to be exposed. This
technique is especially suitable for older patients with severe flexion contractures and
therefore inadequate skin for closure. This method allows hand soaking and immediate
exercises to improve the range of motion (33). The complication rate has been found to be
low with the McCash method (45), but it does not have any beneficial influence on the long-
term outcome, i.e. recurrence (46). One of the ongoing debates in the treatment of DD is
therefore on the issue whether to close or not to close. In any kind of surgery MCP joint
contractures are usually easier to correct than PIP joint contractures.
There are other forms of non-surgical treatment for DD. One of the most recently developed
treatments is collagenase injection therapy, which is still experimental. Collagenase is a
combination of two enzymes derived from the microorganism Clostridium Histolyticum,
which has been found to have collagenolytic properties. Collagenase is injected into a
palpable cord, where its enzymatic activity dissolves the pathologic tissue and therefore
weakens the cord. The following day the contracted joint can be passively extended until the
weakened cord ruptures, with anaesthesia if necessary. Just as surgical treatment collagenase
injection therapy is indicated for flexion contractures of the MCP and PIP joints of at least
20°. A cord can only be injected at one site during one session, this procedure can be repeated
at 30 day intervals (33, 47). Hurst et al. have shown collagenase to release 77% of the MCP
joint contractures and 40% of the PIP joint contractures by 0-5°. This in comparison to 7.2%
and 5.9%, respectively in the placebo group. Also the range of motion was improved by an
average of 41° in MCP joints and 29° in PIP joints. Less severe contractures have an overall
better response rate. The reported adverse events have been peripheral oedema, pain,
haemorrhage, skin lacerations and pruritus at the site of injection (48).
Other less practised, but nevertheless potentially promising treatment forms are continuous
traction and radiotherapy. Messina et al. have described continuous skeletal traction of a cord
through an external fixator. They have shown that preoperative implementation of this
treatment can improve the results of fasciectomy afterwards (49). The results of some studies
suggest that radiotherapy of the affected area can prevent disease progression and achieve
symptomatic improvement (50), but the effectiveness of radiotherapy remains controversial.
As of yet no form of therapy has been developed to completely eradicate DD. Recurrence and
extension of the disease are more rule than exception. There is no one suitable approach for
all forms of Dupuytren’s contracture, the chosen surgical approach must be fitted to the
individual patient.
Having provided some general knowledge of DD, we now embark on the main concern of this
study, the underlying microanatomy in DD, maybe one of its most elusive aspects.
Microanatomy
DD follows anatomical pathways (51, 52) transforming ‘bands’ into ‘cords’, the normal
microanatomy of the hand therefore is an important aspect in the interpretation of the
contractures caused by the fibrotic cords in DD. We give a general overview of palmar as well
digital fascial structures. Since the palmodigital junction is situated in between, palmar as well
as digital structures have potential relevance to it.
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The palmar aponeurosis is the core of the pathologic activity in DD (figure 1). This is a
triangular shaped condensation of fascia which is connected to the overlying skin on the volar
side of the hand by small fibres described by Grapow (53) and is situated volarly to the
superficial palmar arch. Proximally the apex of this structure is continuous with the tendon of
the palmaris longus muscle, if present, and otherwise just attaching to the flexor retinaculum.
The palmar aponeurosis is extended between the thenar and hypothenar eminences and
distally ends at the transverse ligament of the palmar aponeurosis (TLPA) along a line that
joins the proximal and distal palmar creases. The palmar aponeurosis is part of the palmar
fascia of the hand, which can be divided into three categories, the fibres running
longitudinally, transversely and vertically.
Figure 1: Illustration of the fascial structures of the palm of the hand. The palmar aponeurosis is indicated with
PA, the transverse ligament of the palmar aponeurosis with TLPA and the natatory ligament with NL. The
pretendinous band and the spiral bands for ray 2 are indicated. In the upper right corner a magnification of NL is
shown. Next to the transverse fibres, the arciform fibres in the interdigital skin fold are seen to extend into the
digital fascia (from Rayan GM. Palmar fascial complex anatomy and pathology in Dupuytren’s disease. Hand
Clin. 1999;15:75)
Longitudinal fibres
The longitudinal fibres of the palmar aponeurosis are called pretendinous bands and radiate
distally along mainly the rays of digits II, III, IV and V (figure 1). The pretendinous bands
overlie the flexor tendons and the prelumbrical bands overlie the lumbrical muscles in
between the pretendinous bands. The prelumbrical bands are less dense than the pretendinous
ones. These longitudinal bands pass from the apex of the palmar fascia to just beyond TLPA.
Pretendinous bands give rise to pretendinous cords in DD resulting in MCP joint flexion
contractures. Pretendinous cords can continue in the digit as central cords, resulting in PIP
joint contractures (51).
According to McGrouther, after passing TLPA volarly, the pretendinous bands almost
immediately divide into three layers as shown in figure 2 (52). The first layer of pretendinous
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extensions is most superficial and consists of cutaneous insertions which insert into the
palmar skin contributing to the formation of the palmar creases. Some of these cutaneous
extensions of the pretendinous band have been reported to pass to the volar skin of the
proximal phalanx, superficial to the natatory ligament (NL) (54). The second layer is heralded
by the bifurcation of the pretendinous extensions, they have therefore been called the
bifurcating fibres by Legueu and Juvara in 1892 (55). From the bifurcation point distally to
the TLPA, they pass dorsally to NL and the neurovascular bundle to the finger, where they
join the lateral digital sheet (LDS) in the lateral plane of the finger (51, 56, 57). Because of
the spiralling motion these fibres make from their origin at the termination of the pretendinous
band, passing deep to the neurovascular bundle in the palm and coming about superficially to
the neurovascular bundle in the finger, they are also called spiral bands. The third layer is
made up of the deepest pretendinous extensions. These dive deep on both sides around the
MCP joint to insert dorsally in the extensor sheet. According to Legueu and Juvara and also as
described by McGrouther, these fibres perforate the DTIL on their way to the extensor sheet
and are therefore also known as perforating fibres (52, 54, 55). In DD the spiral bands become
spiral cords usually causing PIP contractures. The rigidity of the cords causes the
neurovascular bundle to spiral around this cord. The spiral cord endangers the neurovascular
bundle through medial and proximal displacement (51).
Figure 2: Illustration of McGrouther’s three layers of the pretendinous extensions distal to TLPA. Left side of
the illustration is proximal and right is distal. Layer 1 is indicated by the cutaneous insertions, layer 2 by middle
fibres (spiral bands) and layer 3 by the deep fibres (perforating fibres) in the figure. Note the location of the septa
of Legueu and Juvara dorsal to TLPA and proximal to layer 3 (from McGrouther: The palm. In McFarlane RM,
McGrouther DA, Flint MH (eds): Dupuytren’s Disease: Biology and Treatment (vol 5, The Hand and upper limb
series). Edinburgh: Churchill Livingstone 1990).
