University of Groningen

Revision of the carpal tunnel syndrome ( a computed tomographic study)Jessurun, Winston

IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite fromit. Please check the document version below.

Document VersionPublisher's PDF, also known as Version of record

Publication date:1983

Link to publication in University of Groningen/UMCG research database

Citation for published version (APA):Jessurun, W. (1983). Revision of the carpal tunnel syndrome ( a computed tomographic study). [s.n.].

CopyrightOther than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of theauthor(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons).

Take-down policyIf you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediatelyand investigate your claim.

Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons thenumber of authors shown on this cover page is limited to 10 maximum.

Download date: 14-02-2021

REVISION OF TH� CAH'PAL TUNNEL SYNDROME

(a computed tomographic study)

w. jessurun

REVISION OF THE CARPAL TUNNEL SYNDROME (a computed tomographic study)

Stellingen

1. Een arts kan alleen dan een goede dokter zijn indien hij/ zij ook

een goed mens is (R.W. Jessurun sr.).

2. Ieder individu denkt in een eigen taal; de mate waarin die taal

wordt beheerst, bepaalt de kwaliteit van her resultaat van het

denken.

3. Elke vorm van medisch handelen dient te warden geplaatst in het

kader van prospectief onderzoek.

4. Een volk dat een ander volk onderdrukt, is zelf niet vrij (Karl

Marx); die geldt ook voor individuen.

5. De algemene mening dat 'bowstringing' van de buigpezen aan de

pols, niet zou optreden na klieving van her flexor retinaculum, is

onjuist.

6. Hee primaire carpale tunnelsyndroom is een beroeps- of bezig­heidsziekte.

7. Een grocer aantal medici in Suriname is nog geen waarborg voor

een betere gezondheidszorg.

8. Er bestaat een duidelijke correlatie tussen handenarbeid, tendinitis

nodosa en her primaire carpale tunnelsyndroom.

9. Voor verantwoord opereren aan de hand is bloedleegte een voor­

waarde.

10. Bij decompressie van de nervus medianus is naast klieving van

her flexor retinaculum, partiele reseccie van die ligament niet nodig.

11. De leerplicht is een direkte aantasting van het zelfbeschikkings­

recht van de mens.

12. Na- en herscholingscursussen zouden verplicht moeten worden

gesteld aan iedere praktizerende medicus.

13. Het begrip 'cosmetische' chirurgie zou vervangen moeten

worden door 'psychofunctionele' chirurgie.

Stellingen behorende bij het proefschrift van

W. Jessurun

Revision of the carpal tunnel syndrome

(a computed tomographic study)

Groningen, 1983

RIJKSUNIVERSITEIT TE GRONINGEN

REVISION OF

THE CARPAL TUNNEL SYNDROME (a computed tomographic study)

PROEFSCHRIFT ter verkrijging van het doctoraat in de Geneeskunde

aan de Rijksuniversiteit te Groningen

op gezag van de Rector Magnificus Dr. L. J. Engels

in het openbaar te verdedigen op woensdag 29 juni 1983

des namiddags te 4.00 uur

door

WINSTON JESSURUN geboren te Friendship, Suriname

1983

DRUKKERIJ VAN DENDEREN B.V.

GRONINGEN

Promotores

Coreferenten

Paranymfen

Prof. Dr. A. J. C. Huffstadt Prof. Dr. J. W. F. Beks

Drs. B. Hillen

Ir. F. W. Zonneveld

Drs. A. de Boer

Drs. P. H. M. Spauwen

"Imagination is more important than knowledge"

Albert Einstein

to: Hedy

Quicilia

Janvier

Contents

Chapter I

Introduction

Chapter II History

Chapter III

Anatomy

Chapter IV

3.1. 3.2.

Median nerve

Carpal tunnel

A peripheral nerve . . . . . . . . . . . .

Chapter V

4.1. Structure of a peripheral nerve

4.2. Regeneration

4.3. Compression

The carpal runnel syndrome

5.1. Introduction

5.2. Aetiology 5.3. Symptomatolgy

5.4.

5.5.

Chapter VI

Investigation

6.1.

Examination

5.4.1. Introduction 5.4.2. Thenar atrophy 5.4.3. Sensory disturbance 5.4.4. Electrophysiological examination 5.4.5. Radiographs . . . .

5.4.6. Laboratory examination

Treatment

Introduction

1

5

13

13

16

19

19

21

21

25 25 25

27

28

28

28 29

30

30

31

31

33 33

Chapter VII

Results

Chapter VIII

6.2.

6.3.

7.1. 7.2. 7.3.

Preliminary investigation

6.2.1. Materials

6.2.2. Methods and results

Investigation

6.3.1. Materials

6.3.2. Methods

General data . . . . . .

Morphology and topography

Dimensions of the carpal tunnel

Discussion and conclusion

Summary

Summary in Dutch (Samenvatting)

References

Acknow ledgemencs

34 34 34 44 44 44

51 51 51 54

61

69

73

77

85

Chapter I Introduction

The median nerve is a mixed nerve, which enters the hand by passing through the carpal tunnel, dorsal to the flexor retinaculum and volar to the flexor tendons to the index finger. Within this fibro-osseous tunnel, repeated mechanical irritation or compression of the median nerve can result in a neuropathy known as the carpal tunnel syndrome, or other­wise known as median neuritis, acroparaesthesiae, compression neuro­pathy or entrapment neuropathy. The carpal tunnel syndrome is a painful and often disabling affliction of one or both hands. The patients are awoken by painful paraesthesiae in the area supplied by the median nerve, often accompanied by stiffness and numbness of the fingers and thumb. Persistence of the irritation or compression might result in impairment of sensation and atrophy of part of the thenar musculature (fig.l).

Fig. l. Bilateral thenar atrophy in a patient suffering from carpal tunnel syndrome. 1

At this stage, it is important to distinguish between a primary (idiopathic or spontaneous) and a secondary carpal tunnel syndrome. The primary carpal tunnel syndrome commonly affects hands bilaterally in both sexes, with a predominance in middle-aged women and the pathogenesis is unknown. The secondary carpal tunnel syndrome can be defined as a condition caused by any space-occupying lesion within the carpal tunnel (Phalen 1951, Robbins 1963 ). Paraesthesiae, pain and atrophy of the hand muscles may be caused by a central, radicular or peripheral lesion. Modem functional, electrophysiological and radiological examination help to establish the diagnosis, but the history and the clinical examina­tion are of decisive importance. Abbott and Saunders ( 193 3) suggested that the median nerve is compressed between the proximal edge of the flexor retinaculum and the radius. Brain et al. (1947), Tanzer (1959), Smith et al. (1977) and Gelberman et al. (1981) found elevated pressures within the carpal tunnel in relation to flexion and extension of the wrist and they suggested that these alterations in pressure might give rise to compression of the median nerve. Matricali and Kauer ( 1970) found an abnormal muscle belly of the thenar muscles, originating from the flexor retinaculum on the ulnar side of the median nerve, which could compress the median nerve underneath a thin part of the flexor retinaculum. Most observers agree that unaccustomed intensive manual work may precipitate symptoms or might aggravate them. The importance of the dimensions of the carpal tunnel and its anatomical relationship in relation to the contents, in various positions of the wrist, has never been clearly demonstrated. ,For this purpose, computed tomography was used in this study. With this technique cross-sections (CT-scans) of the carpal tunnel were obtained. In these CT-scans the cross-sectional areas of the tunnel and its tendons were measured and the mutual anatomical relationship in the "living" hand was recorded, with the hand in various positions. By comparing the data of male and female patients with controls, an attempt has been made to elucidate: 1. the role of the anatomical relationships, 2

2. the importance of the dimensions of the carpal tunnel in relation to the pathogenesis of the carpal tunnel syndrome,

3. the reason for the predominance in women.

3

Chapter II

History

In his "Lectures on Surgical pathology", Sir James Paget (1853) descri­bed 2 patients with median nerve compression symptoms: - "The median nerve, where it passes under the annular ligament, is enlarged, with adhesions to all the adjacent tissues and induration of both it and them. A cord had been drawn very tight round this man's wrist seven years before the amputation of the arm. At this time it is probable, the median and other nerves suffered injury; for he had constant pain in the hand after the accident, impair­ment of the touch, contraction of the fingers and constantly repea­ted ulceration at the back of the hand". - "A man was at Guy's Hospital, who, in consequence of a fracture at the lower end of the radius, repaired by an excessive quantity of new bone, suffered compression of the median nerve. He had ulceration of the thumb and fore and middle fingers, which resis­ted various treatment and was cured only by so binding the wrist that, the parts on the palmar aspect being relaxed, the pressure on the nerve was removed. So long as this was done the ulcers became and remained well; but as soon as the man was allowed to use his hand, the pressure on the nerves was renewed and the ulceration of the parts supplied by them returned".

Forty years later Schultze ( 1893) described 8 middle-aged patients with paraesthesiae and nocturnal pain at the distal ends of the upper limbs. While some patients had remissions, the majority continued to have symptoms particularly when performing "hard work" or in "cold water". The condition was equally distributed among men and women, although he was aware of what had already been written by other observers (Putman 1880, Ormerod 1883) on this subject, that it was more frequent in women. Because the paraesthesiae are mainly found at the distal ends of the upper limbs, he introduced the term acroparaesthesiae. The cause was not identified but was attributed to a "vasomotor neu­rosis".

5

Hunt ( 1911) was the first to describe the unilateral and bilateral atro­phy of the thenar muscles. He believed that it was due to compression of the motor branch of the median nerve as it emerged at the distal border of the flexor retinaculum. Marie and Foix ( 1913) classified 'Tatrophie isolee non progressive" of the small muscles of the hand, as being of central, radicular or peri­pheral origin. When dissecting a cadaveric hand with atrophy of the thenar muscles, they found interfascicular fibrosis and segmental demyelination of the median nerve. They were unable to determine, whether it was due to the effects of direct compression or impairment of the blood supply of the affected nerve segment. They were probably the first to recommend that cutting the flexor retinaculum could arrest this process. Sir James Learmonth (1930) was the first surgeon to divide the flexor retinaculum. Abbott and Saunders ( 1933) pointed out the possibilities of damaging the median nerve by fractures of the distal radius. They demonstrated that in acute flexion of the wrist, Berlin Blue or Lipiodol injected into the sheath of the median nerve, was arrested at a point opposite the proximal border of the flexor retinaculum. If however, the wrist was held in moderate flexion or extension, the dyes flowed easily into the palm of the hand. Woltman ( 1941) mentioned the assooat10n of acromegaly and neuritis of the median nerve. He attributed the neuritis to a compres­sion of the median nerve in the carpal tunnel by tissue proliferation. The condition improved by dividing the flexor retinaculum. Denny-Brown and Brenner (1944) showed that if pressure on a nerve is continued, conduction in motor fibres may be selectively damaged. The more rapid recovery of sensory fibres could be the explanation of the frequent dissociation of motor disability and sensory disturbance. Zachary ( 1945) presented 2 typical cases of compression of the median nerve in the carpal tunnel. The diagnosis was verified at the 6

operation and the flexor retinaculum was divided. In both cases "old bone formation" could be noted radiologically. One year later Cannon and Love (1946) operated upon 9 of the 38 patients who they diagnosed as having a "tardy median palsy". They divided the flexor retinaculum and performed an epineural neuro­lysis. At the operation they found a fusiform swelling of the median nerve, just proximal to the flexor retinaculum and a narrowing and discolouration of the nerve in the carpal tunnel. The results of the operative treatment were very satisfying. Three of the 9 operated patients had no history of injury nor previous illness. They probably belonged to the group of patients with spontaneous median neuro­pathy. Brain et al. (1947) discredited the theory that flexion of the wrist is an important factor in the carpal runnel syndrome. They demonstrated that flexion of the wrist only raises the pressure in the carpal tunnel to 100 mm.H

20, but extension raised it well over 300 mm. H20. They found the performance of unaccustomed work to be a precipitating factor, particularly if it involved extension of the wrist.

Meadoff (1949) re-emphasized the fact that the median nerve carries with it most of the sympathetic nerve supply of the hand, accounting for the frequency of trophic disturbances when it is injured. Michaelis ( 1949) found compression of the median nerve in patients with rheumatoid arthritis caused by thickening of the flexor retina­culum. Thickening of the ligament developed, according to him, by overloading the palmaris longus muscle, which would serve to elevate the ligament. Kendall ( 1950) noted that unilateral cases of the carpal tunnel syn­drome tended to occur in younger subjects, male or female. He belie­ved that for treatment the wearing of a splint to protect the median nerve from direct pressure would usually suffice, in case where motor symptoms and muscle wasting were not pronounced, although a change of occupation might be indicated. Bilateral involvement was

7

more likely to occur in middle-aged women, who had taken up heavy

house-hold duties rather late in life. The condition in these cases was

more severe and surgical treatment was usually necessary. Trophic

disturbances tended to occur in the areas supplied by the median

nerve.

Phalen ( 1951) summarized the aetiological factors, related to the

carpal tunnel syndrome and he pointed out that any condition which

might decrease the size of the carpal tunnel or which might increase

the volume of the structure .contained within it, would tend to compress the median nerve.

He found it more difficult to understand how the median nerve can

undergo spontaneous compression beneath the flexor retinaculum

without any antecedent history of injury co the wrist. The apparent

rarity of the syndrome is probably due co the physician's failure to

consider this condition when making the differential diagnosis.

In 1953 Gillian and Wilson introduced the tourniquet-test as a help­ful diagnostic test. They found by chance, that the symptoms became

very much worse when the circulation to the arm was arrested by a

pneumatic cuff above the elbow.

The differential diagnosis of paraesthesiae and other disturbances of sensation and atrophy of the thenar muscles was still a problem in cli­

nical neurology.

The general opinion was that the condition could be due to

compression of the nerve or a disturbance of its vascularization.

With this knowledge Simpson ( 1956) measured the conduction time

of the median nerve between the wrist and the thenar musculature. In

11 of the 15 patients with a carpal tunnel syndrome, he found delayed conduction along the median nerve. In 3 of these hands, the conduc­

tion time improved after decompression of the median nerve.

