Algodystrophy: Diagnosis and Therapy of a Frequent Disease of the Locomotor Apparatus

171 Pages·1981·7.034 MB·English

by  Professeur Paul Doury, Dr. Yves Dirheimer, Dr. Serge Pattin (auth.)

P. Doury Y Dirheimer S. Pattin
Algo dys trophy
Diagnosis and Therapy of a Frequent Disease
of the Locomotor Apparatus
With a Foreword by IVilliaumey
Translated by M.-Th.Wackenheim
With 46 Figures
Springer-Verlag Berlin Heidelberg New York 1981
Professeur PAUL DOURY
Service de Rhumatologie des Armees, H6pital Begin
F-94160 Saint-Mande
Dr. YVES DIRHElMER
Service de Neuroradiologie, Centre Hospitalier Universitaire
F-67091 Strasbourg Cedex
Dr. SERGE PATTIN
Service de Rhumatologie des Armees, H6pital Begin
F-94160 Saint-Mande
Translator
MARIE-THERESE W ACKENHEIM
Institut de Radiologie, Universite de Strasbourg, II, rue Humann
F-67085 Strasbourg Cedex
The cover design shows a classical algodystrophy of the wrist and of the hand
ISBN-13: 978-3-642-67991-9 e-ISBN-13: 978-3-642-67989-6
DOl: 10.1007/978-3-642-67989-6
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© by Springer-Verlag Berlin Heidelberg 1981
Softcover reprint of the hardcover 1st edition 1981
The use of registered names, trademarks, etc. in this publication does not imply, even in the absence of
a specific statement, that such names are exempt from the relevant protective laws and regulations and
therefore free for general use.
Reproduction of the figures: Gustav Dreher GmbH, Stuttgart
2127/3130-543210
Foreword
It is with great pleasure and ,much interest that I accepted to write the
foreword to this book by Paul Doury, Yves Dirheimer, and Serge Pattin
on the subject of "algodystrophy." First, because I know the extent of
their personal experience, from which they have selected the best for this
book. Second, because it seemed to me that their detailed analysis of the
numerous works on the subject, works which have been published all over
the world and which provide diverse physiopathologic interpretations, would
provide a comprehensive study meeting a real need.
Algodystrophy, to adopt the term used by the authors, merits rheumatolog
ists' careful attention. It is indeed a frequent condition and, as is now well
known, occurs in the most varied etiologic circumstances; it is not solely
posttraumatic, a notion on which diagnosis had long been based. This variable
etiology suggests the complexity of algodystrophy's pathogenic mechanism.
The condition usually shows a pseudoarthritic inflammatory pattern and/or
localized and painful demineralization of the bones, which naturally leads
the patient to consult a specialist. Recently much has been learned about
algodystrophy, on the one hand as a result of modern investigation techniques
such as bone scintigraphy, which make possible a more accurate diagnosis
of the early stages or of the localized forms of the disease, and, on the
other hand, with regard to the possibilities of a better adapted therapy,
liable to modify markedly the evolution of the disease. The opening chapter
of this book demonstrates the recent escalation of progress in this field.
This brief preface can unfortunately not provide an exhaustive account
of the authors' personal contribution. I would, nevertheless, like to place
special emphasis upon their essential conceptions. I feel that their governing
thought has been to show the basic unity of the various types of algodystro
phy, the clinical features and the mode of occurrence of which are so variable
that one cannot wonder that so many authors have attempted to dismember
this pathologic group and to individualize several related but nevertheless
distinct entities. Doury, Dirheimer, and Pattin's approach is quite different
and leads them to investigate uniting characteristics found in the fields of
physiopathology and pathology and in the clinical picture of algodystrophy.
First of all, what is the genesis of this painful condition and of the trophic
changes that characterize it? Many factors, from almost all fields of medicine
and of surgery, seem to provoke or to favor algodystrophy. It seems, however
that this condition never has one particular cause, but that it is nearly always
the result of several pathogenic mechanisms occurring on receptive ground.
This explains the absence of a strict or exclusive parallelism between the
provoking or favoring factor and the resulting symptomatic and evolutive
patterns. This is particularly so in cases following trauma, since the latter
can be of vastly differing nature and severity, and it is far from true that the
most severe always cause the most severe and most extended algodystrophic
VI Foreword
syndrome. The posttraumatic forms are considered to be the consequence
of a pathologic reflex leading to direct lesion of the cutaneous, subcutaneous,
muscular, tendinous, capsular, or bony tissues, or to the development of
a large locoregional vascular disturbance with a complex evolution responsi
ble for multiple alterations. - But it seems that such a reflex mechanism
can also be the consequence of very diverse and non traumatic affections
of the locomotor apparatus or of visceral, coronary, mediastinal, and pleuro
pulmonary irritative stimuli. This mechanism can be determined or governed
by central nervous system lesions or by neurosympathetic disturbances. Also
involved are biochemic agents, such as serotonin, liable to be mobilized
by metabolic disturbances or drug intoxications. Many unknowns still persist
on the nature and evolution of the pathogenic process of algodystrophy,
but it is very likely that there is a common response pattern to these very
diverse stimuli.