Transverse fibres
The transverse fibres in the palm of the hand consist of TLPA and NL. TLPA is the
transverse and most distal portion of the palmar aponeurosis and forms the proximal
commissural ligament in the first web space. The transverse fibres of TLPA pass dorsally to
the longitudinal fibres of the palmar aponeurosis and form a continuous fibrous band of
approximately 1 cm wide in the midpalm between the palmar creases. Skoog has described
13
TLPA to have a close relation to the underlying vertical paratendinous septa of Legueu and
Juvara, with which they form a fibrous tunnelling system or palmar pulley (58). TLPA is
usually not involved in DD, but the proximal commissural ligament can be (53).
NL is the ligament extending from the ulnar border of the little finger to the radial border of
the index finger at the base of the fingers (figure 1). It lies superficially underneath the skin
and volar to the neurovascular bundle. Proximally this ligament crosses the A1 pulley while
attaching to it. Distally it extends into the digital fascia, i.e. Grayson’s ligament, through the
arciform arches, which are fibres forming the interdigital skin folds. NL forms the distal
commissural ligament in the first web space. DD commonly affects NL, which results in
restriction of the abduction of the fingers (58). NL is also believed to send deep fibres to the
sides of the fingers, making it a three-dimensional entity (59, 53). NL is situated more distally
and volarly than TLPA (figure 1), the area in between is called the distal palm and consists of
a prominent fat pad. In this area, also called the interdigital lacunae, the neurovascular
bundles are relatively unprotected (58) and therefore easily accessible to function as
orientation points during surgery or dissection. TLPA and NL are not to be confused with the
deep transverse intermetacarpal ligament (DTIL), which runs between the volar plates of the
MCP joints on a much deeper level. For all three of them are commonly referred to as
transverse ligaments by various authors.
Vertical fibres
The paratendinous vertical septa have been first described by Legueu and Juvara (55). TLPA
gives rise to fibres passing deep to attach to DTIL and forming septa in between the flexor
tendons and lumbrical muscles shown in figure 3 (60, 61). The distal borders of TLPA and
DTIL are at the same level. These two ligaments lie on top of each other separated by the
central compartment of the hand, but still connected through the vertical paratendinous septa.
The studies of Bojsen-Moller and Schmidt revealed nine vertical septa, of which seven
intermediate and two marginal. These septa form eight canals, through four of them pass
flexor tendons to digit II through IV and through the other four pass lumbrical muscles with
the arteries and nerves (60).
14
Figure 3: Illustration of the cross section of the palm of the hand at the level of the transverse ligament of the
palmar aponeurosis (TLPA). Top of the illustration is the volar side of the hand and the bottom is the dorsal side.
Shown is the way the vertical paratendinous septa of Legueu and Juvara form flexor tunnels for the flexor
tendons and lumbrical tunnels through which pass the lumbrical muscles and the nerves and arteries. Dorsal to
the deep transverse intermetacarpal ligament (DTIL) the metacarpals and the interosseous muscles can be found.
Digital fascia
Next to the palmar fascia the palmodigital junction probably also has anatomic relations with
the digital fascia. Cleland’s and Grayson’s ligaments are the most known and important
structures of the digital fascia. Cleland describes a strong ligament arising from the sides of
the phalanges near the interphalangeal articulations and inserting into the laterovolar skin,
dorsal to the neurovascular bundle (54, 62). Grayson described another cutaneous ligament
volar to the neurovascular bundle superficially underneath the skin. Grayson’s fibres originate
on the flexor tendon sheaths and also insert in the digital skin (63). Both ligaments have been
attributed a skin retaining function and together they form the neurovascular tunnel (figure 4).
A recent study (64) has found Grayson’s ligament to be a fibrous network originating from
the flexor tendon sheath volar to the neurovascular bundle. The fibres in this network have the
appearance of running in an inverted V-configuration. Cleland’s ligament has been found to
consist of 4 ligaments: 1A and 1B running approximately at the level of the PIP joint and 2A
and 2B at the level of the DIP joint. 1A and 2A run from the flexor tendon sheath distally in
an oblique fashion to insert in the lateral skin. 1B and 2B have a comparable course in the
proximal direction.
Figure 4: Simplified illustration of the cross section of the finger at the PIP joint level. Top of the illustration is
the dorsal side of the digit and bottom is the volar side. Cleland’s ligament dorsally and Grayson’s ligament
volarly can be seen to surround the neurovascular bundle which is marked with red and green. In the lateral
plane of the digit the lateral digital sheet is indicated.
The lateral digital sheet (LDS) is another digital structure commonly known as the line of
union of the dorsal and volar skin laterally in the finger, where the dorsal and volar fascia join
together to form a thickened strand, i.e. LDS (53). It is assumed to run between the lateral
digital skin and the neurovascular bundle (figure 4), along the entire length of the finger (56,
15
57). The spiral bands have been reported to continue into LDS (51). In DD the lateral cord
arises from LDS. Rarely, if this cord extends distally it can cause a DIP contracture (51).
Research question
The structures that are of particular relevance to the palmodigital junction are situated in
between a line connecting the proximal and distal palmar crease and the PIP joint crease, that
is between TLPA and the PIP joint. In this area distal to TLPA structures as the spiral bands
and NL are of particular interest since they have been described to continue into the digit
merging with digital structures among which LDS. However the existing literature does not
provide any conclusive statements on the palmar origins, the digital insertions and the course
of the transitional structures between the palmar and digital fascia. The palmodigital junction
is probably one of the most understudied areas in the fascial microanatomy of the hand, which
is strange considering the fact that the transition of the cords in DD from the palm to the digit
is essential to the development of flexion contractures. Better knowledge of the anatomy of
the palmodigital junction might improve the understanding of the clinical findings in DD and
contribute to its surgical treatment. Therefore the aim of this study was to describe the
anatomical structures of the palmodigital junction and their dynamics through a literature
study and a dissection study on human cadaveric material.
16
Materials and Methods
Study design
In order to elucidate the microanatomy of the palmodigital junction of the hand a literature
study and a dissection study were performed.
Literature study
The databases Pubmed and Embase were searched in order to identify all available articles on
Dupuytren’s Disease (DD) or the normal microanatomy of the hand, mentioning anything
about the cutaneous ligaments of the palm, digits or palmodigital junction. The following
using key terms were used: Dupuytren, Dupuytren’s, Dupuytren’s disease, (micro)anatomy
hand/palm/digit, dissection hand/palm/digit, palmar fascia/aponeurosis, natatory
ligament/cord, lateral digital sheet/cord, spiral band/cord, retrovascular band/cord,
pretendinous band/cord, Grayson’s ligament, Cleland’s ligament. Additionally relevant books
on the surgical anatomy of the hand from the Plastic Surgery department and the Central
Medical Library of the University Medical Centre of Groningen (UMCG) were used.
