[Surgery of the sympathetic nervous system in diseases of the extremities, of the heart and of the lungs. Tumors of the sympathetic nervous system].
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Heart Diseases↗
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Benign angiopathy of the central nervous system.
Apparent central nervous system vasculitis could have a benign course in a subset of patients and is referred to as benign angiopathy of the central nervous system (BACNS). This is mostly is seen in young women and presents with acute onset of neurologic symptoms, usually in the form of severe headache and/or a focal neurologic event. Cerebrospinal fluid analysis could be normal or nearly normal. Brain angiogram typically shows segmental narrowing, ectasia, or beading in multiple vascular territories on brain angiogram. Like in all cases of CNS vasculitis, exclusion of other systemic diseases or its mimickers associated with cerebral involvement is important.BACNS could respond favorably to treatment with corticosteroids alone or in combination with a calcium channel blocker, thereby avoiding unnecessary and prolonged treatment with other immunosuppressants like cyclophosphamide with their side effects. Little is published in the literature about BACNS, but is a rapidly emerging concept. It is thus important to recognize. We report a patient with classic presentation of BACNS to highlight the significance of distinguishing benign angiopathy from the more aggressive form of CNS vasculitis, because the treatment and response varies in these 2 entities.
Journal Article↗
Influence of alkylamides of glutamic acid and related compounds on the central nervous system. II. Syntheses of amides of gutamic acid and related compounds, and their effects on the central nervous system.
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Amides↗
Increased intrathecal immunoglobulin synthesis of both kappa and lambda types in patients with systemic lupus erythematosus and central nervous system involvement.
The concentration of immunoglobulins in paired serum and cerebrospinal fluid (CSF) specimens from 15 patients with systemic lupus erythematosus (SLE) and central nervous system (CNS) involvement (CNS-SLE) were determined based on their light chain properties. Eight patients with SLE without CNS involvement and 20 patients with noninflammatory neurological diseases were also studied for comparison. We found that both of the CSF Ig-k (immunoglobulin kappa) and Ig-1 (immunoglobulin lambda) indices were significantly elevated, indicating the increased intrathecal immunoglobulin synthesis of both kappa and lambda types in patients with CNS-SLE. Moreover, the CSF Ig-k and Ig-1 indices correlated well with each other, and both indices were found to decrease remarkably when the CNS manifestations subsided after successful treatment. In 4 of 15 patients, intrathecal synthesis of free light chains in addition to Ig bound light chains seemed to be increased. These observations provide substantial evidence for polyclonal B lymphocyte activation within the CNS.
Adolescent↗
Biological effects of aging on bone and the central nervous system.
The skeletal and nervous systems express conspicuous signs of aging in humans in the form of osteoporosis and senile dementia, the most common diseases affecting the elderly population. Although the prevalence of these diseases progressively rises with advancing age, especially in females, the interrelationship between the degenerative changes of the skeletal and nervous systems has not been studied in detail. Defective 1,25(OH)2D synthesis in chronic renal failure is known to cause renal osteodystrophy and is also associated with the appearance of dialysis encephalopathy and a decrease of the conduction velocity of peripheral nerves. Calcium content of the nervous system is increased in this condition, suggesting the existence of generalized abnormalities of calcium metabolism, which affect both the skeletal and nervous system. The mild, chronic renal failure of aging, and the consequent secondary hyperparathyroidism, might therefore contribute to the development of nervous degenerative diseases.
Aging↗
[Clinical and experimental studies on central nervous system control of free fatty acids in the blood, with special reference to ketosis due to central nervous system diseases].
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Acidosis↗
Members of the Plag gene family are expressed in complementary and overlapping regions in the developing murine nervous system.
In the developing nervous system, cell fate specification and proliferation are tightly coupled events, ensuring the coordinated generation of the appropriate numbers and correct types of neuronal and glial cells. While it has become clear that tumor suppressor genes and oncogenes are key regulators of cell division in tumor cells, their role in normal cellular and developmental processes is less well understood. Here we present a comparative analysis of the expression profiles of the three members of the pleiomorphic adenoma gene (Plag) family, which encode zinc finger transcription factors previously characterized as tumor suppressors (Zac1) or oncogenes (Plag1, Plag-l2). We focused our analysis on the developing nervous system of mouse where we found that the Plag genes were expressed in both unique and overlapping patterns in the central and peripheral nervous systems, and in olfactory and neuroendocrine lineages. Based on their patterns of expression, we suggest that members of the Plag gene family might control cell fate and proliferation decisions in the developing nervous system and propose that deciphering these functions will help to explain why their inappropriate inactivation/activation leads to tumor formation.
Animals↗
Low concentrations of hydrogen sulphide alter monoamine levels in the developing rat central nervous system.