A critical analysis allows the authors to describe a general symptomatology
which is common to the different varieties of algodystrophy. They also under
line the importance they attach to this unity by devoting a chapter to the
general data on which the diagnosis of algodystrophy is based:
- A clinical syndrome comprising painful, mechanical, and inflammatory
or mixed manifestations which affect more or less intensely the articular
regions and are sometimes accompanied by synovial effusion of the me
chanical type;
- Absence of any biologic changes of an inflammatory type;
- Radiologic changes not involving the interspaces and consisting predomi-
nantly of locoregional demineralization in differing degrees and times of
occurrence;
- Almost constant and usually early occurring increased uptake of isotopes.
This is, of course, not a specific but nevertheless a significant sign, especially
when there is no radiologic evidence of the changes, in contrast to the
clinical findings;
A very peculiar cyclic development leading to spontaneous regression of
the pseudoinflammatory clinical syndrome and of the scintigraphic and
radiologic anomalies, occurring slowly with sometimes very marked
tendinoaponeurotic sequels.
Quite naturally~ this comprehensive study has led the authors to elaborate
diagnostic criteria, the value and usefulness of which they have pertinently
established. All this is the result of a detailed study of all clinical types
of algodystrophy aimed at throwing light on the less well-known pecularities
of the most classic forms as well as describing the hitherto undescribed
features of the disease. The authors' personal experience makes this chapter
a very original contribution. The description of the radiologic and scintigraphic
anomalies is very carefully given, and abundant and accurate illustrations of
remarkable quality are provided, for which the Editor must be congratulated.
In spite of their concern to demonstrate the unity of the disease, the
authors also emphasize its polymorphism and describe in detail its many
clinical forms, particularly their topography, evolution, symptomatology, and
etiology. They thus draw attention to the localized variants of the algodys
trophic syndrome, involving only the coxofemoral area and the knee. The
latter forms, the diagnosis of which is difficult, have been made known
thanks to the authors' personal studies. Equally fascinating is the description
of the atypical evolutive forms, such as those which are immediately plurifo
cal, in a patent or latent manner, or secondarily plurifocal, in an extensive
or recurrent way.
Foreword VII
Finally, the authors rightly emphasize the incomplete or atypical forms,
hyperinflammatory or pseudophlegmonous forms, and fibrous or pseudo
sclerodermal forms, demonstrating the extreme variability of the clinical fea
tures of the disease without casting doubt upon its fundamental unity. This
polymorphism justifies the comprehensiveness of the chapter on differential
diagnosis, which makes reference not only to the effusional type of rheumatic
disease but also to the many conditions which may mimic, clinically or
radiologically, some of the features of algodystrophy in their classic forms
or in their unusual aspects.
Trauma remains by far the most frequent cause of algodystrophy, but
several diseases as well as certain drugs can also be held responsible, as
has already been shown. This has very important theoretical and practical
implications. The authors have made a detailed review of such facts, providing
an exhaustive summing up of all the available data.
The reader will also be interested by the other chapters of this book,
for instance the pathologic study which includes an original description of
a synovial involvement. The latter is all the more interesting as such documen
tations are very rare.
Finally, the treatment of algodystrophy has been dealt with in detail;
the authors describe the drug and physical treatments which are applied
simultaneously and the results which can be expected. Neither prevention
nor medicolegal considerations are neglected, proof that Doury, Dirheimer,
and Pattin wish to provide their readers with a complete handbook, combin
ing theoretical data and the most useful practical indications. We can but
congratulate them on their eclecticism and wish their book the success it
deserves.
J. VILLIAUMEY
Acknowledgements
We are grateful to Prof. J. Villiaumey, president of the French Society of
Rheumatology for having accepted to write the foreword for this book.
We wish to thank Prof. A. Wackenheim, Head and Chairman of Radiology,
University of Strasbourg for his advices and constant support.
We thank also Mrs. M.-Th. Wackenheim for her English translation of
our text and for her kindness and disponibility.
Many people in a variety of ways have made this volume possible and
it gives us pleasure to identify them here: Prof. J. Arlet, rheumatology,
Toulouse; Prof. R.P. Delahaye, radiology, Paris; Dr. R. Granier, nuclear
medicine, Paris; Dr. L. Heraut, neurophysiology, Paris; Prof. R. Lagier,
pathology, Geneva; Prof. P.J. Metges, radiology, Paris; Prof. P. Meunier,
rheumatology, Lyon; Dr. B. Moyses nuclear medicine, Strasbourg; Dr. A.
Norton, general practitioner, London; Dr. A. Ramsheyi, general practitioner,
Teheran.
We thank also our technical assistants Mrs. C. Butterlin, L. Fischer, M.
Reinheimer, R. Walter.
