Document NG6x1dbQ7ew8ye6xYEvRror5D

t- - Ui 0016819 I, AGBs SO NP-43-39 M-43-44 AOTOFSf DATS? ' 1/38/45 HOURS POST BQHV3H* DATE BBABI COT* 2/10/43- : . raMt.OF-MEH# X2S0 grans GLIMIC.&L DlACHGSlSi Hypertensive encephalopathy; possible lead poisoning. MJTOMiaAL DI&dfGSISs Confluent lobular pnsuscaia. b s p o r t m t b s mb c b j So s t o f mmDmmGWGt GROSS DBSCMPTIOHs Ths dural cap has not been preserved. The right frontal pole has been removed for lead studies. Viewed from above the right posterior parietal region . appears, a little, fuller than the corresponding region on the left, and the gjii are somewhat flattened. &t the right parietal occipital region there is a little grayiA discoloration of the sulci, suggestive of a localised meningeal reaction. The mesial portion of the lobe Just anterior to th parietal occipital fissure is soft to touch. This region is broadened and the sulcal markings ar less prominent. The leptoaaninges are not otherwise remarkable. The vascular pattern is norsal, the distribution of veins not being r markable. Inspection of the median cleft shows nothing remarkable, except for a definite fullness of the mesial portion of the parietal lob running: backward to the occipital parietal junction. The occipital lobes are not remarkable* The cerebellum has a suggestion of a pressure eon. The lamia stem has been cat very short, but what there is left, is not remarkable in appesraase. The pons is not neteworfehy. The leptoaejunges at the base are slightly thleksnsd. There is- no rascal herniation. The vessels at the base are of large calibre, the walls re moderately thickened, test there are no frank plaques. The distribution of the vessels of the circle is norasl. Vertical coronal sections were mads through the brain at 1.5 ss. thicknesses. The left hemisphere throughout appears normal, and the left lateral ventricle is of about normal sis, perhaps somewhat small. Throughout all the sections of the right hemisphere, the Ait matter sppears broader than the corresponding whit matter on H- 001^820 yionosGOPIC* -2 HP*43-3t the left sad the white jitter is soft to touch on this side* Use demarcation between grey and white is sharp, except' in. the posterior pwrittMt; t^gtos# .In Blocks PW* 2, 3* and "4 there :!is:, superficial soietmingliOf":t: tisia%; th last- mated.. block the#, 4.4 coapa In Slack. ?*I there is a striking disappearing of the upper the. mesial portion, of the tempore! .lot of the obliterated... fissure- there ig: a corresponds roughly to a eia&2iar son Multiple coronal sections were mad through the disarticulated csrebollua sad brain stem, files shoe th presence of a sassiw kimrrkdge irnrolt&tg 'the region of tho loft, dentate nuclei and spraed^:'Si^ll|i!^hiEt'S8. the aldlis. The greatest asur^sts are 4 x 1. Sections 'Pokes* Survey froa the light hemisphere of ?-l and frost the' sons of hesorifcas in the cerebellum. Photographic Indications* Coronal sections from the cerebellum to show the general nature of the dears of .the sight hemisphere and the extent of the hemorrhage &a the cerebellum. State of Hmtions-.ysir Braiu saved. Gross Feuropatholcgisal Diagnosis? Passive left istraeerebsilar hssorrhago; '-sdssa. of the ri^st hemisphere, associated with softening in. the right parietal region* - ' Survey sections ware taken from the fronto-tesporel region of the cortex, from the centrum seaiavalo, basal ganglia, pons, sad cerebellum. All sections were stained with cresyl violet and II. & 3. The microscopic examination revealed the following changes* (1) heptpaeningss? Tt pis arachnoid res\ thickened md hjparpl&gfets in so areas* The thickening was dus to distention of the meshes, infiltratioa with a variety of cells and hyperplasia of connective tissue, Th@ distended noshes contained many scattered cellular elements, most of the fibroblastic in nature* la sou' areas there Tore large acsmixlations of Kacropiiagos. The larger blood vessels appeared thickened sad soderstely a slerosed. The smaller vein dis closed a marked preliferation of the endothelial and adventitial cells, (g) Psr@aoh.ytaa* xho changes in the parenchyma, consisted of scattered areas of softening, .and hemorrhage. She former were, localised.chiefly within th subcortsx and were in different stages of organisatiom Some of then disclosed the characteristic feature of aetrts anemic infarction,! others more advanced organization and glial repair. 