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PubMedDate not supplied

Possible models for multiple chemical sensitivity: conceptual issues and role of the limbic system.

Conceivably, chemicals contacting olfactory nerve projections in the nose could either be transported into or relay electrical signals to the limbic region, leading to a vast array of symptoms. Likewise, thought processes and mood states may trigger or interrupt pre-existing limbic activity. At present, however, no evidence suggests that limbic activity triggered by environmental exposures can be entirely overcome by psychologic interventions. One important ramification of a limbic hypothesis, if true, is that no convenient biologic marker for multiple chemical sensitivity may exist at the present time. Ten years from now, we may finally confirm the existence of multiple chemical sensitivities (by careful, blinded challenges) but still have no single mechanism to explain it; that is, after all avenues of biochemical and immunologic inquiry have been exhausted, no single cause or marker for this disorder may be apparent. The theory that adaptation plays a role in MCS is based on the observed responses of patients in a deadapted state who have been housed in an environmental unit. Although adaptation is only an observation at this time, not a mechanism, biologic limits might regulate how much an organism can adapt. Such limits could be highly individual and vary by orders of magnitude. Certainly adaptation occurs at all levels of biologic systems, from enzyme systems to cells, tissues, organs, and even behavior (Fregly, 1969). Theoretically, a major insult or the accumulation of lower-level injuries within these systems could lead to a kind of "overload" or "saturation" effect with respect to adaptive capacity. This might cause an individual to have environmental responses, which, instead of being flexible and fluid, would become fragile and overly responsive. Many MCS patients report that years, and in some cases decades, after the onset of their problems, they have recovered only a portion of their former energies and tolerance for their environment. Their descriptions seem to suggest the loss of an intangible capacity to adapt, parts of which may be temporary and recoverable and other parts of which may not. Perhaps our patients have been telling us the diagnosis.

Adult↗
PubMed2003

[Influenza-associated encephalopathy--pathophysiology and disease mechanisms].

From the middle of 1990's, there repeated in winter season an outbreak of encephalopathy in Japan that appeared to be associated with influenza. A national survey was conducted, and a total of 507 patients was diagnosed as having influenza-associated encephalopathy during 1998-2002 on the basis of virologic analysis. Type A influenza was more pathogenic than type B, and A: H3 type was more invasive than A: H1 type. Encephalitis developed mainly in children below 5 years of age, either on the day that influenza signs appeared or on the next day. We hypothesized that the replicated viruses at nasopharyngeal epithelium disrupt the olfactory mucosa. Via olfactory nerve system, the stimuli may be transmitted to the brain eventually to activate glial cells, and to induce the production of pro-inflammatory cytokines. The cytokine storm results in neural cell damage as well as apoptosis of glial cells due to TNF-induced mitochondrial respiratory failure. The disruption of blood-brain barrier progresses to the systemic cytokine storm, resulting in DIC and MOF.

Animals↗
PubMed1992

Primary olfactory terminations in the forebrain of amphibia: a comparative study with soybean agglutinin.

Ambystoma and Xenopus were used to investigate olfactory terminations in the forebrain by exploiting the selective binding of soybean agglutinin to primary olfactory projections. Lectin binding and tridimensional reconstruction provided new information on the distribution of olfactory glomeruli and on regional and interspecific differences. Ambystoma showed an uniform labelling of all olfactory terminations, which were localized in the rostro-lateral forebrain without obvious segregation of different terminal fields, except at dorsal levels. On the contrary, the binding pattern of Xenopus confirmed the existence of three sets of primary olfactory neurons characterized by clear differences in lectin binding. Selective soybean agglutinin binding and a detailed tridimensional reconstruction provided evidence for the existence of a set of neuronal projections, described for the first time, which terminate in a discrete bilateral region of the forebrain localized below the main olfactory bulb. The presence of three different sets of primary olfactory neurons, the experimental potentials and the possible functional significance of SBA binding sites are discussed.

Ambystoma mexicanum↗
PubMed1992

Quantitative enzyme radioautography with 3H-Ro 41-1049 and 3H-Ro 19-6327 in vitro: localization and abundance of MAO-A and MAO-B in rat CNS, peripheral organs, and human brain.