The central nervous system is one of the primary target organs for hydrogen sulphide (H2S) toxicity; however, there are limited data on the neurotoxic effects of low-dose chronic exposure on the developing nervous system. Levels of serotonin and norepinephrine in the developing rat cerebellum and frontal cortex were determined following chronic exposure to 20 and 75 ppm H2S during perinatal development. Both monoamines were altered in rats exposed to 75 ppm H2S compared with controls; serotonin levels were significantly increased at days 14 and 21 postnatal in both brain regions, and norepinephrine levels were significantly increased at days 7, 14, and 21 postnatal in cerebellum and at day 21 in the frontal cortex. Exposure to 20 ppm H2S significantly increased the levels of serotonin in the frontal cortex at day 21, whereas levels of norepinephrine were significantly reduced in the frontal cortex at days 14 and 21, and at day 14 in the cerebellum.
Animals↗
Control of gastrointestinal motility by the "gut brain"--the enteric nervous system.
The enteric nervous system (ENS) as the "brain of the gut" is pivotal for normal muscle activity in the gut. Neuronal circuits within the ENS are designed to control gut motility independent of central inputs. To fulfill this task the ENS contains all necessary elements for coding mechanical and chemical stimuli, interneuronal communication and efferent output to the muscle. This review provides a summary of the ENS circuits that control muscle activity, the main transmitters and neuromodulators involved and the functional implications for the normal and diseased gut.
Digestive System↗
V. Genes, lineages, and tissue interactions in the development of the enteric nervous system.
The enteric nervous system is derived from the vagal, rostral-truncal, and sacral levels of the neural crest. Because the crest-derived population that colonizes the bowel contains multipotent cells, terminal differentiation occurs in the gut and is influenced by both the enteric microenvironment and the responsivity of multiple lineages of precursors. Enteric growth factor-receptor combinations, which promote the development of enteric neurons and/or glia in most of the gastrointestinal (GI) tract, include glial cell line-derived neurotrophic factor-GFRalpha-1-Ret, NT-3-TrkC, a still-to-be-identified neuropoietic cytokine-ciliary neurotrophic factor receptor-alpha, serotonin (5-HT)-5-HT2B, and LBP110, a 110-kDa laminin-1 binding protein. A qualitatively different effect is shown by the peptide-receptor combination ET-3-ETB, which inhibits neuronal differentiation and appears to prevent the premature differentiation of enteric neurons before colonization of the GI tract has been completed (resulting in aganglionosis of the terminal colon).
Animals↗
[Morphogenesis of neuronal systems in tissue culture repeats the evolution of simpler nervous systems].
Comparison of simpler nervous systems of invertebrates and plexiganglionic systems cultivated in tissue culture was conducted for the first time. Their principal resemblance was discovered. By following up the kinetics of neuronal behaviour in culture similarity between mechanisms underlying the evolution of simpler nervous systems and processes of self assembly of neuronal systems was revealed. In both cases isolated nerve cells are replaced by primitive (archaic) nervous plexus that, in turn, becomes a plexiganglionic neuronal system. Final individual architecture of ganglia and mechanisms of formation of nerve ganglia and trunks coincide. Highly specialized unipolar neurons transform into archaic unipolar cells and display signs of chemotaxis. Resemblance of stages and mechanisms of the formation of all elementary nervous systems and neuronal systems in culture is explained by integrity of the neuron properties (adhesion and mobility of neuron bodies, extrusion and retraction of their processes and autotomy of nerve endings). Similar neuron potentialities in evolution and tissue culture underly the abundance of parallelisms between nervous systems in animals of unrelated phyla. In this aspect a possibility appeared to formulate another biogenetic postulate concerning general mechanisms of neurogenesis: morphogenesis of plexiganglionic neuronal systems in tissue culture represents fast and simplified repetition of the evolution of elementary nervous system of invertebrates.
Animals↗
An antiserum to locust adipokinetic hormone reveals a novel peptidergic system in the rat central nervous system.
Using an antiserum to locust adipokinetic hormone I, a novel peptidergic system was identified in the rat central nervous system. Immunoreactive fibers were present in the hypothalamic median eminence and periventricular nucleus and the spinal cord dorsal horn, intermediolateral cell column and sacral parasympathetic nucleus. Immunoreactive cells were present in the dorsal gray commissure of lumbosacral spinal cord, the hypothalamic periventricular nucleus and cerebral cortex.
Animals↗
[Systemic lupus erythematosus and the central nervous system].
The central nervous system (CNS) manifestations of the chronic autoimmune disease systemic lupus erythematous (SLE) are reviewed. SLE-CNS dysfunction is broadly divided into neurologic and psychiatric clinical categories. The distinct clinical entities within these broad categories are fully described. Diagnostic criteria employed to verify the presence of SLE-CNS dysfunction, including laboratory serum and cerebral spinal fluid analyses as well as radiologic and other multimodality diagnostic tools, are compared and contrasted with respect to sensitivity and specificity.
