[The autonomic nervous system in thyroid diseases. I. Reactivity of the autonomic nervous system in thyrotoxicosis].
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Adult↗
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Understanding and controlling the enteric nervous system.
The enteric nervous system or the 'Little Brain' of the gut controls gastrointestinal motility and secretion, and is involved in visceral sensation. In this chapter, new developments in understanding the function of the enteric nervous system are described. In particular, the interaction of this system with the interstitial cells of Cajal, the pacemaker cells of the gut, is highlighted. The importance of the interaction between the enteric nervous system and the immune system is discussed, especially in relation to functional bowel disorders and post-operative ileus. Evidence is also provided that neurones can change their function and phenotype, a phenomenon called neuronal plasticity, which contributes to the pathogenesis of visceral hypersensitivity. Finally, new developments in stem cell transplantation are described. All these new insights should lead to a better understanding of the enteric nervous system and hopefully to better ways of controlling it.
Coiled Bodies↗
[Sympathy and heartache: new information on the sympathetic nervous system].
The sympathetic nervous system is an important regulator of the circulation. Interactions with other regulating systems, e.g. the renin angiotensin system, play important roles. By means of microneurography, sympathetic activity in humans can be assessed directly in the nerve. Insights into the dynamic regulation of the circulation under physiological and pathophysiological conditions are possible. Activation of the sympathetic nervous system in cardiovascular diseases affects course, prognosis, and therapy. Prognosis in heart failure depends on sympathetic activation, which can be decreased by inhibition of angiotensin II synthesis by ACE-inhibitors. In contrast to nitrates, these drugs do not increase sympathetic activity. The sympathetic nervous system is also heavily involved in the pathogenesis of hypertension. Borderline hypertensives and offspring of hypertensive parents show increased sympathetic nerve activities. Investigation of the sympathetic nervous system under physiological and pathophysiological conditions may serve as a basis for new therapeutic strategies.
Cardiovascular Agents↗
The effects of convective cooling and rewarming on systemic and central nervous system physiology in isoflurane-anesthetized dogs.
Recent studies have demonstrated that small (i.e., 2-5 degrees C) reductions in temperature may protect the brain and spinal cord from ischemic injury. The present study evaluated the physiologic response of anesthetized animals to convective-based cooling and warming. Six shaved, isoflurane-anesthetized (1.50% end-expired; 1 MAC), pancuronium-paralyzed dogs were subjected to temperature manipulation. The flow of cool (13-14 degrees C) or warm (39-41 degrees C) air was uniformly applied to the the dorsal and lateral surfaces of the dog using an inflatable blanket with perforations in the interior surface. Convective cooling reduced pulmonary artery temperature (Tpa) from 37.0 +/- 0.2 degrees C (Mean +/- S.D.) to 33.0 +/- 0.0 degrees C over a 93 +/- 18 min period. Thereafter, the active cooling was discontinued and passive cooling resulted in a further reduction in Tpa to 32.4 +/- 0.3 degrees C over the next 60 min. Institution of convective warming resulted in an increase in Tpa from 32.4 +/- 0.3 to 33.0 +/- 0.0 degrees C in 23 +/- 14 min and from 33.0 to 37.0 +/- 0.0 in an additional 137 +/- 26 min. During the periods of active cooling, passive cooling and active warming, there were strong correlations between Tpa and temperature within the brain, cisterna magna, parietal epidural space, lumbar subarachnoid space and other commonly used temperature measurement sites non-invasively monitored (e.g. tympanic membrane, esophagus, rectum) r greater than or equal to 0.97; P less than 0.0001). The combination of isoflurane anesthesia (a potent EEG-suppressor) plus mild hypothermia (less than 34 degrees C) resulted in an EEG attenuation in five dogs, two of which progressed to burst suppression. The magnitude of EEG changes correlated with the degree of temperature reduction. Upon rewarming to 37 degrees C, all dogs had normal EEG activity and normal brain concentrations of high energy phosphates, glucose and lactate. Blood pressure and cardiac output did not change during the study and no dog exhibited acid-based anomalies or blood lactate accumulation. Whole body oxygen consumption and heart rate decreased in a temperature-dependent fashion. Cardiac rhythm disturbances were rare. The authors conclude that convection-based corporeal cooling and rewarming are efficacious methods for non-invasively and uniformly altering CNS temperatures without adversely affecting cerebral or systemic physiology.
