Yoshinari Kamijyo

Cerebral infarction. Evolution of histopathological changes after occlusion of a middle cerebral artery in primates.

Occlusion of a middle cerebral artery is performed with a surgical clip which is placed through a transorbital approach. This results in a reproducible cerebral lesion (infarction) which was analyzed sequentially in a group of primates at intervals ranging from 2 1/2 hours to 16 days. The earliest cytological alterations, involving neurons, neuropil and astrocytes, can be demonstrated convincingly 2 1/2 hours after the arterial occlusion in paraffin-embedded sections, stained with hematoxylin and eosin. A detailed description of the topographic-cytologic abnormalities and the sequence of inflammatory changes elicited by this form of cerebral ischemia, as well as a delineation of the beginning of the post-ischemic healing processes are provided. A three-zone separation of the histological features is suggested. In addition, we illustrate the cellular alterations in the hemisphere opposite to the arterial occlusion and discuss the axonal changes observed in the different zones of the evolving ischemic encephalomalacia. Abnormalities in the microcirculation are also discussed.

Temporary regional cerebral ischemia in the cat. A model of hemorrhagic and subcortical infarction.

A comparison was made on some of the effects that temporary and permanent occlusion of the middle cerebral artery may have on the circulation to the ipsilateral hemisphere in the cat. Reperfusibility of the corresponding capillary bed was unimpaired for the initial six hours after occluding the vessel, as demonstrated by in vivo intravenous injection of carbon black. Short-term occlusion of the middle cerebral artery, followed by re-opening of the vessel, resulted in either (a) no demonstrable parenchymal lesions (i.e., areas of softening), (b) smaller lesions, or (c) infarctions that were either hemorrhagic or confined to the subcortical white matter of the ipsilateral hemisphere.

Cerebellar hemangioblastoma: Histogenesis of stroma cells

Light and electron microscopic features of a cerebellar hemangioblastoma were evaluated with special emphasis on the matter of the origin of interstitial (stroma) cells. Many of the capillary components were of embryonal type, and the stroma cells shared several morphological features with them. It was concluded that the stroma cells originate from vasoformative elements (endothelium and pericytes) and that the endothelial cells are active components of the neoplasm. No convincing morphological counterpart for the erythropoietic activity of this neoplasm was uncovered. Structures identical to ciliary rootlets were identified in many endothelial cells.

Carotid Arterial Supply of the Feline Brain: Applications to the Study of Regional Cerebral Ischemia

A study of the supply to the feline brain by the carotid-middle cerebral arteries was conducted using in vivo transcardiac injection with a mixture of micropaque and carbon black. Modifications in the filling pattern of the arterial vessels were visualized following short-term occlusion of a middle cerebral artery. A modified surgical method to induce occlusion of the M-1 segment of the middle cerebral artery is also described.

Cellular events during partial cerebral ischemia

SummaryThe feline right cerebral hemisphere was subjected to regional (incomplete) ischemia after clipping the middle cerebral artery for 5, 10, 15, 30 or 60 min, respectively. After each ischemie episode, a 10-min recirculation period was allowed, following which the brain was fixed and processed for electron microscopy.The earliest alterations, detected in the cerebral cortex after 15 min, increased in severity with longer ischemic episodes and were distributed multifocally. There was: (a) marked neuronal mitochondrial matrical swelling and progressive condensation of cytoplasm and nucleoplasm; (b) cytoplasmic swelling of astrocytes with preservation of glial mitochondrial volume; (c) capillaries, oligodendrocytes, myelin sheaths and axis cylinders did not change significantly, even after the longest interval studied: 60 min.This type of tissue reaction appears to be common for those forms of cerebral ischemia, in which circulation is either sustained partially (via collateral arteries) or restored after a period of absolute ischemia. Under these conditions, as yet undefined permeability changes in cell membranes lead to pronounced volumetric alterations of cellular compartments. Although no softening is detectable by digital examination, we suggest that such a set of structural abnormalities constitutes encephalomalacia, or the earliest stage of a lesion which is designated infarction, once it reaches irreversibility.

The ultrastructure of “brain death”

SummaryPermanent, complete global cerebral ischemia was induced in cats by filling the cardiovascular system with a plasma substitute (37° C). At variable intervals and up to 120 min thereafter, these feline brains were perfused with aldehydes and processed for electron microscopy. The resulting cellular alterations were homogeneous and uniform throughout the entire brain; they included early chromatin clumping, gradually increasing electron lucency of the cell sap, distention of endoplasmic reticulum and Golgi cisternae, transient mitochondrial condensation followed by swelling and appearance of flocculent densities, and dispersion of ribosomal rosettes. The marked contrast between the structural alterations in permanent, complete ischemia and incomplete cerebral ischemia, suggest differences in their pathogenesis. A basic determinant factor of the structural changes appears to be the volume of flow (serum, plasma, other) which is available at the time of the injury. This analysis of global cerebral ischemia provides some insight on the nature of cellular changes occurring shortly after somatic death.

Unusual demyelinating disease: A form of diffuse‐disseminated sclerosis

A young man, in good health until the age of 22, developed progressive personality changes, lethargy, motor difficulties, urinary bladder dysfunction, and convulsions. Spinal fluid abnormalities included monocytic pleocytosis and selective increase of gamma globulins. The clinical features and the structural lesions in the central nervous system are reminiscent of disseminated-diffuse sclerosis. Oligodendrocytes appeared normal in number and showed nonspecific abnormalities. Comparison of the structural lesions found in this case with those described in several reports of demyelination indicates that the separation of this syndrome, as a distinct entity, may not be justified. We suggest that such cases be classified as myelinoclastic disorders, in the same category with multiple sclerosis and its variants.