Antibodies, Antinuclear↗
Mechanisms of immune regulation in the peripheral nervous system.
The peripheral nervous system (PNS) is a target for heterogenous immune attacks mediated by different components of the systemic immune compartment. T cells, B cells, and macrophages can interact with endogenous, partially immune-competent glial cells and contribute to local inflammation. Cellular and humoral immune functions of Schwann cells have been well characterized in vitro. In addition, the interaction of the humoral and cellular immune system with the cellular and extracellular components in the PNS may determine the extent of tissue inflammation and repair processes such as remyelination and neuronal outgrowth. The animal model experimental autoimmune neuritis (EAN) allows direct monitoring of these immune responses in vivo. In EAN contributions to regulate autoimmunity in the PNS are made by adhesion molecules and by cytokines that orchestrate cellular interactions. The PNS has a significant potential to eliminate T cell inflammation via apoptosis, which is almost lacking in other tissues such as muscle and skin. In vitro experiments suggest different scenarios how specific cellular and humoral elements in the PNS may sensitize autoreactive T cells for apoptosis in vivo. Interestingly several conventional and novel immunotherapeutic approaches like glucocorticosteroids and high-dose antigen therapy induce T cell apoptosis in situ in EAN. A better understanding of immune regulation and its failure in the PNS may help to develop improved, more specific immunotherapies.
Animals↗
Astrocytes in infectious and immune-mediated diseases of the central nervous system.
The central nervous system (CNS) can be invaded and damaged by a variety of microbes. The host response to such injury involves CNS cells, and in many cases hematogenous cells also. Recent experiments indicate that astrocytes, macroglial resident cells of the CNS, play key roles in this process. The astroglial production of trophic factors and elimination of neurotoxins are likely to fulfill important protective and reparative functions during CNS infection. In addition, astrocytes could, in concert with microglial cells, regulate the recruitment and activity of infiltrating hematogenous cells through their expression of cytokines, proteases, protease inhibitors, adhesion molecules, and extracellular matrix components. Although previous experiments suggested that astrocytes might initiate inflammatory demyelinating disease by presenting CNS antigens to autoreactive immune cells, current evidence points against such a detrimental activity. In view of the generally beneficial role of astrocytes, impairments of astroglial function by microbes or host-derived factors have the potential to contribute to neurologic disease. Diseases in which this pathogenetic process may be relevant include HIV-1-associated cognitive/motor complex and spongiform encephalopathies.
Animals↗
[Selected methods for evaluating the autonomic nervous system].
Dysfunction of autonomic nervous system, accompanying different diseases of central and peripheral nervous system, is manifested by cardiovascular, gastrointestinal, genitourinary, thermoregulatory, respiratory and pupillary disorders. In the paper the methods of autonomic nervous system evaluation are reviewed, in particular the most popular cardiovascular and thermoregulatory tests.
Autonomic Nervous System Diseases↗
The role of the sympathetic nervous system in hypertension.
The sympathetic nervous system plays an important role in the regulation of arterial pressure, and increased sympathetic nervous system activity has been implicated as a primary precursor of hypertension in both humans and animal models of the disease. To date, the mechanism that potentiates the increase in sympathetic nervous system activity has not been fully elucidated. Imbalances in several neurotransmitters and neuromodulators are present during the development of hypertension, and these directly and indirectly contribute to increased release of noradrenaline onto the postsynaptic targets of the sympathetic nerves. In sodium chloride-sensitive hypertensive subjects, dietary sodium chloride increases sympathetic nervous system activity both directly and indirectly. Bidirectional interactions among the immune system and the sympathetic nervous system also appear to play a role in the development of hypertension. Finally, recent studies suggest that insulin-glucose excess and nitric oxide deficiency may increase the sympathetic nervous system's contribution to some forms of hypertension.
Animals↗
The radiographic diagnosis and treatment of paraneoplastic central nervous system disease.
Paraneoplastic nervous system syndromes are being identified with increasing frequency because of greater physician awareness and the availability of serodiagnostic tests for some syndromes. Frequently, paraneoplastic syndromes develop in the setting of an indolent, limited stage, or otherwise occult malignancy. As a result, the paraneoplastic disorder often becomes the most disabling part of a patient's disease. Effective treatment appears to require early identification. For these reasons, the ability to diagnose a paraneoplastic syndrome, follow its course, and treat it successfully are important. The authors describe four patients with neurologic paraneoplastic syndromes and identical magnetic resonance imaging abnormalities. Three patients responded to immunosuppressive or immunomodulatory therapy, and in one, corresponding radiographic improvement was documented. Strategies for early diagnosis and options for treatment of paraneoplastic nervous system disorders are discussed.
Aged↗