Anesthesia↗
The neurovascular unit and its growth factors: coordinated response in the vascular and nervous systems.
The nervous and vascular systems contain many common organizational features and develop similarly in terms of anatomical patterning. During embryogenesis and in regions of the brain undergoing postnatal neurogenesis, neural stem cells and endothelial cells are found in close proximity, or within a so-called vascular niche. The similarities in patterning and proximity may reflect coordinated development based on responsiveness to similar growth factors such as vascular endothelial growth factor, semaphorin, and ephrins/Ephs: molecules involved in the development and maintenance of both the nervous and vascular systems. Despite the blatant similarities between the vascular and nervous systems, little is still known about the co-dependence and/or interactions between the two systems during development and following alterations in metabolic demand as seen during aging, exercise, and disease processes. The interactions between the two systems involving common growth factors suggest these two systems have evolved in an interconnected way.
Animals↗
Difference in calcium sensitivities of the sodium transporting systems in the nervous system of susceptible and kdr-resistant houseflies, Musca domestica L.
1. The synaptosomal preparations from the kdr-resistant strains have lower responsiveness to externally applied Ca2+ than the susceptible counterparts with respect to their Na+/Ca2+ exchange, Na+ uptake, Na+-Ca2+ protein kinase-phosphatase and its phosphorylation activities. 2. In vivo toxicity tests support the above in vitro observation in that the kdr-resistant strain shows a significant cross-resistance to agents known to affect the Na+ channel operations, those which increase intracellular Ca2+ or act as effective Ca2+ substitutes. 3. Such evidence indicates a possibility of a causal relationship between kdr resistance and the reduction of Ca2+ sensitivity by these ATP-utilizing systems including the Na+ transporting systems in the resistant insects.
Animals↗
Central nervous system lymphoma.
Central nervous system involvement with malignant lymphoma whether primary or secondary is an uncommon but not rare complication observed in the management of patients with hematological malignancy. Its importance lies in the considerable morbidity and mortality with which it is associated and the inadequacy of therapy. In Section I, Dr. Lauren Abrey addresses the totality of the problem of primary central nervous system lymphoma, with emphasis on strategies increasingly dependent on systemic chemotherapy. In Section II, Dr. John Sandlund reviews the success of sequential clinical trials of overall therapy for acute lymphoblastic leukemia in childhood, identifying those patients at high risk of central nervous system leukemia and the development of a rational therapeutic strategy for prevention. In Section III, Dr. Andrew Lister discusses the issue of secondary central nervous system involvement with lymphoma and the indications for prophylaxis.
Antineoplastic Agents↗
Connections between the immune system and the nervous system.
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Animals↗
Hematologic neoplasia and the central nervous system.
Central nervous system (CNS) involvement with malignant cells is a well recognized complication of hematologic neoplasms. A number of disorders such as acute lymphoblastic leukemia and high grade lymphoma frequently involve the CNS and prophylactic therapy is advised. Disorders such as acute myeloid leukemia (AML) and multiple myeloma are less likely to be associated with CNS involvement. This series describes three cases of CNS involvement by malignant hematologic disease: myelomatous meningitis, CNS chloromas complicating AML, and primary lymphomatous meningitis.
Adult↗
Cellular abnormalities and synaptic plasticity in seizure disorders of the immature nervous system.
The nervous system has an enhanced capacity to generate seizures during a restricted phase of postnatal development. Studies in animals and particularly in in vitro brain slices from hippocampus and neocortex have been instrumental in furthering an understanding of the underlying processes. Developmental alterations in glutaminergic excitatory synaptic transmission appear to play a key role in the enhanced seizure susceptible of rodents during the second and third week of life. Prior to this period, the number of excitatory synapses is relatively low. The scarcity of connections and the inability of the existing synapses to release glutamate when activated at high frequencies likely contribute importantly to the resistance of neonates to seizures. However, at the beginning of week 2, a dramatic outgrowth of excitatory synapses occurs, and these synapses are able to faithfully follow activation at high frequencies. These changes, coupled with the prolonged nature of synaptic potentials in early life, likely contribute to the ease of seizure generation. After this time, seizure susceptibility declines, patterns of local synaptic connectivity remodel, and some synapses are pruned. Concurrently, the duration of excitatory postsynaptic potentials shortens due at least in part to a switch in the subunit composition of postsynaptic receptors. Other studies have examined the mechanisms underlying chronic epilepsy initiated in early life. Models of both cortical dysplasia and recurrent early-life seizures suggest that alterations in the normal development of excitatory synaptic transmission can contribute importantly to chronic epileptic conditions. In the recurrent early-life seizure model, abnormal use-dependent selection of subpopulations of excitatory synapses may play a role. In experimental cortical dysplasia, alterations in the molecular composition of postsynaptic receptor are observed that favor subunit combinations characteristic of infancy.