3 - BP-43-3 1-43-44. Tn addition there vss to be seen a diffuse ischemia degeneration of the narve cells? sots# of ..than especially in. the deeper layers uror ru'roundcd end partly invaded'by glia ffciis (c'-tclxitocir cud rjrr,,TO'^"-~ ph--gia). In. oor-6 ereor '.he ;y-.a'2.i.on cell:: disclosed e fer &c-.*'.noed lln-cf-Oticr*.. Sr of the cortr-- r scored ohujged r.i'.d '03.*'=0" 'piiEnJlr io vr?v. ;j ij regions* Sir rhito svbrSf.nce shored a narhad swelling of che oj-igcdcu::roold.c ccl3.fr, cssoci'.'--cd with -t. rAref-ic-5.on c..< the tic-vui. In. w.( s'"sac she;*' vers ?3t s s of pro gressive changes of '-ho glia, avcllisr; of She suclci t/roocietrS "ith :/r. cuce of ohrroui.V, ead CT'-opluoj'o process?s rith 0 t'-.r.co:.-7 do prelif.'. ration end mcTr Cation in row or clusters, flv V&rcul&r rr^'osn Ter/ striking ehs-uges rere disdocr-d rithin the eud-llaries. ihey Bhrred nested -.roliftr/tive cad progressive phenrosaar ca e/W-nced 1/ erdstbclisl cad cdv-'niiticl proliferation ar.d norr fora'dloa r.f c:~;illoriGS, Sic -c 'Griuy r.f ihc 00. H7.cri.rs ve.ro uef.o'20 of c'-'lltrii t-arl . rolifcrated er.dsthc23.cl coll r;;!cb contained chr.-natin- ps ,,-;p7.r-;. \ith :n -\4 roouni of epicpicon sS their role,?. The/ -era- ir'7'"j'_S3^r fl32c-d uir*i groupie?' provoles r.rc ronotiuivf; curro'.:::dr-rl ];, r Jc: rocrrol~.rojw. Ir. sou- erw f-'re vow to be s&on iivvlj fernra c-. "III mice vita bri:5rM,r etcire-1 Ir.prrli'O'-hiof endothelial OiTlc vith clrro/viv d Mro;' rf thcr. c isclosed ="-.er,"sc bv.cYing forr:.d;cn-- row '../o';' '> -.-..si---, vivid appeared do h& covered viih. ui ;,'.,.rdi ::c~' oQ.f -nlif. reded sr.pill. ri;s ccr.dcfif.ro hyper- _-3 nr tic erasi'-d o !voi.';Isirl et-llr. 11/. ~rJ.~.p of the ler^cr .w/j " vrs*e c,p- roci-ely -hicl:*--,r-d, Ur' U. rohrroi-.-j rciar tv. tj -,r>- llfnifsisn of \/.o r-ddroaSIbl'ii cells. .c :1 colic vsrc ssldoa i.:c: rcs'-id iu _3.:.o c i >iiJ r'd r ,voal :"rod .rclc.sr di/s chm ps. 1c ' the- larver blood vraorlc cimlvceC & .ads.".t* ce.rsc of cJ^crio- 50'L.U'ocis. .. fer cf dhc rrel?.vr vc i'.c f., v.i s si`.yc* fibroeiri and 3<:.'a:i:V osdisa of di*.*' veccr? -.i-Jf,. Ic'v; ;a csoil 1; ^.cc uhe jr.rjor jco'-ol/ c id .vc-r. di*s? T--. ^civ^..c'J.2.ar *.r.f:.2.*cj;':dio:i v itii Ivnoruo rv-o'is tdeaeats. SXMiM&s Tb& changes in different areas of the brain, tissue are both paxeachjastoas and interstitial. The former, diffuse degenerative charges of the serve cells throughout associated with circumscribed areas of softening and tissue necrosis, are essentially regressive or degenerative. Sh inter stitial changes are definitely progressive and proliferative in character, (li/perpiagtis end prdiiferstive phenomena* in; the:* endothelial sad. adven titial cells, new formation of capillaries, hyperplastic changes of the leptoaemnges) . t DlACHCSISs .ihilo the paremhyaatoas changes are raid specific in their character and nay resemble those to be found in any type of structural vascular lesions, (arteriosclerosis, hypertensive encephalopathy) the mesodermal changes of the capillaries and leptoneninges are nor characteristic and signi ficant and are compatible with lead encephalopathy. The latter ia characterised chiefly by prevalence of productive and proliferative phenomena in the endothelial and adventitial vascular tissue and in the leptoaaningos. Load encephalopathy* KE 0P168|2 I. Mart: Scheinker, 23. D.