In the same year Dawson ( 1956) introduced the sensory conduction time. The advantage of this technique is that possible sensory nerve

damage can be determined, before the motor branches are affected.

In an effort to resolve differences of opinion, regarding the position of

the wrist producing the greatest compression of the median nerve in

8

the carpal tunnel, Tanzer (1959) investigated a large number of cases during surgery and at autopsy. He found that with the wrist extended and the fingers forcefully flexed, the median nerve within the carpal tunnel is relatively free of compression, with the tendons hugging the osseous arch. On the other hand, with the wrist and the fingers flexed, the long flexor tendons are displaced volarly and the median nerve is compressed. He also demonstrated, that both in flexion and extension the pressure in the proximal part of the carpal tunnel was raised and that in the distal portion of the tunnel the pressure was only raised in extension. Osborne ( 1959) expressed the opinion that venous stasis may be a cause of "acroparaesthesiae". Blunt (1959) has shown that the blood supply of the median nerve is segmental and he found nothing to suggest a local predisposition to neural ischaemia. In 1960 Crow and Forster treated patients suffering from the carpal tunnel syndrome with local injections of steroids. These injections gave temporary relieve of symptoms, but the symptoms returned within a year. Heathfield and Tibbles (1961) treated pregnant women with the carpal tunnel syndrome with diuretics (chlorothiazide) and 90% of these women was freed from their symptoms. After an anatomical study of the carpal tunnel, Robbins ( 1963) con­cluded, that any space-occupying lesion within the carpal tunnel might compress the median nerve. Certain positions of the wrist, such as acute Hexion and extension, would decrease the volume of the car­pal tunnel. In a comparative study of 114 patients, Goodwill (1965) concluded that with a distal motor latency of 8 msec. or more, non-operative treatment will always fail. With a distal motor latency of 7 msec. or less, approximately 10% of the patients will receive permanent relief with local steroid therapy or splints, but 85 % of those with an initial response will relapse in one to four years.

9

A year later Phalen (1966) published his experience with 439 patients suffering from the carpal tunnel syndrome and he described the wrist-flexion test. Acute flexion of the wrist would compress the median nerve between the radius and the proximal edge of the flexor retinaculum. In healthy hands paraesthesiae will occur after some time, but in the carpal runnel syndrome, paraesthesiae occur within 30 - 60 seconds. The Tinel-test was positive in 73% and the wrist-flexion test in 74% of the examined hands. Folkerts (1969) emphasized that the carpal and tarsal tunnel syndrome can be complicated by a "vegetative dysregulation" and the symptoms can extend along the whole limb and even to a quadrant of the body. An abnormal muscle belly of the thenar muscles in relation to the flexor retinaculum was found by Matricali and Kauer (1970) at opera­tion in primary carpal tunnel syndrome and in dissections of cadaveric hands with atrophy of the thenar muscles. They found an abnormal muscle belly pressing a groove into the ligament and so compressing the median nerve. Curtis and Evermann (1973) operated upon 96 hands with compres­sion of the median nerve. After dividing the ligament, they perfor­med an interfascicular neurolysis under magnification, which impro­ved their results. This technique would not be necessary in patients with transient symptoms of numbness and without thenar atrophy. Simple division of the flexor retinaculum in the last mentioned group, gave a high percentage of good results. Smith et al. (1977) substituted the median nerve in cadaveric hands by a balloon-transducer. They measured pressures of 300 mm.Hg. with the wrist in flexion and with tension on the long flexor tendons. They suggested that these pressures could play an important part in the development of carpal tunnel syndrome or may aggravate the symptoms. 10

Dekel et al. ( 1980) used computed tomography to measure the cross­sectional areas of the carpal tunnel in normal controls in both sexes and in females suffering from the primary carpal tunnel syndrome. They found significantly smaller cross-sectional areas of the carpal tunnels in the female controls, as compared with those in the male controls and also smaller cross-sectional areas in the female patients, when compared with the female controls. The differences in cross­sectional areas of the carpal tunnels would explain the predilection for primary carpal tunnel syndrome in women. They concluded that the condition manifests itself in later life, be­cause of space-occupying degenerative changes in the wall of the tunnel, which would compress the median nerve. Gelberman et al. ( 1981) utilized a Wick-catheter to measure the pres­sures within the carpal tunnel in 15 patients with the carpal tunnel syndrome and in 12 controls. In the patients the average pressure with the wrist in a neutral position was 32 mm.Hg., with the wrist in 90° flexion the pressure increased to 94 mm Hg. and in 90° extension to 110 mm.Hg. In the controls, with the wrist in a neutral position, the average pres­sure was 2.5 mm.Hg., with flexion of the wrist it increased to 31 mm. Hg. and in extension it increased to 30 mm.Hg. The pressure within the carpal tunnel decreased after decompression. However, some of their patients did not have pressures elevated above 30 mm.Hg.; therefore factors other than increase in pressure within the carpal tunnel must be considered in the pathogenesis of the syndrome. Over the last decades numerous data were published about the causa­tive mechanisms as well as the treatment of the carpal tunnel syndrome. It is commonly accepted that unaccustomed manual work plays an important role in inducing or aggravating the clinical symptoms. Certain positions of the wrist could lead to recurrent mechanical irritation or compression of the median nerve, which might lead to inflammation, fibrosis, narrowing, paresis and paralysis of the nerve. One must bear in mind, that no common factor concerning the aetio­logy of primary carpal tunnel syndrome can be found.

11

i I

Chapter III

Anatomy

3 . 1 . Median nerve.

The median nerve arises from the medial and lateral cords of the brachia! plexus (C5 ,6,7,8,Tl) and descends as part of the neurovas­cular bundle of the arm. It passes deep to the bicipital aponeurosis, between the two heads of the pronator teres and descends on the deep surface of the superficial flexors . In the upper arm it gives off no branches, but in the forearm it innervates all the muscles of the volar side, except the flexor carpi ulnaris and the ulnar portion of the deep flexors. It gives sensory branches to the elbow joint and more distally, a cutaneous branch to the palm. The palmar cutaneous branch supplies the skin lying between the thenar, hypothenar and the distal palmar sulcus, the so called "palmar triangle". Carroll ( 1972 ) and Taleisnik ( 1973 ) described various origins and courses of this particular branch (fig.2 ) .

V I+ 2

Fig. 2. The various anomalous origins and courses of the palmar branch of the median nerve (see text) .

1 3

1. The palmar branch arises from the ulnar side of the median nerve proximal to the wrist : most uncommon origin. 2. The most common origin of the palmar branch: arising from the radial side of the median nerve, 3 to 6 cm. proximal to the wrist, proceeding superficial to the flexor retinaculum, towards the centre of the palm. 3. This branch arises more proximally than the one mentioned in case 2. 4. Thi� branch arises just proximal to the wrist and passes through the flexor retinaculum. 5. Before this branch becomes subcutaneous, it travels deep to the flexor retinaculum.

The median nerve enters the hand by passing through the carpal tun­nel and divides into sensory and motor branches. The thenar branch is a motor nerve that innervates the abductor pollicis brevis, the opponens and the superficial head of the flexor pollicis brevis. Various anomalies of this branch are described by Lanz (1975), Das and Brown (1976) (fig.3).

V

6

'- �·----� ......... I--- 3 r���,,--- 4

Fig.3. The various anomalous origins and courses of the thenar branch of the median nerve (see text) 14

1. The motor branch comes from the radial side of the median nerve, beneath the flexor retinaculum and passes straight through to the thenar muscles. This is the most common bran­ching pattern. 2. Two or more branches are given off and supply the thenar muscles directly.

3. This branch separates proximal to the flexor retinaculum and passes through it. 4+5. These branches separate proximally and run either superficial or deep to the flexor retinaculum before supplying the thenar mus­cles. 6. This branch arises from the ulnar side of the median nerve and then curves towards the thenar muscles, either superficial or deep to the median nerve.

The median nerve also supplies the first and second lumbrical muscles. The sensory branches usually supply the volar side of the thumb, index, middle and the radiovolar part of the ringfinger and the dorsal sides of the distal phalanges of these fingers (fig.4). There are many variations in the relative distributions of the median and ulnar nerve.

/2 � �· ··

� rad ial nerve ... :,;., CJ median nerve �

CJ ulnar nerve � palmer cutaneous

branch of the median nerve

Fig.4. Distribution of nerves for skin sensibility. 1 5

3.2 . The carpal tunnel. The carpal tunnel is a fibro-osseous tunnel, formed by a concave arch of the carpal bones and a tough fibrous ligament tightly strung across the base. The four chief attachments of this ligament or flexor retinaculum are at the radial side the tubercle of the scaphoid and trapezium and at the ulnar side the triquetrum, pisiform and the hook of the hamate. The hook of the hamate and the tubercle of the trapezium lie further dis­tally and form the ulnar and radial walls of the carpal tunnel. The carpal bones are arranged in two rows of four. The carpal bones are bound together by ligaments. Each carpal, with the exception of the pisiform, has several facets for articulation with the neighbouring bones. The proximal surfaces of the scaphoid, lunate and triquetrum are convex from side to side and from volar to dorsal. They articulate with the radius and the convexity extends further dorsally than volarly. The range of extension is greater than flexion at this joint. The hamate and the head of the capitate occupy a socket formed by the scaphoid, lunate and triquetrum. The proximal surface of the capitate is anchored to neighbouring bones by radial ligaments and its ulnar surface co the hamate by a strong interosseous ligament. The capitate is in line with the third metacarpal. The distal row of carpal bones forms a fixed unit together with the second and third metacarpal. Movement between these bones is limited by strong ligaments. The movement provided by the radiocarpal and midcarpal joints are fle­xion, extension, abduction, adduction and combinations of these. On cross-sections the carpal tunnel has an oval shape. The osseous part of the carpal tunnel forms an ulnar eminence, the pisiform and hook of hamate and a radial eminence, the tubercles of the scaphoid and the trapezium. The concavity of the carpus is partly sustained by the flexor retinaculum. The average thickness of the flexor retinaculum in the proximal third is 2 mm. and 3.6 mm. for the middle and distal third (Tanzer 1959). The long flexors of the fingers and thumb pass through the carpal tunnel together with the median nerve. The long flexors are surroun­ded by their synovial sheaths. The median nerve lies just dorsal to the flexor retinaculum, radio-1 6

volar to the superficial flexor tendon of the index finger and ulnovo­lar to the flexor tendon of the thumb. The median nerve has a constant topographical relationship to the long flexor tendons along the whole length of the carpal tunnel. At the hook of the hamate the carpal tunnel is at its narrowest. The length of the carpal tunnel is between 2.5 - 4 cm. (Robbins 1963 ). The median nerve flattens out during its course from proximal to distal in the carpal tunnel and finally divides at the distal edge of the flexor retinaculum into motor and sensory fibres. A superficial layer volar to the flexor retinaculum extends from the trapezium volar to the hypothenar muscles. This layer is called the volar carpal ligament and forms together with the palmaris brevis the roof of Guyon's space, through which the ulnar artery and the nerve pass. On the radial side, the flexor retinaculum divides into a superficial and deep part. Between these layers passes the tendon of the flexor carpi radialis. On the ulnar side, the flexor retinaculum extends into the pisohamate ligament. The ulnar artery and nerve pass over the volar side of this ligament. The abductor pollicis brevis, flexor pollicis brevis and opponens pollicis form the thenar eminence and arise from the volar side of the flexor retinaculum and the tubercle of the trapezium. The abductor also arises from the tubercle of the scaphoid and usually receives a slip from the tendon of the abductor pollicis longus. The abductor pollicis brevis is the most superficial muscle and forms the radial side of the thenar eminence.

1 7

Chapter IV

A Peripheral Nerve

4. 1 . Structure of a peripheral nerve.

A peripheral nerve is a collection of nerve fibres and is composed of neuro-epithelial conducting structures and the mesenchyme, which supports and protects it. A nerve fibre consists of an axon and its sheath. The axon is the prolongation of the nerve cell. It contains in its cytoplasm a semi-liquid gel, filaments and neurotubules. The axon is sur­rounded by a membrane: the axolemma. The axons may be called myelinated or unmyelinated. The former possesses a sheath of myeline, formed from the cytoplasmic membrane of the Schwann cell. Since Schwann cells are arranged in a chain of which each link is approximately 1 mm. long, the sheath cannot be a continuous cylinder. It is formed of segments and the short unsheathed area found between the segments is called a Ranvier's node. Only at this point can the axon membrane be stimulated through the propagation of an impulse, whereas the interme­diary segment is isolated by the sheath (Robertson 1955) . In the unmye­linated fibre, the sheath is lacking. Each peripheral nerve is surrounded by a re-enforcing sheath of delicate connective tissue: the endoneurial sheath (sheath of Henle, or of Key and Retzius) . It is composed of delicate collagenous fibres disposed longi­tudinally for the most part, a homogeneous ground substance and cells among which the fibroblasts are the most numerous. The endoneurium protects the nerve fibres against traction, compression and crushing. Most of the capillaries supplying the peripheral nerve fibres are located in the endoneurium. A group of nerve fibres forms a fascicle and is ensheathed in its own perineurium (fig.5 ). The epineurium comprises all the connective tissue of the nerve trunk outside the perineurium. It is composed of fibroblasts and bundles of col­lagenous fibres, arranged partly in a circular manner and partly longitudi­nally, forming a trelliswork. The epineurium provides good mechanical protection. Arteries, which provide nourishment to a peripheral nerve, penetrate the epineurium and divide into several branches. The vascularization consists of two longitudinal networks, with abundant anastomoses.

19

Fig.5. Cross-section of a median nerve (fixation Os 04 2%, slice thick­ness 7 µm.) A= 16.7 times enlarged, B= 167.2 times enlarged, l= fascicle containing nerve fibres ensheathed by endoneurium, 2= perineurium, 3= epineurium, 4= blood-vessels, 5= connective tissue.