Dissection study: materials
The main part of this research project consisted of a dissection study in order to elucidate the
microanatomy of the palmodigital junction and its possible role in the transition of the palmar
fascia into the digital fascia. The anatomical dissections were performed on human cadaveric
hands obtained from the Department of Neuroscience, Anatomy of the University Medical
Centre of Groningen (UMCG). The cadaveric material was used in full agreement of this
department’s regulations on working with human cadaveric tissue. The cadaveric hands were
obtained from adult cadavers fresh frozen at a temperature of -24ºC and thawed at +3ºC for 16
hours. A total number of 26 cadaveric digits was dissected, thirteen middle fingers and
thirteen ring fingers. These digits were taken from thirteen cadaveric hands, of which ten
female and three male. The cadaveric hands showed no signs of injury or prior surgery. Also
none of the specimens exhibited any sign of pathology such as Dupuytren’s disease or
inflammatory arthritis after macroscopic examination prior to dissection. During dissection
one hand however seemed to show the early beginnings of Dupuytren’s disease in the
pretendinous band of the ring finger. The age of the used cadavers ranged between 59 and 91
years, with a mean age of 79 years. The dissections were performed with regular size surgical
instruments. A 20 times maginification was obtained from a ZEISS universal S2 surgical
microscope (Zeiss, Oberkochen, Germany). Photographs were taken and videorecordings and
drawings were made throughout the dissections to record the findings. A Canon EOS 500 D
photo camera with macro lens was used for making detailed pictures (Canon, Oita, Japan).
Measurements on the dissected fingers were taken using a calibrated digital slide gauge.
Additionally a number of 3 dissections was performed on cadavers conserved using Thiel’s
embalming method. Because of the flexibility of Thiel’s embalmed cadavers, these
dissections were particularly suitable to study the dynamics of the cutaneous ligaments in
question.
Dissection study: methods
The dissections were performed on digits III and IV only. Prior to the definitive dissection
method performed on the earlier mentioned 26 digits, pilot dissections were performed on 6
digits to verify which dissection method was the best. This also made it possible to get a clear
17
insight in the anatomic relations of the fascial structures with the flexor tendons, pulley
system, neurovascular bundles, intrinsic muscles and joints. Before dissection the lengths of
digits III and IV of the just thawed cadaveric hands were measured from the palmodigital
crease to the tip of the digit. To study the palmodigital structures and also their possible
relations with palmar and digital structures the entire ray of the digit was dissected. A
longitudinal midline incision was made on the palmar skin of the digit, running from halfway
the distal phalanx to the midpalm (approximately four centimetres distal to the distal wrist
crease). After making a transverse incision halfway the distal phalanx up to the midlateral line
on both sides and one in the midpalm the skin was released from the underlying fibrofatty
tissue by blunt dissection and was gently reflected sideways. The fibrofatty tissue, especially
abundant in the distal palm was removed carefully by blunt dissection with blunt tipped
scissors trying to preserve the underlying fibrous condensations.
Consequently the palmar fascia was relieved of adipose tissue to visualize the pretendinous
bands, the natatory ligament was dissected free of adipose tissue and more distally Grayson’s
ligament as well, to the extent that it was possible without perforating it. The excessive
adipose tissue in the distal palm was removed carefully to visualize the neurovascular bundle
(specifically the arterial bifurcation) and the underlying fibrous condensations of the
palmodigital junction. Next the neurovascular bundle was followed distally in to the finger
underneath natatory and Grayson’s ligaments, lying volarly, to free it from this volar layer. In
the course of following the neurovascular bundle in the neurovascular tunnel with blunt tipped
scissors, the neurovascular tunnel was opened from the midline, slowly exposing the proper
digital nerve and artery. The adipose tissue that was encountered in the neurovascular tunnel,
impeding the view, was removed. After exposing the volar aspect of the neurovascular bundle
it was also freed from the underlying structures, being mainly Cleland’s ligament, dorsally.
After studying an intact neurovascular bundle and the relation of the arterial bifurcation at the
palmodigital junction to the underlying and adjacent structures, it is cut and reflected
proximally or distally. In doing so, the fibrous condensations of the palmodigital junction and
the dorsal aspect of the neurovascular tunnel could be visualized. When the entire digital ray
was exposed, special attention was paid to the fibrous condensations of the palmodigital
junction and their connections with palmar structures proximally and digital structures
distally.
Every microanatomic structure hitherto described in the hand and relevant to the palmodigital
junction was searched for and studied. To be more precise, palmar fascia, transverse ligament
of the palmar aponeurosis (TLPA), pretendinous bands, distal extensions of the pretendinous
bands: cutaneous insertions, spiral bands, perforating fibres, septa of Legueu and Juvara,
natatory ligament, lateral digital sheet (LDS), retrovascular band, Grayson’s and Cleland’s
ligament and the interrelations between all these structures. The variations of these structures
and their interrelations as found in digits III and IV during different dissections were also
noted.
Subsequently the fibrous condensations in question were measured with a calibrated digital
slide gauge on both sides of the finger. The proximal and distal boundaries of the palmodigital
fibrous condensations and their width were measured in the midline of the finger at origin and
radially and ulnarly. Both sides (radial or ulnar) of each dissected digit (III or IV) were scored
for the characteristics of the structures found at the palmodigital junction such as origin,
insertion and course. Also both sides were scored for the presence of and relations with
18
surrounding structures, such as the relations with the spiral bands and natatory ligament, with
the pretendinous bands proximally and with Cleland’s and Grayson’s ligaments distally.
A dorsal approach was also used additionally to a volar approach to study the palmodigital
fibrous condensations and their possible dorsal continuations and insertions. Dorsally also the
same midline incision was used. The overlying skin was also dissected bluntly and reflected
laterally. After removal of the adipose tissue, the palmodigital fibrous condensations became
visible. Variations in the volar approach were used to study the interrelations between certain
microanatomic structures. To see the transition of the palmodigital fibrous condensations into
the neurovascular tunnel and to see the course of the fibres within the tunnel, it was left intact
with small gaps cut out parallel to the course of Grayson’s fibres (in an inverted V shape),
revealing small parts of the interior of the neurovascular tunnel instead of cutting the entire
tunnel open. On occasion the tunnel was not cut open in the midline of the digit, but instead at
the insertion of Grayson’s ligament in the lateral skin to study the fibres in the midline of the
digit.
Dynamics of the fibrous structures at the palmodigital junction
After visualizing the fascial structures at the palmodigital junction, the changes in
arrangement and the degree of tension of these structures during flexion and extension of the
MCP, PIP and DIP joints and during abduction and adduction of the finger were observed.
Statistics
A student’s t-test and wilcoxon square test was used for the statistical analysis of the
performed measurements. Digits III and IV were compared to each other. Statistical
significance was set at a p-value of less than 0.05.
19
Results
Palmodigital spiralling sheet
The anatomy was found to be same, radially and ulnarly, in all digits. The pretendinous band
as mentioned earlier was found to divide in three layers distal to TLPA as described by
McGrouther (52). The structure known as the spiral band or McGrouther’s layer 2 could be
identified bilaterally. It was found to pass underneath the neurovascular bundle, running in a
slightly oblique fashion towards the side of the digit. In contrast to what had been described
earlier, in this study it was found to insert on the deep surface of natatory ligament (NL).
Through the remainder of the paper we will call this structure the spiral band. The spiral band
is of particular relevance to our study, since, together with fibres originating more distally
from the A1 and A2 pulleys, a structure is formed which to our knowledge has not been
described before. We have chosen to call this structure the palmodigital spiralling sheet (PSS).
In the undissected condition PSS as a whole makes a complete spiral around the
neurovascular bundle, which proximally is covered by NL and distally by Grayson’s
ligament, because the fibres of PSS blend with these ligaments. When the natatory and
Grayson’s ligaments are opened from the midline and reflected laterally, the neurovascular
bundle is exposed and PSS can be seen to fan out dorsally to it towards the side of the digit.