P. DOURY
Y. DIRHEIMER
S. PATTIN
Contents
Introduction
Chapter 1 Historical Review .... 2
Chapter 2 Why Study this Condition? 7
Part 1 Symptomatology
Chapter 1 General Data in Algodystrophy 10
A. Clinical Syndrome . . 10
B. Biochemical Syndrome 10
C. Radiological Syndrome 10
D. Scintigraphic Syndrome 11
E. Clinical Course 11
Chapter 2 Clinical Description 11
Chapter 3 Topographic Forms 12
A. Algodystrophy of the Upper Limb 12
I. Onset ......... . 13
II. First Stage . . . . . . . . 13
1. Involvement of Hand and Wrist 13
2. Involvement of the Shoulder 13
III. Second Stage . . . 13
1. Hand and Wrist 13
2. Shoulder 14
3. Elbow ..... 14
IV. Evolution 14
V. Topographic Forms 14
1. Isolated Involvement of the Hand 14
2. Isolated Involvement of the Shoulder 14
3. Associated Involvement of the Elbow 15
4. Associated Involvement of the Sternoclavicular
Articulation .............. . 15
5. Algodystrophy Localized to Two or Three Fingers
of One Hand ....... . 15
6. Bilateral and Extensive Forms 15
B. Algodystrophy of the Lower Limbs 15
I. Algodystrophy of the Foot 15
II. Algodystrophy of the Knee 17
1. The Classical Form . . 17
2. Partial Algodystrophy . 18
3. Highly Localized Algodystrophy 18
XII Contents
III. Algodystrophy of the Hip 18
1. General Data 19
2. Clinical Signs 19
3. Clinical Course 20
C. Algodystrophy of the Spine 21
D. Other Localizations 23
Part 2 Complementary Investigations
Chapter 1 Biochemistry 26
A. Nonspecific Indicators of Inflammation . . . . . . 26
B. Calcium and Phosphorus Levels in Blood and Urine 26
C. Calcitonin Test ..... . 26
D. Hydroxyproline in the Urine 27
E. Parathormone 28
F. HL-A Antigen . . 28
G. Synovial Fluid . . 29
H. Muscular Enzymes 29
Predisposition to Algodystrophy in Certain Preexisting Metabolic
Disturbances . . . . . . 29
1. Diabetes Mellitus 29
2. Hyperlipidemia 29
Chapter 2 Radiology . . . . 29
A. Techniques ..... . 30
I. Magnification Radiology 30
II. Tomography .... 31
III. Xeroradiography 31
IV. Electron Radiography 31
V. Logetronography 31
B. Involvement of Soft Tissues 31
C. Involvement of Bone . . . 32
I. Elementary Radiographic Signs 32
1. Osteopenia . . . . . . . . 32
2. Subchondral Lysis .... 32
3. Resorption of Cortical Bone 32
4. Juxta-articular Erosions 33
II. Association of Primary Lesions Producing Different
Types of Image . . . . . 33
III. Evolution Features .......... . 34
1. Early Demineralization ...... . 34
2. Evaluation of the Radiologic Intensity of
Algodystrophy . . . . . . . . . . . 34
3. Classification into Stages ..... . 34
4. Forms Without Bone Demineralization 35
D. Topographic Forms ........... . 35
I. Partial Algodystrophy . . . . . . . . . 35
II. Highly Localized or Parcellar Algodystrophy 36
III. Algodystrophy of the Upper Limb 36
IV. Algodystrophy of the Foot 37
V. Algodystrophy of the Knee . . . . 37
Contents XIII
VI. Algodystrophy of the Hip 38
VII. Algodystrophy of the Spine 38
E. Articular Involvement 38
F. Arthrography . . . . 44
G. Arteriography . . . . 52
H. Pertrochanteral and Intra-femoral-head Phlebography 53
Chapter 3 Scintigraphy 53
A. Bone Scanning . 53
I. Technique 55
II. Results 55
1. Increased Uptake 55
2. Iso and Hypofixation 56
3. Usefulness of Bone Scanning for Diagnosis
of Algodystrophy . . . . . . . 59
4. Limits of Bone Scanning . . . . . 60
5. Significance of Scintigraphic Data . 60
B. Isotopic Exploration of the Vascular Sector 61
C. Isotopic Exploration of the Interstitial Area 61
D. Joint Scanning . . . 61
Chapter 4 Densitometry 61
Chapter 5 Thermography 63
Chapter 6 Vascular Investigations 64
A. Oscillometry . 64
B. Capillaroscopy . . . . . 65
C. Doppler Effect . . . . . 65
Chapter 7 Electromyography 66
Chapter 8 Pathology 67
A. Synovia. 68
B. Cartilage 68
C. Bone .. 71
I. Macroscopy 71
II. Microscopy 71
III. Electron Microscopy 73
IV. Microradiography . . 74
V. Static and Dynamic Histomorphometry 74
VI. Attempt at a Histodynamic Interpretation of the
Algodystrophic Mechanism 76
D. Periarticular Tissues ..... 80
I. Capsule . . . . . 80
II. Aponeuroses, Bursae and Tendons 80
III. Muscles . . . . . 81
IV. Cutaneous Tissues 81
V. Vessels 82
VI. Nerves 82
Part 3 Clinical Forms
Chapter 1 Topographic Forms 86
Chapter 2 Evolutive Forms . 86