Pachymeningitis Interna Hemorrhagica, with Report of Eight Cases. By E. D. BONDURANT, M. D., Tuskaloosa, Ala., REGARDING the nature of the affection variously described as Pachymeningitis Interna Hemorrhagica, Hæmatoma Dura Matris, Subdural Hæmatoma, Arachnoid Hemorrhage, etc., the older anatomists and pathologists entertained most widely varying and even diametrically opposite opinions, and appear to have transmitted with interest these differences and contentions to their successors of the present time. Probably the greater number of living pathologists, following Durand-Fardel, Heschl and Virchow, insist upon the inflammatory nature of the disease, the initial stage in the morbid process being, they assert a chronic inflammation of the inner layers of the dura, attended by the exudation of fibrino-plastic material, which becomes the basis of the characteristic false membrane. On the other hand, the majority of those who have recently written upon the subject in England (Bevan 1 Lewis, Clouston,2 Wiglesworth3), and America (Dercum, 4 Hoyt, Whittaker" ), subscribe to the opinion, advocated early in the present century by Abercrombie, Andral, Houssard and others, and reaffirmed and ably defended by Huguenin' in 1876, that simple hemorrhage into the subdural space is in every instance the initial lesion. A long and convincing array of facts have been adduced in support of this theory. It has been shown, and it is not now denied by anyone, that effusion of blood beneath the dura, with subsequent organization of the resulting clot, does in certain cases occur; and that its developmental course differs in no respect from that noted in cases of alleged inflammatory origin. As a result of experimental research upon animals, it is stated that irritation of the dura never produces a hemorrhage, but only a purulent inflammation. Sperlings has reproduced the anatomical lesion of pachymeningitis interna hemorrhagica in lower animals by injections of blood into the subdural space. He finds furthermore, as evidencing the necessary part played by the fibrinous clot, and showing the inadequacy of the slight dural irritation resulting from such introduction of fluid, that the injection of defibrinated blood is not followed by the formation of a false membrane. These statements find quite recent confirmation in the report by Goodall of the accidental production, in course of experiments upon the lower animals requiring incision of the dura and application of irritants to the cerebral cortex, of a hemorrhagic false membrane as a result of effusion of blood from a wounded dural vessel. It is claimed by the advocates of the hemorrhagic theory that inflammatory changes in the dura are slight, 3. Journal of Mental Science, Jan., 1888, and article in "Dictionary of Psychological Medicine," 1892. 4. Report of State Hospital, Norristown, Penn. 5. Medical Record, April 30th, 1892. 6. Article "Meningitis" in "Reference Hand-Book," Vol. IV. 7. 8. "Ziemssen's Handbuch der Pathologie und Therapie," Leipzig, 1876. "Reference Hand-Book," quoted by Whittaker, loc. cit. 9. Journal of Mental Science, July, 1892. or, in recent cases, entirely wanting; that when present, the inflammation is secondary to the irritation caused by the extravasation, the changes being compared by Wiglesworth to those occurring in the walls of bloodvessels following the formation of a thrombus. Eliminating minor differences, the two schools are virtually agreed as to the structure of the resulting pseudo-membrane and the subsequent course of the affection. The blood clot or fibrinous exudate, as the case may be, becomes partially organized by the conversion of its leucocytes into spindle-shaped connective tissue cells, and the development of large but weak-walled capillaries; rupture of these newly-formed vessels accounting for the, in many cases, repeated hemorrhage. Within the past eighteen months, among ninety-two autopsies upon insane patients at the Alabama Insane Hospital, this condition has been met with eight times. As these cases are collectively of some interest, and illustrate not inaptly some of the varying phases of this singular malady, a short account of each is given, as a small contribution towards the elucidation of the problem above indicated. CASE I.