The opening of the fascias that lie volar to the neurovascular bundle (i.e. NL and Grayson’s
ligament), and it’s lateral reflection are shown stepwise in figures 5 through 9.
20
Figure 5: Left is proximal and right is distal. The volar skin has been incised in the midline and reflected
laterally. Underneath the skin from proximal to distal the neurovascular bundles and their bifurcations can be
seen in the distal palm, the natatory ligament (NL) covering them at the palmodigital junction and Grayson’s
ligament covering them in the digit.
Figure 6: The fascia on top of the nv bundle is step by step cut open from the midline, starting with NL and
reflected laterally by the left upper clamp. While reflecting NL the proximal part of the palmodigital spiralling
sheet (PSS) can be seen to appear at NL’s dorsal aspect. The scissors have been placed underneath Grayson’s
ligament, which is to be opened from the midline next.
21
Figure 7: Grayson’s ligament has been released at the midline from the tendon sheath and is on both sides of the
finger reflected laterally. The distal part of PSS on the dorsal side of Grayson’s ligament, is now also visible.
The neurovascular bundles are seen to pass volarly to PSS. The blue mark proximally on the flexor tendon
sheath has been set at the level of the proximal border of NL. PSS is indicated in the picture as the fascia in
between the arrows.
Figure 8: The neurovascular bundles have been cut distally and reflected proximally. Now there is a clear view
of the underlying fascia, in particular of PSS at the palmodigital junction. In this laterally reflected condition PSS
has the appearance of running in a slightly oblique fashion towards the side of the digit.
22
Figure 9: Left is proximal and right is distal. A set of schematic drawings to further illustrate the opening of the
volar fascia, as described in figures 5 through 8. Drawing a. shows the intact volar fascia after removal of the
skin. The proper digital nerve in yellow and the proper digital artery in red can be seen to enter their
neurovascular tunnels. PSS marked in blue can be seen to be continuous with the pretendinous band through the
spiral band. PSS makes a complete spiral around the neurovascular bundle. The volar half of this spiral is
covered by the natatory ligament (NL) proximally and Grayson’s ligament distally. Natatory and Grayson’s
ligaments have been marked in green and black respectively. The dotted lines perpendicular to the digit indicate
the MCP, PIP and DIP joints from proximal to distal. In drawing b. the right half of the volar fascia has been
opened from the midline and reflected laterally a bit. This partially reveals the proper digital nerve. Further
23
reflection of natatory and Grayson’s ligaments in drawing c. exposes the entire neurovascular bundle and
Cleland’s ligaments at the PIP and DIP joints dorsally to the neurovascular bundle. Lateral reflection also further
unfolds PSS from its spiralling position at the dorsal aspects of natatory and Grayson’s ligaments.
PSS origins
The origin of PSS can be subdivided in three parts. Firstly the most proximal fibres of PSS
consist of the spiral bands originating in the pretendinous band distal to TLPA. Since they
emerge from the pretendinous band, their origin lies usually just proximal or distal to the
proximal border of the A1 pulley. Secondly the most distal fibres originate from the flexor
tendon sheath just distal to the proximal border of the A2 pulley. Thirdly the intermediate
fibres, which are situated in between the just described proximal and distal borders of PSS.
They also originate from the flexor tendon sheath mostly over the A1 pulley. By applying
tension the course of the fibres of the proximal and distal borders of PSS can be made clearly
visible (figures 10, 11 and 12).
Figure 10: Left is proximal and right is distal. When lifting the proximal and distal borders of the palmodigital
spiralling sheet with the forceps in the midline of the digit, tent like formations appear clearly marking these
borders bilaterally. PSS is seen to fan out slightly in the lateral direction between the proximal and distal borders
of PSS. The transverse ligament of the palmar aponeurosis (TLPA) is situated just proximal to the forceps
holding up the proximal border of PSS. The natatory ligament (NL) is held by the most proximal clamps.
24
Figure 11: Right is proximal and left is distal. The neurovascular bundles are seen to overlie the palmodigital
spiralling sheet (PSS). The natatory ligament (NL) is divided, reflected and clamped on both sides of the digit.
Figure 12: Right is proximal and left is distal. The neurovascular bundles have been cut and removed. The
palmodigital spiralling sheet (PSS) can be seen on both sides of the digit.
25
In addition to McGrouther’s layer 2/the spiral bands, also fibres known as McGrouther’s layer
3/the perforating fibres have been identified. They have been observed to lie adjacent just
proximally to the proximal border fibres of PSS or spiral band. These fibres have been
observed to originate in the termination point of the pretendinous band and pass dorsally
around the sides of the MCP joint (figure 13).
Figure 13: Left is proximal and right is distal. This is a lateral view of the MCP joint of digit III. Perforating
fibres are seen to pass dorsally proximal to the proximal border of the palmodigital spiralling sheet (PSS)
underneath the forceps lifting the pretendinous band.
26
PSS insertions
In their distal course, the proximal border fibres or the spiral band pass the A1 pulley
sideways and are joined by intrinsic fibres, originating on the fascia of the intrinsic muscle
(lumbrical or interosseous). In our dissections these fibres have been found to insert together
on the dorsal aspect of NL to form the volar half of the spiral around the neurovascular bundle
(figure 14). Through this continuity between the proximal border fibres and the intrinsic fibres
on one hand and NL on the other, the spiral can be said to be completed in the midline by
NL’s attachment on the A1 pulley. Between the origin of the proximal border fibres of PSS
and the origin of the fibres from the intrinsics, a triangularly shaped space is usually found.
Figure 14: Left is proximal and right is distal. This photo shows the proximal content of the radial neurovascular
tunnel of the ringfinger of the right hand. Volarly the neurovascular tunnel is seen to be covered by the natatory
ligament (NL) and its attachment to the A1 pulley in the midline of the finger, held by the left upper clamp. The
proper digital nerve and artery are seen to enter the neurovascular tunnel. The proximal border of the
palmodigital spiralling sheet (PSS) originates distal to TLPA and passes from the ulnar side of the neurovascular
bundle (left lower clamp) to the radial side of the neurovascular bundle, forming the floor of the neurovascular
tunnel at its entrance (lower arrow). While passing radially and volarly to the neurovascular bundle the proximal
border of PSS is joined by the intrinsic fibres (upper arrow). Together they insert into NL on its dorsal side (right
clamp).
The distal border fibres do not spiral around the neurovascular bundle as the more proximal
fibres do. From their origin just distally to the proximal border of the A2 pulley, they remain
dorsal to the neurovascular bundle to arch into Cleland’s 1B ligament while this ligament
attaches on the flexor tendon sheath at the level of the PIP joint. The dorsal border fibres
therefore appear to contribute to the floor of the neurovascular tunnel formed by Cleland’s
ligaments 1A and 1B at the level of the PIP joint.
27
The intermediate fibres of PSS do not blend with natatory, nor with Cleland’s ligaments.
Instead they pass distally in an oblique fashion and continue as the fibres of Grayson’s
ligament. Through the continuity of these intermediate fibres with Grayson’s ligament, they
can be said to insert at the level of the A2 pulley after having created the volar half of the
spiral around the neurovascular bundle, because the fibres of Grayson’s ligament insert there.