The outer network is connected via nutrient arteries with the vascular trunks. The number of nutrient arteries increases in areas where the nerves are exposed to possible mechanical extension or compression. Peripheral nerves contain fibres of various categories: myelinated and unmyelinated, large and small, visceral and somatic, sensory and motor. A lesion of the motor fibres results in complete paralysis of all muscle fibres supplied by these branches and may be seriously disabling. The importance of sensory loss varies according to the distribution. A nerve itself has relatively little sensory perception, which means that if a 20

nerve is stimulated along its course, the sensation is felt, not at the point of stimulation, but in the areas supplied by the fibres. This phenomenon is known as projection of sensation or phantom sensation.

4.2. Regeneration. The cell body of a neurone is an irregular star-shaped structure, about 1/ 10mm. in diameter. Attached to this is the axon process, which is 1/50 mm. in diameter or less and may reach as much as 1 metre in length. The cell body exerts an immediate influence on this extended fibre to which it is attached. If a nerve fibre is cut, the isolated peripheral portion will begin to show differences, when compared with the proximal part, within a few hours. Disintegration occurs in the axon severed from its proximal nucleus. This also occurs in the proximal part, but not proximal to the adjacent node of Ranvier. The disintegration is followed by loss of conduction, metabolic changes, morphological alteration, myelin disruption, Schwann cell hypertrophy and hyperplasia and macrophage activity. This highly complex phenomenon is called the Wallerian degeneration. At the same time the axoplasm moves from the proximal portion of the nerve fibre in a distal direction and is conveyed into the empty distal endoneural tubes. The regeneration of nerve fibres progresses at a rate of 1 to 3 mm. per day. When the fibre reaches the periphery, the linear growth ceases, but the increase in diameter continues, until the original thickness is approximated. Initially the axons are thin and unmyelinated and they have a slow conduction velocity, which improves after enlargement and remyelination (Weiss and Hiscoe 1948).

4.3 . Compression.

Local increases in pressure on a nerve cause displacement of substance into zones of lower pressure, thus producing reduction in diameter. This implies a gradual reduction in the diameter at the zone of constriction and slight dilatation at either end of the constriction. 21

•

The degree of narrowing varies not only with the degree of compression of the nerve, but also with: a. the topography of the fibres, b. the consistency of the surroundings, c. the fibre diameter. -a. The effect of compression is not evenly distributed over the whole cross-section of the nerve, but is most marked at the surface and declines rapidly towards the interior. -b. Since interstitial fluid around a nerve fibre can shift more easily than the content of the fibre, it acts as a shock absorber. The nerve sheath likewise has a cushioning effect. -c. The larger fibres of a constricted nerve suffer a greater propor­tional reduction of diameter than do the smaller ones. After more than 300 experiments, Weiss and Hiscoe ( 1948) concluded that synthesis of new axoplasm occurs exclusively at the nuclear site and this is equally true for the incremental growth of immature or regenera­ting axons and for the anabolic renewal of the axoplasm in mature axons. This axoplasm has a constant proximal to distal movement and if the nerve fibre is constricted, the axoplasm is blocked and will accumulate proximal to the constriction. Progression of compression might cause a discontinuity of the axoplasm, which results in degeneration of the distal portion of the nerve fibre. Later studies demonstrated that segmental axonal kinking above a nerve constriction reflects axonal transection and retraction. Segmental axonal dilatation in this nerve segment was usually due to formation of axonal growth cones (Pinner-Poole and Campbell 1969, Spencer 1972). Guinea pigs, as they grow older, may develop entrapment lesions of both median nerves under the flexor retinaculum and the cartilaginous bar, which overlies it at the wrist. In these median nerves, single fibres immediately proximal to the site of entrapment, show a consistent asymmetry of the myelin sheath, which appears to be thinned at one end of the internodal segment and thickened or swollen at the other end (Anderson et al. 1970).

22

Ochoa and Marotte ( 1973) found these changes in very mildly affected animals, on either side of the entrapment sites, but with reversed pola­rity, so that the thin myelin was always at the end of the internodal seg­ment, closer to the centre of the lesion. In the centre, completely demye­linated internodal segments were present. In many cases, this change is only seen on the proximal side of the lesion with degeneration of the axon occuring distal to this. The initial stage of this process is asymmetry of the myelin sheath, leading to retraction from one end, thus to paranodal demyelination. At a later stage, myelin loss from the complete internodal segment will occur or, in the most severe cases, complete degeneration of the fibre. These changes suggest that the demyelination and nerve fibre degeneration are the result of mechanical deformation rather than ischaemia. This interpretation is not favoured by the fact that directly after decom­pression of the nerve, most of the subjective complaints disappear, which appears to suggest rather a vascular insufficiency as the primary cause. Hargens et al. (1979) demonstrated that the time required to produce conduction block in peripheral nerves, was inversely proportional to the intra-compartmental fluid pressure. At pressures between 80 and 120 mm.Hg., nerve conduction was completely blocked in less than two hours. Complete block of conduction was also obtained at a pressure as low as 50 mm.Hg. The conduction block was incomplete after 6 to 8 hours of pressurization at 40 and at 30 mm.Hg. At pressures of 20 mm.Hg. or less, for 8 hours, conduction remained normal. Rydevik et al. (1981) observed changes in intraneural microcirculation (intrafascicularly and extrafascicularly) when graded compression was applied. Interference with venular flow was observed already at a pressure of 20 to 30 mm.Hg., while arteriolar and intrafascicular capillary flow was impaired at about 40 to 50 mm.Hg. At 60 to 80 mm.Hg., no blood flow could be observed in the nerve. Depending on the duration and magnitude of the compression, a discon­tinuity of the axoplasm may occur, which results in degeneration of the distal portion of the nerve fibre. After decompression of the nerve, the axoplasm moves freely into the intact endoneural tubes, unless the rubes are narrowed by fibrosis.

23

1

Chapter V

The carpal tunnel syndrome

5 . 1 . Introduction.

Lesions of nerves may be manifested by paraesthesiae, pain, impairment of sensation, paresis or paralysis and muscle atrophy. Paraesthesiae are subjective pathological sensations. The paraesthesiae can be caused by local disease of the rami or peripheral nerves or more centrally located lesions. They can also be the initial symptoms of a general disease. The brachialgy is a frequently occurring complex of symptoms, in which paraesthesiae can be included. Muscle atrophy may either be isolated or a sign of a generalized condition. It can have a central as well as radicular or peripheral origin. While establishing the diagnosis "carpal tunnel syndrome", other lesions must be excluded. In addition, a peripheral nerve can be compressed along its entire course. 5.2. Aetiology.

Certain anatomical circumstances may produce mechanical irritation (either by stretching, compression or angulation) of a periphal nerve re­sulting in a chronic inflammatory or ischaemic condition. Such circum­stances may occur at certain specified sites in the course of a peripheral nerve. The distal part of the median nerve passes the carpus through a narrow tunnel, together with the nine flexor tendons of the fingers and thumb. The median nerve has no chance of escaping the effects of either space­occupying lesions or when that space is otherwise decreased. It is obvious that any space-occupying lesion will lead to compression of the median nerve, which manifests itself by paraesthesiae, pain, paresis, paralysis and atrophy of a part of the thenar muscles. Generally this is called secondary carpal tunnel syndrome (table I). However, in the majority of cases there is no such condition which could explain compression. The pathophysiology of this condition is unknown and generally it is called primary, idiopathic or spontaneous carpal tunnel syndrome.

25

1. Congenital

2. Tumors 3. Trauma

4. Inflammation 5. Metabolic and endo­crine imbalance

6. Disturbances of circu­lation

- persistently large median artery. - abnormal muscle bellies (superficial flexors, lumbricals, palmaris profundus) . - ganglia, lipomas, haemangiomas, neurofibromas, neurinomas. - fractures of the distal radius. - fractures or dislocation of the carpal bones. - swelling of intercarpal structures resulting from an extensive hand injury. - burn oedema. - rheumatoid disease, gout, amyloidosis, tendinitis nodosa, De Quervain. - mucopolysaccharidosis, acromegaly, pregnancy, diabetes mellitus, hypothyroidism. - Raynaud, diabetes mellitus.

Table I. Conditions, producing or related to a secondary carpal tunnel syndrome.

The median nerve has, as already mentioned, a rich vascularization and the distal 7.5 cm. of this nerve has an exceptional fascicular structure. The interfascicular connective tissue contains relatively large arteries, which can resist compression very well (Denny-Brown and Brenner 1944). Blunt ( 1959) found no evidence in the local vascular architecture of the median nerve that is directly suggestive of any particular local predispo­sition to neural ischaemia, such as has been suggested as the cause of the carpal tunnel syndrome by Dorndorff ( 1931 ), Pritchard ( 1950) and Kremer et al. (195 3). Bentley and Schlapp ( 1943) demonstrated that the oxygen requirements of a nerve trunk may be supplied by oxygen diffusion from surrounding well-vascularized tissues, after occlusion of its regional nutrient arteries. 26

The rapid relief of complaints after decompression of the median nerve, indicates that the disturbances in nerve function are rapidly reversible. This reversibility supports the hypothesis that a process of vascular insufficiency rather than morphological changes within the nerve, is the primary abnormality in the carpal tunnel syndrome. Gelberman et al. (1981) measured pressures within the carpal tunnel in patients and controls and they recorded pressures less than 30 mm.Hg. in both groups. They concluded that elevated pressures within the carpal tunnel could not be the only cause of the carpal tunnel syndrome. Since the disease often occurs in the menopause and during pregnancy, some investigators wonder to what extent neurohumoral and endocrine factors have influence in the pathophysiology of the carpal tunnel syn­drome. Most observers agree, that unaccustomed manual work may induce or aggravate the symptoms.

5 .3 . Symptomatology.

Primary carpal tunnel syndrome is the most frequent affection of the median nerve. It affects both men and women, but with a predominance in middle-aged women. Almost always affecting both hands, the condition usually manifests itself initially in the dominant hand. The complaints begin with prickling in the tips of the thumb, index, middle and sometimes the ringfinger or occasionally with pain in the shoulder and neck. The prickling or paraesthesiae are subjective sensations and are often reproduced as pin-pricks, tinglings, burning sensation, formication or numbness. The effect on sensation varies remarkably, from being just annoying to a very disturbing and unpleasant sensation or even pain. Often the patients go to sleep without complaints, but after a couple of hours, they wake up with an intense prickling sensation of burning quality and pain in the hand and fingers. Many patients say that all the fingers are affected, but on being directly questioned, they often decide after some thought, that the little finger escapes.

27

Most patients describe manoeuvres, which they adopt to obtain relief: hanging the arm out of bed, shaking the wrist, massage with the unaffec­ted hand, walking round the room and bathing the hand(s) with warm or cold water. These manoeuvres often give temporary relief of symptoms, but when they lie down again, the symptoms return. The symptoms may be induced or aggravated by Hexion or extension of the wrist or by direct pressure upon the flexor retinaculum. The symptoms are localized in the areas supplied by the median nerve, but they can also be manifest in a retrograde manner (Phenomenon of Valleix) or even involve a quadrant of the body (Folkerts 1969). This often hampers the establishment of the diagnosis. The clinical signs may be complicated by dysregulation of the vegetative nerve system and can be manifested by trophic changes, vasomotor and secretory disturbances, pain, disturbance of sensation and muscle wasting. Eventually, the initial reversible hypaesthesia and anaesthesia becomes irreversible. In damage of the motor branch, the patients complain of becoming clumsely and have loss of power in the thumb. Finally, damage to the motor branch results in atrophy of a part of the thenar musculature and may give rise to a disturbance of opposition. 5 .4. Examination. 5.4. 1 . Introduction.

It is superfluous to state that every specific examination of the hand should be preceded by the history and a general examination of the shoulder, arm, forearm and hand. The diagnosis of the carpal tunnel syndrome is established on the history and clinical findings and a delayed conduction velocity of the median nerve across the flexor retinaculum may confirm it. 5.4.2. Thenar atrophy.

Muscle wasting is best detected by comparison with the other hand, while viewing the thenar eminence in profile. The strength of the abduc­tor pollicis brevis is tested with the hand of the patient flat on the table, palm upwards. The patient should be asked to touch with his thumb the examiner's finger, held above the hand, while slightly pressing down­wards. 28

5.4.3. Sensory disturbance.

The sensory disturbance is mapped out using light touch. Sensory distur­bance initially takes the form of intermittent numbness and tingling or paraesthesiae. These are invariably within the exact sensory distribution of the median nerve, although not necessarily throughout it. Any indis­putable extension beyond the boundaries of that distribution should make the examiner beware. He may be dealing with anomalous distribu­tion, compression of more than one nerve, or most probably, compres­sion located more proximally than initially suspected. Loss of sensation in median nerve distribution causes clumsiness in fine manipulation and this may be the patient's sole or major complaint. Loss of sensation is not commonly so advanced as to cause a detectable difference in two point discrimination. It follows that sweating is often present, in which event those sensory tests based on its absence, are not applicable. In performing the examination, repeated comparison should be made with ulnar innervated digits and with those on the other hand. The dysaesthesia does not often involve the entire median nerve distribution and this does not cast doubt on the diagnosis. If sensation is lost in the area of the palmar triangle usually innervated by the palmar cutaneous nerve, a diagnosis of carpal tunnel compression should be made with reservation and with the knowledge, that it is only tenable if the palmar triangle is not supplied by the palmar cutaneous nerve. This is also the case if the palmar cutaneous nerve originates as has been described, deep to the flexor retinaculum, piercing it to supply the palmar triangle. A Tinel's sign can be frequently elicited in carpal tunnel syndrome. Tap­ping with the flexed finger or with a tendon hammer over the course of the nerve at the flexor retinaculum or more commonly just proximal to it, produces paraesthesiae radiating into the median nerve distribution. The paraesthesiae may be provoked because demeylinated axons are easily stimulated (Robertson 195 5 ). The Phalen test "increases compression" on the median nerve by pla­cing the wrist in acute Hexion. This is achieved by placing the dorsum of one hand against that of the contralateral side and lowering the elbows as far as possible while maintaining that contact. By examining both

29

hands simultaneously, the normal acts as a control for the affected hand. However, both hands may be involved, either with the patient's know­ledge or subclinically. Therefore a timed Phalen test is of more value and onset of numbness in less than one minute being considered diagnostic of carpal tunnel syndrome. The reversed-Phalen test is performed by placing the palms of the hands together and raising the elbows as high as possible. Occasionally, when the Phalen test is negative, the reversed test is positive, producing numbness and tingling in the median nerve distribution by placing the nerve on stretch. The tourniquet test is based on the fact that a damaged nerve is very sus­ceptible to ischaemia. In normal people arrest of the circulation in the arm by the inflation of a pneumatic cuff above the elbow is followed within one or two minutes by a faint fluttering or vibrating sensation in the hand or fingers, which usually develops into a diffuse tingle, uniform in quality. In patients with the carpal tunnel syndrome, the paraesthesiae and numbness become very much worse within 30 - 60 sec. after the circu­lation is arrested by a pneumatic cuff above the elbow. 5.4.4. Electrophysiological examination.

