Published online by Cambridge University Press: 06 July 2023
In one of the four patients with apoplexy, Wepfer described in 1658 the excess of fluid in the brain was not blood, but ‘serum’ – a gelatinous form of it covered the entire surface. Wepfer therefore distinguished ‘serous apoplexy’ from the sanguineous form, even though the apoplectic state had occurred as part of a protracted illness. Later he reported similar cases. In retrospect, thanks to Wepfer’s meticulous recording, a retrospective diagnosis of chronic infectious disease seems inescapable. In the eighteenth century, Boerhaave and van Swieten implicated the accumulation of brain lymph as a cause of apoplexy, but without providing anatomical proof. In Morgagni’s large series of dissections, patients classified as having ‘serous apoplexy’ showed a variety of lesions; in a patient with ‘paralysis’, he found unilateral ‘erosion’ of the striate body, like Willis before him. In the decades around 1800, once it had become fashionable to diagnose apoplexy in a variety of attacks, the ‘serous’ form was considered less often.
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