A dorsal dissecting approach has revealed the intermediate fibres of PSS also to insert into the
dorsal skin. Figures 15 and 16 show an overview of the origins and insertions of PSS.
Figure 15: Left is proximal and right is distal. This photo gives an overview of the palmodigital spiralling sheet
(PSS) from above. Proximal border fibres are seen to originate from the pretendinous band and insert into the
divided and reflected natatory ligament (NL), held by the most proximal clamps on both sides of the finger. The
intermediate fibres originate from the flexor tendon sheath mostly over the A1 pulley and continue as Grayson’s
ligament. The distal border fibres originate from the flexor tendon sheath just distal to the proximal border of the
A2 pulley and arch into Cleland’s 1B ligament while it attaches on the flexor tendon sheath at the PIP joint.
TLPA = transverse ligament of the palmar aponeurosis.
28
Figure 16: Left is proximal and right is distal. This is a schematic drawing of figure 15. It can be seen as the final
step in the lateral reflection of the volar fascia in figure 9. The proximal and distal border fibres of the
palmodigital spiralling sheet (PSS) are marked in blue and the intermediate fibres in green. Note the semilunar
hiati alongside the proximal and middle phalanges. The dotted lines perpendicular to the digit indicate
consecutively the MCP, PIP and DIP joints from proximal to distal. The A1 pulley consists of the two most
proximal bands encircling the flexor tendon. NL = natatory ligament, TLPA = transverse ligament of the palmar
aponeurosis.
On their way to Cleland’s ligaments the distal border fibres have been found to border a
semilunar hiatus via an arch like shape at the level of the A2 pulley (figures 16, 17 and 18).
We found it to be present bilaterally in almost all digits. On rare occasion the distal border
fibres have been seen to continue distally as Cleland’s 1A ligament inserting in the lateral
skin, instead of arching with Cleland’s 1B ligament towards the flexor tendon sheath at the
PIP joint. This made the shape of the hiatus more triangular. One digit showed complete
absence of the semilunar hiatus bilaterally and one unilaterally. In these cases Cleland’s
ligaments and PSS have been found to form one joined continuous plane of fibres. Mostly at
the same level as the semilunar hiatus the dorsal branch of the proper digital nerve has been
observed to pass dorsally after perforating PSS (figures 16 and 23). Akin to the semilunar
hiatus alongside the proximal phalanx a similar hiatus was found distally along the middle
phalanx, situated between the distal border of the distally running Cleland’s 1A ligament and
the A4 pulley (figures 16, 17 and 18).
29
Figure 17: Left is proximal and right is distal. This photo shows the semilunar hiati at the level of the A2 and A4
pulleys.
Figure 18: Left is proximal and right is distal. This photo gives the same image as figure 17, except for the
proximal hiati, which become more clear when PSS is put under tension.
30
Through PSS’ insertions in natatory and Grayson’s ligaments at their dorsal sides, PSS forms
the most dorsal layer of the roof (i.e. the volar coverage) of the neurovascular tunnel. And
through PSS’ continuity with Cleland’s ligament it also contributes to the floor (i.e. the dorsal
lining) of the neurovascular tunnel. Deep to PSS, multilayered or not, the tendon of the
intrinsic muscle can be seen to pass dorsally (after PSS has been removed that is).
Dynamics of PSS
The tension in PSS does not seem to change during flexion and extension of the finger, apart
from some degree of relaxation during MCP joint flexion. This probably accommodates the
movement of the neurovascular bundle during flexion. With finger abduction the contralateral
PSS was found to tighten. A continuous structure such as PSS, encircling the neurovascular
bundle, seems most effective in stabilising the neurovascular bundle during various finger
movements. Additionally the semilunar hiati can be said to accommodate the lateral bulging
of fat on the proximal and distal phalanges during flexion of the finger.
31
Statistics
In tables 1 and 2 the mean and standard deviations of the measured variables for the middle
and ring fingers are shown, respectively. With α = 0.05 none of these variables were found to
be significantly different between the middle and ring fingers, except for the length of the
fibres at the most distal border of PSS (P = 0.014). The length of these fibres was significantly
greater in the (longer) middle finger.
Table 1 Measurements on PSS in the middle finger
Mean with SD (mm) Range (mm)
Width 13.6 ± 1.7 10.2 – 16.0
Length fibres at most
proximal border
30.3 ± 3.9 24.1 – 38.2
Length fibres at most distal
border
21.1 ± 3.1 16.1 – 28.9
Distance between borders (=
width of PSS at origin)
16.6 ± 2.9 11.7 – 21.6
Length digit 75.5 ± 4.1 66.8 – 80.0
Ratio distance between
borders/length digit
0.2 ± 0.03 0.2 – 0.3
Table 2 Measurements on PSS in the ring finger
Mean with SD (mm) Range (mm)
Width 12.6 ± 2.7 8.0 – 19.9
Length fibres at most
proximal border
27.5 ± 4.9 18.4 – 33.8
Length fibres at most distal
border
18.5 ± 2.8 12.1 – 21.9
Distance between borders (=
width of PSS at origin)
14.5 ± 3.6 11.5 – 21.2
Length digit 69.3 ± 2.3 65.0 – 72.7
Ratio distance between
borders/length digit
0.2 ± 0.05 0.2 – 0.3
32
Natatory ligament
The structure known as NL at the palmodigital crease has been found to be continuous with
Grayson’s ligament volarly through u-shaped fibres in the interdigital skin folds (figure 19).
These u-shaped fibres, distally to the transverse fibres of NL, have the same upward oblique
direction as Grayson’s fibres fitting the earlier described inverted V configuration, and was
also found to be present in our dissections. When lifting up NL by its proximal border the
crossed attachment of NL on the A1 pulley can be seen on a cross sectional plane. Also when
looking in this plane at the openings of the neurovascular tunnels, the two neurovascular
bundles have repeatedly been seen to pass through a shape most resembling an infinity
symbol as shown in figures 20 and 21. Through this infinity symbol shape there seems to be
contralateral continuity between the fibres of NL (volarly to the neurovascular bundle)
attaching on the A1 pulley and the intermediate fibres of PSS (dorsally to the neurovascular
bundle) originating from the A1 pulley (figure 28).
Figure 19: Bottom of the photo is proximal and top is distal. This photo shows the natatory ligament (NL) across
the distal palm of rays III and IV, consisting of transverse fibres and u-shaped fibres through which NL is
continuous with Grayson’s ligament. Grayson’s fibres can be seen to run in an oblique upward fashion on both
sides of the digit (asterisks), forming an inverted V configuration, as indicated distally in the middle finger.
33
Figure 20: Bottom of the photo is proximal and top is distal. This photo shows the natatory ligament in the
natural position, covering the neurovascular bundles on both sides of the digit.
Figure 21: Bottom of the photo is proximal and top is distal. This photo focuses on the opening of the
neurovascular tunnels after having lifted the natatory ligament (NL) (from figure 20) by its proximal border. The
neurovascular bundles can be seen to pass through their corresponding neurovascular tunnels in an infinity
symbol like shape. Note the continuity between fibres of NL and intermediate fibres of the palmodigital
spiralling sheet (PSS) in the middle of this infinity symbol.