Delayed distal sensory and motor conduction times of the median nerve across the flexor retinaculum confirm the diagnosis carpal tunnel syn­drome. However, 40% of the patients with typical symptoms and signs may nave median motor conduction times within normal limits and 2-5 % have sensory conduction times within normal limits. Buchthal et al. (1974) presented a formula to determine the normal distal latency: 2.85 +(0.009 Xage in years)msec. A normal conduction velocity only means that at least one of the examined nerve fibres is unaffected. 5.4.5. Radiographs.

Standard and special carpal views of the hand should be taken, as they may reveal an unsuspected lesion producing the pressure in the carpal tunnel. 30

5.4.6. Laboratory examination.

All patients with a carpal tunnel syndrome should have the most likely systemic causes eliminated by basic laboratory investigation: -sedimentation rate: if elevated, this should be followed with more sophisticated tests for rheumatoid disease and collagen disorders, -two-hour postprandial blood sugar, -serum uric acid, -T3 and T4 estimation, -vitamin B 1,6 and 12 bloodlevels, -pregnancy test if in doubt. 5 .5 . Treatment. The first line of treatment of the carpal tunnel syndrome is decompres­sion of the median nerve by dividing and partially resecting the flexor retinaculum. Non-operative treatment such as a wrist splint in slight extension, diuretics or injection of the carpal tunnel with cortisone preparations are especially indicated in pregnant patients, in whom the compression can be expected to diminish spontaneously after delivery. If the synovium around the flexor tendons is thickened and hypertro­phic, some surgeons undertake synovectomy. Great care must be taken to protect the palmar cutaneous and the thenar (motor)branch when performing release of the carpal tunnel (fig.2 and 3) .

3 1

Chapter VI

I nvestigation

6. 1 . Introduction.

The pathophysiology of primary carpal tunnel syndrome is unknown, as is the reason for its predominance in middle-aged women. Abbott and Saunders (1933) demonstrated that Berlin Blue or Lipiodol injected into the sheath of the median nerve, was arrested at a point opposite the proximal border of the flexor retinaculum, if the wrist was held in arute flexion or extension. If however, the wrist was held in moderate flexion or extension, the dyes flowed easily into the palm of the hand. Since the work of Abbott and Saunders there has been little or no change in viewpoint concerning the aetiology. Brain et al. (1947), Tanzer (1959), Smith et al. (1977) and Gelberman et al. ( 1981) measured elevated pressures within the carpal tunnel, in relation to arute flexion and extension of the wrist. Most observers be­lieve that these pressure-increases are the most important factors in the pathogenesis of the carpal tunnel syndrome. Matricali and Kauer (1970) described an abnormal muscle belly of the thenar musculature, originating from the flexor retinarulum on the ulnar side of the median nerve and compressing the median nerve beneath the flexor retinarulum. This muscle, however, is not consistent­ly found in patients suffering from carpal tunnel syndrome. Using computed tomography, Dekel et al. (1980) suggested that primary carpal tunnel syndrome is caused by inherited rather than acquired carpal tunnel stenosis. Until now, the relevance of the cross-sectional areas of the carpal tunnel in the pathogenesis of the carpal tunnel syndrome, particularly in rela­tion to the position of the wrist and according to the sex of the patient, has not been clearly demonstrated. Using computed tomography, transverse sections (CT-scans) of the carpal tunnel (as described by Hillen and Zonneveld) were performed in the "living" hand at different levels and in various positions of the wrist. High resolution CT-scans reveal mutual anatomical relationships of the walls of the carpal tunnel as well as the contents and surroundings,

33

therefore we used this technique for this purpose. The cross-sectional areas of the carpal tunnel and its contents may be measured accurately, because of the recent developments in computed tomography. In this study we obtained CT-scans of the carpal tunnel in male and female patients suffering from the primary carpal tunnel syndrome and in normal males and females. By comparing the observed images and measured data of the patients and controls, an attempt was made to elucidate: 1. the role of the morphology and topography of the carpal tunnel, the surrounding structures, the flexor tendons and the median nerve in the pathogenesis of primary carpal tunnel syndrome, 2. the role of the transverse dimensions of the carpal tunnel and its contents in the pathogenesis of primary carpal tunnel syndrome, in relation to the position of the wrist, 3. the reason for the predominance in women. To obtain a standardization of the CT-procedure in patients and con­trols, a preliminary investigation was performed, using cadaveric hands (forearms and hands). 6.2. Preliminary investigation.

6.2. 1 . Materials.

Ten (10) cadaveric hands were used in the preliminary investigation. The cadaveric hands were placed at our disposal by the Laboratory of Embryology and Anatomy (head: Prof. Dr. A.G. de Wilde) of the University of Groningen.

6.2.2. Methods and results.

The purpose of the preliminary investigation was to obtain a standardi­zation of the CT-procedure to be performed on patients and controls and also to identify the anatomical structures in transverse CT-scans. Some of the studies were performed using a Philips Tomoscan 300, because the Tomoscan 310 was not available at that time, but the spatial resolution (1.2 mm.) was sufficient for this purpose. 34

Specification of the Tomoscan 310: -tension 120 KV. -slice thickness 1.5 mm. -scan time 9.6 sec. -exposure time 2.4 sec. -spatial resolution 0.6 mm. -attenuation scale -1000 to +3095 Hounsfield units -computer system Philips P857 with 128Kl6 of memory.

The computer data were stored on magnetic tape and flexible disks. The measurements were performed with the "Stand Alone Viewing Console" (S.A.V.C.), a digital image viewing console, equiped with image analysis functions. All CT-scans and measurements were performed in the Department of Radiology (head: Dr. R. Ubbens) of the Roman Catholic Hospital, Gro­nmgen. The cadaveric hands were positioned in the gantry of the Tomoscan using a preformed cuff of polyethylene foam. Frontal (fig.6a and b) and lateral scanograms (or Scoutview®, Pilot-scan, Radio, Topograph, Planar Densitograph) were performed prior to scanning. A scanogram is a radiograph produced by a stationary X-ray tube and translation of the object through the patient aperture. The distal border of the hook of hamate was selected as the point of reference, because of its good definition on the scanogram and the rela­tively constant position in relation to the carpal tunnel. In performing the CT-scans, the principle of geometrical enlargement was used. This meant, that beam width and sample interval could be reduced simultaneously for small objects, which resulted in better spatial resolution. The field of view (F.0.V.), that is the diameter of the area represented in the reconstructed image, was 80mm. The matrix size, that is the number of rows and columns that describe the reconstructed image used, was 256. The CT-scans were obtained with the scan-plane always perpendicular to the 3rd metacarpal by making use of the gantry angulation. This bone forms together with the 2nd metacarpal and the distal row of the carpal bones, a fixed unit (see section 3.2).

35

A

Fig. 6 a. Frontal scanogram. b. Identification of the various bones: 1 = radius 2 = ulna 3 = scaphoid 4 = lunate

7 = trapezium 8 = trapezoid 9 = capitate 10 == hamate

5 = triquetrum 11 == metacarpals 6 = pisiform I, II, III and IV are the scan planes (levels). 36

In this manner, four (4) cadaveric hands were scanned throughout the entire carpal tunnel with the wrist in neutral position, at slice index distances of 3 mm., beginning at the point of reference. All scanograms and CT-scans were filed on magnetic tape and flexible disks for subsequent analysis. After scanning, anatomical cross-sections of one of these cadaveric hands were performed at corresponding levels and compared with the CT-scans in order to identify the structures on the CT-scans. The CT-scans and the anatomical cross-sections at four levels of the carpal tunnel (fig.6) are shown in fig.7a through h. The various struc­tures within the carpal tunnel were clearly defined (fig.7i), although the presence of glycerol in the tissues increased their X-ray attenuation and consequently decreased the contrast between tissues. The tendons and the flexor retinaculum had a higher attenuation value than the median nerve and the synovium. The CT-number of the tendons ranges from 100 to 120 and that of the synovium from 40 to 60 Hounsfield units (H). The digital image data may be recalled from the flexible disks on the S.A.V.C., displaying the CT-image on the monitor. After outlining the cross-sectional areas on the monitor using the lightpen, the computer calculated these areas and displayed the results on the monitor. Sources of errors in the measurements can be due to: a. The performance of the investigator and measuring in CT-scans with poor definition. The most important artefacts that occur are those due to movement and they take the form of linear radiating streaks. These artefacts hindered the determination of the tendons boundaries in the subsequent investigation of patients and controls. The error in outlining the exact contour of the cross-sectional areas could be reduced by enlarging the image. The 95% confidence

intervals of 10 times measured cross-sectional areas of the carpal tunnels in a 2 times enlarged image, is shown in fig.9. These measurements showed errors of less than 4.5 % . Measurements ( 10 times) of the cross-sectional areas of the flexor tendons within the carpal tunnels in a 2 times enlarged image, showed an error of 6.7 %. b. It is difficult to scan the wrist exactly perpendicular to the longitudinal axis of the carpal tunnel. Considering other sources of error, a positioning error of about 1 % would be acceptable, this

37

I

a

II

b

m

C

d

e

g

h

Fig. 7. CT-scans (a through d) and corresponding anatomical cross-sec­tions (e through h) at levels of the carpal tunnel shown in fig.6. A design of corresponding cross-sections b and f is shown in i to identify the anatomical structures. 38

LEVEL II

.. �.\ - . :-

39

means an angular positioning error of 8° or less (angle a �8° in fig.8). Positioning the wrist perpendicular, within an accuracy of 8° , is easily obtained.

Fig. 8. Correction factor for oblique CT-cross-sections 1s cos a, assuming that the carpal tunnel has a cylindrical shape.

c. Carpal tunnel length. Because of the choice of the reference point, errors due to variations in length of the carpal tunnel are rather small in the distal CT-scans, but increase proximally. For instance, the same distance from the point of reference in carpal tunnels of different lengths will result in different scanned levels. All the measurements at the S.A.V.C. were performed with consistent window width (WW) and window level (WL). Fig.9 shows the results of the measurements of the 4 cadaveric hands. The carpal tunnels showed a shape like a Venturi-tube, which means that they are narrow in the centre and flare out proximally and distally. The narrowest part of the carpal tunnel appeared between 6 and 9 mm. proximal to the point of reference, at the midportion of the hook of ha­mate, according to the findings of Robbins (1963 ) . In the subsequent study CT-scans of the carpal tunnel were selected at four levels, initiating at the point of reference and 6, 12 and 18 mm. pro­ximal to this point, because these levels appeared fairly representative of the dimensions of the carpal tunnel (fig.6 and 9) . At these four levels, 6 cadaveric hands were scanned with the wrist in a neutral, 70° flexion and 70° extension position (fig.10). In all these positions the cadaveric hands were positioned into a preformed cuff of polyethylene foam. 40

300

i 2so l/)

0 a., 0

o 2 20 C: 0

� 180 0 I... u

140

II level III

I

1-,,,,_

i

o--' __ 3.....__6..._____,9..______.,, �-____._,s __ l ..... �-m-m

s l i c e po s i t i o n

Fig.9. Graphic representation of the cross-sectional areas of 4 cadaveric hands (Cl-4). The representation of C4 shows the mean and the 95% confidence intervals of the 10 times measured cross-sectional areas in a 2 times enlarged CT-image (see fig. 6 for the various levels).

A B

\ \

C

Fig. 10. Positioning of the wrist during CT-examination, A = neutral C = extension B = flexion

\

4 1

� 260

� 220 ex: ct ..J ct z 0 t== u LU en � 140 0

o :CS • = ca 6:C6 •= C9 □:C7 ■ : C 10

260

OL I

level I I I

JI m rz o"f I

S L I C E P O S I T I O N

f

level I I I

Il m N

260 .s. /

220 �

180 � �

140 �

level I I I

II m I2:

Fig.11. Graphic representation of the cross-sectional areas of 6 cadaveric hands (C5-10), measured at 4 levels. N= neutral F= flexed E= extended position of the wrist.

The results are shown in f ig.11. The narrowest part of the carpal tunnel seemed to be constant at 6 mm. proximal to the point of reference in both the neutral, flexed and exten­ded positions of the wrist. The dimensions of the carpal tunnels showed the same Venturi-tube like shapes, similar to the 4 cadaveric hands described above, in all positions of the wrist. Anatomical cross-sections of one of these cadaveric hands were made at corresponding levels to the CT-scans, with the wrist in the flexed posi­tion (fig.12). This was done to give a better understanding of the struc­tures in the CT-scans and to demonstrate the outlines of the carpal tunnels with the wrist in a flexed position. It was remarkable that the antero-volar portion of the radius, located dorsal to the carpal tunnel, transformed the oval shape of the tunnel into a bean-shape (fig.12d and h). In the cadaveric study, no distinction was made between male and female cadaveric hands. 42

I

a

b

m

C

d

e

g

Fig.12. CT-scans and corresponding anatomical cross-sections at levels shown in fig.6, with the wrist in flexion. 43

6.3. Investigation. 6.3 .1 . Materials.

The patient-group consisted of 38 hands in 24 patients suffering from primary carpal tunnel syndrome, who attended the Department of Plas­tic and Reconstructive Surgery (had: Dr. G. Heybroek, Drs. E.W. Sauer and Drs. A. de Boer) of the Roman Catholic Hospital, Groningen, the Department of Plastic and Reconstructive Surgery (head: Prof. Dr. A.J.C. Huffstadt) and the Department of Neurosurgery (head: Prof. Dr. J.W.F. Beks) of the University Hospital, Groningen, between September 1981 and January 1983. The control-group consisted of 10 male and 10 female hands of indivi­duals without signs or symptoms of median nerve compression or neu­ropathy. The ages of the controls varied between 40 and 70 years. The CT-scans of patients and controls were performed in the Depart­ment of Radiology (head: Dr. R. Ubbens) of the Roman Catholic Hospital, Groningen. 6.3.2. Methods.

