Functional inhibition and release: unilateral tachistoscopic performance and stereoelectroencephalographic activity in a case with left limbic status epilepticus

During prolonged nonconvulsive unilateral left limbic status epilepticus, a natural model of functional hemispheric inhibition, we performed two tachistoscopic experiments, a lexical decision task associated with a RVF (left hemisphere) superiority and a facial matching task associated with a LVF (right hemisphere) superiority. We found that epileptic activity in the left hemisphere, especially rhythmic high-frequency "tonic" discharges, inhibited performance on the lexical task but not on the facial matching task. This suggests that only cognitive activity in the discharging hemisphere is inhibited. Strikingly, the best performance of the right hemisphere was obtained while the left hemisphere was most inhibited, suggesting a functional balance of inhibition and release.     

Sensitivity to eye gaze in prosopagnosic patients and monkeys with superior temporal sulcus ablation

Accuracy at perceiving frontal eye gaze was studied in monkeys and human subjects using a forced-choice detection task on paired photographs of a single human face. Monkeys learned the task readily, but after bilateral removal of the banks and floor of the superior temporal sulcus (STS) they failed to perform the task efficiently. This result is consistent with the conclusion, based on recordings from single cells in awake, behaving monkeys [Perret et al., Physiological Aspects of Clinical Neuro-ophthalmology, Chapman & Hall, London, 1988] that this region of the temporal lobe is important for coding information about eye-gaze of a confronting animal. Human subjects were given identical stimuli in a task where they were asked to detect "the face that is looking straight at you". Human performance is sensitive to the degree of angular deviation from the frontal gaze position, being poorest at small angular deviations from 0 degrees. This was also true of monkeys viewing these stimuli, pre- and post-operatively. Compared with normal controls, two humans prosopagnosics were impaired at this task. However the extent of impairment was different in the two patients. These findings are related to earlier reports (including those for patients with right-hemisphere damage without prosopagnosia), to normal performance with upright and inverted face photographs, and to notions of independent subsystems in face processing.     

Serum influences the differentiation of membrane structure in cultured astrocytes

The membranes of mammalian astrocytic processes apposed to blood vessels or forming the surface of the brain contain high concentrations of a characteristic intramembrane particle aggregate, termed "assemblies." In order to identify developmental processes which contribute to this remarkable regional specialization of membrane structure, we have devised culture conditions which support the differentiation of assemblies in secondary cultures of astrocytes derived from neonatal rat forebrain. We report here that different lots of fetal calf serum vary dramatically in their capacity to support the differentiation of assemblies. Fetal calf serum thus appears to exert two distinct influences on astrocyte development: it promotes the differentiation of type 2 astrocytes from bipotential precursor cells, as shown by others, and it influences the density of assemblies in type 1, flat, GFAP-immunoreactive astrocytes in our secondary cultures. Horse serum and defined media also support the appearance of assemblies in flat, GFAP-immunoreactive astrocytes. The separate effects of serum supplementation upon cell lineage and membrane differentiation have to be carefully considered in studies designed to examine factors influencing astrocytic development in vitro.     

THE EFFECT OF PROSTAGLANDIN E1 ON PULMONARYBLOOD FLOW AFTER RETROGRADE FLUSH ANDCOLD STORAGE OF LUNGS

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CLINICO-EPIDEMIOLOGICAL ALGORITHM FOR PREDICTING SYSTEMIC ARTERIAL HYPERTENSION AT HIGH ALTITUDE THROUGH MATHEMATICAL MODELLING

A population based hybrid design combining element of cohort and cross-sectional approach was used to develop a simple clinical algorithm to predict individual probability of developing hypertension (systolic BP > 140 mm Hg and/or diastolic BP > 90 mmHg). 3615 soldiers initially normotensive at the time of induction into high altitude, were studied by systematic random sampling. Multiple logistic regression analysis showed a high significant association between hypertension and age, body mass index (BMI), tobacco smoking and alcohol consumption. Using the constant/coefficient values obtained from the logistic model and the receiver operating characteristics (ROC) curve analysis, the following predictive rule was developed – To the age in years, add (BMIx 3.86); also add 5.53 if he is a smoker; and add 19.81 if he consumes alcohol. If the total exceeds 142, the individual is at high risk of developing hypertension. This algorithm carries a sensitivity of 68.2% and specificity of 78.5%.KEY WORDS: Hypertension, High altitude     

Autoimmune haemolytic anaemia in a child with MHC class II deficiency

A 3 year old Turkish girl is described who was suffering from major histocompatibility complex (MHC) class II deficiency syndrome, which is characterised by the lack of expression of HLA class II antigens on mononuclear cells. The presence of HLA class II genes was demonstrable at the DNA level. Combined immunodeficiency was indicated by hypogammaglobulinaemia and the absence of delayed type hypersensitivity on skin testing. Further, she was unable to produce specific antibodies towards foreign antigens and suffered from recurrent pulmonary, gastrointestinal, and septic infections from the third month of life. The clinical course was complicated by a Coombs test positive haemolytic anaemia due to the production of autoantibodies against the rhesus "e' antigen, a non-glycosylated protein antigen. Haemolysis could be controlled by oral steroid treatment. This case is of interest as it shows that despite the absence of HLA class II antigens and combined immunodeficiency autoimmune reactions with production of specific autoantibodies directed to protein antigens are possible.     

From cortical plasticity to unawareness of visual field defects.

