Brain function is severely disturbed in ischemia. Within seconds, consciousness and spontaneous activity is lost, whereas interstitial concentrations of major ions are kept near normal levels. After a few minutes, there is a dramatic increase of potassium and a lowering of sodium, chloride, and calcium concentrations. Similar ionic changes are observed during spreading depression, however, that is spontaneously reversible and may be elicited in the otherwise normally perfused brain. In focal ischemia, the two events occur simultaneously. The central core of very low flow displays the ischemic increase of interstitial potassium concentration, whereas the surrounding tissue exhibits repeated episodes of spreading depression. This may induce energy failure by stimulating metabolism in areas with depressed flow thereby causing cell damage outside the ischemic core.

Animals↗

PubMedDate not supplied

In vitro neuronal production and differentiation by precursor cells derived from the adult human forebrain.

It has traditionally been held that the adult brain is incapable of significant self-repair, due in part to its inability to generate new neurons. Nevertheless, rodents and birds have been found to harbor neural precursor cells in adulthood. We asked whether the adult human brain might retain such precursors, by culturing samples of temporal lobe under conditions permissive for neuronal differentiation, while exposed to 3H-thymidine. Adult human temporal lobe cultures, derived from cortex, subcortex, and periventricular subependymal zone (SZ), were incubated for 7-28 d, stained for neuronal and glial antigens, and autoradiographed. Neuron-like cells were found in explant outgrowths and monolayer dissociates of SZ and periventricular white matter, but not cortex; they expressed neuronal antigens including MAP-2, MAP-5, NF, and N-CAM, and were GFAP-. Neurons responded to K+ depolarization with rapid and reversible increases in intracellular Ca2+, with much greater increments than those noted in glia. Although most neurons were not 3H-thymidine labeled, a small number of MAP-2+ and MAP-5+/GFAP- cells did incorporate 3H-thymidine, suggesting neuronal production from precursor mitosis. Rare 3H-thymidine+ neurons were also found in cultures of subventricular white matter; in these, GFAP+ astrocytic mitogenesis was common, while O4+ oligodendrocytes, although the predominant cell type, were largely postmitotic. Thus, the adult human forebrain harbors precursor cells that retain the potential for neuronal production and differentiation in vitro.

Adolescent↗

PubMedDate not supplied

Secondary brain stem hemorrhage in stroke.

The occurrence of secondary brain stem hemorrhage was studied in 435 autopsies from patients with recent cerebral hemorrhage, infarction or ruptured cerebral aneurysms. The frequency of secondary brain stem hemorrhage was found to be 45% in cerebral hemorrhage, 15% in cerebral infarction, and 36% in ruptured aneurysms. In the majority of cases the secondary brain stem hemorrhage occurred a few days after the onset of cerebral hemorrhage or infarction. Ruptured aneurysms showed a more widespread temporal distribution of secondary brain stem hemorrhage. The median survival time was 2 days in cases of cerebral hemorrhage, 4 days in ruptured aneurysm and 4 days in cerebral infarction. The frequency of secondary brain stem hemorrhage was significantly lower in patients younger than 20 years. No significant difference was found in its distribution between the sexes. Secondary occipital lobe infarction was present in 3.5% of the patients. It is concluded that secondary brain stem hemorrhage is a common major contribution to the cause of death in stroke.

Adolescent↗

PubMedDate not supplied

Cell density and cortex thickness in the border zone surrounding old infarcts in the human brain.

Six cases of completed ischemic stroke in the middle cerebral artery territory of more than two months' duration were selected for this study of neuropathology. Coronal brain slices of the entire brain were cut for histology and stained with Klüver-Barrera's stain. Neuronal and glial cell density, and cortex thickness were measured at various distances from the border of the infarct. Corresponding counting points in the contralateral hemisphere served as control in all cases. The density of histologically intact neurons was in all cases normal at a distance of 0.5 cm or more from the border of the infarcts. In one half of the cases the border zone between infarcted and normal tissue was less than a few cells in thickness. This study of old brain infarcts confirms the commonly held view that there is an abrupt transition between infarcted and normal tissue. This observation suggests that the wide zone of low blood flow and metabolism surrounding cerebral infarcts is not caused by selective loss of neurons. Instead, we hypothesize that such change in blood flow and metabolism is the result of neuronal disconnection and cortical deactivation.

Aged↗

PubMedDate not supplied

Cell density in the border zone around old small human brain infarcts.

Nine brain autopsy cases of small old cerebral infarcts were selected for neuropathological studies. Eight of the patients had cortical infarcts, in two cases with extension into the striate body. In one case the infarct involved the striate body only. The density of neurons and glial cells was measured in the coronal and the horizontal planes at various distances from the margin of the infarct. Corresponding counting points in the contralateral hemisphere served as control. On light microscopy, the infarcted cortex was irregularly shaped, but on serial sections the bulging parts appeared to be cut off from the infarcted tissue ("pseudo-infarct islands"). The zone of transition from infarcted to normal brain tissue was less than a few mm wide. In one patient, tomographic measurements of the cerebral blood flow (CBF) and a CT scan could be compared with the neuropathological findings. In this patient, CBF in the surroundings of the infarct was decreased despite a normal neuronal density. The study supports the traditional view held by pathologists that a sharp transition exists between infarcted and normal brain tissue and suggests that the hypoperfusion zone surrounding the region of complete infarction may be due to mechanisms other than selective loss of neurons.

Brain↗

PubMedDate not supplied

[Hydroquinone-sulfuric acid reagents. 3. Colorimetric determination of diethylstilbestrol].

Explore the source record for details and available documents.

Chemical Phenomena↗