Brain-stem auditory evoked potential monitoring. Variations of stimulus artifact in brain death

Brain-stem auditory evoked potentials (BAEPs) were recorded in 20 subjects with brain death (mean age, 33.2 ± 15.1 years) and 20 healthy volunteers (mean age, 29.8 ± 6.8 years). Brain death was due to head injury (n = 14), encephalitis (n = 3), brain-stem hemorrhage (n = 1), cerebellar hemorrhage (n = 1) or cerebral infarction (n = 1). The presence, latency and amplitude of the individual BAEP components and variations of the stimulus artifact were evaluated. The mean ( ± S.D.) amplitude of the stimulus artifact was 0.26 ± 0.12 μV in the brain-dead subjects and 0.09 ± 0.05 μv in the control group (P < 0.001, t test). The causes of the phenomenon of increasing stimulus artifacts in the evolution of brain death remain unclear.     

SEP testing in deeply comatose and brain dead patients: the role of nasopharyngeal,scalp and earlobe derivations in recording the P14 potential

Median nerve somatosensory evoked potentials (SEPs) were tested in 50 patients (20 brain dead, 18 comatose and in 12 progessing from coma to brain death, i.e., 32 cases with brain death and 30 cases with coma were recorded).Derivations were taken from nasopharynx, earlobes, scalp, and neck using cephalic and non-cephalic references. Cortical and subcortical SEP components were evaluated, focussing on the P14 potential. There is evidence that rostral and caudal parts of the P14 generator (lemniscus medialis) are differently affected in brain death, resulting in an abolition of the rostral part, while occassionally leaving intact for some time the caudal part. Non-cephalic referenced scalp records pick up the whole P14 dipole, whereas nasopharyngeal and earlobe derivations pick up different parts of P14, depending on the reference used. Scalp-to-nasopharynx records derive the most rostral part of P14; this “rostral P14” was bilaterally lost in all brain dead patients, but preserved in all deeply comatose patients with diffuse brain-sttem injuries. Scalp-to-earlobe records in contrast, picked up a P14 dipole segment reaching more caudally, resulting in a P14 potential also in brain dead patients. It is concluded that midfrontal scalp-to-nasopharynx derivations give the moset valuable contribution to the electrophysiological assessment of brain death versus deep coma.     

Chromosome aberrations and radiation-induced cell death. II. Predicted and observed cell survival

The surviving fraction of synchronous V₇₉ Chinese hamster cells was measured in two post-irradiation generations after a 300-rad X-ray dose in G₁ by comparing the colony multiplicity in irradiated and control cultures. In addition, the ability of the irradiated population to form colonies was measured immediately after G₁ irradiation or at 6, 32, 75 or 96 h after X-irradiation. Formulae were used in conjunctionwith previously observed transmission and survival parameters of chromosome aberrations² to predict the amount of cell death at any given time after irradiation. The results indicate that the survival pattern of these cells can indeed be predicted on the basis of cell loss from chromosome aberrations.It is likely that an asymmetrical chromosome exchange (dicentric, centric ring, or tricentric) and a chromosome deletion are equally capable of causing cell death, whereas translocations or inversions apparently do not lead to inviability. Furthermore, cell death is rapid: 45% of the total observed death occurs in the first two post-irradiation generations. The initial decrease in viability is caused predominantly by the formation of anaphase bridges, while cell death from fragment loss becomes increasingly important in later generations. In fact, it is probable that, on the average, a cell that loses a single acentric fragment will survive one generation.     

Developmental changes in brain angiotensin II receptors in the rat.

AII binding and distribution were measured in rat brain during development by autoradiographic techniques using radioiodinated [Sar1,Ile8]AII. At all ages, from 2 days to 7 weeks, binding was present in the circumventricular organs, and areas related to pituitary hormone secretion and modulation of sympathetic activity. At early stages of development, AII binding was transiently expressed in a number of motor- and sensory-related areas. These findings support a role for AII in the control of water intake and autonomic activity at all stages of development, and suggest that the peptide may be involved in the maturation of neuronal function during development.     

The ultrastructure of "brain death". II. Electron microscopy of feline cortex after complete ischemia.

Permanent, complete global cerebral ischemia was induced in cats by filling the cardiovascular system with a plasma substitute (37 degrees 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.     