Age Factors↗
Vasculitis of the central nervous system.
Central nervous system (CNS) involvement and management in primary vasculitis (giant cell arteritis, primary angiitis of the CNS, Takayasu's disease, periarteritis nodosa, Kawasaki disease, Churg-Strauss syndrome, Wegener's granulomatosis) and vasculitis secondary to collagen vascular diseases, Beçhet's disease and other systemic conditions (excluding those secondary to infections) and the use of illicit drugs are reviewed. Vasculitis is an infrequent cause of stroke even in the young age groups, and routine screening of stroke patients for vasculitis is not cost-effective. CNS vasculitis may present with isolated CNS symptoms and signs (headaches, meningeal signs, encephalopathy, psychiatric syndromes, dementia, cranial nerve palsies, seizures, strokes), neuropathy or muscle damage, multiorgan involvement or non-specific systemic symptoms or a combination of the above. Magnetic resonance is the most sensitive ancillary procedure to detect CNS damage. Many of the angiographic features found in vasculitis are non-specific. Autoantibodies and tissue biopsy are also useful to the diagnosis. There are few controlled studies on the treatment of vasculitis. Usually a combination of steroids and cytotoxic drugs is used, but there is considerable variation between centres on current therapeutic regimens.
Brain↗
Leukemias and lymphomas: treatment and prophylaxis of the central nervous system.
Central nervous system (CNS)-directed therapy is required for many acute leukemia patients and for nearly all aggressive or high-grade non-Hodgkin's lymphoma patients as part of an overall chemotherapy plan for disease eradication. The CNS therapy decisions differ for overt disease treatment versus prophylactic treatment and take into consideration the type of leukemia or lymphoma, the age of the patient, and other prognostic factors. A variety of CNS-directed therapies are used for prevention or treatment of CNS disease in acute leukemias or aggressive lymphomas: intrathecal medications (cytosine arabinoside, methotrexate, or both in combination with hydrocortisone) with or without cranial or craniospinal irradiation, intrathecal medication only with intensive systemic chemotherapy, or high-dose chemotherapy specifically chosen for CNS penetrance. Any type of CNS-directed therapy, whether intrathecal chemotherapy, high-dose systemic chemotherapy, or irradiation, may cause acute or delayed (late) toxicity. Ongoing clinical trial research aims to reduce the risk of toxicity from CNS-directed therapy while preserving or improving treatment efficacy.
Journal Article↗
Ontogeny of the erythroid/HepG2-type glucose transporter (GLUT-1) in the rat nervous system.
Central nervous system (CNS) microvessels of adult mammals have an unusually high density of the facilitative glucose transporter GLUT-1. Most systemic microvessels and those of the brain's circumventricular organs, which lack 'barrier' properties, do not express a high density of GLUT-1. Thus, a high GLUT-1 density is a marker of adult brain endothelium. To determine the stage at which CNS microvessels acquire GLUT-1, we studied by immunocytochemistry GLUT-1 ontogeny in the rat CNS from embryonic day (E) 11 to senescence. At E11, before blood vessels invaded the neuroectodermal tube, GLUT-1 immunoreactivity was already evident in the perineural plexus of vessels and in most of the vascular endothelium of the embryo. GLUT-1 immunoreactivity was also evident in the neuroectoderm. The neuroectoderm gradually lost GLUT-1 expression, and at about E16, GLUT-1 immunoreactivity was no longer detectable in most of the neuroectodermal epithelium, while CNS microvessels had increased their GLUT-1 immunoreactivity. By birth, GLUT-1 immunoreactivity in the CNS was restricted to the endothelium, the epithelium (but not the endothelium) of the choroid plexus, and tanycytes. This cellular distribution of GLUT-1 did not change much between birth and senescence despite considerable postnatal brain development and the increased brain capillary density. Our results suggest that while a CNS factor(s) may not have a role in the induction of the high expression of GLUT-1 in CNS endothelium, such a factor(s) is probably important in maintaining the high level of GLUT-1 in these endothelia.