The 38 patient-hands (33 female and 5 male) studied, belonged to patients (21 female and 3 male) suffering from primary carpal tunnel syndrome. The patients were selected on history, clinical and laboratory data. The diagnosis was confirmed by electrophysiological examination and the operative findings. Patients with secondary carpal tunnel syndrome were excluded. The control-hands, 10 male and 10 female, belonged to individuals with ages varying between 40 and 70 years. This age range was utilized to minimize the factor changes in volume of the carpal tunnel with aging. In order to scan the patients and controls, they were positioned behind the gantry of the Tomoscan, sitting or standing, depending on their body length. Their hands were immobilized into the gantry with a preformed cuff of polyethylene foam. Scanning in the neutral position of the wrist, the hand, wrist and forearm were in line, with the palm of the hand turned laterally. With the wrist in flexion, the palm of the hand and the elbow were turned downwards, while with the wrist in extension, the 44

palm of the hand was turned upwards and the elbow downwards (fig.10). All patients could maintain these positions during scanning very well; some noticed aggravation of the symptoms. The CT-scans were performed in both groups at four levels in the carpal tunnel, beginning at the distal border of the hook of hamate (point of reference), according to the preliminary study (fig.6a and b). Level of the CT-scan I : the point of reference,

,, II : 6 mm. proximal to the point of

" "

reference, III : 12 mm. proximal to the point of reference, IV : 18 mm. proximal to the point of reference. The four CT-scans were performed with the wrist in three positions: -1st neutral 0°

-2nd Hexion 70°

-3rd extension 70°

The computed tomography was performed using the Philips Tomoscan 310. See section 6.2.2. for technical data. As a result from the knowledge obtained from the preliminary study, the anatomical structures were easily recognized in the CT-scans (fig.7i and 13 ). Initially the shape and anatomical relationships of the carpal tunnel, its walls and contents were observed at different levels and in the various positions of the wrist. Subsequently, the origin of the thenar musculature from the flexor retinaculum was determined. The part of the flexor retinaculum covered by these muscles, was recorded in percentages of the transverse length of the ligament. The last mentioned was only performed in the CT-scans with the wrist in neutral position. Determination of the position of the median nerve was performed by using co-ordinate registration. In order to achieve this, the shortest dis­tance between the centre of the median nerve and the hook of hamate (x) and the shortest distance between the centre of the median nerve and the flexor retinaculum (y) was measured on the S.A.V.C. (fig.14).

45

a I b n

neutra l

f

f lexion

j

extension

Fig.13. CT-scans of the carpal tunnel of a patient at the 4 levels (fig.6) and with the wrist in the various positions. 46

C m d

neutral

g h

f lexion

k

-� -..: .;e;_ ...

✓'

4.

extension

47

y X

Fig. 14. Definition of distance between the hook of hamate and the centre of the median nerve (x) and distance between the flexor retinaculum and the centre of the median nerve (y). This was done in the narrowest part of the carpal tunnel (level II) in the neutral and flexed positions of the wrist. The measurements of the cross-sectional areas were carried out using a method similar to that used for the cadaveric hands. Both the observed images and measured data will be compared between the four groups (female patients and controls and male patients and controls) . The difference of the cross-sectional area of the carpal tunnel (Cc) and the tendons (Ct) is the space available for the median nerve and synovmm. The synovial tissue consists of a double membrane, surrounding each tendon separately and around groups of tendons. The thickness of the synovial membrane is too small to be measured accurately on the CT­scan. Hence the space available for the median nerve and the synovium will be regarded as one entity. The Relative Space available for the median nerve and synovium (R.S. ) is:

Cc - Ct x 100% Cc Because of differences in cross-sectional areas of the carpal tunnels (Dekel et al. 1980 and Gelmers 198 1 ) and most probably of the tendons in various individuals, the R.S. will be compared between the four 48

groups in order co rule our the influence of the different diameters of the tendons. In addition, the errors of measurements in oblique CT-scans will be decreased by com paring the R.S. All data of patients and controls were compared using the Standard Student's t test for statistical analysis.

49

I

l .J

Chapter VII Results

7 .1. General data. In this study 696 CT-scans were performed of the hands of 24 patients suffering from the primary carpal tunnel syndrome and 10 controls. The patients involved in this study had a mean duration of symptoms of 7.6 years. Bilateral involvement was found in 91.7% of the patients. The incidence of sex distribution was 87.5 % for females and 12.5 % for males. The mean ages of the various groups are shown in table II. female patients male patients female controls male controls

52.9 ± 1 .55 43.4 ± 3.40 49.6 ± 1.10 55 .2 ± 3.34

Table II. Mean ages ± S.E.M. in years of the various groups concerned in this study. All patients involved in this study had occupations involving fairly intensive manual work, such as housewife (15), secretary (4), farmer (milker) (2), auxiliary nurse (2) and cook (1). All laboratory data were within normal ranges (see section 5.4.6.). During operation, in none of these patients aberrant muscles (as descri­bed by Matricali and Kauer 1970) or other anomalies were found. All patients had delayed motor or sensory latency times of the median nerve across the wrist. 7.2. Morphology and topography.

The initial CT-scan (level I, fig.13a) showed the distal edges of the hook of hamate and the trapezium. At this level, the carpal tunnel had an oval shape. The dorsal and lateral bony boundaries were formed by the meta­carpal bases. Between the dorsal wall of the carpal tunnel and these bones there is a layer of low density tissue and the proximal part of the adductor pollicis.

51

The median nerve was situated just dorsal to the flexor retinaculum in the radial part of the carpal tunnel, surrounded by the long flexor tendons. The second CT-scan (level II, fig. 13b) showed a cross-section through the midportion of the hook of hamate. In this cross-section the carpal tunnel was tightly enclosed by a concave arch of carpal bones on the dorsal and lateral sides. From radial to ulnar these were the trapezium and trapezoid, the capitate and hamate. The flexor retinaculum extended from the hook of hamate to the tubercle of the trapezium. The third CT-scan (level III, fig.Be) showed a cross-section through the proximal portion of the hamate. The most proximal CT-scan (level IV, fig.13d) dissected the pisiform, triquetrum, capitate, hamate and scaphoid. The flexor retinaculum was slightly curved and ran to the dorsal base of the pisiform. Some low density tissue was observed (fat in Parona's space), between the dorsal wall of the carpal tunnel and the bones. The thenar muscles originated from the flexor retinaculum and partly covered this ligament (table III) .

level I level II level III level IV

Patients n=38 69.08 ± 2.65 64.15 ± 2.68 40.46 ± 2.19 7.90 ± 2.46

Controls n=20 65.63 ± 3.00 60.00 ± 3.35 36.88 � 2.31 3.13 ± 2.20 Table III. The part of the flexor retinaculum covered by the thenar mus­cles expressed in percentages of the transverse length of the ligament, according to the level of the carpal tunnel (mean ± S.E.M.). No significant differences in origins of the thenar muscles were found between patients and controls. Flexion of the wrist (fig. 13e through h) increased the concavity of the carpal arch at all levels, while the flexor retinaculum became convex towards the volar side. The median nerve moved dorsally away from the flexor retinaculum ( table IV). The increased distance between the centre of the median nerve and the flexor retinaculum in flexion of the wrist indicated that this nerve was not compressed between the flexor tendons and the ligament.

52

This phenomenon was statistically significant for both patients and controls (p<0.01 ) .

Position of the wrist

Patients n=38 X

y Controls n=20 X

y

neutral

1 1 .358 ± 0.275 2 . 195 ± 0.075

12 .025 ± 0.602 2 .095 ± 0. 1 50

flexion

10.97 1 ± 0.5 19 3 .968 ± 0.3 18

12 .705 ± 0.737 4. 175 ± 0.463

Table IV. Determination position of the median nerve using co-ordinate registration (mean ± S.E.M.), x= mean distance between the centre of the median nerve and the hook of hamate (mm.) , y= mean distance between the centre of the median nerve and the flexor retinaculum (mm.) .

However, in 8 patient-hands (2 1 . 1 % ) this phenomenon could n9t be observed. In 5 of these patient-hands the median nerve maintained its position and in 3 patient-hands the distance of the centre of the median nerve and the flexor retinaculum decreased by flexing the wrist. In the control-hands only l hand (5 % ) showed a median nerve that did not become displaced dorsally. No significant correlation was found between the duration of symptoms and the dorsal displacement of the median nerve (fig. 15 ) . At the level of the third (fig. 13g) and fourth CT-scan (fig. 13h) the carpal tunnel became convex volarly and flattened dorsally in flexion of the wrist. In the third CT-scan the disto-volar portion of the lunate was located on the dorsal side of the carpal tunnel and in the fourth CT-scan the disto-volar portion of the radius was placed volarly to this lunate projection. Direct compression of the median nerve by the distal radius was not observed. Extension of the wrist decreased the concavity of the carpal arch and straightened the flexor retinaculum (fig.1 3i through k) . The median nerve was situated just dorsal to the flexor retinaculum in all CT-scans with the wrist in extension.

5 3

E a E -

� 7

� 6 .Q 5

I

� 0 . E 4 a, •

£ 3 • 0 • •

• 0 • 0 • •

• = � 0 = cl'

•

•

• •

• •

• 0

• . - - - - - - - - -•- - - - • • 0

10 20 30 years

Fig.15. Dispersion diagram showing the relationship between duration of symptoms and dorsal displacement of the median nerve.

7.3. Dimensions of the carpal tunnel.

The results of comparison of the (absolute) cross-sectional areas be­tween the various positions of the wrist, in each group individually, are shown in fig. 16a. There was a statistically significant increase of the cross-sectional areas in the female patients at the third and fourth level of the carpal tunnel with the wrist in flexion. In the other groups there was an increase of the cross-sectional areas at these levels, but this was not significant. In none of the four examined groups was there a significant decrease of the cross-sectional areas in flexion or extension of the wrist. 54

-N

§ -=-(/) < UJ a: < --' < z Q I-0 UJ (/)

Cf) Cf) 0 a: 0

-N

E

..§. Cf) < UJ a: < --' < z 0 j:: () UJ en en en 0 a: 0

260

I 95¼ conf idence interval

220

I

NFE 300 I 1

I

female patients

II m

male patients

II m S L I C E P O S I T I O N

NF E

m: level I

l N FE

nz: level I

female controls

n m

male controls

II m

Fig.16a. Comparison of the cross-sectional areas between the various positions of the wrist, in each group individually. N= neutral, F= flexion, E= extension. 5 5

-N

E

380

340

...§, 300 Cl) <{ UJ cc <{ ....J 260 <{ z 0

n _ 3

1-(.) LU en

u n 220 - -�- . en

0 cc u 180

140

100 0

..

I

S L I C E PO S I T I O N

I 95'/, conf idence i nterval

--...

II level l[

Fig.16b. Comparison of the cross-sectional areas of the carpal tunnels between the four groups in neutral position of the wrist. Pf = female patients Cf = female controls Pm = male patients Cm = male controls

The cross-sectional areas of the carpal tunnels and the flexor tendons showed a significant correlation in the female patients (p<0.001). Statistically significant correlation in the other groups could not be arri­ved at, because of low numbers (fig.17). 56

N

Cl) <t: UJ

<t: _J <t: z Q I-

Cl) Cl) 0 a: u

N

Cl) <t: a:

z Q

u UJ Cl)

Cl) 0 a: u

C t C t 170 170 r =0-.70518 r = 0.57366

130 130 female patients • • female controls • •

. .. :-� 90 90 , . ,. • • • • • • • 50 50

Cc Lf " I I I 240 -YI I I I , 1 20 160 200 120 1 60

170 Ct 170 C t

r = 0.70668 • r =0.61 43

130 male patients • .130

male controls

• 90 • 90 • • • •

so 50 L/' I I I i 1 20 160

Cc

200 I 240 YI I I 120 I 160

•

Cc I I 200 240

• • • • •

Cc I I 200 240

C ROSS SECT ION A L A R E A S (mm2 ) C ROSS SECT ION A L A R E AS (mm2 )

Fig.17. Dispersion diagrams showing the relationship between the cross-sectional areas of the carpal runnels and the flexor tendons. Cc= cross-sectional areas of the carpal tunnels, Cr= cross-sectional areas of the flexor tendons, Pf= female patients Cf= female controls Pm= male patients Cm== male controls.

The results of comparison of the R.S. between the four groups in the neutral position of the wrist are shown in fig.18. There was a statistically significant difference (p<0.05) between female patients and female controls at level II, the narrowest part of the carpal tunnel. 57

I 95°

1o conf idence i nterval

70

60

- 50 � -

en 40 a:

30

20

10

I level II

s l i c e pos i t ion

Fig. 18. Comparison of the relative space available for the median nerve and synovium (R.S.) in the neutral position of the wrist, Pf= female patients Cf= female controls Pm= male patients Cm= male controls.

, By comparing the (absolute) cross-sectional areas between female patients and controls, no significant differences were found (fig. 16b ) . Consequentially, the flexor tendons of the female patients had larger dia­meters than the female controls. There was no significant difference in the RS. between the female patients and male controls and there was also none between female controls and male patients or controls. Only the two distal levels were compared, because these levels included the narrowest part of the carpal tunnel (level II) and they were the most

5 8

reliable ones as far as the measurements were concerned (see section 6.3. 1 . ) . The comparison of the R.S. was only performed in the neutral position of the wrist, because the position of the wrist exerted no influence upon the cross-sectional areas of the carpal tunnel (fig.16a).