-White female, aged 36. Died of chronic pulmonary tuberculosis, with a complicating chronic nephritis. Had suffered from melancholia with persecutory and religious delusions for eleven years, accompanied during the last several of these years by gradually advancing dementia. Was confined to bed for two months before death, and during this time was extremely dull and confused. Urine contained albumin and casts, and was diminished in quantity. No heart lesion. The autopsy shows tubercular disease of the lungs, pleuræ, bronchial and mesentric lymph nodes; tubercular ulcers in small intestine; a parenchymatous nephritis. In the aorta are seen, scattered sparingly throughout its entire length, pale yellow atheromatous patches. The brain is atrophied, the convolutional shrinking being especially noticed in frontal and motor regions. Weight of right hemisphere 17; of left 181; of cerebellum, pons, and medulla 5 ozs.; together 41 ozs. For near a quarter inch, at posterior edge of the pons, the pyramidal tracts are superficial, being destitute of the normal covering of transverse fibers. The pia is, over the entire convexity, thickened, very tough, very cedematous, and shows irregular areas of opalescence. The dura is seemingly normal. Covering its inner surface is, in each parietal region, an exceedingly thin, pale yellow, friable, false membrane, dotted here and there with small hemorrhagic spots. This membrane is of scarcely more than gelatinous consistency, but can with care be raised in sheets of some size. Microscopic examination shows a normal dura. The false membrane is almost structureless; there are shreds of fibrin, leucocytes, a few spindle-shaped cells, a few brownish pigment masses, and some collections of red blood cells. There is slight thickening of the intima of many of the vessels of the pia. CASE II.-Negro woman, twenty-six years of age, died of tuberculosis pulmonum. At the time of puberty had an attack of acute dementia, terminating in three weeks in entire recovery. Three years before death symptoms of tubercular disease of the lungs were first seen, and almost at the same time an acute melancholia developed, attended by numerous and rapidly systematized religious delusions, the emotional disturbance eventually giving place to dementia. Casts and albumin were absent from the urine until a few weeks before death, when both were detected. There was no heart lesion. At the necropsy tubercular disease of lungs, intestinal tract and lymph glands is found, together with a parenchymatous nephritis of mild grade. There are a few small scattered atheromatous patches in aorta and its larger branches. Upon the inner surface of the dura, both sides, but thicker on the left, is a soft, straw yellow membrane, exhibiting brownish discolorations in places, but no distinct hemorrhagic foci. The membrane has no organic connection with the dura, the inner surface of which is smooth and apparently unaffected. Upon the pia, in right parietal region, is a circumscribed area of reddish-brown staining, unaffected by washing, and visible after pia has been removed and floated in water. The pia is thickened and shows some cloudiness and oedema. The brain is atrophied; the sulci in anterior lobe gape widely and the ventricles are dilated. Weight of right hemisphere 17, of left 17, of cerebellum, pons and medulla, 5 ozs.; total 39 ozs. The microscopic appearance is that of Case I., minus the aggregations of red blood cells. In these two cases the severe bodily disease favors the occurrence of the hæmatoma at an earlier age than is usual. There is commencing arterio-sclerosis in each case. Wiglesworth10 comments upon the frequency with which tuberculosis is found as a complication. CASE III.-Male, white, æt. 73. Died of a general marasmus, the most important factors in its production being senility, chronic renal disease, and a large eroding ulcer of the face. Patient has been very intemperate for years, and had used tobacco to excess. Following several years of gradually progressing impairment of intelligence, an attack of maniacal excitement occurred. This quickly gave place to profound dementia, which persisted during the two years which elapsed before death. Towards the close utter fatuity and somnolence were noted. Urine contained casts and albumin. Autopsy. "Brown atrophy" of heart. Weight 61 ozs. Atrophy and softening of ribs and other bones. Cirrhotic liver and kidneys. A general endarteritis chronica. The dura showed no trace of inflammatory action. Lying beneath it, and covering the convexity of right hemisphere is a thin, bright red sheet of coagulated blood, too friable to admit of handling; no false membrane. On left side no trace of either false membrane or hemorrhage is discoverable. In the meshes of the pia, on each side, are several dark red ecchymotic spots. There is thickening, opalescence and oedema of the pia, and all of its larger blood-vessels are atheromatous. The brain weighs 42 ozs., and is much atrophied. CASE IV.-White man, aged 71, died of senility and renal disease, having been greatly demented for five years previous. No symptoms of heart lesion. Urine contained casts and albumin. Post-mortem examination.-Small circumscribed area of pneumonic consolidation in one lung; contracted kidney, 10. Loc. cit. |