Aging↗
Netrin-1 is required for commissural axon guidance in the developing vertebrate nervous system.
During nervous system development, spinal commissural axons project toward floor plate cells and trochlear motor axons extend away from these cells. Netrin-1, a diffusible protein made by floor plate cells, can attract spinal commissural axons and repel trochlear axons in vitro, but its role in vivo is unknown. Netrin-1 deficient mice exhibit defects in spinal commissural axon projections that are consistent with netrin-1 guiding these axons. Defects in several forebrain commissures are also observed, suggesting additional guidance roles for netrin-1. Trochlear axon projections are largely normal, predicting the existence of additional cues for these axons, and evidence is provided for a distinct trochlear axon chemorepellent produced by floor plate cells. These results establish netrin-1 as a guidance cue that likely collaborates with other diffusible cues to guide axons in vivo.
Alleles↗
Acute injury to the central nervous system.
Central nervous system (CNS) trauma is divided into brain and spinal cord injury. A basic understanding of the pathophysiology of CNS trauma helps the practitioner more accurately evaluate, treat, and prognose cases of CNS trauma. The progressive nature of CNS injuries and the contribution of microvascular ischemic are explored.
Animals↗
Measles infection of the central nervous system.
Central nervous system (CNS) complications occurring early and late after acute measles are serious and often fatal. In spite of functional cell-mediated immunity and high antiviral antibody titers, an immunological control of the CNS infection is not achieved in patients suffering from subacute sclerosing panencephalitis (SSPE). The known cellular receptors for measle virus (MV) in humans, CD46 and CD150 (signaling lymphocyte activation molecule, SLAM), are important components of the viral tropism by mediating binding and entry to peripheral cells. Because neural cells do not express SLAM and only sporadically CD46, virus entry to neural cells, and spread within the CNS, remain mechanistically unclear. Mice, hamsters, and rats have been used as model systems to study MV-induced CNS infections, and revealed interesting aspects of virulence, persistence, the immune response, and prerequisites of protection. With the help of recombinant MV and mice expressing transgenic receptors, questions such as receptor-dependent viral spread, or viral determinants of virulence, have been investigated. However, many questions concerning the human MV-induced CNS diseases are still open.
Animals↗
Fetal brain progenitor cells transdifferentiate to fates outside the nervous system.
Central nervous system stem cells give rise to neurons and glia when exposed to specific trophic factors. In our studies with rat fetal brain-derived stem cells (RSCs), we showed that they could be induced to express the developmentally regulated transcription factors and cell markers characteristic of cells derived from another germ layer, e.g. pituitary cells. Therefore, rat fetal brain-derived stem cells do not seem to be restricted to a defined developmental fate. They may retain pluripotentiality and can be redirected to develop into other cell types not found in the brain provided the correct set of stimuli is present. This multipotent developmental behavior also suggests that instructive signals are operative.
Animals↗
[Lupus erythematosus and the central nervous system].
Central nervous system (CNS) involvement in early stages of systemic lupus erythematosus (SLE) and even before it's precise diagnosis is increasingly observed. Clinically predominant are non - focal neuropsychiatric symptoms (migrainous phenomena and depressive disorders ). Actual literature on their features, and - beside the classical - recent pathophysiological models of cerebral Le including evidence of autoimmunological processes are reviewed. In patients with doubtful diagnosis the "classical signs of SLE" are evidently of decreasing diagnostic value, whereas extended neuroimmunological laboratory investigations and 15O-positron emission tomography contributed a great deal towards detection of CNS-disease. At present, in pharmacotherapy of CNS-Le corticosteroides alone are preferably used rather than their fixed combination with immunosuppressive agents like azathioprin . In spite of an improved prognosis of SLE complications from CNS-involvement become the main cause of SLE-patients' deaths beyond the fifth year after diagnosis.
Azathioprine↗