59

Chapter VIII Discussion and conclusion

Using computed tomography it was possible to obtain CT-scans of the carpal tunnel in vivo, at different levels and with the wrist in various positions. In these CT-scans the carpal tunnel, its contents and surroun­dings were clearly represented. This technique allows discrimination of detail, with dimensions in the order of 0.6 to 1.2 mm. by which it was eminently suited for the purposes of this study. Previous investigators (Zucker-Pinchoff et al. 1981) used computed tomography (Ohio-nuclear Delta 50 scanner with 8 mm. slice thickness and a GE. CT/T8800 scanner with 5 mm. thick sections) to study the carpal tunnel and its morphological relationships in cadaveric hands. However, it might be possible that they removed the median nerve from the specimen, because a round hypodense area can be seen in the CT­scan, representing the place of the median nerve. Another possibility is, that the median nerve was encircled by air and in this case may not have been represented in the CT-image, because of the partial volume effect. Dekel et al. (1980) also used computed tomography (CT 1010F35), but they were not always able to define the outlines of the carpal tunnel. As a result of the recent developments in this technique it was possible to image very fine details using the Philips Tomoscan 300 and 310, as described by Hillen and Zonneveld (1982). The patients involved in this study showed a mean age and sex distribu­tion, comparable to that commonly found in the literature (table V). Table V. mean ages female bilateral

incidence involvement this study 51.7 87.5% 91.7% Crow (1960) more than 50% be-tween 40 and 59 88.9% 60.5% Phalen ( 1966) more than 50% be-tween 40 and 60 67.0% Linscheid et al. ( 1967) 51 75.0% 75.0% van Rossum et al. ( 1980) 84.0% 35.5%

61

The age range ( 40 - 70 years) in the controls was used to eliminate pos­sible changes in volume of the carpal tunnel during life, although Dekel et al. ( 1980) found no evidence of this. The pathogenesis of primary carpal tunnel syndrome has long been controversial.

Abbott and Saunders (1933) suggested that with the wrist in acute flexion, the median nerve is compressed between the anterior part of the radius and the flexior retinaculum. However, in our morphological study no evidence of direct compression of the median nerve could be observed by surrounding anatomical struc­tures in the examined part of the carpal tunnel, neither in flexion nor in extension of the wrist. At the fourth (IV) level of the carpal tunnel, with the wrist flexed, the anterior part of the radius was situated volar to the lunate and flattened the carpal tunnel dorsally, while the flexor retina­culum became more convex towards the volar side.

Michaelis (1949) and Watson-Jones (1949) suggested that the condition resulted from the thickening of the flexor retinaculum which compres­sed the median nerve, while Phalen and Kendrick (1957) and Lipscomb (1959) believed that the condition was due to tenosynovitis within the carpal tunnel. Tanzer ( 1959) measured the thickness of the flexor retinaculum in patients suffering from the carpal tunnel syndrome and compared his measurements with those found at routine autopsy in the same number of patients with pressumably normal hands. He found no difference between the two groups, nor was there any difference in the synovium.

Tanzer (1959), Smith et al. (1977) and Armstrong and Chaffin (1978) continued with the idea that the median nerve was damaged by repetitive direct compression. They suggested that the median nerve was compressed between the long flexor tendons and the flexor retinaculum, especially when the tendons were subjected to tension. 62

In both our patients and controls, significant dorsal movement of the median nerve was observed, when the wrist was flexed and no evidence was found suggesting that the nerve was compressed between the flexor tendons and the ligament. In addition, with the wrist flexed, the path of the long flexor tendons is shortened, by which the flexor tendons become relatively too long and hence it appears unlikely that they are subjected to much tension. However, in 8 patients and in 1 control the dorsal displacement of the median nerve could not be observed and we have no explanation for this fixed position. There was no evidence of a relationship between the duration of symptoms and the dorsal displacement. It could not be determined, whether the fixed position in these 8 patients was the primary cause of compression.

Brain et al. (1947), Kendall (1950), Tanzer (1959) and Gelberman et al. (1981) believed that extreme positions of the wrist (90° Hexion or 90°

extension) would decrease the volume of the carpal tunnel, resulting in compression of the median nerve. They demonstrated this by inserting a catheter into the carpal tunnel and they measured the pressures in acute flexion, acute extension and neutral positions of the wrist. Apart from the fact that this catheter might be compressed between the tendons alone or between the tendons and the carpal tunnel walls, these extreme positions of the wrist are very uncomfortable and rarely necessary in normal daily activities. In addition, this study showed no significant decrease of the cross-sectional areas of the carpal tunnels in any of the four groups, neither in Hexion nor in extension of the wrist.

Dekel et al. (1980) and Gelmers (1981) measured the cross-sectional areas of the carpal tunnel in female patients and male and female controls. They found significantly smaller cross-sectional areas in female patients as compared with the male and female controls. The female controls had significantly smaller cross-sectional areas as compared with the male controls and they concluded that this difference was the expla­nation of the predominance of carpal tunnel syndrome in women.

63

Their results cannot be compared with our results, because they are not standardized at one specific level. Furthermore, these investigators compared the cross-sectional areas of the carpal tunnel, but they omitted to take the co-incidental differences in cross-sectional areas of the long flexor tendons into account. In this study a statistically significant correlation was found (p<0.001) between the cross-sectional areas of the carpal tunnels and the flexor tendons in female patients. Statistically significant correlation in the other groups could not be arrived at, probably because of low numbers. By comparing the relative space available for the median nerve and sy­novium (R.S. ) , significant smaller dimensions were found in female patients as compared with female controls.

Matricali and Kauer (1970) believed that an abnormal muscle belly of the thenar muscles, originating from the flexor retinaculum, on the ulnar side of the median nerve, would compress the median nerve underneath a thin part of the flexor retinaculum. Our study of the origins of the thenar muscles from the flexor retina­culum, showed no significant differences between patients and controls. These results do not support their opinion. In addition, these abnormal muscle bellies were not found in our patients during surgery.

This present study showed no evidence of direct compression of the median nerve, neither by decrease in dimensions of the carpal tunnel in flexion and extension of the wrist, nor by a stenosis of the carpal tunnel. Furthermore, Sunderland (1945) and Blunt (1959) found no abnormali­ties in the local vascular architecture of the median nerve, which were directly suggestive of any particular local predisposition to neural ischaemia. The possibility that primary carpal tunnel syndrome is caused by a multi­plicity of mechanisms rather than one condition has to be considered. Hypothesis.

In this study, compression of the median nerve by movable space-occu­pying structures could not be excluded. 64

Touborg-Jensen (1970) published a case of carpal tunnel syndrome cau­sed by an abnormal position of a lumbrical muscle. The origin of the lumbrical muscle from the deep flexor tendon of the middle finger, was proximal to the carpal tunnel. In most textbooks (Spalteholz 1959, Grants 1959, Verdan 1979, Gray 1980) the lumbrical muscles are descri­bed as originating from the deep flexor tendons just distal to the carpal tunnel. These lumbrical muscles show variations in number as well as in origins from the associated flexor tendons. The amplitude of the deep flexor tendons in this area varies between 7 and 8.5 cm. according to Bunnell (1944), 4.5 and 6 cm. according to Con­verse (1978) and 4.5 and 8.5 cm. according to Verdan (1979). Carpentier Alting (1978) found an amplitude ranging from 28 to 36 mm. with the wrist in the neutral position and 39 to 48 mm. with the wrist in flexion. The deep flexor tendons pull the lumbrical muscles into the carpal tunnel during contraction. Obviously, these muscles reduce the space available for the median nerve. The lumbrical muscles serve the purpose of a moderator unit between the extrinsic flexor and extensor system of the interphalangeal joints (Kaplan 1953) and hypertrophy of these muscles will occur in indivi­duals performing intensive manual work. The hypertrophied muscles occupy more space and the space available for the median nerve is fur­ther reduced and as a result, irritation or compression of this nerve may occur. At rest the lumbrical muscles are outside or in the distal part of the carpal tunnel. The irritated synovial tissue could become oedematous, which may result in "night" pain. The abnormal position of the lumbrical muscle which Touborg-Jensen described, was possibly due to a normal variation in the origin of this muscle. In the anatomical dissections (3) and during the operations (6) a varia­tion in origins of the lumbrical muscles was observed. (fig. 19) These origins were located on the deep flexor tendons within the carpal tunnel or just distal to it with the fingers in extension. The lumbrical muscle, originating from the deep flexor tendon of the index finger, appeared to have the largest volume. This is probably due to its greater activity, compared to the other fingers. Obviously, hypertrophied lumbrical muscles, entering the carpal tunnel, decrease the space available for the median nerve and they will disturb the anatomical relationships. This could be so great that irritation or compression of the median nerve may occur.

65

Fig. 19. A lumbrical muscle in one of the hands during operation; with the fingers flexed. 1 = dis to-volar wrist fold 2= thenar 3= hypothenar 4= lumbrical muscle of the middle finger.

The predisposition to primary carpal tunnel syndrome is possibly deter­mined by several different conditions and one of these, the variations in the origins and number of lumbrical muscles, may play an important role. The higher incidence in females is possibly contributed by the smaller overall hand dimensions, in which the anatomical relationships could be easily disturbed. Undoubtedly, the significant difference in R.S. between female patients and controls and the difference in diameters of their flexor tendons (larger in female patients) will play a role in the pathogenesis of primary carpal tunnel syndrome. Conclusions.

- Computed tomography appeared to be a very valuable technique as a method of investigation of the hand in vivo. 66

- The morphological study showed a dorsal displacement of the median nerve in flexion of the wrist. This phenomenon has never been demonstrated before. In 15.5% of the hands, this phenomenon could not be observed. It was not possible to determine whether the fixed position of the median nerve in these hands was primary or secondary to the carpal tunnel syndrome. In this study no evidence of direct compression could be demonstrated. - The study of origins of the thenar muscles and the findings during the operations did not support the opinion of Matricali and Kauer (1970). - The study of the dimensions of the carpal tunnels showed no signifi­cant decreases in cross-sectional areas in 70° flexion or 70° extension of the wrist. There was no evidence of carpal tunnel stenosis in the patient-groups. The relative space available for the median nerve and synovium (RS.) was significantly smaller in the female patients when compa­red with the female controls. This was due to the larger cross-sectio­nal areas of the flexor tendons in the female patients. - All things considered, the aetiology of the carpal tunnel syndrome seems to be multicausative. A contributory factor may be the lumbri­cal muscles which hypertrophy with intensive manual work. Finally, the predominance in females is possibly due to variations in the number and origins of these muscles, combined with smaller overall hand dimensions in which the anatomical relationships are more easily disturbed. The incidence among females could be due to the larger diameters of the flexor tendons in the (female) patients. Further study on this subject is required.

67

Summary

The carpal tunnel syndrome is the most common affection of the median nerve. It is a painful and often disabling affliction of one or both hands. The usual complaints are paraesthesiae, burning pain, impairment of sensation in the area supplied by the median nerve and weakness in the thumb. A typical symptom of this condition is that the patients are awakened by painful paraesthesiae after a couple of hours sleep. Progression leads to permanent impairment of sensation and muscle wasting of a part of the thenar musculature. The carpal tunnel syndrome affects both males and females, with a predominance in middle-aged women. The condition is caused by compression of the median nerve in the carpal tunnel. The aetiology of this compression is unknown. Patients who have a space-occupying lesion within the carpal tunnel, have what may be defined as the secondary carpal tunnel syndrome. However, in most cases no such lesion is found and this condition is called the primary carpal tunnel syndrome. The opinions among previous investigators is controversial with regard to the aetiology. Generally it is agreed that manual work may cause the symptoms or aggravate them. Cross-sections (CT-scans) of the carpal tunnels were obtained in patients and controls, at different levels and with the wrist in various positions, using computed tomography (Philips Tomoscan 300 and 310) . The CT-scans were performed at 4 levels of the carpus with the wrist in 70° flexion, 70° extension and in the neutral position. In these CT-scans the anatomical relationships were recorded and the cross-sectional areas of the carpal tunnel and the flexor tendons were measured. By comparing the observed images and measured data of patients and controls, an attempt was made to elucidate the following: 1. whether the condition is caused by direct compression of the sur­rounding structures, 2. the role of the cross-sectional areas of the carpal tunnel in the pathogenesis of the carpal tunnel syndrome and the influence of Hexion and extension upon these cross-sectional areas, 3. the reason for predominance in women.

69

A preliminary study, using cadaveric hands, was carried out to stan­dardize the investigation. As previously mentioned, 696 CT-scans were performed on 58 hands (38 hands of 24 patients and 20 hands of 5 male and 5 female controls). The morphological study showed no evidence of direct compression of the median nerve by surrounding structures in the carpal tunnel. Both in patients and controls a dorsal displacement of the median nerve was observed with the wrist in flexion. The conclusion that may be drawn from this observation is that the median nerve is not compressed between the long flexor tendons and the flexor retinaculum. However, in 8 patients no dorsal displacement of the median nerve could be observed. Whether this was the primary cause of the carpal tunnel syndrome could not be established. The relative space available for the median nerve (R.S.) (Cc - Ct/Cc) in the female patients was significantly smaller, compared with the female controls. Flexion and extension did not decrease the cross-sectional areas of the carpal tunnels. The predominance in females could not be explained by a stenosis of the carpal tunnels. Taking all factors into consideration, it may be assumed that the primary carpal tunnel syndrome is of multifactorial aetiology. It would appear that the lumbrical muscles play an important role. These muscles have an origin on the deep flexor tendons, just distal to, or within the carpal tunnel. It has been observed chat the deep flexor tendons pull the lumbrical muscles into the carpal tunnel during contraction. As a result, the space available for the median nerve will be reduced. The lumbrical muscles serve the purpose of a moderator unit between extensor and flexor apparatus. By performing intensive manual work, these muscles will hyper­trophy and as result the space available for the median nerve will be further reduced, resulting in irritation or compression of the median nerve. Differences in incidence are probably determined by variations in origin and number of the lumbrical muscles, hand size and the inten­sity of manual work. 70

The significantly smaller relative space available for the median nerve (R.S.) in female patients compared with female controls, may contribute to the incidence among women.

