Rev Neurol France
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The long history of sciatica is recalled from the 18th century observations through the contributions of Lasègue (a philosopher who worked with Claude Bernard), Valleix, Brissaud, Dejerine, Sicard, Forestier, Alajouanine and Petit-Dutaillis. Two papers by professor de Sèze on the significance of herniations of lumbar disks were published in December 1939 and June 1940, a most unfavourable period in France. Since then many advances are to be recorded among which the use of metrizamide instead of the old lipiodol and, most of all, the advent of CT Scan.
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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. ⋯ 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.
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Case Reports Biography Historical Article
[Gustave Flaubert's illness].
All those interested in Gustave Flaubert's illness, during his lifetime as well as after his death, have agreed that he had epilepsy. The one important exception is Jean-Paul Sartre, who, in the 2800 pages of his "Idiot de la famille" claimed that Flaubert was a hysteric with very moderate intelligence who somatized his neurosis in the form of seizures. These, in Sartre's views, were moreover probably hysterical, but possibly epileptic resulting from the existence of a psychogenic epilepsy bred from the neurosis. ⋯ But, unable to carry out his wishes and desiring both to die and to survive, Gustave, adolescent, might have chosen the pathway of "false deaths", as exemplified by the seizures. Modern epileptology data enables not only to confirm the epileptic etiology and to discount the hysterical nature of the fits, but also: 1. to establish precise details of the site and nature of the cerebral lesions responsible for the attacks: neonatal atrophy or vascular malformation of the occipitotemporal cortex of the left hemisphere, the only lesion capable of provoking: a) the phosphenes marking the onset of the seizures; b) the intellectual manifestations (forced thoughts or flight of ideas), affective features (panic terror), and psychosensory (ecmnesic hallucinations) or psychomotor (confusional automatism) symptoms accompanying some attacks; c) the loss of speech preceding the loss of consciousness and terminal generalized convulsions. 2. to establish the consequences of the lesion and of the temporal fits on the behaviour of the writer; a) associated hypoactivity (slowness of ideation and writing) and paroxysmal impulsiveness (violent unmotivated angry outbursts); b) disturbed verbal functions (difficulty in finding words); and c) diminished sexuality. As a conclusion, it must be admitted; a) that Flaubert suffered from an organic and not a psychogenic epilepsy, the existence of the latter currently being disputed; b) that this epilepsy modified the behaviour of the author without affecting his genius; c) that, as a result of this, the epilepsy of Flaubert, as that of Dostoïevski, should serve as a defense witness for the unfortunate epileptics thought to be destined for intellectual deterioration only because of the repetition of their seizures.