Monoamine oxidases A and B (MAO-A and MAO-B) oxidatively deaminate neurotransmitter and xenobiotic amines. Since the cellular localization of the isoenzymes in the CNS and peripheral organs determines to a large extent which substrate has access to which isoenzyme, knowledge of their tissue distribution and cellular localization is essential. Here we describe how reversible and selective inhibitors of MAO-A and MAO-B [Ro 41-1049 and Ro 19-6327 (lazabemide), respectively] can be used, as tritiated radioligands, to map the distribution and abundance of the enzymes in microscopic regions of the rat CNS and peripheral organs, and human brain by quantitative enzyme radioautography. The in vitro binding characteristics of both radiolabeled inhibitors revealed them to be selective, high-affinity ligands for the respective enzymes. KD and Bmax values for 3H-Ro 41-1049 in rat cerebral cortex were 10.7 nM and 7.38 pmol/mg protein, respectively, and for 3H-Ro 19-6327 were 18.4 nM and 3.45 pmol/mg protein, respectively. In accordance with their potencies as enzyme inhibitors, binding to MAO-A and MAO-B was competitively inhibited by clorgyline (IC50 = 1.4 nM) and L-deprenyl (selegiline; IC50 = 8.0 nM), respectively. The capacities of various rat and human tissues to bind the radioligands correlated extremely well with their corresponding enzyme activities. As revealed by the respective binding assays, the distribution and abundance of MAO-A and MAO-B in the tissues investigated differed markedly. MAO-A was most abundant in the locus coeruleus, paraventricular thalamus, bed nucleus of the stria terminalis, median habenular nucleus, ventromedial hypothalamus, raphe nuclei, solitary tract nucleus, inferior olives, interpeduncular nucleus, claustrum, and numerous peripheral tissues, including liver, vas deferens, heart, superior cervical ganglion, and exocrine and endocrine pancreas. In contrast, MAO-B was most abundant in the ependyma, circumventricular organs, olfactory nerve layer, periventricular hypothalamus, cingulum, hippocampal formation, raphe nuclei, paraventricular thalamus, mammillary nuclei, cerebellar Bergmann glia cells, liver, posterior pituitary, renal tubules, and endocrine pancreas. The cellular localization of the isoenzymes in both rat and human brain differs markedly and does not reflect the distribution of the presumed natural substrates, for example, absence of MAO-A in serotoninergic neurons. Indeed, the present evidence suggests that, whereas MAO-A is found in noradrenergic and adrenergic neurons, MAO-B occurs in astrocytes, serotoninergic neurons, as well as ventricular cells, including most circumventricular organs. The physiological roles of the enzymes are discussed in the light of these findings, some of which were unexpected.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2005

Death by sewer gas: case report of a double fatality and review of the literature.

Hydrogen sulfide (H2S), the toxic gas associated with the smell of "rotten eggs," is an important cause of work-related sudden death. The gas is particularly insidious due to the unpredictability of its presence and concentration and its neurotoxicity at relatively low concentrations, causing olfactory nerve paralysis and loss of the warning odor. We report a double fatality involving 2 surveyors working near a man-hole, who fell into the sewer and died due to sudden exposure to hydrogen sulfide gas. Key historical, physical, and toxicologic findings are described. Additionally, we present a discussion of the clinical presentations and differential diagnosis, mechanism of injury, metabolism and toxicology, incidence, and scene and safety concerns in fatal hydrogen sulfide exposures.

Accidental Falls↗
PubMed1992

[Evaluation of the surgical results of the interhemispheric approach in comparison with the pterional approach for anterior communicating artery aneurysms].

From 1986 to 1990, 77 cases of ruptured anterior communicating artery (Aco) aneurysms have been operated on through an interhemispheric approach or a pterional approach. In this study, we mainly investigated the following factors: surgical outcome, surgical complications, degree of evacuation of subarachnoid clot, and frequency of symptomatic vasospasm. The difference of outcome between the two surgical groups was not statistically significant. Each operating method had characteristic surgical complications. Pterional approach had a tendency to complicate premature rupture, sacrifice small vessels around the aneurysm, and to result in Korsakoff syndrome and inadequate clipping. Interhemispheric approach was apt to complicate cerebral contusion, bilateral olfactory nerve injury and hemorrhagic infarction due to sacrifice of the bridging veins. The pterional approach could evacuate more of the subarachnoid clot than could the interhemispheric approach, but there was no significant difference in frequency of symptomatic vasospasm depending on which method was used.

Adult↗