[From Morbus Sudeck to complex regional pain syndrome]. / Vom Morbus Sudeck zum komplexen regionalen Schmerzsyndrom.

Burning pain and autonomic disorders, such as change of skin color, hyperhidrosis, edema and stiffness in joints of extremities were first described in 1864 by Silas W. Mitchell. The German expression "Morbus Sudeck" takes its name from the surgeon Paul Sudeck from Hamburg who described spotty decalcification in x-rays in 1900. In the Anglo-Saxon world, the theory that the sympathetic nervous system was involved in the generation and sustention of these alterations was based on the observations of the French surgeon René Leriche and in 1846 James A. Evans introduced the expression sympathetic reflex dystrophy. As doubts arose that the sympathetic nervous system could not be the sole culprit, the descriptive phrase of complex regional pain syndrome was introduced to substitute for more than 60 synonyms focusing on the fact that the disease develops after minor trauma or nerve lesions and does not correlate with the severity of the trauma. Diagnosing this syndrome is still hampered by the fact that no specific laboratory or radiological marker has yet been identified. Multidisciplinary and interdisciplinary approaches to therapy seem to be inevitable. Since Sudeck first described the disease, 110 years have passed. The underlying hypothesis and theories as well as the development during this time period are summarized.

ACTUALIZACIÓN EN MEDICINA DE FAMILIA: Síndrome de Sudeck (distrofia simpático refleja) / UP-DATE IN FAMILY MEDICINE: Sudeck's syndrome (reflex sympathetic dystrophy syndrome)

Desde que Mitchel en 1864 la denominara causalgia y en1909 Paul Sudeck la bautizara, a día de hoy continúa siendoun reto para la clínica médica. Su inespecificidad diagnóstica,añadida al gran número de factores precipitantes y a suetiopatogenia no claramente esclarecida y de terapéuticacontrovertida hacen de esta enfermedad un cuadro clínicocomplejo tanto para el paciente como para quien lo asiste.Llegar a un diagnóstico precoz es el eje principal del tratamientodel síndrome de Sudeck.Puede afectar a cualquier edad y tanto a hombres como amujeres, aunque estadísticamente es más frecuente en mujeresjóvenes.La incidencia de la enfermedad es variable, oscilando entreel 2 y el 25% de la población, aunque en nuestro país noconocemos cifras. Indudablemente es una entidad que pasahabitualmente desapercibida para nuestra comunidad médicaen general (AU)

Since Mitchell coined the term causalgia in 1864 and PaulSudeck baptized it in 1909, this disease continues to be achallenge for the medical clinician. Its non-specific diagnosisas well as its large number of precipitating factors, this alladded to its etiopathogenesis that cannot be clearly clarifiedand its controversial treatment, makes this disease a complexclinical picture for both the patient and treating clinician.Reaching an early diagnostic is fundamental in the treatmentof Sudeck’s syndrome. It can affect any age group andboth men as well as women, although it is more frequent inyoung women statistically.The incidence of the illness is variable, ranging from 2%to 25% of the population. Although there are no known valuesin our country, it is undoubtedly a condition that generallygoes unnoticed in our medical community (AU)

[Wars in the history of rheumatology]. / Le guerre nella storia della reumatologia.

Some important discoveries in the history of rheumatology happened during war periods. It is well known that arthritis associated with conjunctivitis and urethritis, following dysenteric episodes, has been described during the First World War from the German Hans Reiter and, nearly contemporarily, from the French Nöel Fiessinger and Edgar Leroy. Less known is instead the fact that the first cases of sympathetic algoneurodystrophy have been reported by the American Silas Weir Mitchell in soldiers wounded by fire-arms, during the Civil War of Secession. Other war episodes have been crucial for the development of some drugs now abundantly applied to the care of rheumatic diseases. The discovery of therapeutic effects of immunosuppressive agents, in fact, happened as an indirect consequence of the use of poison gas, already during the First World War (mustard gas), but above all after an episode in the port of Bari in 1943, where an American cargo boat was sunk. It had been loaded with a quantity of cylinders containing a nitrogenous mustard, whose diffusion in the environment provoked more than 80 deaths owing to bone marrow aplasia.Moreover, the history of the cortisone shows a strict link to the Second World War, when Germany imported large quantities of bovine adrenal glands from Argentina, with the purpose of producing some gland extracts for the Luftwaffe aviators, in order to increase their performance ability.

Sudeck atrophy.

This paper reviews the contribution of Sudeck to the understanding of the condition commonly referred to as 'Sudeck's atrophy' and which is commonly used as a synonym for a condition variously called reflex sympathetic dystrophy, causalgia, algodystrophy and others. Sudeck came to show in his later papers that the so-called atrophy was, in the majority of cases, a normal inflammatory process of bone change in the course of healing after an inflammatory/infective or traumatic insult. Contrary to the views of much current literature, the vast majority of such cases had a good prognosis. In those cases which became pathological and had a correspondingly poorer prognosis, the characteristic clinical picture becomes associated with radiological and pathological changes, which, uniquely, are described by Sudeck. A knowledge of such radiological and pathological substrate for clinical symptomatology is important in the analysis of pain following trauma.

[Sudeck's syndrome. Was Sudeck right?]. / Sudeck-Syndrom. Hatte Sudeck recht?