7 1

Samenvatting

Het carpale tunnelsyndroom is de meest voorkomende aandoening van de nervus medianus. Het is een pijnlijke, invaliderende aandoening van een of beide handen. Het klachtenpatroon wordt gekenmerkt door para­esthesieen, brandende pijn of dove gevoelens in het verzorgingsgebied van de n. medianus. Zeer kenmerkend is dat na enkele uren slaap de patienten worden gewekt door paraesthesieen of brandende pijn in de hand. Progressie van de aandoening kan leiden tot blijvend verlies van gevoel in het verzorgingsgebied van de zenuw met oppositiebeperking en krachtsverlies van de duim door parese of paralyse van de thenar mus­culatuur. Het carpale tunnelsyndroom komt merendeels voor bij vrouwen van middelbare leeftijd. De pathogenesis van de aandoening berust op een irritatie of compressie van de n. medianus in de carpale tunnel. Het mechanisme van het ont­staan van de compressie is onbekend. Die gevallen waarin de compressie wordt veroorzaakt door een ruimte-innemend proces, noemt men een secundair carpaal tunnelsyndroom. In de meeste gevallen echter wordt er geen anatomisch substraat gevonden dat de compressie kan ver­klaren; dit wordt het primaire (essentiele of idiopathische) carpale tunnelsyndroom genoemd. De opvattingen over het mechanisme van de compressie zijn controver­sieel. De meeste onderzoekers zijn van mening dat handwerkzaam­heden een belangrijke rol spelen en in ieder geval de klachten verer­geren. Dankzij de recente ontwikkelingen in de computer tomografie kunnen dwarse doorsneden (CT-scans) warden verkregen van de carpus in vivo op elk gewenst niveau en met de pols in verschillende posities. In dit onderzoek werden met de Philips Tomoscan 300 en 310, CT-scans gemaakt van de carpus bij patienten, lijdende aan het primaire carpale tunnelsyndroom en bij "gezonde" individuen. De CT-scans werden op 4 niveaus gemaakt met de pols in de flexie, extensie en neutrale stand. In deze CT-scans werden de oppervlakten van de carpale tunnels en de buigpezen gemeten. Het doel van dit onderzoek is, door vergelijking van de metrische en niet-metrische gegevens, duidelijkheid te verkrijgen in: 1. de gesuggereerde direkte compressie van de n. medianus door omgevende structuren,

73

2. de rol van de oppervlakten van de carpale tunnel in de pathogenesis van het carpale tunnelsyndroom en de invloed van flexie en extensie van de pols op de oppervlakten van de carpale tunnel, 3. de reden van het vaker voorkomen bij vrouwen.

Voorafgaand aan dit onderzoek werd een kadaver-studie uitgevoerd om het onderzoek te standaardiseren. Op bove ngenoemde wij ze werden 696 CT-scans gemaakt van 5 8 handen (38 handen van 24 patienten en 20 handen van 5 "gezonde" vrouwen en 5 "gezonde" mannen). Her morphologische onderzoek leverde geen aanwijzingen op, die suggestief waren voor direkte compressie van de n. medianus door omgevende structuren in de carpale tunnel. Zowel bij de patienten als bij de "gezonde" individuen werd een dorsale verplaatsing van de n. medianus waargenomen als de pols was geflec­teerd. Hetgeen betekende dat deze zenuw niet werd gecomprimeerd tussen de buigpezen en het retinaculum flexorum. Bij 8 patienten was dit niet het geval. Het was niet duidelijk of de gefix­eerde positie van de zenuw bij deze 8 patienten de oorzaak was van de compressie of dat deze het resultaat hiervan was. Het onderzoek naar de rol van de oppervlakten van de carpale tunnel leverde een statistisch significant verschil op van het relatieve oppervlak voor de n. medianus (oppervlakte carpale tunnel - oppervlakte pezen / oppervlakte carpale tunnel) tussen de vrouwelijke patienten en "gezonde" vrouwelijke individuen. Tussen de vrouwelijke patienten en "gezonde" mannen was geen significant verschil. Het vaker voorkomen bij vrouwen kon niet warden verklaard door een stenosis van de carpale tunnel. Flexie en extensie van de pols bleken de oppervlakten van de carpale tunnel niet te verkleinen. In de beschouwing wordt gesteld dat de pathogenesis van het primaire carpale tunnelsyndroom waarschijnlijk multicausaal is. Aandacht moet warden besteed aan de mm. lumbricales, die hun oorsprong op de diepe buigpezen hebben. De variatie in aantal en oorsprong is groat. Zij dragen zorg voor de balans van strek- en buigapparaat in de vingers. Gezien de amplitudo van de diepe buigpezen in de handpalm en de oorsprong van de mm. lumbricales, zullen zij de tunnel warden 74

ingetrokken bij comractie van de m. flexor digitorum profundus. Zij reduceren de beschikbare ruimte voor de n. medianus in de carpale tunnel en bij hypertrofie (tengevolge van intensieve handenarbeid) kunnen zij her evenwicht in de carpale tunnel verstoren en zodoende de zenuw irriteren en zelfs comprimeren. De verschillen in voorkomen worden waarschijnlijk bepaald door de variatie in aantal en oorsprong van de mm. lumbricales, de grootte van de hand, de diameters van extrinsieke buigpezen in de carpale tunnel en de handwerkzaamheden van her individu.

75

References

Adams, W.E. 1943. The blood supply of nerves. J. Anat. 77:243-250. Adson, A.W. 1951. Cervical ribs: symptoms, differential diagnosis and indications for section of the insertion of the scalenus anticus muscle. J. Int. College Surgeons 16: 546-559. Aiache, A.E. and E.F. Delagis. 197 4. A pure sign of lumbrical function. Plast. Reconstr. Surg. 54: 312-315. Aiache, A.E. 1978. An early sign of carpal tunnel syndrome. Plast. Reconstr. Surg. 61: 130-131. Anderson, M.H. et al. 1970. Changes in the forearm associated with median nerve compression at the wrist in the guinea-pig. J. Neural. Neurosurg. Psychiatry 33: 70. Armstrong, T J. and D.B. Chaffin. 1979. Some Biomechanical aspects of the carpal tunnel. J. Biomechanics 12 : 567-570. Bell, G.E. and J.L. Goldner. 1956. Compression neuropathy of the median nerve. Southern Med. J. 49: 966-972. Bennet, J.B. and C.C. Crouch. 1982. Compression syndrome of the recurrent motor branch of the median nerve. J. Hand Surg. 7: 407-409. Bentley, F.H. and W. Schlapp. 1943. Experiments on the blood­supply of nerves. J. Physiol. 102: 62-71. Bergh, R. van de and J.F. Folkerts. 1972. Neurologie voor de alge­mene praktijk, 2nd ed. Agan Elsevier, A'dam/Brussel. Biemond, A. 1972. Hersenziekten: diagnostiek en therapie, 4th ed. De Erven F. Bohn N.V., Haarlem. Blodgett, R.C. et al. 1962. Incidence of hematologic disease in pa­tients with carpal tunnel syndrome. J.A.M.A. 182: 814-815. Blunt, M.J. 1959. The vascular anatomy of the median nerve in the forearm and hand. J. Anat. 93: 15-22. Bourrel, P. and M. Chickly. 1980. Anomalous muscle causing tunnel syndromes. Anatomia Clinica 2 : 75-81. Brain, W.R. et al. 1947. Spontaneous compression of both median nerves in the carpal tunnel: six cases treated surgically. The Lancet 8: 277-282. Buchthal, F. et al. 197 4. Electrophysiological findings in entrapment of the median nerve at wrist and elbow. J. Neural. Neurosurg. Psychiatry 37 : 340-360.

77

Bunnell, S. 1944. Surgery of the hand. J.B. Lippincott Company, Philadelphia. Campbell, E.D.R. 1962. The carpal tunnel syndrome: investigation and assessment of treatment. Proc. R. Soc. Med. 55: 401-405. Cannon, B.W. and J.G. Love. 1946. Tardy median palsy: median thenar neuritis amenable to surgery. J. Surg. 20: 210-216. Cappell, D.F. and J.R. Anderson. 1971. Muir's Textbook of Pathology, 9th ed. Richard Clay L.T.D., Bungay, Suffolk, G.B. Carpentier Alting, M.P. 1978. Enige functioneel anatomische as­pecten van vingers, p. 20-22, thesis State University, Groningen, the Netherlands. Carroll, R.E. and D.P. Green. 1972. The significance of palmar cutaneous nerve at the wrist. Clin. Orthop. Rel. Res. 83: 24-28. Converse, J.M. 1977. Reconstructive Plastic Surgery, 2nd ed., vol. VI, W.B. Saunders Company, Philadelphia/London/Toronto. Crow, R.S. 1960. Treatment of the carpal tunnel syndrome. Br. Med. J. 2: 1611-1615. Curtis, R.M. and W.W. Eversmann. 1973. Internal neurolysis as an adjunct to the treatment of the carpal tunnel syndrome. J. Bone Joint Surg. 55-a: 733-740. Das, S.K. and H.G. Brown. 1976. In search of complications in carpal tunnel decompression. The Hand 8: 243-249. Dekel, S. et al. 1980. Idiopathic carpal tunnel syndrome caused by carpal stenosis. Br. Med. J. 280: 1297-1299. Denman, E.E. 1979. The volar carpal ligament. The Hand 2: 22-27. Denny-Brown, D. and C. Brenner. 1944. Lesion in peripheral nerve resulting from compression by spring clip. Arch. Neurol. Psychiatry 52: 1-19. Dorndorff, G. 1931. Ueber isolierte Lahmungen im Daumenballen. Mschr. Psyschiatry Neurol. 80: 331-341.

Eisen, A. et al. 1977. The application of F-wave measurements rn the differentiation of proximal and distal upper limb entrap­ments. J. Neural. 27: 662-668. Elliott, F.W. and A.F. Little. 1977. Median entrapment neuro­pathies. Br. Columbia Med. J. 19: 48. Fissette, J. and A. Onkelinx. 1979. Treatment of carpal tunnel syn­drome: comparative study with and without epineurolysis. The Hand II: 206-210. 78

Folkerts, J.F. 1969. Het carpale en tarsale tunnelsyndroom: her kwadranten syndroom. Ned. T. Geneesk. 1 1 3 : 1629-1634.

Forster, J.E. 1959. Acroparaesthesiae and the carpal tunnel. Br. Med. J. 2: 369.

Fullerton, P.M. 1963. The effect of ischaemia on nerve conduction in the carpal tunnel syndrome. J. Neural. Neurosurg. Psychiatry 26: 385.

Gardner, E. et al . 1969. Anatomy, 3rd ed., a regional study of human structure. W.B. Saunders Company, Philadelphia/London/Toronto.

Gelberman, R.H. et al. 1980. Carpal tunnel syndrome: results of a pros­pective trial of steroid injection and splinting. J. Bone Joint Surg. 62-a: 1 181 - 1 184.

Gelber man, R.H. et al. 1981 . The carpal tunnel syndrome, a study of car­pal canal pressures. J. Bone Joint Surg. 63-a: 380-383.

Gelmers, H.J. 1981 . Primary carpal tunnel stenosis as a course of entrap­ment of the median nerve. Acta Neurochirurgica 5 5 : 3 17-320.

Gilliatt, R.W. and T.G. Wilson. 1953. A pneumatic-tourniquet test in the carpal tunnel syndrome. The Lancet 2 : 595-597.

Goodman, H.V. and R.W. Gilliatt. 1961 . The effect of treatment on me­dian nerve conduction in patients with the carpal tunnel syndrome. Ann. Phys. Med. 6: 1 37-155 .

Goodwill, G.J. 1965. The carpal tunnel syndrome long-term follow-up showing relation of the latency measurements to response to treat­ment. Ann. Phys. Med 8: 12-2 1 .

Hargens, A.R. e t al. 1979. Peripheral nerve-conduction-block by high muscle-compartment pressure. J. Bone Joint Surg. 61 -a : 192-200.

Haussmann, P. von. 1980. Isolierte Traumatische Llisionen motorischer Nervenaste an der Hand. Handchirurgie 12 :23-25.

Heathfield, K.W.G. and J.A.R. Tibbles. 196 1. Chlorothiazide in treat­ment of carpal tunnel syndrome. Br. Med. J. 1 :29-30.

Hillen, B. and F.W. Zonneveld. 1982. CT-scanning of the carpus and tar­sus. Acta Morphologica Neerlando Scandinavica 20:273.

Hunt, G.M. et al . 1960. The median nerve and carpal tunnel syndrome. Bull. of the Los Angeles Neurosurg. Soc. 25 :2 1 1 -222.

Hunt, J.R. 1911 . The thenar and hypothenar types of neural atrophy of the hand. J.A.M.A. 141 :224-241 .

Inglis, A.E. e t al. 1972. Median nerve neuropathy a t the wrist. Clin. Or­thop. Rel. Res. 83 :48-54.

