J. Neurol. Neurosurg. Psychiat., 1954, 17, 295. CASE REPORT: PRENATAL OCCLUSION OF THE INTERNAL CAROTID ARTERY BY R. M. CLARK and ERIC A. LINELL From the Department of Pathology and the Division of Neuropathology, University of Toronto erythroblastic series. The liver, kidneys, adrenals, and spleen showed extramedullary haematopoiesis. There were enormous numbers of erythroblasts and a diminution in formation of lymphocytes. The latter finding was considered to account for the hypoplasia of the thymus. The presence of a small infarct in the spleen was confirmed microscopically, but an arterial embolic occlusion could not be demonstrated even by interrupted serial microscopic sections. A detailed histological examination of the placenta She was the fourth child of an Rh-negative mother and an Rh-positive and homozygous father. The first confirmed oedema of the villi. The capillaries contained child was born at full term. The second was stillborn at numerous erythroblasts. A few small areas of infarction, full term. The mother was given A.C.T.H. before the with necrosis of placental villi, were found, a possible birth of her third infant, who was born alive at full term site of origin of an embolism of the foetal circulation. but required a replacement transfusion and had a Examination of the Head.-The scalp tissues were positive Coombs test. and haemorrhagic. There was subperiosteal oedematous For five weeks before the premature delivery of this and slight extradural haemorrhage in relation to the fourth infant the mother had received 100 mg. of bones of the cranial vault. There was no subdural cortisone daily. The pregnancy was normal and there haemorrhage and the tentorium cerebelli was grossly was no antenatal haemorrhage to suggest premature normal. separation of the placenta. Her albumin antibody titre Brain.-This was examined after fixation in 10% was 1 64. The infant was born by mid-forceps delivery. The very large, oedematous placenta was manually formol-saline for 48 hours. The organ showed preexpressed. The obstetrician considered it otherwise maturity, weighing only 215 g. but the convolutions (Fig. 1) were moderately well formed throughout. There grossly normal. was palpable softening of the cortical distribution of the Necropsy left middle cerebral artery (Fig. 1), and a horizontal Necropsy was performed three hours after death. The section through the cerebral hemispheres (Fig. 2) coninfant was immature, weighing only 2,250 g., in spite of firmed early softening in the complete distribution of this severe generalized oedema of subcutaneous and muscular vessel. A dissection of the left internal carotid and tissues and large effusions in the serous cavities. There middle cerebral arteries showed the lumen of the internal was also oedema of the larynx. The placenta was very carotid to be occluded by well-defined, white, solid much enlarged by oedema and weighed 945 g., whereas material. This occluding tissue extended to the terminathe weight of the normal placenta is considered to be tion of the internal carotid and for a short distance into one-seventh the weight of the infant, which would be its posterior communicating, anterior and middle cerebral about 320 g. in this case. No further gross pathological branches. The extent of the occlusion was determined by lesions were found in the placenta to account for its limited serial histological sections and satisfactorily accounted for the softening in the distribution of the enlargement. The large spleen weighed 45 g. and contained a small left middle cerebral branch. The white colour and the infarct. The liver was also enlarged. The hypertrophied sharp limitation of the occluding tissue were much more heart weighed 31 g. and its cavities were dilated, possibly suggestive of embolus than of thrombus forming in situ on due to increased blood volume. The foramen ovale was the vessel wall, as the softening in the middle cerebral widely patent and there was a small patent ductus distribution was estimated as being of only a few days' arteriosus. The lungs were atelectatic. The thymus was duration. The material occluding the lumina of these vessels does hypoplastic, weighing only 1 g. Microscopical examination showed hyperplasia of the not have the histological characters either of a thrombus bone marrow, with marked proliferation of cells of the formed in situ or of a blood embolus from a distant The following case is reported as a contribution to our knowledge of the aetiology of " congenital" hemiplegia. Case Report A baby girl, I. (NP. No. 363/53, A. 168/53), died about one and a half hours after her birth on May 13, 1953. The pathological findings were those of erythroblastosis foetalis. 295 296 R. M. CLARK AND ERIC A. LINELL ~~ ~ ~ ~ ~ ~ ~~~~~.,7~ 4* _ .*... b. r X; . FIG. I.-Cerebral hemispheres seen fr om above, showing early cortical softening with a few pete4 chial haemorrhages in the distribution of the left middle cerebra1l artery. FiG. 3.-Transverse section of the left internal carotid artery at its bifurcation. The lumen of the vessel is occluded by embolic material, the exact origin of which could not be determined. FIG. 2.-Upper cut surface of horizontal section of cerebral hemispheres. This shows softening of a few days' duration in the complete distribution of the left middle cerebral artery (to the right of the photograph). There is a large fifth ventricle. FIG. 4.-Medium-power photomicrograph of the embolic tissue (Fig. 3). It appears to be composed of "dead" cells with degenerating hyperchromatic nuclei. Some of the nuclei are those of erytbroblasts from the circulating blood. This occluding material may be dead tissue from the infant's severely diseased placenta. PRENATAL OCCLUSION OF INTERNAL CAROTID ARTERY focus (Figs. 3 and 4). The main mass of the material appears to be dead tissue, the origin of which cannot be determined. It is infiltrated with moderate numbers of red blood corpuscles, many of which contain nuclei. The vessel wall shows early reactive inflammatory changes, maximum in amount at the point of adhesion of the occluding material to the intima (at bottom of Fig. 3). This suggests the possibility of thrombus formation in situ but such changes could be produced by the pressure of an embolus. The extent of the reaction indicates that the occlusion had been present for at least some days. The softened cortex and white matter in the left middle cerebral distribution shows the severe vacuolation of early softening. Fully formed lipoid-filled histiocytes are seen in the cortical tissue and white matter, and there are similar microglial cells, filled with lipoid, in the 297 subarachnoid space overlying the softened cortex. Sections stained with Scharlach R confirm early phagocytosis of fatty degenerative products by microglial cells in the white matter. This would date the softening as being of three days to one week of age. It seems likely, therefore, that the middle cerebral occlusion occurred, in this case, during the last few days of pregnancy. Embolism appears more probable than thrombosis in situ, and, in the absence of another source, an embolus of infarcted, necrotic placental tissue is suggested. The infarct found in the spleen was probably also due to arterial embolic occlusion, although an occluded artery could not be found even after detailed microscopical examination.