It was long held that, following alterations in sensory input, structural changes in the primary visual cortex take place only in early life, during so-called "critical periods." Recently, however, it has been established that, in adults, cortical maps in the brain are not fixed, and the cortex does not perform stereotyped operations. Instead, neuronal receptive fields in the cortex can reorganize following deactivation or an altered pattern of activation. Plasticity is essential for the normal adjustment of the brain to modifications in the sensory environment, and for improving perceptual skills and sensorimotor performances. It also plays a crucial role in recovery from damage to the visual system. Cortical remapping generates a filling-in of visual field defects. Consequently, it alters the image perceived. Cortical rearrangement following lesions in the visual pathways does not restore function to the destroyed tissue, but it helps to compensate for gaps in perception. In this review article, we focus on effects of plasticity in the adult visual cortex which are of major importance in the daily practice of neuroophthalmology. Cortical reorganization, together with resulting filling-in, affects the early recognition and evaluation of visual field defects. The importance of brain remapping in these matters is still largely underestimated by clinicians.     

Plasticity in the adult visual cortex: implications for the diagnosis of visual field defects and visual rehabilitation

It has recently been shown that, contrary to long-held beliefs, sensory and motor maps are not stable in the adult cerebral cortex. Alteration of input from the periphery results in changes in topography in the cortex, including the primary visual cortex. Mechanisms involved consist mainly of reshaping the receptive field of cortical cells and increasing the sensitivity of deprived cells in the visual cortex. Cortical plasticity allows the brain to adapt to background modifications or to damage of the nervous system. It also underlies learning and attention processes. Cortical changes occurring after focal visual differentiation modify visual perception by filling in visual field defects with information from the area surrounding the scotoma. This modification causes affected subjects to ignore or underestimate their defects. With visual field defects, cortical plasticity also causes distortion in spatial perception. Although the effects of cortical plasticity are prominent in neuro-ophthalmological daily practice, they are usually unrecognized or greatly underestimated. These effects cause delay in recognizing visual field defects, and hence in receiving therapy, while affecting the results of some procedures for testing the visual field. Affected individuals who are unaware of their defects may have increased difficulty in coping with activities in everyday life. Up to now, phenomena related to plasticity in the visual system have been investigated mainly by psychophysicists and neurophysiologists. It is essential to start considering the various effects of cortical reorganization in clinical practice. It is especially important to introduce into clinics the concept of dissociation between actual and perceived defects in the visual field, resulting from the filling-in process, and the need to measure it. This dissociation should also be demonstrated to the affected subjects.     

Further Evidence that Most Luteinizing Hormone-Releasing Hormone Neurons are not Directly Estrogen-Responsive: Simultaneous Localization of Luteinizing Hormone-Releasing Hormone and Estrogen Receptor Immunoreactivity in the Guinea-Pig Brain

Gonadotropin secretion from the pituitary is regulated in large part by steroid action on the brain. An important question concerns whether luteinizing hormone-releasing hormone (LHRH) neurons themselves transduce steroid signals, or whether, alternatively, steroid-sensitive interneuronal populations regulate their activity. A previous study in the rat employing steroid autoradiography combined with LHRH immunocytochemistry revealed that only an exceedingly small percentage of LHRH-immunoreactive (ir) neurons was estrogen concentrating. This study has examined the relationship of estrogen receptive and LHRH-ir cells in the male and female guinea-pig brain with double label immunocytochemistry. Since estrogen receptor-ir, as demonstrated with antibody H222, is known to be confined predominantly to the cell nucleus, whereas LHRH-ir is localized mainly in the cytoplasm, single cells can be double-labeled. Diaminobenzidine tetrahydrochloride was used for localization of LHRH-ir while nickel-enhanced diaminobenzidine tetrahydrochloride was used for localization of estrogen receptor-ir. The results revealed that there were many brain nuclei that contained both LHRH and estrogen receptor-positive cells, including the preventricular periventricular nucleus, the anterior subcompact nucleus of the medial preoptic nucleus (MPNa), the remainder of the medial preoptic nucleus, the retrochiasmatic area, and the anterior, dorsomedial, ventrolateral and arcuate nuclei. However, of a total of 2,604 LHRH-ir cells that were examined, we observed only 5 double-labeled cells (<0.2%). The double-labeled cells were not restricted to a single nucleus; they were present in the MPNa, the retrochiasmatic area and the arcuate nucleus. Moreover, at the light microscopic level, LHRH cells quite frequently appeared to be apposed to estrogen receptor-positive cells (8.8% in the female), especially in the MPNa. These results lend further support to the notion that estrogen-mediated regulation of the LHRH system is achieved primarily through estrogen receptive interneurons. However, due to the existence of LHRH-LHRH synaptic interactions, the possibility also exists that a small population of estrogen-sensitive LHRH neurons could contribute to generalized activation of the LHRH system.     

Effects of dexamethasone on the differentiation of membrane structure in cultured astrocytes.

Astrocytic processes investing vascular structures or forming the surface of mammalian brain have large numbers of orthogonally packed aggregates of intramembrane particles, termed "assemblies." Similar particle aggregates are expressed by astrocytes derived from neonatal rat forebrain in secondary culture, but they are much more uniformly distributed across the membranes of the cultured cells. Dexamethasone, a potent glucocorticoid, affects the differentiation of astrocyte membrane structure in two patterns, depending on the rate of proliferation in the culture. When confluent secondary cultures of astrocytes are exposed to 5 microM dexamethasone, the densities of assemblies increase, and in some cells approach the values present in the glial limitans in vivo. However, when rapidly proliferating astrocytes are exposed to dexamethasone during the first week of secondary culture, most of the astrocytes fail to express any assemblies. The rate of astrocyte proliferation is slowed, and a lower cell density is reached during the first 2 weeks of secondary culture in dexamethasone. The suppression of assemblies is transient: as the cultures approach confluence, the proportion of cells expressing assemblies increases to nearly control levels, and the density of assemblies increases to greater than control values in some astrocytes. Certain of the effects of dexamethasone on cultured astrocytes may have relevance for understanding the mechanism(s) of its action in treating cerebral edema.