79

Johnson, E.W. et al. 198 1. Sensory latencies to the ring finger: normal values and relation to carpal tunnel syndrome. Arch. Phys. Med. Re­habil. 62 :206-208. Kaplan, E.B. 1953. Functional and surgical anatomy of the hand.J.B. Lip­pincott Company, Philadelphia. Kendall, D. 1960. Aetiology, diagnosis and treatment of paraesthesiae in the hands. Br. Med. J. 2 : 1633-1640. Kopell, H.P. and W.A.L. Thompson. 1958. Pronator syndrome: a confir­med case and its diagnosis. The New England ]. Med. 259:7 13-715. Kremer, M. et al. 1953. Acroparaesthesiae in the carpal tunnel syndro­me. The Lancet 2 :590-595. Kreuzer, K.B. von and P. Haussmann. 1979. Ungewohnliche Ursachen des Karpaltunnelsyndroms. Handchirurgie 1 1 : 173-175. Langloh N.D. and R.L. Linscheid. 1972. Recurrent and unrelieved carpal tunnel syndrome. Clin. Orthop. Rel. Res. 83:41-47. Lanz, U. 1975. Variationen des Nervus Medianus im Bereich des Kar­palkanals. Handchirurgie 7: 159-162. Lavey, E.B. and R.M. Pearl. 198 1. Patent median artery as a cause of car­pal tunnel syndrome. Ann. Plast. Surg. 7:236-238. Linscheid, R.L. et al. 1967. Carpal tunnel syndrome associated with vaso­spasm. J. Bone Joint Surg. 49-a: 1 141- 1 146. Lipscomb, P.R. 1959. Tenosynovitis of the hand and wrist: carpal tunnel syndrome, De Quervain disease, trigger digit. Clin. Orthop. Rel. Res. 13: 164- 181. Lister, G. 1977. The hand: diagnosis and indications. Churchill Living­stone, Edinburgh/London/New York. Mantero, R. et al. 1981. Trois cas rares de compression du nerf median clans le canal carpien. Ann. Chir. 35:804-806. Marie, M.M.P. and Faix. 1913. Atrophie isolee de !'eminence thenar d'origine nervritique. Role du ligament annulaire anterieur du coupe clans la pathogenie de la lesion. Seance, Nov. 1913 p. 647-649. Matricali, B. et al. 1970. Aspects anatomiques du syndrome du carpal carpien. Bulletin de !'Association des Anatomistes 55th congres, no. 148, Nancy 22 -26 March 1970. May, J.W. and H. Rosen. 198 1. Division of the sensory ramus communi­cans between the ulnar and median nerves: a complication following carpal tunnel release. J. Bone Joint Surg. 63-a:836-838.

80

Mechelse, K. 1969. Het carpale tunnelsyndroom, elektromyografisch onderzoek tijdens de operatie. A'damse Neurologen Vereniging, May 1st 1969. Melville, J.D. 1972. The differential diagnosis of nerve compression syn­dromes in the arm and hand. The Hand 4:111-114. Melvin, J.L. et al. 1966. Sensory and motor conduction velocities in the ulnar and median nerves. Arch. Phys. Med. Rehabil. 47:511-519. Melvin, J.L. et al. 1969. Median nerve conduction in pregnancy. Arch. Psys. Med. Rehabil. 50:75-80.

Michaelis, L.S. 1950. Stenosis of carpal tunnel, compression of median nerve and flexor tendon sheaths combined with rheumatoid arthritis elsewhere. Proc. of the R. Soc. Med. 43:20-23. Michon, J. and E. Moberg. 1975. Traumatic nerve lesions of the upper limb, 1st English ed., Churchill Livingstone, Edinburgh/London/ New York. Nicholas, G.G. et al. 1971. Carpal tunnel syndrome in pregnancy. The Hand 3:80-83. Ochoa, J. and L. Marotte. 1973. The nature of the nerve lesion caused by chronic entrapment in the guinea-pig. J. Neural Science 19:491. Osborne, G. 1959. Acroparaesthesiae and the carpal tunnel. Br. Med. J. 2 :98. Paget, ]. 1853. Lectures on surgical pathology. I : 42-43, Longman, Brown Green and Longmans, London. Peacock, E.E. and W. van Winkle. 1976. Wound repair, 2nd ed. W.B. Saunders Company, Philadelphia/London/Toronto. Phalen, G.S. 1951. Spontaneous compression of the median nerve at the wrist. J.A.M.A. 145: 1128-1133. Phalen, G.S. and JI. Kendrick. 195 7. Compression neuropathy of the median nerve in the carpal canal. J.A.M.A. 164: 524. Phalen, G.S. 1966. The carpal tunnel syndrome: seventeen years expe­rience in diagnosis and treatment of six-hundred fifty-four hands. J. Bone Joint Surg. 48-a: 211-228. Phalen, G.S. 1972. The carpal tunnel syndrome: clinical evaluation of 598 hands. Clio. Orthop. Rel. Res. 83: 29-40. Phalen, G.S. 1981. The birth of a syndrome. J. Hand Surg. 6: 109-110. Pinner-Poole, B. and J.B. Campbell. 1969. Effect of low temperature and colchine on regenerating sciatic nerve. Exp. Neural. 25: 603.

81

Pritchard, E.A. 1950. Acroparaesthesia. Br. Encyclopedia of Med. Prac­tice, 2nd ed. , Butterworth, London.

Reinstein, L. 1981 . Hand dominance in carpal tunnel syndrome. Arch. Phys. Med. Rehabil. 62 : 202-203.

Robbins, H. 1963. Anatomical study of the median nerve in the carpal tunnel and aetiologies of the carpal tunnel syndrome. J. Bone Joint Surg. 45-a: 953-966.

Robbins, S.L. 1967. Pathology, 3rd ed. W.B. Saunders Company, Phila­delphia/London.

Robertson, J.D. 1955 . The ultra structure of adult vertebrate peripheral myelinated nerve fibres in relation to myelinogenesis. J. Biophys. Biomechan. Cyt. p.27 1 .

Rossum, J . van et al. 1980. Management in the carpal tunnel syndrome. Clio. Neurol. Neurosurg. 82-3 : 169-176.

Rydevik, B. et al. 198 1 . Effects of graded compression on intraneural blood flow. J. Hand Surg. 6: 3 - 12.

Schiller, F. and F.O. Kolb. 1954. Carpal tunnel syndrome in acromegaly. J. Neural. 4: 27 1-282.

Schivde, A.J. et al. 1981 . The carpal tunnel syndrome: a clinical-electro­diagnostic analysis. Electromyogr. Clio. Neurophysiol. 2 1 : 143-153 .

Schorn, D. et al. 1978. Bone density and the carpal tunnel syndrome. The Hand 10: 184- 186.

Schultze, F. 1893. Ueber Akroparasthesie . Deutsche Zeitschrift fiir Ner­venheilkunde 3: 300-3 19.

Simpson, J.A. 1956. Electrical signs in the diagnosis of carpal tunnel and related syndromes. J. Neural. Psychiatry 19: 275 -280.

Smith, E.M. et al. 1977. Carpal tunnel syndrome: contribution of flexor tendons. Arch. Phys. Med. Rehabil. 58 : 3 79-385.

Spalteholtz, W and R. Spanner. 1959. Handatlas der Anatomie des Men­schen, erster Teil, p.267-277. Scheltema and Holkema N.V. , A'dam.

Spencer, P.S. 1972. Reappraisal of the model for "bulk axoplasmic flow". Nature (New Biol. ) 240: 283.

' Stewart, J.M. 1972. Nerve entrapment in the upper limb. The Hand 4: 1 15 - 1 18.

Stopford, J.B.S. 1918. The variation in distribution of the cutaneous ner­ves of the hand and digits. J. Anat. 5 3 : 14-25.

Sumner, A.J. 1980. The physiology of peripheral nerve disease, 1st ed., W.B. Saunders Company, Philadelphia/London/Toronto.

82

Sunderland, S. 1945. Blood supply of the nerves of the upper limb in man. Arch. Neural. Psychiatry 53: 91-115. Sunderland, S. 1976. The nerve lesion in the carpal tunnel syndrome. J. Neural. Neurosurg. Psychiatry 39: 615-626. Taleisnik, J. 1973. The palmar cutaneous branch of the median nerve and the approach to the carpal tunnel. An anatomical study. J. Bone Joint Surg. 55a: 1.212-1.217. Tanzer, R.C. 1959. The carpal tunnel syndrome: a clinical and anatomi­cal study. J. Bone Joint Surg. 41-a: 626-634. Thomas, P.K. and P.M. Fullerton. 1963. Nerve fibre in the carpal tunnel syndrome. J. Neural. Neurosurg. Psychiatry 26: 520-527. Touborg-Jensen, A. 1970. Carpal tunnel syndrome caused by an abnor­mal distribution of the lumbrical muscles. Scand. Plast. Reconstr. Surg. 4: 72-74. Trojaborg, W. 1970. Rate of recovery in motor and sensory fibres of the radial nerve: clinical and electraphysiological aspects. J. Neural. Neu­rosurg. Psychiatry 33: 625-638. Truex, R.C. and M.B. Carpenter. 1969. Human neuro-anatomy, 6th ed., the Williams and Wilkins Company, Baltimore. Uriburu, I.J.F. et al. 1976. Compression syndrome of the deep motor branch of the ulnar nerve. J. Bone Joint Surg. 58-a: 145-147. Verdan, C. and J. Michon. 1961. Le traitement des plaies des tendons flechisseurs des doigts. Revue de Chirurgie orthopedique et repara­trice de l'appareil moteur 47: 301-308. Verdan, C. 1979. Tendon surgery of the hand. Churchill Livingstone, p. 10-23, Edinburgh/London/New York. Vuursteen, P J. 1976. De Chirurgische behandeling van het carpale tun­nelsyndroom. Ned. T. Geneesk. 47: 2058-2063. Walshe, F.M.R. 1951. In "modern" trends in neurology, 1st series, p.542, A. Ferling, Butterworth, London. Watson-Jones, R. 1949. Leri's pleonostenosis, carpal tunnel compres­sion of the median nerves and Morton's metatarsalgia. J. Bone Joint Surg. 31-b: 560-571. Weiland, W. von and U. Lanz. 1979. Ungewohnliche Ursache eines Kar­paltunnelsyndrams. Handchirurgie 11: 169-171. Weiss, P. and A.S. Burt. 1944. Effect of nerve compression on Wallerian degeneration in vitro. Proc. Soc. Exp. Biol. Med. 55: 109-112. Weiss, P. and H.B. Hiscoe. 1948. Experiments on the mechanism of nerve growth. J. Exp. Zoology 107: 315-395. 83

Williams, P.L. and R. Warwick. 1980. Gray's anatomy, 36 th ed. p. 586-593, Churchill Livingstone, Edinburgh/London/New York.

Wissinger, H.A. 1975 . Resection of the hook of the hamate. Plast. Re­constr. Surg. 56: 501 -506.

Woltman, H.W. 1941 . Neuritis associated with acromegaly. Arch. Neu­ral. Psychiatry 45 :680.

Wood, M.R. 1980. Hydrocortisone injections for carpal tunnel syndro­me. The Hand 2 : 62-64.

Young, J.Z. 1945 . Structure, degeneration and repair of nerve fibres. Nature 156: 1 32- 136.

Zachary, R.B. 1945. Thenar palsy due to compression of the median nerve in the carpal tunnel. Surg. Gynaec. Obstet. 8 1 : 2 13 .

Zonneveld, F.W. 1980. Computed Tomography. Philips Medical Sy­stems. Eindhoven, the Netherlands.

Zucker-Pinchoff, B. et al. 1981 . Computed tomography of the carpal tun­nel: a radio-anatomical study. J. Computer assisted Tomography 5 ( 4) : 525 -528.

84

Acknowledgements

The completion of this work has been made possible by the coope­ration of: - the Laboratory of Embryology and Anatomy (head: Prof. Dr. A.G. de Wilde) of the University of Groningen, - the Department of Radiology (head: Dr. R. Ubbens) of the Roman Catholic Hospital Groningen, - the Department of Neurosurgery (head: Prof. Dr. J .W.F. Beks) of the University Hospital Groningen, - the Department of Plastic and Reconstructive Surgery ( Dr. G. Heybroek, Drs. E.W. Sauer and Drs. A. de Boer) of the Roman Catho­lic Hospital Groningen, - the Department of Plastic and Reconstructive Surgery (head: Prof. Dr. A.J.C. Huffstadt) of the University Hospital Groningen. I am delighted to have the opportunity to express my gratitude to everyone, who devoted much time and effort during completion of this thesis. This acknowledgement seems hardly adequate to express my gratitude. First of all, I would like to express my thanks to Prof. Dr. A.J.C. Huff­stadt. It has been a privilege to me, receiving training in Plastic and Reconstructive Surgery under his supervision. His criticism, advice and inexhaustible scientific inspiration were a great stimulus at the onset and during completion of this manuscript. I am grateful to Prof. Dr. J.W.F. Beks for taking me into his confi­dence in carrying out this study. His skillful advice was a great support. The patient and accurate way in which Drs. B. Hillen supported this study, deserves sincere appreciation. I wish to thank Ir. F.W. Zonneveld for his valuable criticism and advice concerning the technical details of this study. Prof. Dr. A.G. de Wilde I would like to thank for his pertinent remarks, advice and pleasant cooperation. I would like to express my special appreciation to Miss L.Y. Mann for the pleasant cooperation and the patient and accurate way she perfor­med the typography.

85

Drs. P.H. Robinson F.R.C.S. and Dra. I.F. Brown F.R.C.S. , plastic sur­geons, I would like to thank for correcting the English text and giving me valuable advice.

I would like to thank all the others, who supported and stimulated this study:

- the plastic surgeons Dr. G. Heybroek, Drs. E.W. Sauer and Drs. A. de Boer of the Department of Plastic and Reconstructive Surgery of the Roman Catholic Hospital Groningen, - the radiologists Dr. R. Ubbens, Dr. S.P. Keyser, Drs. W.J. Over­beek, Drs. P . Gravendeel and Drs . F.J.B. Williams and their assistents R. Zuiderveld, J. Remijn , M. vd. Port, N. van Bakel, A. Maaskant and M. Kremer, - Dra. W.H.M. Amesz-Voorhoeve for her ass istence in carrying out the computerized statistical analysis, - mr. T.A.J. Deddens for the skillful performance of the cover design and graphs, - mr. A.J.H. Deddens for carrying out the photography of the anatomical cross-sections, - the Medical Photographic Service of the Univers ity Hospital Groningen: A. Huiser, K.H. Roggen, Th. Hersevoort, S. Noorman and F .P . Hoffs , - all the patients and ' healthy' controls, who were involved in this study, - my colleagues, who were charged with my daily duties, affording me the time and opportunity to complete this manuscript.

I would like to thank my mother-in-law and my late father- in-law for the support they gave me. My parents deserve a special place in these acknowledgements. I am very grateful to them, affording me the opportunity to reach this goal.

86