After opening NL in the midline and reflecting it laterally, part of PSS could be seen almost
immediately to lie underneath the neurovascular bundle and insert into NL as stated
previously (figures 6 and 9). We found some anatomical variation in the level of insertion of
34
the proximal border fibres into NL. Usually this was somewhere in the proximal half of NL as
shown in figures 22 and 23. However in two digits the proximal border fibres have been
observed to pass NL diagonally and insert directly into Grayson’s fibres. The proximal border
fibres of two adjacent PSS’s in the interdigital space joined by intrinsic fibres have been
found to attach before inserting in NL (figure 24).
Figure 22: Bottom of the photo is proximal and top is distal. This photo shows the intact natatory ligament. It is
put under tension by the left clamp.
35
Figure 23: Bottom of the photo is proximal and top is distal. This photo shows the palmodigital junction after
opening the natatory ligament (NL) in the midline and reflecting it laterally with the right two clamps. Proximal
border fibres of the palmodigital spiralling sheet (PSS) can be seen immediately, to insert into NL. Digital nerve
and artery are seen to overlie PSS and the dorsal branch of the digital nerve can be seen to pass distally before
perforating PSS and passing dorsally.
Figure 24: Bottom of the photo is proximal and top is distal. The interdigital space between digits III and IV is
seen. Proximal border fibres of two adjacent palmodigital spiralling sheets (PSS) joined by intrinsic fibres are
36
seen to attach before inserting into the natatory ligament (NL). The gap in between the PSS’s is an artefact of
dissection.
Three types of continuities
Additionally to the study of the palmodigital junction dissection of the finger has revealed
three kinds of possible continuities between fibres. Firstly the ipsilateral continuity between
Grayson’s and Cleland’s ligament in the lateral plane of the digit (figures 16 and 28).
Secondly the ipsilateral continuity between Grayson’s and Cleland’s ligament on one side of
the digit in the medial plane (figure 25). And thirdly the contralateral continuity between
Grayson’s and Cleland’s ligaments over the flexor tendon sheath at the level of the
interphalangeal joints (akin to the contralateral continuity between the fibres of NL attaching
on the A1 pulley and the intermediate fibres of PSS originating from the A1 pulley, as
described earlier) (figures 26, 27 and 28). More specifically the distally running Cleland’s
ligaments 1A and 2A at the PIP and DIP joints respectively. At these levels fibres have been
observed to cross from one side of the digit to the other running between an intact Grayson’s
ligament on one side and the dissected free Cleland’s ligament on the other.
Figure 25: Left is proximal and right is distal. Shown is the index finger of the right hand. The skin has been
opened from the midline and reflected laterally, held by the lower two clamps. Grayson’s ligament has been
opened from its lateral insertion in the skin and has been reflected medially, held by the two upper clamps. The
neurovascular bundle can be seen and dorsally to it Cleland’s ligament. Continuity between Grayson’s fibres and
Cleland’s fibres can be observed in the midline of the digit.
37
Figure 26: Left is proximal and right is distal. This photo shows digit III of the right hand. The forceps are
placed beneath Grayson’s ligament ulnarly and radially Cleland’s ligaments at the PIP joint have been
visualized.
Figure 27: Left is proximal and right is distal. This photo is a magnification of figure 25, where the ulnar
Grayson’s fibres seem to cross the flexor tendon sheath into the radial distally running Cleland’s 1A ligament.
38
Figure 28: Left is proximal and right is distal. Schematic drawing of the ipsilateral continuity between Grayson’s
and Cleland’s ligaments in the lateral plane of the digit, contralateral continuity between the natatory ligament
(NL) and the intermediate fibres of the palmodigital spiralling sheet (PSS) at the level of the MCP joint and
contralateral continuity between Grayson’s ligament and Cleland’s ligament at the PIP and DIP joints. The
dotted lines perpendicular to the digit indicate the mentioned joints.
39
Discussion
With this study we aimed to elucidate the fascial anatomy at the palmodigital junction as a
first step to explain clinical findings during fasciectomy in Dupuytren Disease. To this end we
performed a literature and a dissection study. The latter was performed on fresh frozen
cadaveric hands and including only ring and middle fingers. Due to their resemblance and
similar positioning in the hand as being both bordered by other fingers, the anatomy of these
fingers was expected to be similar. The volar aspect of each finger was dissected from
midpalm to tip, not only to visualize the palmodigital structures, but also their possible
interrelations with palmar structures proximally and digital structures distally. All the
microanatomic structures so far described in the hand and their possible relevance to the
palmodigital junction were noted during dissections.
At the palmodigital junction, between a line connecting the proximal and distal palmar crease
and the PIP joint crease, we have found a sheet like structure, for which we suggest the name
“Palmodigital Spiralling Sheet” (PSS). The fibres constituting this structure originate from the
pretendinous band (in the form of the spiral band), the fascia of the intrinsic muscle and the
flexor tendon sheath. In its course distally, PSS shows continuity with natatory, Grayson’s
and Cleland’s ligaments through its distal insertions in them. PSS spirals around the
neurovascular bundle at the palmodigital junction completely encircling it, while curving into
NL and Grayson’s ligament. In doing so we believe it forms the most inner and proximal part
of the neurovascular tunnel. The measurements on PSS were performed consistently using the
same orientation points and measuring instrument. The significantly longer distal borders of
PSS in the middle finger can most probably be explained by the middle finger’s greater
length.
Next to the study of the palmodigital junction the dissection of the entire ray also provided
ample opportunity to also study aspects of the digital fascia. This mainly revealed three types
of possible continuity between fibres. The ipsilateral continuities between Grayson’s and
Cleland’s ligaments in the medial plane and the lateral plane of the digit (figures 16 and 28).
The contralateral continuity between fibres of NL and intermediate fibres of PSS and between
Grayson’s and Cleland’s 1A and 2A ligaments at the level of the PIP and DIP joints (figures
21 and 28). These three types of continuity might play a role in the connection of volar and
dorsal structures forming the tunnel around the neurovascular bundle.
Summary of relevant literature
Various accounts have been given in the literature on the structures running in the
palmodigital junction, i.e. the distal extensions of the pretendinous band, natatory ligament
and lateral digital sheet. McGrouther described the pretendinous band to split into three layers
just distal to TLPA (52). Layer 1 constituting the cutaneous insertions. Layer 2 the spiral
bands which pass underneath the neurovascular bundle, blend with NL and continue
longitudinally into LDS in the finger. Layer 3 the perforating fibres, which dive deep around
the MCP joint to perforate DTIL. However there have been some earlier descriptions of these
three layers, slightly differing from McGrouther’s description.
Legueu and Juvara have called layer 2 the bifurcating fibres (55) and so have Zancolli and
Cozzi (54). Zancolli and Cozzi’s bifurcating fibres are described as the more distal group of
deep longitudinal fibres of the pretendinous bands, passing deep between the A1 pulley and
the proper digital arteries and nerves and ending bilaterally on the MCP joint and the base of
proximal phalanx. According to Zancolli and Cozzi the bifurcating fibres form an
40
anteroposterior sheet on both sides of the A1 pulley, which in the same sagittal plane is said to
be continuous with the vertical paratendinous septum proximally and with the dorsal fibrous
septum of the natatory ligament distally, i.e. Cleland’s ligament (54). Zancolli and Cozzi do
acknowledge these fibres to also have been called spiral bands by Gosset (56, 57), but they do
not mention a spiralling aspect of their bifurcating fibres themselves.