Calcium permeability changes and neurotransmitter release in cultured brain neurons. II. Temporal analysis of neurotransmitter release

The coupling between depolarization-induced calcium entry and neurotransmitter release was studied in rat brain neurons in culture. The endogenous dopamine content of the cells was determined by high performance liquid chromatography utilizing electrochemical detection. The amount of dopamine in unstimulated cells was found to be about 16 ng/mg of protein. Depolarization of the neurons by elevated K+ caused a Ca2+-dependent release of dopamine from the cells. Following 1 min of depolarization, the cellular dopamine content and the amount of [3H]dopamine in cells preloaded with the radioactive transmitter were reduced by 35%. The release of [3H]dopamine by the neurons was measured at 1.5-6-s intervals by a novel rapid dipping technique. Depolarization in the presence of Ca2+ (1.8 mM) enhanced the rate of neurotransmitter release by 90-fold (0.072 +/- 0.003 s-1) over the basal release in the presence of Ca2+. The evoked release consisted of a major rapidly terminating phase (t1/2 = 9.6 s) which comprised about 40% of the neurotransmitter content of the cells and a subsequent slower efflux (t1/2 = 575 s) which was observed during following prolonged depolarization. Predepolarization of the cells in the absence of extracellular Ca2+ did not affect the kinetics of the evoked release. The fast evoked release could be re-elicited in the cells after 20 min "rest" in reference low K+ buffer. The effects of varying the extracellular Ca2+ concentrations on the kinetic parameters of the evoked release were measured. The amount of neurotransmitter released during the fast kinetic phase was very sensitive to the external Ca2+ (from 0% in the absence of Ca2+ to 40% of the neurotransmitter content at Ca2+ 0.3 mM). The rate constant of the fast release did not depend on the extracellular Ca2+, whereas the rate constant of the slow release increased from 0.0004 +/- 0.0001 s-1 at 0.4 mM Ca2+ to 0.0012 +/- 0.0002 s-1 at 0.8 mM Ca2+. The fast evoked release was inhibited by verapamil in a concentration-dependent manner. By contrast, verapamil enhanced the basal and the slow release independent of the presence of Ca2+. Both fast and slow phases of the evoked release were blocked by Co2+. Addition of Co2+ within the first 6 s after the onset of depolarization inhibited the fast release but failed to do so when added later on.(ABSTRACT TRUNCATED AT 400 WORDS)     

Analysis of translocations observed in three different populations. II. Robertsonian translocations

A sample of 229 Robertsonian translocations was classified into three groups according to the method of their ascertainment (Group I = couples with repeated abortions; Group II = karyotypically unbalanced probands; Group III = balanced translocation heterozygotes). Statistical analysis showed that the distributions of Robertsonian translocations differed significantly from random in all three groups. Additionally, the distributions were significantly different between couples with repeated abortions and karyotypically unbalanced probands and between unbalanced probands and balanced translocation heterozygotes.     

Metabolic impairment elicits brain cell type-selective changes in oxidative stress and cell death in culture

Abnormalities in oxidative metabolism and inflammation accompany many neurodegenerative diseases. Thiamine deficiency (TD) is an animal model in which chronic oxidative stress and inflammation lead to selective neuronal death, whereas other cell types show an inflammatory response. Therefore, the current studies determined the response of different brain cell types to TD and/or inflammation in vitro and tested whether their responses reflect inherent properties of the cells. The cells that have been implicated in TD-induced neurotoxicity, including neurons, microglia, astrocytes, and brain endothelial cells, as well as neuroblastoma and BV-2 microglial cell lines, were cultured in either thiamine-depleted media or in normal culture media with amprolium, a thiamine transport inhibitor. The activity levels of a key mitochondrial enzyme, alpha-ketoglutarate dehydrogenase complex (KGDHC), were uniquely distributed among different cell types: The highest activity was in the endothelial cells, and the lowest was in primary microglia and neurons. The unique distribution of the activity did not account for the selective response to TD. TD slightly inhibited general cellular dehydrogenases in all cell types, whereas it significantly reduced the activity of KGDHC exclusively in primary neurons and neuroblastoma cells. Among the cell types tested, only in neurons did TD induce apoptosis and cause the accumulation of 4-hydroxy-2-nonenal, a lipid peroxidation product. On the other hand, chronic lipopolysaccharide-induced inflammation significantly inhibited cellular dehydrogenase and KGDHC activities in microglia and astrocytes but not in neurons or endothelial cells. The results demonstrate that the selective cell changes during TD in vivo reflect inherent properties of the different brain cell types.     

Antibody changes in paragonimiasis patients after praziquantel treatment as observed by ELISA and immunoblot

To observe antibody changes after praziquantel treatment in paragonimiasis, a total of 46 serum samples from 13 serologically diagnosed patients was collected for 4-28 months. The specific antibody (IgG) levels were measured by enzyme-linked immunosorbent assay (ELISA). All but one patient who needed retreatment became symptom-free within a week. Antibody levels were dropped near to or below a cut-off absorbance (abs.) of 0.25 in varying intervals from 4 to 18 months. Of 9 patients who were retested within 3 months, 5 revealed temporary elevation of antibody level. After the elevation, the levels began to decline slowly to negative ranges. If treated earlier after symptoms developed, the temporary elevation did not occur and intervals to negative conversion were shorter. By sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE)/immunoblot, antigen-antibody reactions in individual patient faded gradually without significant changes in reacting antigen bands.