Reflex sympathetic dystrophy (RSD) is a syndrome affecting an extremity after a minor trauma or operation. At the moment there is no consensus about the pathogenesis of RSD. In 1942 Paul Sudeck suggested that the signs and symptoms of RSD may be provoked by an exaggerated inflammatory response to injury or operation of an extremity. His theory found no disciples, as most physicians believe that RSD is initiated by an hyperactive sympathetic system. We performed various clinical and experimental investigations, including the effects of antiinflammatory treatment. The results of these studies support the theory of Paul Sudeck.

[Historical review of algodystrophy: part I]. / Rys historyczny algodystrofii: czesc I.

The history of algodystrophy discerning, its recognition as a separate clinical entity and evolution of ideas about its nature is presented on the basis of historical and scientific literature. First cases resembling algodystrophy were described as early as in XVI and XVIII century. A more detailed description of limb dystrophy that followed gunshot injuries was reported by American surgeon Weir Mitchell in 1864, who coined this condition as "causalgia". In the year 1900 Paul Sudeck of Germany described radiological changes secondary, as he believed, to inflammatory process within the limb as patchy osteoporosis. His name is still attached to this syndrome in German and Polish literature. French neurosurgeon Rene Leriche believed, that the syndrome was caused by increased activity of the sympathetic nervous system and introduced a surgical periarterial sympathectomy. Oscar Steinbrocker of the United States separated particular form of algodystrophy known as shoulder-hand syndrome; later, he introduced the treatment of this condition with steroids.

[A historical review of algodystrophy: part II]. / Rys historyczny algodystrofii: czesc II.

Second part of this paper deals with developing of the etiopathological concepts on algodystrophy. Variety of terms have been used to describe the syndrome during over hundred years. The name "reflex sympathetic dystrophy" introduced by J.A. Evans in 1946 is commonly used in English and American literature. French rheumatologists proposed the term "algodystrophy" in 1960; this seemed very satisfactory, because did not imply involvement of any particular tissue, localization or etiology but reflected the combination of pain and dystrophic changes. Current taxonomic concepts were also presented e.g. "complex regional pain syndrome". A discrepancies on the incidence rates of the condition were mentioned and their causes suggested. Current diagnostic criteria of the syndrome were presented. The contribution of Polish authors was reminded. In spite of considerable progress in understanding of the syndrome, its many aspects remain controversial or obscure.

The enduring mark left by Jean-Martin Charcot on rheumatology.

Although Charcot is remembered above all as an outstanding neurologist, he also left a lasting imprint on the study of rheumatic diseases, primarily in two fields. a) He performed a pathologic-nosographic confrontation based on principles that remain relevant in today's era of imaging techniques. His vision as a pathologist allowed him to establish links between nonspecific lesions, which led him to develop a unified concept of chronic rheumatism. At the same time however, his experience as a clinician gave him a sense of the nosologic distinctions that are widely accepted today. b) He analyzed osteoarticular dystrophies associated with neurologic disorders, most notably tabetic arthropathies with epiphyseal fragmentation and in some instances spontaneous fractures. In addition, a constellation of alterations of the synovial membrane, ligaments, and muscles identified in those analyses foreshadowed today's concept of reflex sympathetic dystrophy syndrome.

Reflex sympathetic dystrophies and algodystrophies: historical and pathogenic considerations.

This paper reviews the historical development of the concepts of 'sympathy' of organs and of the sympathetic nervous system. In particular, the afferent function of the sympathetic system is discussed. The attention is focussed on sympathetic reflex dystrophies, known in some European schools as 'algodystrophies'. The pathogenic mechanisms of these affections, especially of causalgia, are discussed, considering the importance of peripheral damage to nerves, lateralisation of pain, 'mirror phenomena', and the relationship between peripheral and central mechanisms of pain.

[Nervous arthropathies]. / Arthropathies nerveuses.

In 1868, J.M. Charcot published his memoir "sur quelques athropathies qui paraissent dépendre d'une lésion du cerveau ou de la moelle épinière "based on 4 cases of tabes dorsalis. This work was subsequently developed and presented in London in 1881 when Sir James Paget acknowledged the significance of this entity. "Charcot's joint" has come in use to mean that particular joint disease which results, from nervous lesions, whatever its nature. A controversy lasted between those who thought, e.g. Volkman, that mechanical trauma is the significant pathophysiological factor and those, e.g. Charcot, who ascribed a trophic role to the spinal cord. At the beginning, Charcot thought that lesions of the anterior horn were responsible but finally concluded that be could not bring a precise answer to that point. Subsequently Raymond, Dejerine (who insisted on the absence of pain), Foix and Alajouanine, Alajouanine and his collaborators extended Charcot's observations. Alajouanine proposed that lesions of the sympathetic nervous system played a major pathophysiological role. In 1960 Castaigne and Cambier proposed a unified theory with complementary roles ascribed to trauma and to nervous lesions. In 1936, diabetic neuropathy was described by W. Jordan. In 1942, Thevenard described "acropathie ulcéro-mutilante" now widely known as hereditary sensory neuropathy. Amyloidosis, familial dysautonomia, congenital insensitivity to pain were added to the list of causes of Charcot's joint. Less well known are the works of Charcot on joint diseases in hemiplegics. These were later studied by Alajouanine and Thurel and de Sèze and Ryckewaert have proposed to call them "algoneurodystrophies décalcifiantes réflexes" a topic which nowadays arises much interest in rheumatology.