As a third layer Zancolli and Cozzi do not mention perforating fibres, but vertical
paratendinous septa. In any case Zancolli and Cozzi do not seem to recognize the perforating
aspect of any of the layers of the pretendinous extensions through DTIL, as described by
Legueu and Juvara. The perforating fibres and the vertical paratendinous septa, both
originally described by Legueu and Juvara (55) have often been confused because of their
deep nature. According to McGrouther the vertical septa lie dorsally to TLPA and have a
largely vertical orientation perpendicular to the plane of the palm, merging with TLPA volarly
and with DTIL dorsally surrounding the flexor tendons. The perforating fibres on the other
hand are distal extensions of the pretendinous bands and pass dorsally distal to TLPA (65).
Gosset has suggested the perforating fibres and vertical septa to be in continuity with each
other and LDS laterally in the finger (56, 57). This might have contributed to the confusion
(65). According to Bojsen-Moller and Schmidt distally the vertical septum is continuous with
the digital fascia (60).
Holland and McGrouther have subdivided layer 3 of pretendinous bands into 3a, deep fibres
passing dorsally distal to TLPA, and 3b, fibres passing dorsally proximal to TLPA into the
vertical paratendinous septa (66). However a personal communication has revealed this article
to have been submitted without McGrouther’s final agreement.
The natatory ligament is classically known for the transverse fibres running across the distal
palm at the palmodigital junction and the arciform fibres. These are u-shaped fibres forming
arches lining the interdigital skin folds and they extend to the fingertips (53, 54). Zancolli and
Cozzi describe the natatory ligament as a far more extensive structure. According to them the
natatory ligament consists of Bourgery’s transverse subcutaneous band, the volar digital
septum and the dorsal digital septum. These septa are formed respectively by Grayson’s
ligament and Cleland’s ligaments. In this view these digital ligaments are considered
components of the natatory ligament (54).
The lateral digital sheet is described in the literature as a longitudinal structure found in the
lateral plane of the digit at the confluence of the volar and digital fascia. Other than that LDS
has not been clearly specified in the existing literature. Many authors have described LDS to
receive palmar fibres in the form of fibres of vertical septa, spiral bands and deep fibres of NL
(51, 53, 54, 56, 57, 60 ). Thomine describes a similar retrovascular structure also running over
the entire length of the finger, which he calls ‘la bandelette digitale’. Thomine states not to
agree with Cleland’s description of a retrovascular formation with a transverse path, i.e.
Cleland’s ligament. Instead he believes it to be ‘a structure with a longitudinal route, which
presents elective zones of fixation on the osteo-articular plane’. This structure is also found to
be in continuity with NL (67, 68). There is some confusion on what structure Thomine means
to describe. Gosset largely agrees with Thomine’s description of what he believes is LDS.
According to Stack Thomine means Cleland’s ligament (68). McFarlane on the other hand
suggests the retrovascular band is an additional structure altogether (69).
Based on our literature and dissection studies we have come to the following conclusions on
the fascial structures relevant to the palmodigital transition being PSS, NL, LDS and the
neurovascular tunnel.
41
Palmodigital spiralling sheet
Our dissections show that the spiral band or layer 2 of McGrouther forms the proximal border
of a complex spiralling structure, which we have called the palmodigital spiralling sheet
(PSS). In contrast to what McGrouther suggested (52), we have not been able to show that his
spiral band continues into LDS in the finger, but ends in NL (figures 2 and 16). However the
intermediate fibres of PSS, which are essentially also spiralling fibres, can give the illusion of
continuing longitudinally in the finger when the volar fascias of the finger are opened in the
midline. We do agree with Zancolli and Cozzi’s description of their bifurcating fibres or spiral
bands forming an anteroposterior sheet on both sides of the A1 pulley (54). Our sheet did not
appear to be continuous with the vertical septum proximally, but distally PSS can indeed be
said to be continuous with Cleland’s ligament since it blends with Cleland’s 1B ligament.
In contrast to the spiral bands, the perforating fibres have been found as described by
McGrouther at MCP joint level. We also agree with MCGrouther’s view that the vertical
paratendinous septa are situated more proximally than the perforating fibres (65). Because of
their adjacency and deep nature the vertical paratendinous septa and perforating fibres might
often be mistaken to be the same. Gosset might have given rise to confusion, but we support
his view about the continuity between the vertical paratendinous septa and the perforating
fibres (56, 57), if continuity implies adjacency. In the same regard the perforating fibres can
be said to be continuous with the spiral bands/proximal border of PSS, through adjacency
(figures 13 and 16).
Natatory ligament
In our study, NL was found to be continuous with Grayson’s ligament through the arciform
fibres, but we have not found arciform fibres or any other fibres originating in NL that extend
to the distal phalanx as described by Zancolli and Cozzi (54). NL has repeatedly been
attributed to be more than just a transverse ligament, but to also have deep fibres passing into
the finger. The fibres that come closest to fit that description in our dissections are the fibres
of PSS, located from approximately halfway PSS to its distal border. They are situated at the
level of the natatory ligament, which overlies them with the neurovascular bundle in between.
Technically these fibres are observed to originate on the flexor tendon sheath and feed PSS.
Location wise though these fibres could also belong to NL instead and could therefore also be
called deep fibres of NL. This is plausible, considering how fluently and imperceptibly one
structure flows over into another. Because the PSS fibres after coming about superficially to
the neurovascular bundle insert in NL and Grayson’s ligament at their dorsal aspects (figure
29), PSS can be said to form the most inner and proximal part of the neurovascular tunnel, as
stated previously. In concordance with Zancolli and Cozzi’s view on NL (54), we found PSS
in addition to being continuous with Cleland’s ligament to be continuous with Grayson’s
ligament as well through its insertion in it. If PSS is to be considered part of NL, NL can be
said to contribute to the formation of the neurovascular tunnel through these digital
prolongations (i.e. Grayson’s and Cleland’s ligaments).
When reviewing the pattern of Cleland’s ligaments at the PIP and DIP joints and the
semilunar hiati at the proximal and middle phalanges (figure 16), PSS can alternatively be
regarded as some proximal form of Cleland’s ligament at the MCP joint.
42
Lateral digital sheet
Almost all authors have described some form of palmar contribution to LDS, but
unequivocally. As stated previously we have not found the spiral band or proximal border of
PSS and deep fibres of NL to make a longitudinal contribution to LDS. For in our dissections
LDS has neither appeared as an autonomous nor as a longitudinally running structure. Instead
we believe Grayson’s and Cleland’s ligaments are continuous with each other in the lateral
plane of the digit (figures 16 and 28). Employing this definition of LDS, the fibres of PSS
make a more or less vertical contribution to LDS parallel to the transition lines between
Grayson’s and Cleland’s ligaments. That is the fibres of PSS form a proximal LDS laterally to
the neurovascular bundle when they are encircling it (figure 29). Gosset and McFarlane
among others suggest LDS to be a continuation of the vertical paratendinous septum (51, 56,
57). Considering the fact that both LDS and the vertical paratendinous septum are situated
laterally to the flexor tendon and the neurovascular bundle respectively, this is possible
through the earlier mentioned adjacency. But the performed dissections are not sufficient to
corroborate this.
