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Resumen Presentamos la evolución de la terminología y los criterios diagnósticos para el síndrome de fatiga crónica/encefalomielitis miálgica. Este síndrome es una entidad compleja y controvertida, de etiología desconocida, que aparece en la literatura médica en 1988, si bien desde el siglo XIX se identificaron cuadros clínicos de fatiga crónica idiopática con diferentes nombres, desde neurastenia, neuromiastenia epidémica y encefalomielitis miálgica benigna hasta la actual propuesta de enfermedad de intolerancia al esfuerzo (postesfuerzo). Todos ellos aluden a un estado crónico de fatiga generalizada de naturaleza desconocida, con limitaciones al esfuerzo físico y mental, acompañado de un conjunto de síntomas que comprometen diversos sistemas orgánicos. La Clasificación Internacional de Enfermedades (CIE-10) encuadra este síndrome en el apartado de trastornos neurológicos (G93.3), aunque todavía no se hayan encontrado hallazgos anatomopatológicos que lo clarifiquen. Se han documentado múltiples alteraciones orgánicas, pero no se ha establecido una biología común que aclare los mecanismos que subyacen a esta dolencia. Se enuncia como una disfunción neuroinmunoendocrina, con un diagnóstico exclusivamente clínico y por exclusión. Diversos autores han propuesto incluir el síndrome de fatiga crónica/encefalomielitis miálgica dentro de los síndromes de sensibilidad central, aludiendo a la sensibilización central como el sustrato fisiopatológico común para este síndrome y otros. El papel del médico de familia es clave en la enfermedad, para la detección de aquellos pacientes que presenten una fatiga de naturaleza desconocida que se prolonga de forma continua o intermitente durante más de 6 meses, al objeto de realizar un diagnóstico temprano y establecer un plan de actuación frente a una enfermedad crónica con unos altos niveles de morbilidad en la esfera física y mental. Objetivo Realizar una revisión bibliográfica de la terminología y criterios diagnósticos del síndrome de fatiga crónica/encefalomielitis miálgica, al objeto de aclarar conceptualmente la enfermedad, como utilidad en el diagnóstico a los médicos de Atención Primaria.

The widespread psychological disturbances observed during and after epidemics of myalgic encephalomyelitis are briefly reviewed. Two young women are described who developed severe and long-lasting changes in mood and behaviour after this illness. One developed temporal lobe epilepsy and had recurring bouts of depression for eight years, with histrionic, attention-seeking behaviour, hysterical fits and frequent suicidal attempts, both serious and demonstrative. The other had similar recurrent depressions, with a striking restlessness and inability to concentrate, and frequent aggressive and self-destructive out-bursts which are showing no sign of abating five years after her original illness. Though both patients had shown some evidence of neurotic predisposition beforehand, it is argued that damage to the cerebral mechanisms underlying the control of mood and behaviour must be postulated to underlie such severe and prolonged disturbances. Though psychological disturbances have been a prominent feature of all epidemics of myalgic encephalomyelitis they have failed to attract the attention of psychiatrists. It is to be hoped that, if further epidemics of this strange illness occur, comprehensive psychiatric and psychological studies will be instituted.

THE FREQUENCY of papilledema associated with encephalitis varies to some extent from report to report, but usually the condition is described as rare. This variation is due to several factors. Thus, differences in terminology render comparison and classification of the ophthalmoscopic findings in the various series difficult, and some authors have expressed the view that the presence of papilledema is inconsistent with a diagnosis of encephalitis. However, the most important reason seems to be that there is a real difference in the frequency of papilledema in the various types of encephalitis. Thus, in epidemic encephalitis (Economo) papilledema is not uncommon,1-3but considerable differences are seen in the various series reported in the literature. As examples of encephalitides in which papilledema is very rare the following may be mentioned: the Central European type4and, among etiologically nonclassifiable types, benign myalgic encephalomyelitis,5and a number of cases reported

Four cases of encephalomyelitis resembling benign myalgic encephalomyelitis are reported. A Coxsackie B2 virus was isolated from the cerebrospinal fluid in one case and an echovirus type 3 virus from the faeces and the cerebrospinal fluid in another. Serological tests indicated Coxsackie B2 and Coxsackie B5 infection in the other two cases.

The reports of the 15 recorded outbreaks of benign myalgic encephalomyelitis have been reviewed and in one instance the original clinical data studied. We believe that a lot of these epidemics were psychosocial phenomena caused by one of two mechanisms, either mass hysteria on the part of the patients or altered medical perception of the community. We suggest that the name “myalgia nervosa” should be used for any future cases of functional disorder which present the same clinical picture.

In 1955 an epidemic occurred among the staff of a London Teaching Hospital group. The nature of the epidemic remains uncertain. One view is that the illness was a viral encephalomyelitis (Medical Staff Report, 1957); an alternative is that it was a manifestation of anxiety spreading through a population consisting largely of young women (McEvedy and Beard, 1970). This paper reports the results from the follow-up study carried out in 1968–69 on the nuclear group affected by the epidemic and on a matched series of controls.

Ten patients in whom the clinical findings were consistent with the syndrome variously described as 'benign myalgic encephalomyelitis', 'epidemic neuromyasthenia', 'Royal Free disease' and 'Icelandic disease' were investigated for blood levels of myoglobin and various enzymes. Although there is no clinical resemblance between the two diseases, the biochemical pattern bears a close similarity to that found in Duchenne muscular dystrophy (DMD) though differing sharply in that no rise in creatinine kinase levels was found. These findings are discussed with particular reference to recent suggestions that the permeability of cell membranes may be impaired by changes in intracellular energy mechanisms.

Recent technical advances have added greatly to the ease with which virological methods may be applied to the study of poliomyelitis and allied infection of the central nervous system. These techniques have already borne abundant fruit in the development of a vaccine against poliomyelitis. The accurate appraisal of the preventive value of such a vaccine will depend on our ability to diagnose poliomyelitis accurately. It had long been believed that the clinical features of acute paralytic poliomyelitis were sufficiently characteristic for a confident diagnosis to be made on clinical grounds alone. This confidence has recently been shaken by the finding that the virus of louping-ill (Russian spring–summer encephalomyelitis) may produce a similar clinical picture, even in the United Kingdom. There is also suggestive but incomplete evidence that Coxsackie B, Echo and other viruses may occasionally cause acute flaccid paralysis. The position of a “non-paralytic” poliomyelitis is even less secure and the diagnosis can no longer be established on clinical grounds alone. The purpose of this article is to review a number of obscure outbreaks of paralytic illness, the majority of which were at first confused with poliomyelitis but which were later differentiated on clinical and epidemiologic grounds. Although investigations have been restricted by the fact that no deaths have occurred, the most careful virologic studies have failed to incriminate the polio virus, the Coxsackie or Echo groups of organisms, or any other known neurotrophic agent. The outbreaks will be compared, and the basis for the view that they constitute a clinical entity will be discussed. Such information as is available about the etiology, prognosis and treatment will be reviewed.

Ten patients in whom the clinical findings were consistent with the syndrome variously described as ‘benign myalgic encephalomyelitis’, ‘epidemic neuromyasthenia’, ‘Royal Free disease’ and ‘Icelandic disease’ were investigated for blood levels of myoglobin and various enzymes. Although there is no clinical resemblance between the two diseases, the biochemical pattern bears a close similarity to that found in Duchenne muscular dystrophy (DMD) though differing sharply in that no rise in creatinine kinase levels was found. These findings are discussed with particular reference to recent suggestions that the permeability of cell membranes may be impaired by changes in intracellular energy mechanisms.