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The distinction between thrombosis and haemorrhage was unclear until the mid-19th century,1 despite the clinical and pathological descriptions of Abercrombie, Cheyne, Cooke, and, in France, Serres. Small softenings were first designated lacunes by Dechambres in 1838. Van Swieten,2 far ahead of his time, postulated embolism arising in the heart and great vessels.3
After Virchow,4,5 William Senhouse Kirkes (1823–64) published one of the earliest descriptions of cerebral embolism associated with infective endocarditis, which together with the later paper of Samuel Wilks brought this disease to the attention of doctors. Kirkes’ paper6 described three patients.
“Margaret Shaw at 34 was admitted to St Bartholomew’s hospital under Dr Roupell...on account of pains in her lower limbs and general debility. A loud systolic murmur was heard all over the cardiac region.... While sitting up in bed eating her dinner, she suddenly fell back as if fainting...and when attended to was found speechless, though not unconscious, and partially hemiplegic on the left side[sic]. The hemiplegia increased... and gradually became complete...but without loss of consciousness for five days, when she quietly died.”
“On examining the body...the right corpus striatum was softened to an extreme degree...the corresponding optic thalamus was healthy; but a condition of pale softening, similar to that affecting the corpus striatum, existed also in considerable extent in the posterior lobe of the right cerebral hemisphere...all other parts of the brain were healthy. The right middle cerebral artery just at its commencement was plugged up by a small nodule of firm, whitish, fibrinous-looking substance... The right cavities and left auricle [of the heart] contained recent separated coagula; the fibrine firm and whitish. The mitral valve was much diseased, the auricular surface of its large cusp being beset with large warty excrescences of adherent blood-stained fibrine...”
Although, the report did not indicate whether the speechless patient was left handed, it gives convincing details of embolic infarcts in the spleen, right kidney, and right iliac artery.
His second patient was a woman of 24, with mitral valve “fungous condylomatous growths”, who had a right hemiplegia with striatal and left cerebral infarction and middle cerebral artery occlusion. The third was a man aged 24, with left hemiplegia, who died after a fluctuating illness over two months. He had vegetations on the aortic, tricuspid, and mitral valves and right middle cerebral artery occlusion; he also had fibrin clots in the left lateral sinus and left jugular and iliac veins.
Kirkes was physician to St Bartholomew’s Hospital, amiable, and much respected. His Handbook of physiology was popular and was deservedly held as an authority. Together with Virchow, the name of Kirkes stands firmly connected with the subject of embolism, one of the most fruitful inquiries in modern pathology. While attending a meeting (nominated by the Admiralty and Horse Guards) to inquire into venereal disease, he fell ill and met a premature death with pleurisy, pericarditis, and haematuria.
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