Concerning the retrovascular structure described earlier, Cleland and Thomine most likely
have given different interpretations of the same structure. What Thomine probably means
might be a combination of Cleland’s ligament and LDS, with the elective zones of fixation
being Cleland’s formations at the interphalangeal joints. We therefore do not believe the
retrovascular band to exist next to LDS. McFarlane has observed retrovascular cords in
diseased hands (69), but retrovascularly we have not observed enough fascia in healthy hands
to account for Cleland’s ligaments as well as LDS and additionally a retrovascular band.
Neurovascular tunnel
In previous literature the neurovascular tunnel has repeatedly been described to consist of
Grayson’s ligament volarly and Cleland’s ligament dorsally. As far as we know no further
details have ever been provided on the exact arrangement of fibres in the neurovascular
tunnel. Based on the three types of continuity between fibres in the finger described earlier,
we have formed two theories on the possible arrangement of fibres that form the
neurovascular tunnel.
Theory 1: Spiralling network.
The pretendinous band gives off the initiation point for the neurovascular tunnel through the
proximal border of PSS or spiral band which encircles the neurovascular bundle using its
insertion in NL (figure 29). The ipsilateral continuities between Grayson’s and Cleland’s
ligaments in the lateral and medial planes make an ongoing spiral in the neurovascular tunnel
possible, with the volar part of the loop of the spiral being formed by Grayson’s fibres and the
dorsal part of the loop by Cleland’s fibres. This view is in concordance with the observations
of Hettiaratchy et al. They have, in addition to the proximal spiral cord commonly observed in
DD, found a second more distal spiral cord in several of their DD cases (70). Figure 29
shows the neurovascular tunnel externally and in figure 30 the internal arrangement is shown
as it would be in the spiralling network.
Theory 2: Spiralling infinity symbol network.
The possible contralateral continuity between fibres of NL and fibres of PSS and the infinity
symbol like shape which surrounds the neurovascular bundles at this level suggest that the
contralateral continuity between Grayson’s and Cleland’s ligament at the interphalangeal
43
joints possibly results in the same shape. If so, the neurovascular bundles in their distal course
would pass through the loops of a continuous infinity symbol spiral, functioning as
neurovascular tunnels. In this network the fascia in both sides of the digit would be linked
through crossing of fibres over the flexor tendon sheath. Figure 29 shows how this
contralateral continuity and the ipsilateral continuity in the lateral plane of the digit result in
continuous repetitive infinity shapes joining the neurovascular tunnels. The resulting
configuration of fibres is reminiscent of the Spanish ruffs, collars which were very
fashionable in the Western Europe during the 16th
and 17th
centuries.
These spiralling networks should not be seen as anatomically distinct structures, but as
anatomical relations between the fibres of PSS and NL and between the fibres of Grayson’s
and Cleland’s ligaments. Since Cleland’s ligaments are only present at the interphalangeal
joints these theoretical patterns are most prominent at the level of NL and PIP and DIP joints
(figures 29 and 30). The existence of these two patterns in the neurovascular tunnel might not
be directly obvious, nor are they necessarily relevant in the healthy hand. But in the formation
of cords DD might follow whatever fibre paths through anatomical relations are present.
Some fibre paths are “walked” by DD more often than others, what results in the occasional
observation of double spiral cords, as described by Hettiaratchy et al (70). In this case this
possible spiralling network in the neurovascular tunnel became more relevant when DD used
it to cause contractures. Spiral cords are clinically very relevant because of the risk for
neurovascular damage. On the other hand the spiralling infinity symbol network could result
in crossing of diseased tissue from one side of the finger to another.
Figure 29: Left is proximal and right is distal. Schematic drawing of the neurovascular tunnel seen externally and
the arrangement of fibres in the spiralling infinity symbol network. As a consequence to contralateral continuity
between fibres an infinity symbol like shape can be found through which the neurovascular bundles pass at the
level of the natatory ligament (NL)/palmodigital spiralling sheet (PSS) and at the interphalangeal joints. The
dotted lines perpendicular to the digit indicate the MCP, PIP and DIP joints.
44
Figure 30: Left is proximal and right is distal. Schematic drawing of the internal arrangement of fibres in the
spiralling network in the neurovascular tunnel. Cleland’s ligaments have been shaded blue. Shown is how the
ipsilateral continuities between volar and dorsal fibres in the medial and lateral plane of the digit (at the levels of
the natatory ligament and the interphalangeal joints) enable an ongoing spiral in the neurovascular tunnel, which
is iniated by the proximal border of PSS or the spiral band. The dotted lines perpendicular to the digit indicate
the MCP, PIP and DIP joints.
This study gives an extensive overview of the microanatomy of the palmar as well as the
digital fascia. But the results of anatomical studies are always affected by anatomical
variation and dissection itself which is the destruction of the very tissue to be studied (71).
This is a great but inevitable paradox, which must always be taken into account when
performing dissections. Additionally the inconsistent terminology in the literature, the
variability in possible interpretations of anatomical texts and the hardly existent borders
between fascial structures make the representation of the microanatomy of the hand very
challenging and therefore prone to mistakes by authors and misinterpretations by readers.
45
Conclusion
This study has provided new insights into the microanatomy of the palmar, digital and
palmodigital fascia. At the palmodigital junction the palmodigital spiralling sheet has been
found to have an important linking function between the palmar and the digital fascia. The
palmodigital spiralling sheet’s continuity with the pretendinous band, natatory, Grayson’s and
Cleland’s ligaments and the three types of ipsilateral and contralateral continuities between
Grayson’s and Cleland’s ligaments unite the palmar and digital structures to an intertwining
continuum of fibres, with a possible spiralling pattern. None of the fascial structures can
therefore be regarded as independently existing entities, as they are usually implied to be.
This makes every structure in the continuum a potential victim of Dupuytren Disease. The
possible ipsilateral and contralateral continuities between Grayson’s and Cleland’s ligaments
and their role in the formation of the neurovascular tunnels still require additional research.
Also the relation between the vertical septa and the perforating fibres and the dorsal
extensions of the palmodigital spiralling sheet have to be more extensively studied before any
conclusions can be drawn.
46
Acknowledgements
The authors would like to thank the following departments and people in the UMCG.
- The department of Neuroscience, Anatomy, for providing the necessary cadaveric
material, instruments and space for the dissections.
o Dr. P.O. Gerrits, for allowing almost unlimited access to the anatomy lab.
o K.L. van Linschoten, for assistance during dissections and advice.
o P. Veldman, for getting the cadaveric material ready and assistance during
dissections.
o J. Dokter, for assistance during dissections and photographing.
- The medical photo service, for assistance and advice with photographing and the
adjustment of the photos.
o B. Tebbes
o J. Bender
- The Skills lab, also for providing the accommodations for occasional dissections.
o H. Gjaltema
- The department of Plastic Surgery, for the opportunity to do this research and for
providing the necessary accommodations.
- A. Malsagov, for giving SPSS tutorials necessary for the statistical analysis.
47
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