Brain abcess with pathological observations / by Charles Bagley.

  • Bagley, Charles, 1882-
Date:
[1924?]
Catalogue details

Licence: In copyright

Credit: Brain abcess with pathological observations / by Charles Bagley. Source: Wellcome Collection.

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    Fig. 28. P. V. Transverse section through the occipital pole of the brain shown in Figure 5. a, Occipital pole of the lateral ventricle converted into abscess cavity with necrotic wall; b, area of encephalitis, tract of evacuation of pus from the ven¬ tricle cavity to the subarachnoid space; c, thickened pia-arachnoid; d, site of section shown in Figure 29. shown in Figure 18 indicating that the wall was formed within a period of 3 or 4 weeks. The haemorrhages shown in Figure 19 were no doubt due to the very active vascular pro¬ liferation in the soft, cerebral tissue. Type III.—Walls of Varying Thickness, the Result of Glial Proliferation Walls formed almost entirely of glial fibrils may be very heavy, but because of the deli¬ cate character of the fibrils the wall is not so resistant as one in which there is fibrous tissue. In Figure 21 the wall was visible macroscopically and in this picture of low magnification has the appearance of a thick, limiting membrane, but the delicate quality of the tissue is shown in Figure 22. The relative value of this type wall and the firm fibrous tissue wall is perhaps best shown in Figure 13, in which there is a firm fibrous tissue wall at c and at d, the adjacent cerebral tissue with glial proliferation. A photomicro¬ graph of d, given in Figure 15, is similar to the abscess wall shown microscopically in Figure 22. The neuroglial fibrils are again well shown in Figure 23, which was taken from the innermost part of the abscess wall. A large part of the cellular element has fallen out because of the necrosis, leaving the fibrils in plain view. Type IV.—Walls Showing no Evidence of a Protective Reaction Figure 24 shows an abscess which was the result of a virulent streptococcus planted deep in the substance of the cerebellar hemi¬ sphere. There is no evidence of a protective reaction and the lesion marks an intermediate stage between an encephalitis and the usual abscess formation, for though suppuration occurred there was no true barrier between the pus and the brain tissue. At b in Figure 24 there is an area of haemorrhagic extravasa¬ tion, the result of thrombosis, which is also well shown in Figure 25, the destructive process entirely replacing the usual prolif¬ erative reaction. The merely necrotic end- result of the destructive process is shown in Figure 26. Abscesses of this type also occur as second¬ ary lesions to firm wall abscesses. In Figure 27 the primary abscess has a thick wall, the building of which, no doubt, required several weeks, but the extension from this abscess was doubtless more recent due to escape of pus into the substance of the occipital lobe, an invasion altogether too sudden to allow the slowly proliferating glial tissue to form a pro¬ tecting membrane. D. F., age 29. Gunshot wound left hemisphere, July 14, 1918. Constant drainage of pus from the wound. Drainage of abscess, June 22, 1919. Death, June 30.
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